Will this revolutionary material change medicine?
Will this revolutionary material change medicine?
Cryonics is the practice of deep-freezing recently deceased bodies (or even just the brains of those who have recently died) in the hopes of one day reviving them. It has been the subject of serious scientific exploration and study — as well as a fair share of pseudoscience, lore, and myth. Fictional accounts like Batman’s Iceman, and the (untrue) rumors of Walt Disney being cryogenically frozen have, unfortunately, cast a speculative shadow over the field of cryonics.
But recently, for the first time ever in China, a woman has been cryogenically frozen. Zhan Wenlian died at the age of 49 from lung cancer and her husband, Gui Junmin, “volunteered” her for the cryonic procedure. Both he and his late wife wanted to donate her body to science to “give back to society.” He told Mirror UK that he was initially “pitched” the idea of cryonics with it being described as a “life preservation project.”
This procedure — which has Wenlian’s body resting facedown in 2,000 liters of liquid nitrogen — was completed at the Yinfeng Biological Group in Jinan. This project is the collaborative effort of the Yinfeng Biological Group, Qilu Hospital Shandong University and consultants from Alcor Life Extension Foundation, a nonprofit cryonics company based in the United States.
Even with all the faith many have in the procedure, the question remains: how scientifically possible is a project like this? Is this just an experiment to allow us to better understand human biology, or could cryonics one day become a feasible option?
Cryonics is all about timing. The bodies of the deceased are cryogenically frozen immediately after the heart stops beating. “Freezing” is a bit of a misleading term, because cryonic freezing is actually very specifically trying to avoid ice crystal formation — which damages the cells of the body’s tissues. Rapid cooling, rather than freezing, is a more accurate description of the process. A chemical cocktail of preservatives like glycerol and propandiol, in addition to antifreeze agents, are commonly used to get the body into a stable state where it won’t be decaying, but also won’t suffer damage from being stored at low temperatures for, conceivably, a very long time.
From there, the bodies are given specific care that caters to the idea that death is a continuing process; one that can ultimately be reversed. The aim of cryonic preservation would be to one day be able to thaw the bodies and reanimate them at a cellular level — preferably without too many epigenetic changes.
“I tend to believe in new and emerging technologies, so I think it will be completely possible to revive her.”
With our current understanding and technology, this process of reversing death so completely is just not possible. The closest kind of revival we have are the moments after clinical death where patients are revived by something such as cardiac defibrillation. Cryonics acts within this critical, albeit brief, period as well — but works within the belief that death is a grey area. More of a process rather than a definite, final, event.
Just because we haven’t succeeded in reviving the dead yet doesn’t mean the field of cryonics is unnecessary or unimportant. This first case in China is a major step forward for everyone researching in the field of cryonics — and those of us who may, one day, hope to benefit from advancements in it.
We may not be able to reverse death just yet, but it doesn’t seem out of the realm of possibility to imagine that, with such wild scientific advancements underway, technology could one day allow it to be possible. Whether or not it does in our lifetimes, this most recent development is certainly a positive one.
The post For The First Time Ever, A Woman in China Was Cryogenically Frozen appeared first on Futurism.
Newborn infants are some of the most delicate creatures on Earth. As soon as they emerge from their mothers’ wombs, human infants are exposed to an environment they aren’t yet equipped to handle. This could lead to infection which could turn into a life-threatening condition, the most common of which is the extreme infection response known as sepsis.
Fortunately, an inexpensive prevention technique for sepsis might soon be available, thanks to the work of scientists in the United States and in India — and to a bacteria commonly found in Asian kitchens. Probiotic bacteria, which is abundant in kimchi, pickles and other fermented vegetables, could drastically reduce the chances of babies getting sepsis.
The trick was figuring out which probiotic bacterial strain would work most effectively, according to University of Nebraska Medical Center College of Public Health pediatrician Pinaki Panigrahi, who’s been working on a way to prevent sepsis for 20 years now.
“We screened more than 280 strains in preliminary animal and human studies,” he told NPR. “So it was a very methodical process.” Probiotics are also known to be effective in preventing an infection of the intestines of newborns called necrotizing enterocolitis. Best of all, the use of these probiotics could cost as little as $1 per baby, Panigrahi said.
Sepsis remains the primary cause of death from infection globally. It’s known to affect 6 million newborns and children every year, accounting for about 60-80 percent of lives lost annually, including the deaths of about 600,000 babies. Worst of all, it’s not easily detected in newborns. “All the sudden the baby stops being active. It stops crying and breastfeeding,” said Panigrahi, lead author in the report published in the journal Nature, “By the time the mother has a chance to bring the baby to the hospital, the baby dies.”
In this study, the risk of death from sepsis dropped by 40 percent, from 9 percent to 5.4 percent in the 4,000 babies fed with the probiotic microbes. The administration of probiotics was also shown to prevent lung infections, which dropped by about 30 percent. “That was a big surprise, because we didn’t think gut bacteria were going to work in a distant organ like the lung,” Panigrahi said. Abdominal distention was the only significant side-effect observed, affecting just six of the babies tested.
Manufacturing a treatment using probiotics will be remarkably inexpensive. And it might not be long before this treatment is found in common use. “[Probiotics] can promote maturation of the immune system in a healthier way,” neonatologist Pascal Lavoie, from BC Children’s Hospital in Vancouver, British Columbia, told NPR. “Probiotics can be much more powerful than drugs.”
The post A Common Gut Bacteria Could Prevent a Top Killer of Newborns Worldwide appeared first on Futurism.
Australian researchers seem to have found a way to cure children of their peanut allergies. As reported by The Guardian, an immunotherapy trial left a group of children cured for the last four years, allowing them to eat peanuts and other peanut-based foods as part of their diet.
“These children had been eating peanut freely in their diet without having to follow any particular program of peanut intake in the years after treatment was completed,” said Professor Mimi Tang, lead researcher on the study.
Tang created this new form of treatment, known as PPOIT, by combining a probiotic with peanut oral immunotherapy. The treatment reprograms the body’s immune system, allowing it to build up an immunity. According to Tang, the combination of probiotic and immunotherapy provides the body will the small push it needs to combat the allergy.
Following the initial trial in 2013, 82% of the children involved developed a tolerance to peanuts. Four years later, 70% of that group were tested once again, confirming the treatment’s long-term effects.
“The way I see it is that we had children who came into the study allergic to peanuts, having to avoid peanuts in their diet, being very vigilant around that, carrying a lot of anxiety with that and, at the end of treatment and even four years later, many of these children who had benefited from our probiotic peanut therapy could now live like a child who didn’t have peanut allergy,” said Tang.
Peanut allergies are relatively common these days, being the most common form of anaphylaxis, with more than 200,000 reactions requiring emergency medical attention each year. The peanut allergy, specifically, is also largely associated with children, though one-in-five are expected to outgrow it.
If work on Tang’s treatment progresses and is confirmed by larger clinical studies, it could eventually be used to greatly reduce the prevalence of peanut allergies and the medical risk that comes along with them.
The post Australian Researchers May Have Created a Cure for the Peanut Allergy appeared first on Futurism.
Recently, scientists achieved a world first using the genetic editing tool, CRISPR, when they corrected a genetic mutation that causes heart failure in viable human embryos. This means that certain genetic defects may be relatively simple to correct in the near future. The issue that really has people talking, though, is the fact that the same tool could potentially be used to enhance healthy embryos, altering physical traits such as appearance or mental traits like intelligence.
However, the authors of the study firmly point out that the technology’s purpose is to save lives. “This is for [the] sake of saving children from horrible diseases,” lead author Dr. Shoukhrat Mitalipov explained in a Nature podcast. With this “milestone” achieved, humanity is getting closer, Dr. George Church confirmed to The Scientist.
The work in this study solved past problems with embryo editing including the issue of mosaicism, which happens when “fixed” cells contain a mix of the new, repaired DNA and older, damaged DNA. It also conquered the issue of unintended problems in the DNA being passed down in the germline. The technique that made the difference was injecting the CRISPR setup right into the fertilized embryo or egg cell about to be fertilized. It can then be degraded after it does its work, rather than floating around on plasmids in cells where it can do damage over time.
This discovery is significant for anyone suffering from hereditary, genetic diseases. For people with fatal diseases such as Huntington’s, for example, carrying certain genes means they are certain to get the disease, and a 50/50 chance of passing it on. For this reason, many people with Huntington’s don’t have children. If this discovery pans out, these patients won’t have to worry about passing on a genetic disorder.
Of course the specter of the “designer baby” is always raised in this context — but the study demonstrates that the way the cells repair the genes in question, researchers can’t add anything that wasn’t already present in the DNA. In other words, repair is possible, but not adding limitless “super” traits.
Nevertheless, there are critical voices in the fray: former molecular biologist Dr. David King (also founder of independent genetic engineering watchdog group Human Genetics Alert) said in an editorial in The Guardian that, “In fact, the medical justification for spending millions of dollars on such research is extremely thin: it would be much better spent on developing cures for people living with those conditions.” King believes that despite medical cures being the original motivation for developing genome editing, the creation of “designer babies” for the very wealthy is inevitable — as is the deepening class stratification caused by this modern eugenic drive.
In any event, there is significant work left to be done before CRISPR could be used in clinics. Scientists want to increase its accuracy and precision, for one thing. Furthermore, IVF clinics already screen out genetic disease and other abnormalities before implanting embryos; to justify the cost of using CRISPR, it would need to show more benefits unachievable otherwise.
Either way, now is probably the time to start grappling with the ethical issues surrounding CRISPR. Waiting until it is possible to use it — and dying people are waiting for it — seems shortsighted. In any event, more dialogue and research only stands to help resolve the societal issues that remain.
The post Here’s Everything You Need to Know About the Recent Human Gene Editing Trial in the US appeared first on Futurism.
3D-printing technology has made significant strides over the past several years. What started as a tool for producing small objects can now be used to craft food, build houses, and even construct “space fabric.”
One of the tech’s most impressive applications, however, is the creation of artificial tissues and organs, a process known as 3D bioprinting, and now, a team of researchers from the University of Oxford has developed a new method that takes 3D bioprinting to the next level. They published their work in the journal Nature Communications.
A major challenge faced by researchers when 3D printing artificial tissues is getting them to maintain their shape. The cells are apt to move around in the printed structure and collapse in on themselves.
To avoid this, the Oxford team, led by 3D-bioprinting scientist Alexander Graham from Oxford Synthetic Biology (OxSyBio), contained their cells within nanolitre droplets that were wrapped in a lipid coating. These droplets could then be placed one layer at a time into living structures. Thanks to the structural support provided by the container, the tissues would maintain their shape, and the individual cells could survive longer as well.
Because this new method allows tissues to be built one drop at a time, researchers can use it to more accurately mimic natural tissues.
“We were aiming to fabricate three-dimensional living tissues that could display the basic behaviors and physiology found in natural organisms,” Graham said in a press release.
“To date, there are limited examples of printed tissues, which have the complex cellular architecture of native tissue. Hence, we focused on designing a high-resolution cell printing platform, from relatively inexpensive components, that could be used to reproducibly produce artificial tissues with appropriate complexity from a range of cells including stem cells,” he explained.
Researchers across the globe have already made considerable advances in 3D bioprinting and how it can be applied to regenerative medicine. We can now create 3D-printed organs and body parts that resemble and function like their natural counterparts, such as those realistic-looking ears. By enabling the production of complex tissues, the Oxford team’s method could revolutionize regenerative medicine even more, allowing for the repair or replacement of more intricate diseased and damaged body parts.
“There are many potential applications for bioprinting, and we believe it will be possible to create personalized treatments by using cells sourced from patients to mimic or enhance natural tissue function,” OxSyBio CTO Sam Olof said in the press release. “In the future, 3D bio-printed tissues maybe also be used for diagnostic applications — for example, for drug or toxin screening.”
The next step, according to Graham, is to develop complementary printing techniques that will allow for the use of additional kinds of living and hybrid materials. At the same time, they’re exploring the production of their current artificial tissues on an industrial scale.
The post Scientists Have Developed a New Method to 3D-Print Living Tissue appeared first on Futurism.
Leonard Guarente is a molecular biologist and the Director of the Glenn Laboratory for the Science of Aging at MIT. He is one of the world’s leading scientists in the realm of age-related research. He’s also the co-founder of a direct-to-consumer health company called Elysium Health – an impressive list of credentials, to be sure.
If you haven’t heard of Elysium yet, you’ll want to pay attention. They work to take the latest discoveries from health and aging research and translate them into products that consumers can benefit from today. While they might not have found the fountain of youth (yet), they have created a “cellular health pill,” and their product pipeline has been guided by a Scientific Advisory Board that is comprised of seven winners of the Nobel Prize in areas of research including neuroscience, complex chemical systems, and biochemistry — an impressive list of supporters, to be sure.
The pill is called Basis, and it’s a once daily supplement that supports human health at the cellular level.
According to the company, Basis exists thanks to a coenzyme inside each of our cells called nicotinamide adenine dinucleotide, or NAD+, which is involved in metabolism and is known to diminish with age. NAD+ is essential for hundreds of biological processes. As a recent article in The Observer explains, “While Elysium is careful not to make claims about the health benefits of Basis, the coenzyme NAD+ has, for years, been revered among the bio-hacker community.” This is, in part, because NAD+ has been shown to maintain DNA health and improve metabolic function in animal studies — hence the desire for consumers to liken it to the fanciful concept of “a fountain of youth.”
Other preclinical research reveals that an increase in NAD+ levels can improve mitochondrial function, circadian rhythms, and the detoxification of cells, which can help to support a sturdy immune system and feelings of overall health.
As we age, NAD+ levels decline, compromising the systems it supports. But a randomized, double-blind, placebo-controlled clinical trial in humans indicated that Basis is effective at restoring NAD+ levels by 40 percent in adults. An exciting discovery for Elysium, which is continuing to study the various health benefits in humans associated with increasing NAD+ levels.
The pill itself is comprised of two active compounds: pterostilbene (a polyphenol found in blueberries, grapes, and peanuts) and nicotinamide riboside (a form of vitamin B3 naturally found in milk and beer). Together, these compounds, that are generally recognized as safe, work to boost NAD+ levels in the human body — creating an opportunity for the body to experience health benefits as a result.
While the research behind the pill has been over 25 years in the making, and while there are compelling reasons to believe that increasing NAD+ levels can and will increase health function, it is important to remember that this is still early research. That said, the research and clinical trials completed to date have garnered promising results.
To learn more about Leonard Guarente, his insight into healthspan, and the scope of human longevity, check out Elysium Health. For $60, you’ll get a month supply of 60 capsules and play a part in this research. Or, you can subscribe and save up to 33%.
Researchers used autonomous vehicles known as micromotors to cure bacterial infections in the stomachs of mice. Micromotors are only the width of a single human hair, which allows them to negotiate the labyrinthine confines of the human body, and administer precise treatment.
In this study, micromotors were used to provide mice with a dose of antibiotics every day for five days. This regimen was found to be more effective than the standard method of administering the medicine.
Micromotors are a relatively new technology, but they’re coming along in leaps and bounds. Earlier this year, researchers in Germany developed a method of combining the vehicles with sperm cells to help combat tumors.
This particular implementation of micromotors is comprised of a spherical magnesium core that’s coated with specialized layers that perform various different functions,, like protecting the vehicle, carrying the treatment, and giving it the ability to stick the walls of the stomach.
However, it’s the core that’s the really clever part — it propels the micromotor along, but it does so in a way that helps the medicine have the desired effect.
The micromotors are able to move around the stomach thanks to the propulsion provided by the magnesium as it reacts with gastric acid. This reaction actually reduces the level of acidity in the stomach for a short amount of time.
This amounts to more than complementary antacid; antibiotics and protein-based drugs can be rendered useless by the gastric acid in the stomach. As such, it’s essential that the acidity level be dropped before they are released from the micromotor to do their job. This particular layer of the vehicle responds to the acidity around it, and it will only administer the medicine when it detects safe conditions for it to do so.
The acidity level of the stomach is said to return to its normal state within 24 hours. The micromotors themselves are largely biodegradable, so when finished, they simply dissolve within the stomach without leaving anything harmful behind.
“There is still a long way to go, but we are on a fantastic voyage,” said Dr. Joseph Wang, professor at the University of California San Diego and the lead researcher on the project, alongside fellow professor Dr. Liangfang Zhang. Following the success of these tests, the research team plans to engage in a larger study with animals — but the long-term goal is to investigate whether the same technique can be used safely on a human subject.
The post Researchers Used Tiny Autonomous Vehicles to Deliver Medicine to the Stomach of Mice appeared first on Futurism.
Fear comes in both healthy and harmful doses. Healthy fear, for example, teaches one to avoid touching fire or a sharp edge so as not to be harmed. Traumatic experiences also develop fears, and in the case of post-traumatic stress disorders (PTSD) or even some phobias, it can be psychologically and emotionally harmful.
What if you could get rid of such fears? That’s what researchers from the University of Califronia, Riverside have developed, and they published their findings today in the journal Neuron. They’ve developed a method to erase specific fear memories in the brain.
“In the brain, neurons communicate with each other through synaptic connections, in which signals from one neuron are transmitted to another neuron by means of neurotransmitters,” lead researcher Jun-Hyeong Cho said in a press release. “We demonstrated that the formation of fear memory associated with a specific auditory cue involves selective strengthening in synaptic connections which convey the auditory signals to the amygdala, a brain area essential for fear learning and memory. We also demonstrated that selective weakening of the connections erased fear memory for the auditory cue.”
Cho’s team conducted behavioral training tests involving mice, exposing them to a high-pitch and a low-pitch tone. Then, they exposed the mice again to the high-pitched tone, this time accompanied by a mild footshock. Exposing them to the two tones again, the mice stopped moving when it heard the high-pitched one, despite the absence of an actual electric shock on their feet. No such response was noted when it heard the low-pitched sound.
The freezing behavior happened because the experience developed stronger synaptic connections that relayed high-pitch tone signals to the amygdala. The mice learned to fear the sound, in short. This neural connection, the team explained, could be reduced using optogenetics — i.e., exposure to light could weaken the synaptic connection and erase the fear memory.
“In the brain, neurons receiving the high- and low-pitch tone signals are intermingled,” Cho explained. “We were able, however, to experimentally stimulate just those neurons that responded to the high-pitch sound. Using low-frequency stimulations with light, we were able to erase the fear memory by artificially weakening the connections conveying the signals of the sensory cue — a high-pitch tone in our experiments — that are associated with the aversive event, namely, the footshock.”
Traumatic fear memories often lead to unhealthy reactions or even harmful behaviors. For example, a person who suffered from a car accident might develop fear that triggers him to relive that traumatic memory every time he steps inside a car. Such a fear could be debilitating. Now, it’s possible to target such fears.
“This study expands our understanding of how adaptive fear memory for a relevant stimulus is encoded in the brain,” Cho added. “It is also applicable to developing a novel intervention to selectively suppress pathological fear while preserving adaptive fear in PTSD.” It could even be developed into treating addictive behavior, which Cho’s team wants to explore next by studying the mechanisms for “reward learning.”
The post Researchers Have Devised a Method to Erase Memories Associated With Fear appeared first on Futurism.
This revolutionary technology is able to heal organs by injecting them with DNA. This process reprograms healthy cells in one part of the body so that they can become a new type of cell in another.
The post A Revolutionary Device Heals Body Parts by Injecting DNA appeared first on Futurism.
Polio cases have decreased by over 99% since 1988, but a recent breakthrough could lead to this disease’s elimination once and for all.
In an interesting way of using one virus to combat another, scientists at the John Innes Centre in Norfolk, England, “hijacked” a relative of the tobacco plant, and used its own metabolism to turn its leaves into the leafy equivalent of polio vaccine factories. The end result is a virus that looks and acts like the polio virus, but technically isn’t; it has everything needed to train the body’s immune system, but nothing that can pass on the polio virus — which can cause an infected person to eventually become paralyzed or suffer from meningitis.
Scientists began this process by taking the genetic code used to make the outer layer of the polio virus, and combining it with material from various other virus known to effectively infect plants. From there, the resulting combination was inserted into soil bacteria, which then went on to infect tobacco. After the infection took hold, the plants responded to the newly made genetic code and began making the virus-like particles that would later be extracted.
When used in preliminary animal tests, the particles completed prevented polio from occurring.
Speaking to BBC News, John Innes Professor George Lomonossoff called the particles “incredibly good mimics.”
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Researchers have already explored ways to use stem cells to treat everything from diabetes to aging, and now, a team from UCLA thinks they could potentially offer some relief for people suffering from baldness.
During their study, which has been published in Nature, the researchers noticed that stem cells found in hair follicles undergo a different metabolic process than normal skin cells. After turning glucose into a molecule known as pyruvate, these hair follicle cells then do one of two things: send the pyruvate to the cell’s mitochondria to be used as energy or convert it into another metabolite known as lactate.
Based on these findings, the researchers decided to see if inactive hair follicles behaved differently depending on the path of the pyruvate.
To that end, the UCLA team compared mice that had been genetically engineered so that they wouldn’t produce lactate with mice that had been engineered to produce more lactate than normal. Obstructing lactate production stopped the stem cells in the follicles from being activated, while more hair growth was observed on the animals who were producing more of the metabolite.
“No one knew that increasing or decreasing the lactate would have an effect on hair follicle stem cells,” co-lead on the study and professor of molecular, cell, and developmental biology William Lowry explained in a UCLA press release. “Once we saw how altering lactate production in the mice influenced hair growth, it led us to look for potential drugs that could be applied to the skin and have the same effect.”
Based on their study, the researchers were able to discover two different drugs that could potentially help humans jumpstart the stem cells in their hair follicles to increase lactate production.
The first is called RCGD423, and it works by establishing a JAK/STAT signalling pathway between the exterior of a cell and its nucleus. This puts the stems cells in an active state and contributes to lactate production, encouraging hair growth.
The other drug, UK5099, takes the opposite approach. It stops pyruvate from being converted into energy by the cells’ mitochondria, which leaves the molecules with no choice but to take the alternate path of creating lactate, which, in turn, promotes hair growth.
Both of the drugs have yet to be tested on humans, but hopes are high that if tests are successful, they could provide relief for the estimated 56 million people in the U.S. alone suffering from a range of conditions that affect normal hair growth and retention, including alopecia, hormone imbalances, stress-related hair loss, and even old age.
However, as undoubtedly pleased as many of those people would be to stimulate their hair growth, the potential relevance of this research stretches far beyond hair loss. The new knowledge gained regarding stem cells, specifically their relation to the metabolism of the human body, provides a very promising basis for future study in other realms.
“I think we’ve only just begun to understand the critical role metabolism plays in hair growth and stem cells in general,” noted Aimee Flores, first author of the study and a predoctoral trainee in Lowry’s lab. “I’m looking forward to the potential application of these new findings for hair loss and beyond.”
The post We Just Figured out How to Activate Stem Cells to Treat Baldness appeared first on Futurism.
Old hearts may find new life, according to a new study, which shows that stem cells taken from younger hearts can be used to reverse the aging process. This could potentially cause older hearts to act and perform like younger ones.
The study, conducted by the Cedars-Sinai Heart Institute and published by the European Heart Journal, set out to observe the effects of cardiac stem cells on various aspects of the heart, including its function and structure. Prior applications of Cardiosphere-derived cells (CDC) resulted in positive effects, but this was the first time its effects in the aging process were tested. This is different from the tests performed last month at the Albert Einstein College of Medicine, where the hypothalamus region of the brain was discovered to be a key part of aging in mice.
Cedars-Sinai researchers instead took CDC cells from newborn mice and injected it into the hearts of older mice, while another group of older mice were injected with saline. Blood, echocardiographic, haemodynamic and treadmill stress tests were performed on all mice after injections, with the older groups tested 1 month later.
The mice given the Cardiosphere-derived cells saw a number of benefits compared to their saline counterparts. They had improved heart functionality, were able to exercise 20 percent longer, regrew hair at a faster rate, and had longer heart cell telomeres. This is important because telomeres are compounds found at the ends of chromosomes whose shortening is directly correlated to the aging process.
“The way the cells work to reverse aging is fascinating,” said Cedars-Sinai Heart Institute Director and Lead Researcher Eduardo Marbán, MD, PhD. “They secrete tiny vesicles that are chock-full of signaling molecules such as RNA and proteins. The vesicles from young cells appear to contain all the needed instructions to turn back the clock.”
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Cancer is nothing to mess around with. While alternative treatments may seem appealing to patients, some have been found to have more harmful effects in the aftermath.
Skyler Johnson and his colleagues at the Yale School of Medicine in Connecticut discovered this very fact when they decided to look into cancer treatments and cancer survivors. Records from the US National Cancer Database provided data on 281 people who tested positive for four types of cancer — lung, breast, prostate, or colorectal — and sought out alternative methods to deal with the disease, instead of the more conventional and often recommended treatments like chemotherapy, radiotherapy, or surgery.
“[These alternative treatments] could be herbs, botanicals, homeopathy, special diets or energy crystals, which are basically just stones that people believe have healing powers,” said Johnson.
Johnson doesn’t know specifically what treatments this group used, but his team’s results are telling.
Johnson and his team compared the aforementioned 281 people to 560 others of similar ages and race who also had cancer, but chose the conventional route. The alternative treatment group was two and half times more likely to die within five years of being diagnosed. That said, Johnson notes that the nature of prostate cancer makes the comparison a little inaccurate, since it takes longer for this specific form of the disease to progress to the point of becoming life-threatening.
Among breast cancer patients, specifically, those that chose alternate treatment were over five times more like to die within the same span of time. Forty-one percent of lung cancer patients who took conventional treatments survived at least five years, compared to 20 percent of those who eschewed the treatment in favor of alternatives. Only 33 percent of colorectal cancer patients survived five years following alternative treatments; 79 percent survived five years using recommended means.
Interestingly enough, those that decided to try alternative treatments were also people who were considered wealthy or well educated. Alternate treatments like herbs or diets can often be expensive, especially when offered by a large company.
“It’s a multibillion dollar industry. People pay more out-of-pocket for alternative treatments than they do for standard treatments,” John Bridgewater, an oncologist at the University College London Hospital, told New Scientist.
There’s nothing to prove these method work or do not work, however, making it hard to keep people from seeking them out. The fact that people sometimes survive the treatment can also make it difficult to condemn it, though Johnson has speculated they managed to do so because they eventually got the necessary treatments. Secondary treatments are not kept on record, so there’s no official way to tell if this was the case, or if instead the person was incredibly fortunate.
Alternative cancer treatments might sound appealing when compared to methods like chemotherapy, which can have frankly unpleasant side effects. Yet the fact remains that these methods have gone through rigorous scientific testing and peer review, which confers some degree of safety and effectiveness. The scientific process is far from perfect — but it’s still the best we’ve got.
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On August 21, America will experience a total solar eclipse for the first time since 1979. While total solar eclipses occur every 18 months 0n Earth, it has been 38 years since the American mainland has fallen in the path of totality. Unlike “black moons” and “blood moons,” which have been inflated on social media as of late, this celestial event is actually a big deal — especially if you live somewhere between Oregon and South Carolina.
Indeed, the sight has been called “life-changing” and “mind-bending” by even the most seasoned astronomers. Fred Espenak, a retired NASA astrophysicist, recently described his first eclipse experience to Vox, noting that it is “truly spectacular” and that “once in a lifetime [is] not enough.” Astronomer Jay Pasachoff reminisced with Scientific News about his last eclipse viewing experience, discussing the strong emotional reaction viewers had: “People cheer, and people cry.”
And while the best visual experience will be had from the path of totality, the rest of North America and even parts of South America will see a partial solar eclipse, which is still worth stepping outside for. But whether you’re in for a full black-out or partial blockage, you’ll need a pair of protective eyewear. NASA strongly recommends certifiably safe eyewear for viewers of the solar eclipse, meeting the ISO 12312-2 standard.
Staring into the Sun with a naked eye can result in injury to the retina and even blindness. The danger to the eye comes from infrared radiation, ultraviolet radiation, and excessive blue light. And before you ask, yes, it’s more dangerous than looking at the Sun on any other ordinary day.
This danger is due to the fact that our normal built-in ocular safety doesn’t really work the same during an eclipse, thanks to the juxtaposition of the dark shadow of the Moon against the blazing Sun. The combination of extreme brightness against total darkness creates a sharpness that challenges the eye’s safety focus features, causing it to absorb the damaging image on the most sensitive neural tissue.
Of course, even if it didn’t direct this radiation to the most sensitive areas, the eclipse would still be dangerous. Depending on exposure time and other personal health factors, the damage could be temporary or it could last a lifetime. In either case, it’s not a risk worth taking, and proper glasses are a must.
There are lots of solar eclipse branded glasses on the market right now, but NASA warns that many of them fall below the safety standard, so it’s important to make sure you’re purchasing a NASA approved brand.
NASA stands behind Lunt SUNoculars, which have been personally tested on the Sun with a 100% quality and safety guarantee. The lenses reduce the light of the Sun to an ND-5 transmission, blocking all ultraviolet and infrared components. Plus, they’re pocket-sized, include a case, strap, lens cap, cleaning cloth, a one year warranty, and only cost $129.
While there won’t be another total solar eclipse until 2024, you can use your SUNoculars to safely view planetary transits, sunspot activity, magnetic storms, and other astronomical events. To get your pair of SUNoculars, head to Amazon asap—August 21 is almost here.
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A team of engineers at the University of Toronto have created a way to fix damaged organ tissue without surgery. The method involves a needle, a patch the size of the postage stamp, and a bit of time.
The patch itself has shape-memory capabilities, meaning it will always return to its default state when introduced to the right temperature. Once inserted into the needle and injected into the body, the patch unfolds and expands before proceeding to repair and replace missing tissue. Made using a biocompatible, biodegradable polymer, the patch will dissolve over time, and in its wake, leave behind newly-made tissue.
Biomedical engineering Professor Milica Radisic and her team have been working on the project for nearly three years, with a lot of their work devoted to creating a tissue patch that could work via injection. Miles Montgomery, a PhD candidate in Radisic’s group, finalized the patch’s design after a dozen attempts.
“At the beginning it was a real challenge; there was no template to base my design on and nothing I tried was working,” said Montgomery in an interview for Eureka Alert. “But I took these failures as an indication that I was working on a problem worth solving.”
The expanding tissue patch was initially made to treat those that have suffered from heart attacks, and could be used instead of open-heart surgery. And while it could have been an implant, Radisic explains that the risks outweigh the benefits. If the implant required surgery to be implemented, it wouldn’t be easily accessible to everyone that needed it. Since heart attacks are extremely traumatic on the human heart, leaving it in a vulnerable and precarious condition, surgery after the fact could risk the patient’s survival.
Going forward, Radisic and her team are working with researchers from the nearby Hospital for Sick Children. They intend to study the long-term benefits of the patches, as well as their stability. The patch has been tested on rats, to great success, but there is a long way to go before clinical trials. But if things pan out, the patch might also be used for other traditionally damaged organs, such as the liver. To buy more time for these studies, patents on their patch and the injection process have been applied for.
The post New Stamp-Sized Tissue Patch Could Be Used to Regenerate Damaged Organs appeared first on Futurism.
About 15 years ago, Dr. Sue McElroy, a psychiatrist in Mason, Ohio, started noticing a pattern. People came to see her because they were depressed, but they frequently had a more visible ailment as well: They were heavy.
McElroy was convinced there had to be a connection.
“Many of my [depressed] patients were obese. And they were very upset by obesity,’’ McElroy recalled. “I looked into the literature, and it said there was no relationship. It didn’t make sense.”
That sense of disconnect has started to change, promising new avenues for treatment, but also presenting a puzzle: Just how can you chart the mechanics of what ties the two together? And how can treatment be linked for two disorders that exist in totally different parts of the health care system?
Ingrid Donato, a top official in the federal agency that promotes mental health treatment, says that both conditions are on the rise, heightening the need to unlock the connection and develop treatments that address both conditions simultaneously.
“You can’t address obesity in a person that’s struggling with major depression without addressing that major depression,” said Donato, chief of mental health promotion at SAMHSA, the Substance Abuse and Mental Health Services Administration. “When a person’s coming in with depression… or they’re coming in with the struggles on the physical side of obesity, if they’re not having those treated both ways, they’re only going to be having half a treatment plan.”
The relationship between obesity and depression is what researchers call “bidirectional.” Being obese or overweight ups the odds of depression, and vice versa.
For example, about 43 percent of people with depression are obese, according to the federal Centers for Disease Control and Prevention, compared with a third of the general population. People who are obese are 55 percent more likely to be depressed, and people with depression 58 percent more likely to develop obesity, according to one 2010 study. “This is a massive public health issue when you have numbers that large,” Donato said.
While on the surface the two conditions appear very different, they share important similarities. Both are chronic diseases that are tricky to treat, requiring long-term physical and mental health interventions.
In cases in which depression and obesity coincide, those interventions can be even more complex, with research often showing the best results when care involves not only doctors and nurses but also other health professionals such as dietitians, behavioral health specialists and physical therapists.
“We need to find synergistic therapies — or it’s going to be the same kind of messy system in which we spend a lot of money and don’t get any return,” said William Dietz, the director of George Washington University’s Sumner M. Redstone Global Center for Prevention and Wellness, who researches obesity interventions.
A 2011 paper by researchers from the University of Texas-Southwestern found that patients’ depressive symptoms were reduced when physicians gave them prescriptions for weekly exercise sessions, which were supervised at the Cooper Institute in Dallas or at home. And in 2014, a study at Duke University found that simply helping obese women maintain their weight — via small lifestyle changes and monthly dietitian check-ins — cut their rates of depression in half.
Still, this kind of care-syncing is not yet the norm. While the Affordable Care Act promoted coordinated care as part of its efforts to lower costs, those initiatives haven’t yet been directed toward depression and obesity.
But federally funded efforts to coordinate care for diabetes and depression could provide a template, said Madhukar Trivedi, a professor of psychiatry at the University of Texas-Southwestern who was involved in the 2011 study.
“This is going to require a real mindset change. We have to be thinking at a policy level,” Trivedi said.
One reason is cost. Depression and obesity are among the largest drivers of health care cost increases.
Obesity already costs the medical system almost $150 billion per year in direct costs, and the nonprofit Robert Wood Johnson Foundation estimates that by 2030, obesity will sap the U.S. economy of an additional $390 billion to $520 billion in lost worker productivity.
Depression makes the price tag worse. Its most severe variant, major depressive disorder, costs the country more than $200 billion per year in direct costs such as psych visits, medication and other treatments as well as the hours and days in which people afflicted aren’t able to work.
The federal government foots much of this bill.
About 13 million Medicare-eligible senior citizens — an estimated 35 percent of people older than 65 — are obese, according to CDC data from 2012, the most recent year for which statistics are available. It’s estimated that Medicaid pays as much as 30 percent of the total bill for U.S. mental health care.
“These are both incredibly burdensome on the health care system. … They’re both on the rise, and there’s a correlation,” said Dori Steinberg, an assistant research professor at Duke’s Global Health Institute who was involved in the 2014 study.
And resources to tend to patients with each condition, even individually, are limited.
The federal government has worked to expand mental health care access and insurance coverage, but in many parts of the country, few mental health specialists accept insurance, rendering that theoretical benefit useless.
Obesity interventions also fall short. The American Medical Association, a leading trade group for doctors, dubbed the condition a “disease” four years ago and the ACA limited cost-sharing for some preventive obesity treatments. Some critics say the benefit doesn’t go far enough in terms of consultations with more specialized health care providers, such as dietitians and nutritionists, to make a meaningful impact. That means patients may get little help until they have gained enough weight or suffered sufficient health consequences that they qualify for more extreme measures, like bariatric surgery.
And there’s the added challenge of finding a physician able to address both problems at once.
“It’s not a one-shot thing. Both of these are chronic conditions. They don’t lend themselves to episodic treatment,” said Anita Everett, president of the American Psychiatric Association. “It’s not like you take a course of treatment to [make it] go away.”
Already, research suggests primary care physicians, who are on the front lines in providing care, aren’t meeting clinical standards for treating depression. Most psychiatrists aren’t trained in weight management.
“This is an important area, and I don’t think people are trained how to do it,” said Dietz.
Progress has been slow, in part, because of the stigma surrounding both conditions.
Having either is “like having the scarlet letter,” suggested Karen Coleman, a research scientist at Kaiser Permanente’s Southern California branch. (Kaiser Health News is not affiliated with Kaiser Permanente.) Despite a now vast body of evidence to the contrary, even health professionals are more likely to place some blame on the patient. That makes patients more hesitant to seek care, and physicians don’t necessarily make efforts to provide it.
“We have a long, long way to go before we treat obesity like we do … heart failure,” Coleman added.
In her Ohio practice, McElroy says she has seen the benefits of what she called a self-taught approach to treating obesity and depression together. She screens patients for weight and BMI. And, because some of the medications used to treat mental health conditions can cause weight gain, she tailors what antidepressants she prescribes, so that they don’t cause more weight gain.
Her patients vouch for her methods.
Ask 26-year-old Michael Stewart, who has bipolar disorder. He joined her practice within this past year for weight treatment — he sees a psychiatrist separately — and has dropped 20 pounds, or about 6 percent of the 335 pounds he weighed when he started. Treating both conditions isn’t easy, he said, and there’s been some difficulty in finding medications that help his bipolar disorder and his weight problems.
“I’ve had to work harder with my doctor to find something that works — so that I don’t weigh 500 pounds,” he said.
McElroy has prescribed him a new pill that’s helped control his weight, he said. Had his psychiatrist known how to treat both conditions, he added, he would “for sure” had begun addressing weight sooner.
McElroy worries that without broader changes to the health care system, patients like Stewart are just that: individual cases.
“If we addressed this systematically, you would think it would be not only better for patients’ health but also cost-effective,” she said.
Kaiser Health News is a nonprofit health newsroom, an editorially independent part of the Kaiser Family Foundation.
The post Scientists Still Don’t Fully Understand the Connection Between Obesity and Depression appeared first on Futurism.
It’s a problem of leviathan proportions: every year, an amount of food equivalent to roughly 9,553 blue whales — the largest animal that has ever lived — gets thrown in the garbage. (That’s 1.3 billion tonnes, or 2.9 trillion pounds.)
According to the Food and Agricultural Organization (FAO) of the United Nations, as much as one third of all food is wasted before it can be eaten, either by food loss (spilled or spoiled before reaching a store) or food waste (when it gets thrown away or spoils before use).
Food production is already an environmentally costly process: it depletes nutrients and helpful organisms from the soil, adds pesticides and algal-bloom-causing nitrogen to nearby water sources, accounts for 69% of all water use worldwide, and produces greenhouse gases. In fact, agriculture is second only to energy in producing the most planet-warming carbon dioxide and methane worldwide.
Add in the impact of food waste, and the footprint of food production becomes dizzying. The FAO estimates the cost of wasted food is equal to about US $750 billion every year — and that doesn’t take into account costs that can’t be calculated, like impacts on biodiversity and shortages that feed social conflict. In the below video, FAO estimates that nature could charge us at least an additional $700 billion for these hidden side-effects.
However, entrepreneurs all over the world are stepping up to the plate to address food waste in remarkably creative ways.
Barnana produces snacks from dehydrated bananas, sourced from Latin America, that would have been otherwise wasted — either because they’re scuffed, too ripe, or an unappealing size for consumption. The company has even “close(d) the banana waste loop,” as chief marketing officer Nik Ingersoll told Forbes, by powering their dehydrator using pellets made from dried banana peels.
In the Netherlands, Koffiekik is growing protein-rich oyster mushrooms using discarded coffee grounds. In California, Imperfect Produce delivers produce that supermarkets won’t sell in-store, due to their odd shapes and sizes, for 30-50% below market price. Bronx-based Baldor Fresh Cuts uses food scraps from restaurants, like carrot tops and pineapple cores, to make cookies, supplements, breadcrumbs and more.
“The idea is to take an item that normally would be wasted and turn it into a consumer product,” Tom McQuillan, Baldor’s director of food service sales and sustainability, told Popular Science. “It’s a great way to get food into the hands of the food-insecure, and to people who should be eating healthy foods.”
By turning food waste back into food, these entrepreneurs are beginning to tackle one of our planet’s biggest paradoxes: despite producing much more food than we consume, millions of people remain hungry.
According to the World Hunger Education Service, nearly 795 million people suffered from chronic undernourishment in 2014-16.
In developing regions, this impacts about 12.9% of the population, compared to less than 5% of developed countries. Unsurprisingly, the balance of food waste skews in the opposite direction, with hungrier countries producing less waste.
In these countries, food waste usually isn’t due to distaste for bumpy produce, but instead lack of access to the technology needed to keep food fresh. A 2014 study from the University of Birmingham found that India loses 4.4 billion UK pounds, or roughly US $5.8 billion, worth of fruits and vegetables due to the absence of refrigerant technology.
As such, projects are underway in these countries that seek to preserve food before it can spoil. In Kenya, where more than half of the mango crop often spoils before reaching market, Azuri Health is developing a facility to dry the mangoes into fruit leather, a shelf-stable product and dense source of nutrients.
The FAO-partnered SAVE FOOD Initiative is among the biggest organization pursuing this mission. Thirteen African countries already have SAVE FOOD initiatives underway to reduce food loss and bolster small farmers, as do India, Egypt, Iran, Jordan, Lebanon, Malaysia, and Timor-Leste. In January 2017, the initiative launched its first project in Russia, where food waste is lower than the global average, but still estimated, as of 2013, at roughly 56 kilos per person per year.
“If each of us takes a look at their fridge and starts counting the volume of food we throw away each year, we will end up with industrial-scale figures. This is particularly disturbing against the background of the large numbers of people around us who have to save on the essentials and need help,” said Viktoria Krisko, president of Foodbank Rus, at the launch.
The post Reducing Food Waste in Creative Ways Could Help the World’s Hunger Problem appeared first on Futurism.
The placebo effect occupies a liminal space in clinical consideration, somewhere between biological and psychological, therapeutic and phony. Scientists maintain that it is a collective term for a host of processes and mechanisms that effect our experience of our condition — gymnastics of perception — rather than helping to cure the underlying, objective, and measurable causes of it.
Ted Kaptchuk, Director of the Harvard-wide Program in Placebo Studies, summarizes it as “finding out what is it that’s usually not paid attention to in medicine — the intangible that we often forget when we rely on good drugs and procedures. […] The placebo effect is a surrogate marker for everything that surrounds a pill. And that includes rituals, symbols, doctor-patient encounters.”
A study undertaken by Kaptchuk and colleagues that shows the power of perception over objectivity particularly well was published in the New England Journal of Medicine in 2011. Subjects were given the effective drug albuterol, a placebo inhaler, acupuncture, and periods without treatment. They all took each treatment three times, which had the double effect of producing lots of data and allowing subjects to serve as their own controls. While everyone reported a similar level of improvement in their symptoms regardless of which treatment they had most recently undergone, objective measures indicated that only the albuterol improved airflow — but all three options actually increased their lung functionality.
While a significant amount of the placebo effect remains obscured by a lack of research, scientists have been able to discover some of the perception mechanisms behind what allows our brains to fool our bodies into feeling better.
The main cluster is the effect that conditioning has on our body’s responses — the results of a soft-Pavlovian training that has been built up since birth. The most rudimentary form of this is the power of expectation. In an interesting study, Luana Colloca has conducted experiments involving lights. One such experiment involved flashing a red light when a subject was given a high voltage electric shock and flashing a green light when they were given a lower one. She then played with the levels and eventually found that, even when the shocks were equal, when the green light flashed, subjects reported less pain. Conversely, when the red light was on, they exhibited higher pain than the shock would reasonably evoke; this is called the nocebo effect.
The essence of this is manipulated and made more complex by the very presence of clinical procedure — a real world “green light.” It can be seen most pertinently when it comes to drugs.
The body responds positively to any drug because it remembers the healing effect drugs have had on it before. This is reflected in one of the most interesting pieces of placebo research in recent years, in which participants knew they were taking sugar pills but still experienced therapeutic effects. This showed that something beneath our conscious and rational mind believed the administration of drugs was beneficial, and exhibited the positive effects of taking drugs when it received one — despite the conscious mind knowing it was fake. The action taking of a pill, rather than what was in the pill itself, became the signal to release the chemicals that the real pill normally would.
The next stage in the research is to codify the precise natures and mechanisms of the placebo effect. Franklin Miller, a retired NIH bioethicist, asserts that “sooner or later we’ll get rid of the term” because it will be broken down into component parts.
If we can break it down into these parts, these precise mechanisms, it then becomes hypothetically possible to begin to use them in a therapeutic setting. Because the doctor is using the mechanisms of perception, this actually means that manipulating the placebo effect becomes a psychological treatment of biological phenomena — a psychosomatic treatment.
While Miller goes on to say that the effect can never cure an objective disease with definite biological causes — it could, for example, not cure the ebola virus, but may help with symptoms — because “There are real limits to what you can condition.” The placebo has to treat something that the brain can adjust itself, without help, such as pain.
An example of this is irritable bowel syndrome, which Kaptchuk used for an experiment. Two groups got placebo acupuncture, but half were treated with empathy by the doctor, while the other half were treated without any warmth. The half who had been treated kindly reported 15 percent more relief. Experts have also suggested using the effect to reduce America’s current opium crisis, as it could provide an effective pain relief with smaller doses of physically addictive substances being involved.
The placebo effect remains obscured by a lack of research and the enigmas and riddles of the human mind. However, what is clear is that there is huge potential for it to be a part of our medical system.
The post The Placebo Effect Is Real and It Can Lead to Better Healthcare appeared first on Futurism.
Check out this crystal-clear MRI footage
An estimated 270,000 women die from cervical cancers each year, and their primary cause is the human papillomavirus (HPV). Now, a new study by the Royal Women’s Hospital in Melbourne and the Victorian Cytology Service suggests that up to 93 percent of cases of cervical cancer could be prevented by an HPV vaccine that currently isn’t approved for use in Australia.
Around three quarters of HPV infections are caused by just two of the nearly 200 strains of the virus: HPV 16 and HPV 18. Gardasil, the quadrivalent HPV vaccine that’s currently approved for use in Australia, protects against both of these forms.
During their study, which is published in the International Journal of Cancer, the researchers found that 77 percent of the 847 cervical cancer samples tested were caused by HPV 16 and 18. A further 16 percent were linked to HPV 31, 33, 45, 52, and 58. Gardasil 9, an HPV vaccine that was approved for use in the U.S. in 2014, protects against all seven of these strains.
Based on these numbers, the researchers believe the Gardasil 9 vaccine could prevent up to 93 percent of cervical cancer cases.
“The new vaccine still protects against genital warts but is expanded to cover the seven most common viral types that cause cervical cancer,” said the senior author of the paper, Professor Suzanne Garland, in a Royal Women’s Hospital news release. “I do believe that if we continue with this high coverage of vaccination, we could almost wipe out cervical cancer in women.”
With the promising results of the study in hand, the next step is to ensure that as many people as possible have access to the Gardasil 9 vaccine. The Royal Women’s Hospital is hopeful that it will be adopted by Australia’s National HPV Vaccination Program as early as 2018.
Of course, to remove the threat of HPV causing cervical cancer completely, a vaccine would have to protect against the less common strains of HPV that comprise the remaining 7 percent of cases covered by this study. It remains to be seen how feasible that would be, but the extra coverage achieved by Gardasil 9 is definitely a big step forward.
The post New Research Shows That This HPV Vaccine Could Prevent 93% of Cervical Cancers appeared first on Futurism.
New research from a team at MIT indicates symptoms of Alzheimer’s disease (AD) affecting patient’s memories may be reversible. AD causes memory loss by setting up genetic “blockades” formed when the enzyme HCAC2 condenses the genes of the brain responsible for memory. Eventually, those genes become useless; unexpressed, the genes are unable to cause the formation of new memories or retrieval of existing ones.
Clearly, blocking HCAC2 in the brain is an obvious fix; however, it has to date been impossible, in that all prior attempts have negatively affected the internal organs which require other enzymes in the histone deacetylase (HDAC) family for normal function. Researchers at MIT have now found something they hope might be the answer: LED lights which they use to prevent HCAC2 alone from binding with Sp3, its genetic blockade formation partner in crime (and Alzheimer’s).
The post New Research Suggests Memory Loss in Alzheimer’s Patients May be Reversible appeared first on Futurism.
Researchers have made a significant breakthrough in the area of organ transplants, and it brings us remarkably close to being able to safely transplant organs from other species into humans. In this latest work, scientists are working specifically with pig organs.
Notably, teams have been working on interspecies transplants for decades. One of the concerns that halted the previous studies was the 1998 discovery that retroviruses were hiding within pig DNA, which could possibly pose a threat to human recipients.
To combat this threat, a team from Harvard University and a private company, eGenesis, just created gene-edited pig clones that are completely free of the aforementioned retroviruses. Now, without the threat of these hidden diseases, it may be possible to safely transplant pig livers, hearts, and other organs. This adds to the growing number of transplants that are already in relatively widespread use in medicine (heart valves, skin grafts for burn patients, etc.).
Ultimately, these genetically altered pigs could be raised specifically for the harvesting of organs for transplant.
According to Dr. David Klassen, Chief Medical Officer at the United Network for Organ Sharing, last year saw 33,600 organ transplants, with another 116,800 people listed on various lists waiting for sutiable organs. If the research proves sound, Dr. Klassen believes this “…could be a real game changer.”
The post A New Gene Editing Breakthrough Could Allow Us to Transplant Pig Organs Into Humans appeared first on Futurism.
Impossible Foods’ meatless burger uses an ingredient sourced from a genetically engineered yeast to mimic the taste and texture of beef, and the end result has proven very popular among diners at high-end restaurants. However, the Food and Drug Administration remains reticent to issue its approval.
To clarify, soy leghemoglobin is a substance that occurs naturally in the roots of soybean plants. Impossible Foods produces the ingredient in its laboratory, and the company has been actively pursuing confirmation from the FDA that it’s safe for humans to eat.
A document released under the Freedom of the Information Act sheds light on correspondence between the FDA and Impossible Foods. The administration expresses concerns that there’s no precedent for humans ingesting the substance, while the company argues that it’s safe because it’s structurally and functionally equivalent to “other widely consumed globin proteins.”
Impossible Foods can sell its burger whether or not it receives approval from the FDA. However, if the company wants its product to appeal to regular consumers as well as the more adventurous tastes of haute cuisine chefs, getting the go-ahead from the agency would be a big advantage. Plans to resubmit the petition are already in motion.
The FDA feels that Impossible Foods hasn’t yet done enough to find out about soy leghemoglobin’s potential to act as an allergen. For its part, the company has apparently fed the ingredient to rats in larger amounts than are included in its burger, and observed no negative effects on the animals.
In 1958, Congress enacted a Food Additives Amendment that allowed companies to bypass FDA approval if a substance was deemed to be “generally recognized as safe” by experts. This allows Impossible Foods to self-adjudicate, hiring its own consultants without being obliged to appraise the federal agency of the results. A study published in 2013 suggested that around 10 percent of the ingredients used in food are unknown to the FDA as a result of self-adjudication.
However, several parties contest Impossible Foods’ invocation of the Food Additives Amendment. “The exemption was meant to cover ingredients that had long been used in the food supply, so that companies didn’t have to come in every time they made a new product,” said Tom Neltner, chemicals policy director at the Environmental Defense Fund, a plaintiff engaged in lawsuit over the matter, in an interview with The New York Times.
While there are some serious concerns about Impossible Burger’s candor regarding its bypass of the FDA, the burger itself is made entirely from plant-based ingredients, including wheat, coconut oils, and potatoes. It’s suitable for vegans, completely free from hormones, antibiotics, and artificial ingredients, and apparently it tastes great — this means that it ostensibly fits the bill for a sustainable, wholesome alternative to old-fashioned livestock, avoids the potentially devastating development of antibiotic-resistant diseases like MRSA, and could provide impetus for increased investment in domestic agriculture. Yet, since the ingredient still needs some testing, it will take some time to determine just how viable it truly is.
The post The FDA Has Reservations About Impossible Foods’ Meatless Burger appeared first on Futurism.
It is now possible to design bone implants and 3D print them quickly and affordably. Each implant is custom made for the patient, resulting in far better patient outcomes.
“It’s time we provided some critical scrutiny and stopped parroting the gospel of medical progress at all costs,” writes former molecular biologist Dr. David King in a recent Guardian editorial. “…we must stop this race for the first GM baby.”
King wrote in response to the announcement earlier this month that doctors had successfully altered the genomes of single-cell human embryos. Using CRISPR, the doctors removed a gene for hypertrophic cardiomyopathy (HCM), a common heart disease that can cause sudden cardiac arrest and death. Their results are described in Nature.
King is the founder of Human Genetics Alert, an independent watchdog group opposed to certain outcomes of genetic engineering. He argues that genome editing of the type in Nature is not a justified use of medical research dollars, given the ability to avoid the birth of children with such conditions through testing.
“In fact, the medical justification for spending millions of dollars on such research is extremely thin: it would be much better spent on developing cures for people living with those conditions,” King says. He argues that inevitably, even if pioneered for medical reasons, market forces will inevitably push genome editing towards creating “designer babies,” allowing the very wealthy to program desired traits into their unborn children.
King, and others, see this application as unethical and akin to eugenics.
“Once you start creating a society in which rich people’s children get biological advantages over other children, basic notions of human equality go out the window,” King writes. “Instead, what you get is social inequality written into DNA.”
The advent of CRISPR technology has drastically accelerated the field of genetic engineering, and with it the fears of ethicists like King. Yet many say that these worries are overblown.
“We are still a long way from serious consideration of using gene editing to enhance traits in babies,” Janet Rossant, co-author of a report on human genome editing for the National Academy of Sciences (NAS), told the Guardian. “We don’t understand the genetic basis of many of the human traits that might be targets for enhancement.”
If this changes in the future, King argues that it will be impossible to keep the influence of money from directing how that knowledge is used. He bases this prediction of market-based inequality on existing practices — such as the high price tag of ova donated by “tall, beautiful Ivy League students” and the popularity of the international surrogacy market among those with the means to travel for a baby.
Yet existing regulatory systems may be enough to prevent the future King predicts.
In their report for NAS, Rossant and her co-authors emphasized that while caution and ethical oversight are necessary, the US Food and Drug Administration’s system for evaluating medical products could, too, assess potential uses of genome editing. The authors predict that editing for purposes of enhancement — as they put it, “not clearly intended to cure or combat disease and disability” — would not pass muster.
Additionally, King’s argument largely overlooks the potential of gene editing to help children whose conditions are unlikely to have a cure, or whose parents are unwilling to reject a pregnancy.
For Lee and many others suffering from genetic disease, even a selective regulatory establishment may spell collateral damage for the rest of their lives. But the fact stands: caution and oversight will be paramount when playing with the very means nature gave us for life.
The post Expert Argues That Gene Editing Will Widen Economic Class Gap appeared first on Futurism.
Science fiction has often featured technology that’s capable of healing wounds and injuries almost instantly. Such devices could be found in the medical bay of any interstellar ship. Well, now you don’t have to look any farther than Columbus, Ohio, where researchers from the Wexner Medical Center at the Ohio State University have developed a device capable of repairing organs with a single touch.
The chip is put at the surface of the skin, where it uses a technology called Tissue Nanotransfection (TNT) to input a certain genetic code into the skin cells. These turn the skin cells into the type of cell needed to treat a specific injury or condition. By applying a small electrical current, DNA or RNA are injected into the cells, which are then biologically reprogrammed to morph into the kind of cell most needed in situ.
“It takes just a fraction of a second. You simply touch the chip to the wounded area, then remove it,” Chandan Sen, director of the Center for Regenerative Medicine and Cell-Based Therapies at Wexner, said in an OSU press release. “At that point, the cell reprogramming begins.”
The device introduces a new approach to gene therapy and cellular reprogramming, one that isn’t particularly invasive. In a study published today in the journal Nature Nanotechnology, the researchers talked about a series of lab tests that demonstrated the power of the device. Applied to the injured legs of mice, the blood flow in these legs, vascular scans revealed, were initially either limited or completely blocked.
“We reprogrammed their skin cells to become vascular cells,” Sen explained. “Within a week we began noticing the transformation.” Although the injured mice didn’t receive any other form of treatment, active blood vessels formed within two weeks. By the third week, the legs were fully healed. “What’s even more exciting is that it not only works on the skin, but on any type of tissue,” he added.
This OSU research is yet another example of how technological advancement pushes medicine to new frontiers. This goes beyond building better machines and equipment; several hard sciences have proved a boon to medical research and development, including artificial intelligence, from labs-on-a-chip, and even blockchain.
The post Researchers Developed a New Device Capable of Fixing Damaged Tissue with Just One Press appeared first on Futurism.
The CRISPR//Cas9 gene editing tool has quickly earned a reputation as a revolutionary technology, and its merits support the clout. This year has, in fact, seen so many CRISPR-related breakthroughs that it’s worthwhile to take a step back and take in all of the many accomplishments.
1. This week, circulating reports about the successful application of gene-editing human embryos in the US were confirmed by a research paper published in Nature. The researchers “corrected” one-cell embryo DNA to remove the MYBPC3 gene — known to cause hypertrophic cardiomyopathy (HCM), a heart disease that affects 1 in 500 people.
2. This year, scientists successfully used gene editing to completely extract HIV from a living organism, with repeated success across three different animal models. In addition to the complete removal of the virus DNA, the team also prevented the progress of acute latent infection.
3. Semi-synthetic organisms were developed by breeding E.coli bacteria with an anomalous six-letter genetic code, instead of the normal four-base sequence. Additional gene editing was implemented to ensure that the new DNA molecules were not identified as an invasive presence.
4. The CRISPR method successfully targeted the “command center” of cancer — called the hybrid fusion — which leads to abnormal tumor growths. A “cut-and-paste” method allowed the creation of a cancer-annihilating gene that shrinks tumors in mice carrying human prostate and liver cancer cells.
5. Scientists also slowed the growth of cancerous cells, by targeting Tudor-SN, a key protein in cell division. It’s expected that this technique could also slow the growth of fast-growing cells.
6. Gene editing techniques have also made superbugs kill themselves. By adding antibiotic resistant gene sequences into bacteriophage viruses, self-destructive mechanisms are triggered which protect bacteria.
7. Gene editing may even make mosquito-born diseases an extinct phenomenon. By hacking fertility genes, scientists have gained the ability to limit the spread of mosquitoes — a success they credit to CRISPR’s ability to make multiple genetic code changes simultaneously.
8. Using CRISPR, researchers have edited out Huntington’s disease from mice, pushing the symptomatic progression of the condition into reverse. Experts expect this promising technique to be applied to humans in the near future.
9. Outside of the medical field, CRISPR might also provide a more abundant and sustainable biofuel. By connecting several gene-editing tools, scientists engineered algae that produce twice the biofuel material as wild (or “natural”) counterparts.
10. Very recently, the first-ever “molecular recorder” was developed — a gene editing process that encodes a film directly into DNA code — and with this ability, scientists embedded information into an E.coli genome.
11. Last but not least, and on the macro-scale, the US Defense Advanced Research Projects Agency (DARPA) invested $65 million in a project called “safe genes,” designed to improve the accuracy and safety of CRISPR editing techniques. In addition to serving the public interest of avoiding accidental or intentional (cue ominous music) misuse, the seven research teams will remove engineered genes from environments to return them to baseline “natural” levels.
The post 11 Incredible Things CRISPR Has Helped Us Achieve in 2017 appeared first on Futurism.
The potential of the gene editing tool CRISPR just seems to keep growing and growing, and the latest experimental use of the technology is creating skin grafts that trigger the release of insulin and help manage diabetes.
Researchers have successfully tested the idea with mice that gained less weight and showed a reversed resistance to insulin because of the grafts (high insulin resistance is a common precursor to type 2 diabetes).
In fact, the team from the University of Chicago says the same approach could eventually be used to treat a variety of metabolic and genetic conditions, not just diabetes – it’s a question of using skin cells to trigger different chemical reactions in the body.
“We didn’t cure diabetes, but it does provide a potential long-term and safe approach of using skin epidermal stem cells to help people with diabetes and obesity better maintain their glucose levels,” says one of the researchers, Xiaoyang Wu.
If you’re new to the CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats) phenomenon, it’s a new and innovative way of editing specific genes in the body, using a biological copy and paste technique: it can do everything fromcut out HIV virus DNA to slow the growth of cancer cells.
For this study, researchers used CRISPR to alter the gene responsible for encoding a hormone called glucagon-like peptide-1 (GLP-1), which triggers the release of insulin and then helps remove excess glucose from the blood.
Type 2 diabetes comes about due to a lack of insulin, also known as insulin resistance.
Using CRISPR, the GLP-1 gene could be tweaked to make its effects last longer than normal. The result was developed into skin grafts that were then applied to mice.
Around 80 percent of the grafts successfully released the edited hormone into the blood, regulating blood glucose levels over four months, as well as reversing insulin resistance and weight gain related to a high-fat diet.
Significantly, it’s the first time the skin graft approach has worked for mice not specially designed in the lab.
“This paper is exciting for us because it is the first time we show engineered skin grafts can survive long term in wild-type mice, and we expect that in the near future this approach can be used as a safe option for the treatment of human patients,” says Wu.
Human treatments will take time to develop but the good news is that scientists are today able to grow skin tissue very easily in the lab using stem cells, so that won’t be an issue.
If we can make it safe, and patients are happy with the procedure, then the researchers say it could be extended to treat something like haemophilia, where the body is unable to make blood clots properly.
Any kind of disease where the body is deficient in specific molecules could potentially be targeted by this new technique. And if it works with diabetes, it could be time to say goodbye to needles and insulin injections.
Other scientists who weren’t directly involved in the research, including Timothy Kieffer from the University of British Columbia in Canada, seem optimistic.
“I do predict that gene and cell therapies will ultimately replace repeated injections for the treatment of chronic diseases,” Kieffer told Rachel Baxter at New Scientist.
The findings have been published in Cell Stem Cell.
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Around 2% of births in the U.S. are genetically engineered. Would you do it? Learn more: https://www.a360.digital/a/4799/d7LJdNVo
Of the many diseases that have plagued humanity, HIV is proving to be one of the trickiest to cure. The virus’ ability to remain hidden in latent reservoirs makes eliminating it particularly challenging, which is why Chinese researchers decided to test a different approach. Instead of developing a drug to fight HIV, they’re working on a way to make cells immune to the virus.
In a study published in Molecular Biology, a team led by Hu Chen of the 307 Hospital of the Chinese People’s Liberation Army and Hongkui Deng of the Peking University Stem Cell Research Center used CRISPR/Cas9 to induce a homozygous mutation in a gene called CCR5, which encodes receptors in immune cells.
Previous studies have shown that this mutation of CCR5 can prevent HIV from entering cells, but only a small percentage of people have it naturally. Using CRISPR/Cas9, the researchers edited human fetal liver hematopoietic stem/progenitor cells (HSPCs), which were then engrafted into mice. Their research showed that this targeted approach of editing CCR5 was effective at making T-cells more resistant to HIV.
While this study isn’t the first to use edited stem cells to develop HIV-resistance in immune cells, it is the first example of using CRISPR to edit CCR5. “One of the advantages of CRISPR is its high efficiency on difficult to transfect cells,” Cheng and Deng told The Scientist. Using the remarkable method, they achieved a 21 to 28 percent efficiency in editing CCR5.
This isn’t surprising since CRISPR is considered the most effective and efficient gene-editing tool available. One of the most recent and remarkable demonstrations of its precision was the first-ever editing of a human embryo in the U.S.. The tool even gives us the ability to revive extinct species (if we wanted to).
As for this CCR5 study, Kamel Khalili from Temple University told The Scientist that expectation should remain in check: “[It] may not be a complete cure because the virus itself is not eliminated and may shift to using the CCR4 or another receptor to spread.” However, he did add, “CCR5 seems to be the one Achilles heel of HIV. There may be some other targets, but for now, it’s the best target.”
HIV affects more than 36.7 million people worldwide, 1.8 million of whom are younger than 15 years old. An approach that helps humans develop a resistance or immunity to it could be our best chance at future eradication.
The post Researchers Used CRISPR to Successfully Increase HIV Resistance in Animals appeared first on Futurism.
Cancer is one of the leading causes of death worldwide, according to the World Health Organization, claiming 8.8 million victims in 2015. While researchers have made significant progress in the battle against the disease, it remains notoriously difficult to treat. This is due, in part, to the wide variety of cancers known to exist today, but the matter is further complicated by our difficulty preventing cancer cells from spreading.
While treatments such as chemotherapy and immunotherapy are available, they are often rendered ineffective by the fast rate at which cancer cells spread. Now, researchers from the University of Southampton in the United Kingdom, working in partnership with Cancer Research UK, may have found a way to aid such treatments by slowing down the spread of many different types of cancer.
In a study published in the Journal of the National Cancer Institute, the researchers focused on the enzyme NOX4 and a kind of cell called cancer associated fibroblasts (CAFs). When healthy, fibroblasts keep different kinds of organs together. When infected by cancer and turned into CAFs, however, they are known to help tumors grow, spread, and even evade treatment.
“By looking at many types of cancer, we have identified a common mechanism responsible for CAF formation in tumors,” lead research Gareth Thomas said in a press release. “These cells make cancers aggressive and difficult to treat, and we can see exciting possibilities for targeting CAFs in many patients who don’t respond well to existing therapies.”
The researchers found that CAFs decrease patient survival for a number of cancer types, including head, neck, and bowel cancers. “[E]ffective methods to manipulate these cells clinically have yet to be developed,” the researchers wrote. Thankfully, through their research, they discovered that NOX4 and CAFs have a peculiar dynamic.
In many types of cancer, NOX4 enzymes are required for CAFs to form and subsequently facilitate tumor growth. In tests conducted on mice, blocking NOX4 reduced the size of tumors by up to 50 percent. This blocking was made possible using a drug that’s being developed to treat another kind of disease called organ fibrosis.
“Some cancers are incredibly difficult to treat and can use the body’s own cells to help them grow, evade treatment, and spread around the body,” explained Áine McCarthy at Cancer Research UK in the press release. “Researchers have been trying to unlock the secrets behind this for many years, and this study is a big step forward in understanding how some cancers achieve this.”
“These findings show that CAFs can be targeted with a drug and their ‘pro-tumor’ effects can be reversed in mice, giving researchers a starting point to develop new and potentially more effective treatments in the future,” she added.
Thomas and his team believe that their work could help improve a patient’s chances of reacting positively to chemo and immunotherapy. At the very least, it could help slow down the spread of cancer, dealing a critical blow to the disease that affects so many people.
The post Researchers Have Found a Drug That Can Help Slow the Spread of Multiple Cancers appeared first on Futurism.
Advancements in deep learning, virtual reality (VR), and artificial intelligence (AI) may signal an end to issues engrained within the practice of clinical psychology — such as subjectivity and the difficulty of conducting large-scale studies — perhaps leading us into a new era of diagnosing and treating mental disorders.
This new branch of study is known as computational psychiatry. It operates on the tenet that researchers can better understand and treat mental illnesses using the aforementioned technologies. Application vary, but some researchers in the field apply mathematical theories of cognition to data mined from long-standing observations to effectively diagnose and predict cognition, while others use virtual experiments to enable the pure study of human behavior.
Sarah Fineburg of Yale University in New Haven recently published a study that used computational psychiatry to explore borderline personality disorder (BPD), a condition that the National Institute of Mental Health (NIMH) reports includes symptoms such as “ongoing instability in moods, behaviors, self-image, and functioning,” as well as “impulsive actions and unstable relationships.”
For her study, Fineburg observed the responses of people with BPD to events in virtual environments. She used a game called Cyberball in which avatars pass a ball to one another, with the patient in control of one avatar. Though they believe the remaining avatars are controlled by other people, their actions are actually determined by computer systems.
The game allowed Fineburg to monitor the patients’ emotional responses to the frequency with which they were passed the ball. She found that BPD sufferers experienced greater feelings of rejection than non-sufferers when they did not receive the ball, and they also experienced more negative feelings than non-sufferers even when they received the ball more often than the other avatars.
Not only can computational psychiatry be used to study the emotions of BPD patients, it can also help researchers understand their language use, which some have posited was different from that of non-sufferers. However, the data was previously too vast to analyze.“We and others have identified language features that mark psychological states and traits,” Fineberg told MIT Technology Review. “Computational models based on word-use patterns can predict which writers have psychosis or will progress to psychosis.”
The two strands of computation psychiatry explored by Fineburg — using virtual environments as clinical spaces and using AI to find patterns in large swathes of data — are being used by other researchers to study other disorders.
The use of AI to diagnose disorders and recommend treatments has gained traction in the world of apps, which are acting as “virtual psychotherapists” to treat a variety of mental disorders.
A prime example is Woebot, a chatbot that uses cognitive behavioral therapy principles to help combat depression. The results from a small test of the app were promising, with the majority of users reporting a significant reduction in depression symptoms. Alison Darcy, a lecturer at Stanford who pioneered the app, told Business Insider, “The data blew us away. We were like, this is it.”
The app does have the potential to help people, but there are also some inherent problems with it. Due to the novelty of such systems, no one has yet studied whether or not psychiatric interactions with a computer over an extended period of time are beneficial for patients. Darcy’s study only had 70 total participants and lasted just two weeks, which is likely too short a time period to produce any certainty about the app’s impact.
Virtual environments seem to have fewer pitfalls when used for psychiatric studies. The whole idea of psychology is to study how a person’s perception colors empirical data, so if the senses are sufficiently fooled into believing a virtual scenario is “real,” the results of a VR supported study are just as valid as one conducted in the real world.
In fact, these environments give researchers the ability to learn more than they could from a traditional environment as the VR world can be modified in virtually limitless ways. This enables the study of events that may not be possible in the real world, which gives the researchers a more robust data pool and potentially more clarity on their patient’s cognition.
Indeed, virtual realities and digital environments have already demonstrated their ability to help researchers study and even treat mental disorders. VR can be used to help ex-soldiers overcome symptoms of PTSD, and it has also been shown to help people overcome depression by increasing their self-compassion.
Computational psychiatry could potentially help millions of people, but as with anything that involves the brain, we must careful in how we apply this technology. Without knowing precisely what effect these treatments can have on the mind, we set ourselves up to potentially do more harm than good.
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The idea of never growing old is seductive, but it has remained a pipe-dream throughout history. However, that may not be the case for much longer as the scientific community has seen a surge in anti-aging research in recent years. All across the globe, researchers are now exploring different methods to combat aging and extend human health span (the number of years of good health a person experiences).
The avenue that is arguably generating the most support involves telemores. These are the “caps” that sit on the ends of chromosomes. They provide protection for the DNA molecules, and their length has been linked to good health. Unfortunately, they shrink with every division until they can no longer protect the cell and it dies or damages surrounding cells through senescence.
So far, the research on telemores has been promising. Maria Blasco of the Spanish National Cancer Research Centre used gene therapy to extend the telemores in mice, which led to a 40 percent increase in lifespan.
Meanwhile Helen Blau, Director of the Baxter Laboratory for Stem Cell Biology at Stanford, modified the RNA of skin cells to increase telemore length. This caused the cells to divide up to 40 more times than their untreated counterparts did before dying or stagnating.
Another promising avenue of anti-aging research involved targeting senescent cells. These cells pump out chemicals as they deteriorate that are damaging to their neighboring cells, causing many of the diseases associated with aging, so researchers have been looking for ways to either inhibit their development or periodically purge them.
At the Mayo Clinic in Rochester, Minnesota, Darren Baker and his colleagues found that giving mice a drug that destroyed these cells delayed the development of the diseases of aging, as well as made the mice look plumper and younger.
At the slightly more unsettling end of the anti-aging treatment spectrum is the process of transfusing the blood of the young into the old. Despite the vampiric and macabre nature of the treatment, researchers have found evidence that it is effective. Individuals who receive blood from younger donors report health benefits, such as lowered cholesterol levels, while older mice have been shown to be rejuvenated by injections of blood from younger mice or even human teenagers.
While science is moving quickly toward a future in which aging and its consequences are obsolete, the few commercial means of receiving the treatments above are, at present, extremely expensive.
Liz Parrish is not a biologist by training, but she did enlist the help of scientists to develop the telemore-based treatment offered by her company, BioViva. Ostensibly, Parrish has developed an injection based on Blanco’s principles, and she herself is patient zero, having already injected herself with that telomere-extending treatment as well as one designed to preserve muscle mass. While BioViva hasn’t gone to market yet, Parrish told New Humanist that each injection costs between $200,000 to $400,000 to produce.
While no commercial means of senescent cell therapy exists as of yet, individuals can buy young blood transfusions. Jesse Karmazin’s company Ambrosia offers blood plasma transfusions for anyone willing to pay $8,000.
However, Stanford University neuroscientist Tony Wyss-Coray, who has conducted numerous experiments on mice’s reaction to young blood, thinks you’d be better off saving your money. He dismisses the science behind the treatment, telling MIT Technology Review that “people want to believe that young blood restores youth, even though we don’t have evidence that it works in humans.”
For the moment, anti-aging therapies are attainable in theory, but well out of financial reach for all except a wealthy few. Once the science is crystallized, however, the treatments should become exponentially cheaper, and a long, healthy life will be neither a pipe dream nor a hideously expensive commodity.
The post Researchers Are Finding Remarkable Ways to Combat Aging and Extend Human Health appeared first on Futurism.
Glaucoma is a devastating disease of the eye that is typically associated with aging. It’s the leading cause of blindness, along with cataracts, affecting 70 million people worldwide. Specifically, glaucoma comes from the deterioration of retinal nerve ganglion cells. There is currently no cure. For the first time, scientists at the Vision Institute (Sorbonne University) and the National Institute of Health and Medicine have prevented and reversed glaucoma in over 70 mice by injecting them with a single gene.
The ingenious gene that the scientific team injected into the glaucomatous mice is called Ngb, which codes for neuroglobin, a protein that is abundant throughout the brain and eye. Neuroglobin scavenges toxic reactive oxygen species (ROS) such as hydrogen peroxide, nitric oxide, and other radicals that corrode the body. It also protects the mitochondria — the cell’s smoky, ROS-ridden energy producer — in a host of ways. The Paris team showed how in glaucomatous retinal nerve cells, there is significant mitochondrial dysfunction as well as a 50 percent loss of neuroglobin. Unlike most other cells, they are highly dependent on mitochondria for energy supply, since they don’t have the fatty myelin sheath to insulate energy and boost synaptic signaling.
To deliver the Nbg gene into the mice, the scientists used an adeno-associated viral vector (AAV), a virus whose DNA has been removed and replaced with a gene of the scientist’s choice. The Ngb-filled AAV was then proliferated in the lab, and injected into the retina of 55 young mice (aged 2 months with a predisposition for glaucoma) and into 18 old mice (aged 8 months with developed glaucoma). The injected Ngb-AAV virus penetrated surrounding cells, and released its’ Ngb gene into the nuclei where unsuspecting RNA printed it into the eventual neuroglobin protein.
When the mice reached 12 months (their typical lifespan), the results were unprecedented: in all mice, Ngb neuroglobin doubled in their retinas. In mice treated at a young age, glaucoma never developed and their retinal ganglion cell numbers, visual cortex activity, and other vision markers were the same as that of young, healthy mice.
In mice that received the Ngb-AAV injection at the old age of 8 months, glaucoma was reversed: mitochondrial respiratory function, visual cortex activity, retinal cell function, and other vision markers were completely restored. Their retinal ganglion cell numbers, however, were the same as old healthy mice (only 34 percent of young healthy mice), indicating that the AAV didn’t replace cells that had died off with age.
Dr. Corral-Debrinkski, who heads the research team and is now based at the National Institute of Health and Medicine noted, “The data reached in this study is very promising not only for glaucoma but for many conditions in which mitochondrial function is impaired, including a wide range of optic nerve diseases and devastating neurological diseases such as cerebellar ataxias or leuokodystrophies.” Based on these results, her team plans to conduct human cell and primate studies before moving into human trials.
Over the last several years, adeno-associated viral vectors have been preferred over other vectors because of their lower immune response. AAV’s also tend to stabilize near chromosome 19, versus disrupting the DNA strand. They also cannot replicate with cell division. However, significant challenges remain: creating vectors that can avoid an immune response altogether, or can invade a large number of host cells, has not been easy. AAV’s are also tiny and can therefore only accommodate tiny genes. More research is also needed to determine long term toxicity. Even still, as scientists fine tune these masterful genetic envoys, unprecedented results have been achieved in such diseases as hemophilia B, sickle cell disease, muscle degeneration, and now vision.
The post Scientists Reversed Glaucoma in Mice With the Help of a Single Gene appeared first on Futurism.
Myalgic encephalomyelitis/chronic fatigue syndrome, or ME/CFS, affects at least one million Americans. The illness causes sufferers to feel incredibly sick with flu-like symptoms and a deadening sense of fatigue; one that sleep and rest never seems to banish entirely. Now, researchers from Stanford University may have found the key to creating a diagnostic laboratory test for the illness, and possibly the first treatment ever devised.
Symptoms of ME/CFS range from mild to disabling. Around one-quarter of patients are so sick that they’re confined to bed most or all of the time. The new research has uncovered a link between severity of symptoms and variations in multiple biological markers. The researchers tracked links between illness severity and specific cytokines, a kind of immune-signaling protein, rather than focusing on positive or negative results.
In the study of 192 ME/CFS patients and 392 controls, the concentrations of only two of 51 cytokines differed between the groups. However, the levels of 17 cytokines — 13 of which promote inflammation — varied dramatically between patients with mild and severe ME/CFS symptoms. This ties in with findings from previous studies which indicated that chronic inflammation plays a major role in ME/CFS. This research indicates that higher levels of inflammatory cytokines in the patient’s blood correspond with more severe symptoms.
Routine lab tests can miss ME/CFS because what they generally test for (sedimentation rate and C-reactive protein) have not been definitively linked to the disease. The Stanford team is currently developing a commercial diagnostic panel that would assess five of the 17 cytokines. The test alone wouldn’t be enough, however: interpretation of the results would rely heavily on a doctor’s assessment of the severity of patient’s symptoms.
The researchers are also hoping that their work will prompt others in the scientific community to pursue anti-inflammatory and immune-modifying therapies to treat ME/CFS. In recent years, the National Institutes of Health has increased research funding for ME/CFS, and a major drug trial investigating the efficacy of modifying drug rituximab for the treatment of ME/CFS is already underway in Norway.
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It turns out, writing about your investment ideas before actually putting money into them is a nifty strategy for ensuring success. It’s proven to work for British billionaire Jim Mellon, anyways. He hopes to continue the trend with his latest book, Juvenescence: Investing in the Age of Longevity, by using it as the jumping off point for a new biotech company with a focus on putting an end to aging.
Juvenescence Limited is a joint venture between Mellon and longevity researchers Gregory Bailey and Declan Doogan. Under that parent umbrella is Juvenescence AI, a joint venture with Alexander Zhavoronkov, CEO of Baltimore-based Insilico Medicine, Inc., a drug research company that uses artificial intelligence (AI) to explore ways to end aging and age-related diseases.
Research under Juvenescence AI will focus on examining cellular pathways to aging, as well as affecting change in the mitochondria and finding ways to clean senescent cells, which accumulate when the body grows old.
The team at Juvenescence isn’t just hoping to prolong life, however. As Doogan, a former executive at Pfizer, explained to Endpoints News, “Not just longer, but better longer. Healthy aging is the objective here.”
However, as with any drug development research, this process could take time, and Juvenescence Limited hopes to find a shortcut through their use of AI technology.
“We are excited by the potential for AI to streamline the longest and most costly portions of the drug development cycle: clinical trials,” Mellon said in a press release. “With Insilico Medicine’s help, we hope Juvenescence AI will both develop therapeutics that treat the diseases that plague all of us as we age and eventually treat the aging process itself.”
Bailey, the CEO of Juvenescence, sees the company as being positioned for great success in this endeavor: “We are at an inflection point for the treatment of aging. I think this is going to be the biggest deal I’ve ever done.”
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For a phenomenon that affects all living beings, there’s nothing simple about aging. Experiments that focus on understanding aging are as numerous and varied as the aspects of the subject itself. Some look at the roles that the brain or the mitochondria have on aging, while others examine some protein or another. A study from the Houston Methodist Research Institute (HMRI) is focusing on chromosomes.
Specifically, the team led by cardiovascular sciences department chair John Cooke, looked at telomeres — the region located at the tip of every chromosome, the length of which supposedly corresponds to age. Cooke’s team studied the cells of children with a fatal genetic disease called progeria that causes rapid aging.
In their study, published in the Journal of the American College of Cardiology, the researchers discovered that extending the shortened telomeres effectively halted aging in the isolated sample cells taken from the patients with progeria. “What we’ve shown is that when we reverse the process of the telomere shortening in the cells from these children and lengthen them, it can reverse a lot of the problems associated with aging,” Cooke said in an HMRI press release.
Cooke’s team isn’t the first to associate telomeres with aging. The field, however, isn’t considered that precise yet. Medical genetics professor Peter Lansdorp at the University of British Columbia told Motherboard that there’s still a lot to learn in this area. “It is not hard to find a 70-year-old with longer telomeres than a teenager,” he said, noting that the decline in telomeres works as a “tumor suppression mechanism” for the body.
Furthermore, since the study was limited to cell samples — taken from just 17 patients — on a lab dish, the researchers still need to see if it could work in cells functioning inside the body. The next step is to deliver the same treatment directly into patients, beginning with children suffering from progeria.
Still, Cooke is hopeful. “We can at least stall or slow down accelerated aging, and that’s what we’re working toward,” he said in the press release. “I want to develop a therapy for these children. It’s an unmet need.”
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Scientists in Sweden and the U.K. developed a surgical technique to reconnect the spinal cord with sensory neurons after traumatic spinal injuries. Now, by recreating the technique in rats, they have new insights into the cellular processes implicated in the technique. This new knowledge has the potential to assist the development of novel therapies for other spinal cord injuries — even those in which the spinal cord is severed.
The spine is the point of connection between the brain, sensory neurons (which transmit sensory information such as temperature, pain, and touch), and motor neurons (which control the muscles). At junction point between the spinal cord and both types of neurons, bundles of motor neurons form “motor roots” connecting with the cord, and sensory neurons create similar bundles called “sensory roots.” Traumatic injuries, including severed spinal cords, can tear both motor and sensory roots — when they do, the brain loses control of the connected neurons.
To date, it has been relatively simple for surgeons to implant new motor roots where they were torn, prompting them to reconnect, usually successfully. However, this kind of repair for sensory roots has been more problematic — that is, until this recently developed procedure, in which the original sensory nerve cells are cut and removed from the root and the remaining root itself is placed directly into the spinal cord in a deeper structure.
This area, called the dorsal horn, contains secondary sensory neurons that typically don’t connect directly to sensory roots. However, the technique achieved the return of some spinal reflexes in patients, proving that the implanted neuron did form a functional neural circuit with the spine after all.
In a more recent study published in Frontiers in Neurology, some of the same collaborators began working with rodents to try to understand how and why the new procedure worked. The team was able to study the technique and its mechanisms at the cellular level using a rat model of spinal injury.
After severing the spinal cords of the rats surgically, the researchers used the new technique to reattach the sensory roots. Between 12 to 16 weeks after surgery, the researchers tested the neurons with electricity to assess whether they formed a complete neural circuit. They also analyzed the rats’ neural tissue microscopically.
The electrical tests were positive, revealing a complete neural circuit and an integrated root. The microscopic analysis of the dorsal horn showed that small neural offshoots sprouted from the dendrites at the end of neurons inside the dorsal horn and spread into the implanted sensory root, resulting in a complete, functional neural circuit.
If the technique is working in the same way for humans as it did in the rats, the researchers are hopeful that encouraging new growth from spinal neurons might hold promise for repairing other kinds of nervous system and spinal cord injuries, including cases of severed spinal cords — without having to use any “secret glue.”
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TurnAid is a bed system that rotates disabled patients with ease.
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After 25 laborious years of scientific study, researchers in Finland have finally found a connection between viral infection and the onset of Type 1 Diabetes.
The post The First Vaccine for Diabetes Could Be Ready for Human Trials in 2018 appeared first on Futurism.
MIT and Singaporean researchers have developed and deployed a self-driving wheelchair at a hospital.
Scientists at Columbia University discovered during a study published in the journal Hippocampus that the memories of mice with Alzheimer’s disease can be recovered optogenetically — meaning with the use of lights. This could shift our understanding of the disease from the idea that it destroys memories to the concept that it simply disrupts recall mechanisms.
The results were garnered by comparing healthy mice with mice given a disease similar to human Alzheimer’s. First, parts of mice’s brains were engineered to glow yellow during memory storage and red during memory recall. Then, the mice were exposed to the smell of lemon followed by an electric shock — associating the two memories.
A week later, they were given the smell of lemon again: the healthy mice’s red and yellow glows overlapped and they expressed fear, showing they were accessing the right memories. However, the Alzheimer’s brains glowed in different areas, and the diseased mice were indifferent, showing they were recalling from the wrong sections of the brain.
The team, lead by Christine A. Denny, then used a fiber optic cable to shine a blue laser into the mice’s brains. This successfully “reactivated” the lemon and electric shock memory and caused the mice to freeze when they smelt it.
The research could possibly revolutionize Alzheimer’s research and treatment, helping the 5 million Americans who are suffering from the disease. Ralph Martins at Edith Cowan University in Australia told New Scientist that “it has the potential to lead to novel drug development to help with regaining memories.”
However, the crucial question is whether mice brains and the artificial Alzheimer’s disease that the team exposed them to are sufficiently similar to the human variant for the results to be medically significant. In particular, humans loose more neurons than mice during the course of Alzheimer’s, and it would be extremely difficult to target specific memories because our brains are far more complicated.
While further studies must be done, these findings are one of many promising avenues that are currently being developed in Alzheimer’s research. Artificial intelligence is being applied to the condition and has successfully predicted who will develop Alzheimer’s 10 years out, the leukemia drug nilotinib has been shown to help combat the condition — and finally, a “metabolic enhancement for neurodegeneration” treatment has also reversed some of its symptoms.
The post New Evidence Suggests Alzheimer’s Doesn’t Destroy Memories, it Only Blocks Them appeared first on Futurism.
Scientists have come up with a potential new way to treat neuroblastoma, the most common kind of cancer in infants, by targeting it with nanoparticles loaded up with an ingredient of the spice turmeric.
Turmeric is more often used to add flavour to curries, but the curcumin chemical it contains has shown promising progress in tests in destroying neuroblastoma tumour cells resistant to other drugs.
If scientists can work out how to adapt this into a full and safe treatment, it would have the benefit of being less toxic and unpleasant for patients than traditional alternatives like chemotherapy – which is especially important when you’re dealing with young kids.
“High-risk neuroblastoma can be resistant to traditional therapy, and survival can be poor,” says lead researcher Tamarah J. Westmoreland, from the University of Central Florida.
“This research demonstrates a novel method of treating this tumour without the toxicity of aggressive therapy that can also have late effects on the patient’s health.”
Using curcumin to fight cancer isn’t a new idea, but it’s difficult to get the chemical into drugs because of its low solubility and poor stability. Nanoparticles could fix that.
During the study, cerium oxide nanoparticles loaded with curcumin and coated in dextran were shown to cause “substantial” cell death in neuroblastoma cells while having little impact on healthy cells – the perfect combination for a cancer drug.
Even better, the nanoparticles were more effective against the type of cells usually most resistant to conventional drugs, those with an amplification of the MYCN gene.
As neuroblastoma is usually very difficult to treat, that’s a promising start for these spicy nanoparticles. This type of cancer normally takes root near the kidneys, striking 700 people per year in the US, most of whom are under 5.
Not only is it largely resistant to anti-cancer drugs, it’s also known to cause health problems after successful treatment, including hearing loss and other disabilities. It also often returns after treatment.
If we can develop an effective nanoparticle approach to fighting neuroblastoma, it would be yet more evidence of the potential of treating disease at the smallest possible scales: nanoparticles have previously been shown to help kickstart the human immune system to help fight cancer, for example.
Other recent research has looked at how nanoparticles can better target tumours in the brain by squeezing through the blood-brain membrane barrier, as well as reaching other places that conventional drugs can’t get to.
The next step for the researchers behind the latest study is to see if the same positive effects can be observed in animal trials as well as lab tests.
“We are hopeful that in the future, nanoparticles can be utilised to personalise care to patients and reduce the late effects of therapy,” says Westmoreland.
The research has been published in Nanoscale.
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One of the more controversial subjects in professional sports is the possible relationship between time spent playing American football and the development of chronic traumatic encephalopathy (CTE), a degenerative disease caused by repeated blows to the head. The symptoms of CTE, which sometimes don’t present until years after play has stopped, include depression, confusion, memory loss, and dementia.
To explore this potential link, Dr. Ann McKee, chief of neuropathology at the VA Boston Healthcare System and director of the CTE Center at Boston University, examined the brains of 202 deceased former football players. The results of her study, which was just published in The Journal of the American Medical Association, reveal a sobering connection.
At death, the median age of the 202 deceased former football players studied was 66 years old, and of those studied, 177 had a neuropathological diagnosis of CTE. Neither of the two players who quit before high school and only three of the 14 who played in high school (21 percent) received a positive diagnosis, but the rate went up significantly from there.
Forty-eight of the 53 college players (91 percent), nine of the 14 semiprofessional players (64 percent), and seven of the eight Canadian Football League players (88 percent) all appeared to have CTE. Of the 111 National Football League players studied, all but one had a neuropathological diagnosis of CTE (99 percent).
Dr. McKee pointed out that her sample is certainly not random. “There’s a tremendous selection bias,” she mentioned to The New York Times, explaining that many of the donated brains were probably donated specifically because the former players showed symptoms of CTE prior to death.
However, a diagnosis for 110 of 111 brains remains highly significant. As The New York Times’ writers pointed out, “About 1,300 former players have died since the B.U. group began examining brains. So even if every one of the other 1,200 players had tested negative — which even the heartiest skeptics would agree could not possibly be the case — the minimum CTE prevalence would be close to 9 percent, vastly higher than in the general population.”
The neuropathological severity of the CTE varied depending on levels of play. The longer a player stayed with the sport, the more likely they were to experience more severe CTE. A major difference existed between high school and college players, with mild pathology among all three former high school players and severe pathology among the majority of former college players (56 percent). Severe pathology was also present in the majority of semiprofessional players (56 percent) and the vast majority of professional players (86 percent).
Mild CTE pathology is still significant. Among the 27 participants who had mild CTE pathology, almost all suffered from behavioral symptoms, mood symptoms, or both (96 percent). A huge majority of those experienced cognitive symptoms (85 percent), and about a third experienced signs of dementia (33 percent).
Unsurprisingly, the outlook was grimmer for the 84 participants with severe CTE pathology. Eighty-nine percent had behavioral symptoms, mood symptoms, or both; 95 percent had cognitive symptoms; and 85 percent had signs of dementia.
These results lead us to some inevitable questions. First, since the chances of developing CTE increase the longer one plays football, will parents start to feel differently about their children playing the sport? Will adult football players feel differently?
At least one player already does. John Urschel of the Baltimore Ravens, who is also an applied mathematics PhD candidate at MIT, announced his retirement from football at age 26 on July 27, two days after the study was published. Sources told ESPN that he was concerned about the study’s findings.
Undoubtedly, Urschel is not the only player to give the results of the study serious consideration, but will others follow his lead and step away from the sport (even if it means leaving money on the table)? Moreover, given that only one of the 111 NFL players studied didn’t have CTE, will Americans begin to feel differently about watching football and force the league to change how the sport is played?
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Doctors and patients all over the world have long followed the same wisdom when taking antibiotics: it’s important to finish the entire course prescribed. Stopping midway through a course of prescribed antibiotics is said to give bacteria breathing space, which can allow it to mutate and develop immunity to the drug. Researchers from the Brighton and Sussex Medical School (BSMS) are challenging the age-old wisdom with the results of a study that showed this may not necessarily always be the case.
The team, led by Martin Llewelyn, published their findings in the British Medical Journal, asserting there’s no evidence to support the long-held notion. “While the ‘complete the course’ message is one we all know, we have found that it is time for this message to change,” Llewelyn said in a BSMS press release. “The belief that stopping antibiotic treatment increases the risk of antibiotic resistance is not supported by evidence. In fact, this risk is actually increased by taking antibiotics for longer than is necessary.”
The researchers did, however, acknowledged that there are diseases (like tuberculosis) where bacteria can develop antibiotic resistance when not exposed to drugs for a long enough period. However, the most common bugs like E.coli and Staphylococcus aureus, are more likely to become superbugs the longer they are exposed to antibiotics.
Antibiotic or antimicrobial resistance is a growing concern that is becoming increasingly more widely acknowledged within the medical community. In fact, the United Nations has already elevated the issue to the level of a health crisis. In the United States alone, about 2 million people become infected with antibiotic resistant bacteria each year. Some 23,000 of those patients die as a result.
A number of studies have been launched in attempts to find a solution to this crisis. One team has turned to gene-editing, using CRISPR to delete antibiotic resistant strains of bacteria. Another recent study suggested tracking which genes could potentially turn pathogens into superbugs; data which the ream hoped could be used to help develop a new types of antibiotics.
Meanwhile, the new BSMS research suggests a change in mentality may be what’s required — and several other experts agree. Still, further research is required before any official prescribing guidelines could be updated.
Of course, not everyone in the medical community agrees that they should be: chair of the Royal College of GP’s Helen Stokes-Lampard urged caution, however. “We are concerned about the concept of patients stopping taking their medication midway through a course once they ‘feel better’, because improvement in symptoms does not necessarily mean the infection has been completely eradicated. It’s important that patients have clear messages and the mantra to always take the full course of antibiotics is well known,” she told The Guardian. “Changing this will simply confuse people.”
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A two year trial has shown that monthly antiretroviral therapy (ART) injections are as effective at keeping HIV under control — defined as having less than 50 copies of the virus per millilitre of blood — as a daily pill. Of the 286 people who took part in the trial, 269 (94 percent) achieved the desired effect, in contrast to 84 percent of people who used daily pills.
The treatment is a combination of cabotegravir and rilpivirine, which are both antiretroviral drugs — they do not kill or cure the virus but block its growth. After being injected into the buttock, they collect in between muscle fibers where they slowly flow out over the course of a number of weeks. Peter Williams, who helped to lead the project and is part of the pharmaceutical firm Janssen, told New Scientist that “a single dose can last for 48 weeks or more.”
This news was revealed at a conference for the International Aids Society in Paris by Joseph Eron, Director of the Clinical Core at the UNC Center for AIDS Research.
HIV effects 1.1 million people in the US alone, and so any developments in treatment help a huge amount of people. Mahesh Mahalingam, of the United Nations Programme on HIV/AIDS, explained to the New Scientist that “it will help remove the challenge of taking tablets every day and significantly improve the quality of life of people living with HIV.”
Recently, scientists have used cows to determine how the virus invades the human immune system by encouraging the release of broadly neutralizing antibodies; the key to defeating HIV. Additionally, at the same conference that the injection was announced, Anthony Fauci, part of the US National Institute of Allergy and Infectious Diseases, asserted that a nine-year-old South African child was “virtually cured” of the disease due to treatment he had soon after being born.
In particular, due to it being a monthly injection vs a daily treatment, this therapy will help people who live in areas where there is a taboo against HIV. Instead of having to have seemingly constant refills and treatments, it can be a monthly affair that is more easily managed, especially in difficult circumstances.
This development is one of many avenues of exciting new research concerning HIV, some of which could contain the seed that one day grows into a full-blown cure.
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Researchers at the Albert Einstein College of Medicine in New York have successfully tested a new procedure on mice that could help keep age-related diseases, and even aging itself, at bay. Reporting their findings in the journal Nature, the researchers discovered the crucial role the hypothalamus —the region of the brain responsible for the body’s hormonal and metabolic processes— plays in aging.
“Our research shows that the number of hypothalamic neural stem cells naturally declines over the life of the animal, and this decline accelerates aging,” led researcher Dongsheng Cai said in a press release. They found, however, that the process isn’t irreversible.
In order to figure out if the disappearance of stem cells was caused by (or due to) aging, they injected mice with a toxin that killed 70 percent of their neural stem cells. “This disruption greatly accelerated aging compared with control mice, and those animals with disrupted stem cells died earlier than normal,” Cai explained.
In a second experiment, the researchers implanted stem cells ready to become fresh neurons into the brains of older mice. This extended the life of the mice by 10 to 15 percent, and kept them physically and mentally fit for several months.
Previously, other researchers have hinted at the role the hypothalamus has in aging — though it has never before been pinpointed quite so clearly. Cai’s team seems to have provided the missing link, which could significantly pushed anti-aging research forward. “It is a tour de force,” David Sinclair at Harvard Medical School told The Guardian. “It’s a breakthrough. The brain controls how long we live.”
Research in the field of aging has increased over the last several years as scientists warm up to the idea that aging itself is a disease that can, and should, be cured. Perhaps not surprisingly, a lot of these potential treatments have a basis in some function of the brain. One study examines the mitochondria, while others look at drugs that are already being used to treat the effects of aging. One study is even going so far as to explore the anti-aging potential of transfusions using young blood.
For Cai’s research, the next step is to test the procedure on humans, and the team wants to begin clinical trials soon. However, that may be a ways off yet. “Of course humans are more complex,” Cai said, also speaking to The Guardian. “However, if the mechanism is fundamental, you might expect to see effects when an intervention is based on it.”
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Cancer is often difficult to treat because it’s not detected in time. That there are more than 100 types of cancer, each with various possible causes, doesn’t help. This is why a team of researchers led by the National Cancer Center Japan (NCC) in Tokyo, together with Toray Industries, Inc., and other institutions, want to change things. They’ve developed a new method that could detect 13 different cancer types using just a single drop of blood.
The novel method detects differences in the microRNA (miRNA), which can be secreted by cells into the blood as a way to communicate with other cells, between healthy cells and cancer cells. Using just one drop of blood, the test may be able to detect cancers in the breast, lung, stomach, colorectal tract, esophagus, liver, and pancreas.
In a lab test using preserved blood samples from 40,000 patients, the researchers were able to identify miRNA specific to each type of cancer with more than 95 percent accuracy. The researchers noted, however, that the miRNA could have changed while the blood was preserved. As such, clinical tests planned for August would use fresh blood from 3,000 people.
While there are a number of studies in using blood to detect cancer, the Japanese team’s method is the first that’s known to be capable of diagnosing multiple types with a single test, The Japan News reports. This could potentially improve a patient’s chances of being properly diagnosed, while at the same time eliminating the need for separate tests.
“Patients will not need to take multiple tests. In the future, it will become possible to identify cancer stages and characteristics,” said Yet Takahiro Ochiya, head of the Molecular and Cellular Medicine Division at the NCC’s Research Institute, The Japan News reported.
In the same report, Masahiko Kuroda, chief of the Molecular Pathology Department of the Tokyo Medical University, added, “In Europe, research aimed at early detection of diseases using miRNA is being actively pursued, but there haven’t been any studies where analysis was conducted on so many patients like this one. So this should prove very useful.”
The Japanese researchers got a go-ahead to proceed to clinical tests from the NCC’s research and ethics screening committee sometime in the middle of July. They plan on applying for government approval next, which could open their method for practical use in the next three years.
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Amazon is arguable a leader in both the retail industry and the digital market. Leveraging on both strengths, the e-commerce giant is now looking to secure a firm spot in the $3 trillion healthcare industry by setting up a rather stealthy lab called “1492.” It’s a name that seems to be a reference to the year Christopher Columbus stumbled upon the Americas (never mind that Columbus actually brought a host of diseases the New Word was then unfamiliar with).
Sources familiar with the development told CNBC that the new project is based in Seattle, where it would explore opportunities in healthcare technologies. CEO Jeff Bezos previously mentioned how the Echo and Alexa could be tools for both patients and healthcare providers. Bezos has also been clear about how Amazon is banking heavily on artificial intelligence (AI) and machine learning technologies.
Amazon is currently looking for prospective talent to join this team. CNBC reported that there were jobs posted such as a UX designer and a machine learning director that were listed under “a1.492” or “The Amazon Grand Challenge a.k.a. ‘Special Projects’ team.” However, these posts seem to have been taken down from Amazon’s site, although Amazon’s “a1.492” project is still listed on at least one Seattle-based LinkedIn profile.
The secret healthcare project would build on Amazon’s machine learning and data analytics expertise, as well as the familiarity some doctors already have with Amazon’s AI assistant Alexa. It’s not clear whether Amazon would develop new health devices, though, and the company has not responded to CNBC’s request for comment or released a formal statement.
Through 1492, Amazon could be planning to develop a platform that simplifies accessing medical records and patient data — similar to, perhaps, Google’s DeepMind Health. Data could then be made available using the Echo and other Amazon devices. The secret lab is also possibly developing health apps for these and a telemedicine system to connect doctors and patients.
Apart from 1492, Amazon also has other efforts in the works. According to CNBC, Amazon’s also beefing up its cloud services for hospitals through the Amazon Web Services and by investing in a startup called Grail.
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Every year, the world around us moves a little faster, and it’s easy to stumble and get stressed out as we try to catch up with it. Almost every fifth person in the United States has an anxiety disorder, costing the country more than $42 billion a year. Nearly half of those who suffer from depression are diagnosed with an anxiety disorder as well.
While sufferers would be wise to reach out to professionals for help, they can also take certain measures on their own to improve their everyday lives. The following tools may not be as effective as consulting a professional, but they could certainly lead to a less anxious and stress-free life in the future.
Virtual reality (VR) isn’t just for gamers — it can be used as a tool to reduce anxiety and curb the effects of Post Traumatic Stress Disorder (PTSD) as well.
By transporting the user to another time and place inside a virtual 3D-rendered environment, researchers are trying to send PTSD sufferers mentally back to the scenes that first triggered their anxieties and fears. In other clinical trials, virtual reality technology is being used to recreate a setting with a private therapist sitting across from the patient.
The Berkeley Well-Being Institute is trialing its own anxiety-reducing VR method by relaxing the patient through “virtual wellness,” a suite of apps that range from deep-breathing exercises to star flight simulations.
Meditation has been a common practice for thousands of years. Its history is intricately bound to religious practices, but secular forms have become increasingly popular as a way to relax and reduce anxiety.
The popular app Headspace has been developing its own technique through the science of mindfulness. According to their website, “a number of studies […] have initially found that online mindfulness training does produce results similar to in-person training.”
Not only can app-based mindful meditation reduce anxiety, it can sharpen your concentration at work and help you sleep better.
The idea of a weighted blanket aiding in reducing stress and anxiety is a proven concept. Weighted blankets such as the Gravity Blanket have been shown to increase serotonin and melatonin levels, helping users relax and sleep.
The Gravity Blanket is made of high-grade microfiber on the outside for an exceptionally soft feel and maximized comfort. Users will never miss a minute of sleep again.
Rather than reaping the benefits of meditation through an interactive app on a smartphone, a company called Muse is trying to help sufferers reduce anxiety with the aid of a sensing headband. The Muse headband uses EEG-neurofeedback sensors to guide a wearer step-by-step through customized meditation programs.
HeartMath’s emWave2 promises increased athletic performance and a reduction of stress by providing users with real-time heart rhythm feedback. The idea is to be able to act upon this information immediately, thereby “balancing your mind, body, and emotions.”
The Thync wearable is designed to help users overcome negative thoughts and anxiety with daily sessions that last for 10 minutes.
According to their website, the Thync uses low levels of electrostimulation to “activate specific nerve pathways on the head and neck.” The science behind the technology has been developed by a team of neuroscientists from MIT, Harvard and Stanford over the last five years.
Imagine yourself inside a completely dark pod, floating in a pool of high salt content water. Feeling relaxed yet?
The so-called sensory deprivation tank treatment is burgeoning into a cult phenomenon of sorts, and the idea behind it is simple: spend 45 to 90 minutes inside the tank without any external stimuli.
The treatment is said to reduce stress and anxiety, enabling you to forget the hardships of everyday life — assuming you aren’t claustrophobic, that is.
Cryotherapy — spending about three minutes in a -151.1 degree Celsius (-240 degree Fahrenheit) chamber — is no longer reserved for top-level athletes. It’s supposed to help burn calories and leave you in a relaxed state, figuratively freeze-burning the stress away.
A new study published in Scientific Reports has revealed a link between depression and the structure of white matter in the brain, which we use to process our emotions and thoughts. The research, which was conducted by the University of Edinburgh, Scotland, analysed data from 3,461 people in the U.K. Biobank database, making it the largest study of its kind in history.
The scientists used diffusion tensor imaging — which is based on magnetic resonance imaging (MRI) — to create highly detailed maps of the fibers in the brain. When they compared depression sufferers to healthy individuals they realized that there were substantial differences in the “integrity” (or “quality”) of the white matter.
Heather Whalley, who led the team, said in a Biobank press release that “there is an urgent need to provide treatment for depression and an improved understanding of it[s] mechanisms will give us a better chance of developing new and more effective methods of treatment. Our next steps will be to look at how the absence of changes in the brain relates to better protection from distress and low mood.”
Depression is epidemic in today’s society, with 40 million adults — 18 percent of the population — being affected in the U.S. alone. However, only a third of people suffering from anxiety related disorders receive treatment. Research like this study is pivotal to improving the quality of millions of lives by uncovering the physical causes of the disorder.
The study adds to a growing body of research that supports the understanding that depression as a physical condition rather than a chemical or purely psychological one. This has instigated a fundamental change in the way depression is treated.
For example, researchers at UCLA have begun to use magnetic pulses to target the specific parts of the mind that are associated with depression — “actually changing how the brain circuits are arranged, how they talk to each other” as the press release stated.
In order to fight depression these types of research are crucial — let us all hope one of them leads to a cure capable of helping millions.
The post New Study Reveals That The Brains of People With Depression Look Different appeared first on Futurism.
At the on-going Paris conference of the International AIDS Society (IAS), a team of scientists is presenting details of a remarkable development that could improve HIV treatment. The case is that of a nine-year-old South African child who was infected with HIV at birth. After receiving a burst of treatment soon after being born, the child has since been free of any symptoms or active signs of the menacing virus without any further treatment.
HIV, which is known to affect more than 36.7 million people worldwide, is one of the deadliest viruses around today — since it was discovered, it’s taken the lives of more than 35 million victims, according to the World Health Organization. This South African case, however, is a glimmer of hope.
“[T]his new case strengthens our hope that by treating HIV-infected children for a brief period beginning in infancy, we may be able to spare them the burden of lifelong therapy and the health consequences of long-term immune activation typically associated with HIV disease,” Anthony Fauci, director National Institute of Allergy and Infectious Diseases (NIAID), told The Guardian.
While the doctors report detecting tiny fraction of immune cells that still have the virus integrated into them, the child’s immune system remains healthy, and there is no sign of HIV infection.
The South African child was part of a NIAID-funded trial in 2007 for treating infants with HIV. Scientists and doctors, however, have yet to understand why and how the 40-week treatment (which was also given to 142 other children) worked for this child, whose identity remains anonymous.
“We don’t believe that antiretroviral therapy alone can lead to remission,” Avy Violari, pediatric research head at the Perinal HIV Research Unit in Johannesburg, told the BBC. “We don’t really know what’s the reason why this child has achieved remission — we believe it’s either genetic or immune system-related.”
Still, the mere fact that something like this is possible is a cause for hope. Unlike other cases where supposedly cured infants later on demonstrated latent HIV in the immune system, this South African case is the third reported “virtually cured” child. Speaking to The Guardian, Caroline Tiemessen from Johannesburg’s National Institute of Communicable Diseases said, “By further studying the child, we may expand our understanding of how the immune system controls HIV replication.”
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While often misrepresented in the media, schizophrenia is a disease that can have a major impact on the lives of those living with it. Around the world, 21 million people are currently living with the mental illness, the symptoms of which can include paranoia, auditory and visual hallucinations. These symptoms can be severe and debilitating, and can impact every aspect of a person’s life. According to the World Health Organization (WHO), schizophrenia is defined by “profound disruptions in thinking, affecting language, perception, and the sense of self.”
An international team of researchers has found that these life-altering symptoms could be caused by defects in glial cells, the cells that support and insulate nerve cells. By using mice with brains colonized by human-donated glial cells, the team’s discovery could greatly impact the future diagnosis and treatment of schizophrenia.
Lead researcher Steve Goldman, from the University of Copenhagen and the University of Rochester, stated that “It was through studies of mice with human glial cells that we succeeded in testing how dysfunctional glial cells may cause abnormalities in the formation of the brain’s neural networks, which may in turn cause severe anxiety, anti-social behaviour and severe sleep problems.”
Living with schizophrenia can present many challenges for patients, and to further complicate matters, the antipsychotic medications used to treat the mental illness often lead host of side effects themselves: ranging from severe restlessness to the onset of Parkinson’s disease.
The side effects of many conventional, readily available treatments are so severe that patients sometimes discontinue or avoid treatment altogether. As is the case with most neurological diseases, there isn’t likely to be one single cause for the disease — nor a single cure-all. But this discovery marks hopeful progress towards better treatment.
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Throughout the course of human history we’ve developed marvelous means to protect ourselves from illness and injury: ailments and afflictions that once commonly took lives are now a thing of the past, are easily treatable and preventable through modern medical science — and some scourges have been downright eradicated. The one thing we have no seemed to get a handle on – that will ultimately be fatal for humans even if specific diseases are not — is time. Our centuries-long quest for the fountain of youth has led us from myth to magic and now, into the science lab where researchers are unlocking the mysteries of aging — and perhaps getting closer to not only stopping it, but reversing it.
Through DNA, researchers have been able to identify the genes responsible for aging. The genes that are the culprits in human aging can then be manipulated using advanced technologies like CRISPR, with remarkable success. Others are using “young blood” to revitalize the old. Some are harkening back to the legends of our ancestors, who also attempted to devise ways to address the problem of aging: today, researchers are developing anti-aging treatments based on everything from cannabis to a bacteria native to Easter Island.
In recent decades, science and technology has advanced so rapidly that, while human beings may still be inevitably aging in the interim, the prospect of solving the problem of aging is closer in reach than it’s ever been before: back in December of 2016, researchers at the Salk Institute successfully reversed the process of aging in mice and predicted that they would be ready for human trials within ten years. The research at the Salk Institute not only made the mice look younger, it extended their lifespan by an average of 30 percent. This was similar to findings from research by the Buck Institute for Research on Ageing and the University of Washington back in 2015 which found that through deleting particular genes in yeast they could extend the organism’s lifespan by up to 60 percent.
The science at work not just in this altered course of human aging, but the natural course is well, is epigenetics. Throughout life, our genes can be altered in a number of ways; often by things we’re exposed to as a result of our environment (pollution, for example) or lifestyle (like cigarette smoke). As our genes change, so do our bodies —and so do we. Whether it means we develop a condition for which we had a genetic predisposition all along, or we are acquire one our bodies are not able to recover from, these epigenetic changes provide clues as to why, and how, these processes take place. They are also, then, where we are most likely to find the answers we need to stop or reverse them altogether.
Juan Carlos Izpisua Belmonte, an expert in gene expression at the Salk Institute, put it rather frankly when he spoke to Scientific American: “Aging is something plastic that we can manipulate.” The question for researchers was how to do that — and the answer, it turned out, was through transforming adult cells back into an earlier state; a much earlier state. Embryonic, in fact. At this stage, cells possess the capacity to differentiate into any type of cell in the body, which has made them the focus of stem cell research.
At Harvard University, Dr. David Sinclair and his team of researchers determined that an anti-aging compound called nicotinamide adenine dinucleotide (NAD+) was found more frequently in younger mice than older ones. NAD+ is an important part of how our DNA repairs damage — which can occur for a multitude of reasons, including being a somewhat natural part of the cellular division process. The magical DNA-repair compound, PARP1, responds to levels of NAD+ in the body: the higher the NAD+, the more PARP1. Younger people, like mice, have more and our levels decrease as we age — meaning it becomes harder for our DNA to repair itself. That, in turn, leads to aging, illness, and all the other physical inevitabilities of humanhood.
With that in mind, and following the logic behind it, Sinclair and his team gave older mice more NAD+, and soon the older mice began to look younger — biologically, anyway. Sinclair explained the findings to TIME back in March, saying that after the treatment, “We can’t tell the difference between the tissues from an old mouse that is two years old versus a young mouse that is three to four months old.”
Sinclair’s work throughout his career as a molecular biologist has been focused on aging — which he calls “the gravity of life” — and as he told The Washington Post in 2015, he’d like to apply the research he’s lead at Harvard to the development of a drug — an anti-aging pill, in fact. That could conceivably make the possibility of turning back the biological clock closer than ever for those of us alive (and therefore aging) today. Futurism polled readers about when they believed we’d be able to reverse aging, and nearly 40 percent thought we’d be able to achieve it between 2030-2040 — but nearly a quarter of readers thought we may never be able to. Or, at the very least, that it may be impossible to predict: “Anything past the year 2030 is most likely unpredictable,” responded , who pointed out “If our current predictions of Artificial Superintelligence are on par, then we should have achieved this by 2029.” But even if it’s impossible to predict, that doesn’t mean its impossible to achieve: “Giving it one full year to enhance and optimize itself, it can supercharge humanity beyond our wildest dreams in 20 years at most. So yes, achieving immortality is quite literally within our grasp.”
See all Futurism predictions and make your own predictions here.
By the year 2050, it’s anticipated that in the U.S. alone, 5 million people will be diagnosed with Type 1 Diabetes (T1D). This autoimmune disease, which affects children and adults, is currently unable to be prevented or cured. In order to manage T1D, people with the condition must constantly monitor their blood glucose levels, and manage those levels through insulin injection, activity, and diet in order to avoid life-threatening complications.
It has been suggested, for quite some time now, that T1D could be related to viral infection, which has lead some to propose the possibility of creating a vaccine for the disease. In Finland, researchers have been exploring this connection and potential vaccine for approximately 25 years. After such a laborious scientific journey, they believe they’ve found the viral group that can trigger T1D. The hard work seems to have paid off — as the team has created a prototype vaccine which will move into human clinical trials by 2018.
While it’s unlikely that the vaccine would become an immediate cure-all T1D, if the trials prove successful, it will dramatically shift the future of the disease. Up until this point, patients with T1D have been required to vigilantly self-manage. Complications of the disease, which can result when it goes undiagnosed or is ineffectively managed, can range from heart attack to stroke, amputation, kidney failure, and even blindness.
The threat of these complications constantly hangs over the heads of those with T1D. Unfortunately, as the team notes, this vaccine would not be a cure for T1D, but if it proves successful in preventing the onset of the condition, it could change the lives of millions of people around the world.
The post A Vaccine for Type 1 Diabetes is Headed for Human Trials in 2018 appeared first on Futurism.
In a new paper published by Science, Alexey Kondrashov, Professor of Ecology and Evolutionary Biology at the University of Michigan, along with the co-authors of the study, have proposed that a discrepancy between the predicted amount mutations in a species and the actual number is explained by sexual intercourse compounding mutations. When mutations combine and interact, it expedites the time it takes for natural selection to work against negatively mutated individuals.
The study first calculated the theoretical mutation rate of humans and wild fruit flies. Then, it amassed data from around 2,000 people and around 300 flies, in order to ascertain the proportion of real-world individuals with mutations. They found that the real world ratio was far lower than the theoretical one.
Shamil Sunyaev, a co-director of the project, told Phys.Org that this lead them to believe that “natural selection against highly damaging genetic mutations is ongoing in humans, and that it is aided by synergistic interactions between different parts of the human genome.” Essentially, mutation does not work in isolation, but different mutations can impact and worsen each other.
Mashaal Sohail, lead author on the study, went on to state that “sex had to come about in a species such as our own to allow for more effective natural selection because the mutation rate is too high to sustain otherwise.” Sex is the mechanism through which we combine mutations and therefore speed up the rate at which these mutations are eliminated, as they are exposed to other mutations that increase their effect.
This phenomena is called synergistic (or narrowing) epistasis, and the researchers concluded that it is has a more positive evolutionary effect than asexual reproduction, as it allows an organism to eliminate multiple mutations — that are the result of sexual genome mixing — in the death of a single organism that is no longer able to reproduce — or even reach the reproductive stage — due to stacked mutations.
The implications of this study are twofold. First, it gives a causal mechanism that explains why humans continue to reproduce at such a rapid rate — a key question in the field of population genetics. According to the study, rapidly multiplying may in fact be an efficient means of mutation purging.
It also explains why there were fewer people and flies with lots of detrimental mutations. Natural selection continues to exert its influence in a world of effective medicine and adequate infrastructure.
The study, if it proves correct, would change the previous concept of genetic mutations, which saw them as manifesting and being purged on a micro level, with each being eliminated one by one.
This shift in perception towards a synergistic model has serious ramifications on the theories behind gene editing processes like CRISPR. CRISPR functions according to the logic of the micro alteration proposed above, making individual changes in the genome with the hope of altering one aspect or mutation.
This finding shows, however, that genes work in synchronicity, and therefore an alteration in one could be the first domino to fall in a chain reaction, leading to wholly unexpected consequences. It gives ammunition to the scientists who are arguing that CRISPR does cause unexpected genetic mutations in a recent dispute over a paper published in Nature Methods.
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Cancer continues to be one of the major diseases that plagues humanity. Around the world, approximately 1 in 6 deaths is due to cancer, according to the World Health Organization (WHO). The prevalence of cancer is due, in part, to the absence of a universal cure for all forms of the disease. While various treatments are available, each type of cancer generally requires specific treatment.
A new method developed by doctors at the Great Ormond Street Hospital in London presents a hopeful solution. The team has successfully tested their method on two infants with an aggressive form of leukemia. In a study published in the journal Science Translational Medicine, the doctors reported their treatment has succeeded in keeping the two infants cancer-free for 16 and 18 months, respectively.
The team combined a novel but promising cell therapy called chimeric antigen receptor T cell (CAR T) with a gene-editing technique called TALENS. The former uses the patient’s immune system to fight cancer, while the latter is a gene editing tool that allows for direct manipulation of the patient’s genes.
In a CAR T cell therapy, specialized immune cells (T cells) are taken from a patient’s blood and given special surface receptors called CARs. Once ready, the CAR T cells are infused back into a patient’s blood, where they can attach to tumors and destroy them. Clinical trials have demonstrated the effectiveness of CAR T cell therapy, and its worked well for blood cancers in previous studies.
However, as every set of T cells must to be tailored to each individual patient, it’s proven to be a tedious and expensive process. Gene-editing, however, would help make it easier to develop universal T cells. In the study, the doctors made four genetic changes to T cells from donors, which they hoped would prove successful for treating their young patients’ cancers.
Prior to receiving the new treatment, however, both infants were already given chemotherapy and received stem cell transplants. This make it difficult to ascertain how much the novel treatment actually contributed to the infants’ remission. As Stephan Grupp from the Children’s Hospital of Philadelphia told MIT Tech Review, “There is a hint of efficacy but no proof. It would be great if it works, but that just hasn’t been shown yet.”
Still, this doesn’t mean that the combined CAR T cell therapy and TALENS method isn’t promising, and one day if the treatment is perfected, it could potentially lead to cancer cures. Gene-editing is the key, as it allows for CAR T cells to do their job efficiently by preventing the risk of rejection and adding signature receptors that seek out and attack tumors. The British test used TALENS, but other clinical trials of this method combines CAR T with the more popular and easier to use CRISPR gene-editing tool. All that being said, it will still take time and many more trials before this treatment combo could be made available to more patients, or even patients with cancers other than leukemia.
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Warning: Graphic Content* This could save countless lives in emergency situations
The post This Could Save Countless Lives in Emergency Situations appeared first on Futurism.
Researchers have long been looking for ways to help HIV-infected individuals produce more broadly neutralizing antibodies (Bnabs) — antibodies which are known to combat multiple forms of virus. Bnabs are an important topic in HIV research, because the virus alters slightly with every cell division — meaning that a single, specific antibody can’t keep up. A new study has found that cows may provide answers for scientists who have been seeking to better understand how Bnabs can be harnessed.
In terms of their makeup, broadly neutralizing antibodies are notable because they’re big and kind of unruly as far as proteins go. Considering these features, scientists realized that Bnabs bore resemblance to a the types of antibodies found in cows. Cows don’t get HIV, but after researchers injected them with a protein that’s very similar to the virus’s envelope, their bodies produced antibodies to block it. The proteins were then extracted, and tested against multiple strains of HIV as it attempted to infect cells in a petri dish.
Devin Sok, director for antibody discovery and development at the International AIDS Vaccine Initiative, told STAT News that the epiphany was like “an alignment of the stars, where we had veterinarians, cow antibody scientists, and HIV scientists all talking and came up with this.”
While the study is the first to reliably encourage the development of Bnabs, it has not elucidated how to prompt the same growth in humans. However, John Mascola, director of vaccine research at National Institute of Allergy and Infectious Diseases (NIAID), optimistically stated to STAT that while “the study . . . doesn’t tell us how to make a vaccine for HIV in people […] it does tell us how the virus evades the human immune response.”
The discovery may also open up the possibility of using cow blood in a clinical capacity in order to provide short term protection against HIV, or help treat those who are already infected. The move may help alleviate the suffering of patients among the estimated 1.1 million people in the U.S. who are currently living with HIV.
The cow antibodies could be useful in treating numerous other disorders as well, as they appear capable of fighting multiple viruses and diseases. Dr. Vaughn Smider is working with pharmaceutical companies to use them to fight autoimmune disorders, certain cancers, and infectious diseases like malaria. More widely, scientists have used cows to find promising avenues for producing cures for tuberculosis and even breeding the animals to develop resistance to climate change.
The post Cows are Helping Researchers Fight HIV. Here’s How. appeared first on Futurism.
At eight years old, Zion Harvey became the first person to receive a pair of donor hands in a groundbreaking transplant operation. Two years later, his doctors have published an update on his progress, revealing that while the transplant was a success overall, there remain many challenges and risks in this nascent area of medicine.
As a toddler, Zion lost his hands and feet after a bacterial infection he’d contracted developed into sepsis. In addition to his amputations, his kidneys also failed, necessitating a partial kidney transplant. After his body was able to recover from both the sepsis and kidney transplant, doctors decided that he might be the right candidate for something novel and a little bit risky: a bilateral hand and forearm transplantation that took a team of 40 medical personnel almost 11 hours to complete.
The transplantation was a success, although it has been an uphill battle for Zion. By about one year after the surgery, he could hold a baseball bat, and by 18 months after the procedure, he’d made even further marked progress. Today, his movement is more coordinated and powerful, and the motion between his right and left hands is in tandem.
Zion can also write as well as feed, dress, and go to the bathroom himself more independently than before the procedure. Unfortunately, he has also experienced eight rejection episodes, during which his body’s immune system mounted a defense against the transplanted tissues. These episodes have been managed mostly with medications, in addition to Zion’s continuing physiotherapy. Researchers are hoping that, by studying the ways that the child’s body recovers from each setback, they will be able to improve the process for future patients.
Hand transplantation was first attempted, unsuccessfully, in the 1960s. More than 100 people have had one or two donor hands transplanted since that time, with varying degrees of success. A milestone in the process came in 2000, when Malaysian surgeons transplanted the arm of a deceased infant onto her identical twin. Zion’s success in 2015 has provided ample learning opportunities for researchers in the field, especially since he was older than the infant in the Malaysian case, and therefore his brain development was not optimized to adapt as much.
The post The World’s First and Youngest Double Hand Transplant is Declared a Success appeared first on Futurism.
A new blood test has been found to be able to detect buildups of beta-amyloid in the brain, the cause of the plaques that characterize the development of Alzheimer’s disease. Although the role that these clumps of beta-amyloid play in the brains of Alzheimer’s patients is unknown, monitoring their presence has been a reliable way to watch for the disease. Unfortunately, watching for the build-up of these plaques in the brain has only been possible through PET-scans, which are expensive and not widely available, or with spinal tap procedures, which are invasive and can only be administered by a, relatively, select few practitioners.
In this new study, researchers have developed a simple blood test to screen for Alzheimer’s risk that anyone from general practitioners to nurses in clinics could use. This simple to administer screening would be able to identify thousands of at-risk patients, allowing them to start treatment before brain damage and irreversible memory loss occurs. In fact, with this kind of basic screening tool, monitoring for Alzheimer’s disease could be as widespread and quick as checking your cholesterol and blood sugar.
The post New Test Allows For Easier and Earlier Detection of Alzheimer’s appeared first on Futurism.
Doctors recently reported the reversal of brain volume loss in an unresponsive two-year-old cold water drowning victim who had experienced cardiac arrest. After treating the child with hyperbaric oxygen therapy (HBOT) and normobaric oxygen (oxygen at sea level), she experienced marked improvement and reversal of many symptoms.
After resuscitation, an MRI showed that the child experienced cerebral atrophy with white and gray matter loss and deep gray matter injury. At the time she was discharged from the hospital, she was unable to speak, unresponsive to commands, and she exhibited constant head shaking and squirming.
To prevent permanent degeneration of tissue, Dr. Paul Harch, Director of Hyperbaric Medicine at LSU’s School of Medicine, began partial treatment. Fifty-five days post-drowning, the patient began daily short-duration treatment under Dr. Harch’s care with 100% normobaric oxygen.
With treatment, the child became more awake and alert and even stopped squirming. She experienced ongoing neurological improvement throughout her treatment period, characterized by laughing, eye tracking, increased movement of arms, grasp with the left hand, movement of hands, partial oral feeding, and short-sequenced speech at pre-drowning levels, albeit with diminished vocabulary.
The post Medical Researchers Reverse Brain Damage in Drowning Victim appeared first on Futurism.
This tech can potentially identify rare cancer genes in healthy people
The post This Tech Can Potentially Identify Rare Cancer Genes in Healthy People appeared first on Futurism.
The Population Reference Bureau has projected that the percentage of the population over the age of 65 will rise from the current 15 percent to a staggering 24 percent by 2060. This means that research into aging has never been more important.
Eric Verdin is at the forefront of this research and has become the President and CEO of the Buck Institute for Research on Aging. The institute is the world’s biggest independent research facility studying the causes of growing old — and how to combat them. Recently, he conducted an interview with Nautilus to discuss how aging is effecting our lives.
Verdin believes that the explosion in age-related research is due to researchers’ discovery in the 1990s that aging is not necessarily an inevitability. Instead, it is caused by mutations — and scientists could make changes to the genome of other species that led to a lifetimes of up to twice as long. Verdin stated in the interview this resulted in a belief that “there might be pathways to regulate aging, and if there are pathways that means there are proteins, and that means you can eventually develop drugs.”
Despite this, he says, “if you hear the word immortality, just run. There is no drug that can give you that.” While Verdin believes we can increase the average human lifetime significantly, the fountain of youth is still just a fairy tale. “It’s just nonsense from my perspective, and I think we should really resist the I-word.”
The best way to maximize your lifespan, he said in the interview, is to maintain your body well. Good nutrition and exercise are “incredible anti-aging medicine.” His general advice is to treat the cause rather than the symptom with a combination of lifestyle and pharmaceutical treatments — to fight aging itself rather than dealing with Alzheimer’s, Parkinson’s, or macular degeneration when they occur.
The human attraction to immortality has been present in our cultural landscape since the beginning of time — the human mind seems to be unable to resist its lures. There are countless myths and stories based on it: the fountain of youth, the Wandering Jew, the philosophers stone, and the Bible’s Enoch are a few examples.
Recently, this mystical desire has birthed a myriad of promising methods for reversing the aging process which are currently under investigation: from transfusing young people’s blood into older people to give them more osteopontin, to digging into the role telemores play on the aging process, to developing anti-aging, bacteria-based pills.
However, when our increasing life expectancy is combined with the decrease in fertility that many nations are facing, the results are an aging population. In an interview with CNN, Elon Musk pointed out why this is undesirable, saying it causes a “very high dependency ratio, where the number of people who are retired is very high relative to the number of people who are net producers” — an economically detrimental state of affairs.
Due to technological and therapeutic advancements, aging is looking less like an ugly inevitability of our condition and more like a new and exciting epoch in our lives. However, we must ensure that longer lives for people do not come at the expense of the environment, economy, or wellbeing of others.
The post We Will Extend Our Lives but Not Attain Immortality, Says Anti-Aging Researcher appeared first on Futurism.
A new study has investigated what patients themselves prefer when it comes to managing pain — opioids, which are widely distributed for intense pain relief, or medical marijuana.
The researchers found that the patients themselves much prefer medical marijuana, and many believe it is just as effective for their pain.
“This study can conclude that medical cannabis patients report successfully using cannabis along with or as a substitute for opioid-based pain medication,” the team reported in the journal Cannabis and Cannabinoid Research.
“Patients in this study who are using cannabis and opioids report that they are able to use less opioids and that cannabis presents less unwanted side effects than their opioid-based medication.”
The researchers, from University of California Berkeley and Kent State University emailed participants a survey asking them about their pain, and their opioid and marijuana usage.
Out of the 2,810 participants who were currently using cannabis, 828 had used opioids in the last six months to manage their pain.
Of that group, “97 percent of the sample ‘strongly agreed/agreed’ that they are able to decrease the amount of opioids they consume when they also use cannabis. In addition, 89 percent ‘strongly agreed/agreed’ that taking opioids produces unwanted side effects such as constipation and nausea,” the researchers wrote.
But interestingly, the researchers also found that “81 percent ‘strongly agreed/agreed’ that taking cannabis by itself was more effective at treating their condition than taking cannabis with opioids.”
Basically — if given the choice, many of the participants would prefer to use cannabis than opioids. You can see the results from this part of the study in the graph below.
Although opioids are an important part of managing pain, nearly 100 people are dying a day due to abusive opioid usage, according to the Center for Disease Control and Prevention.
This is a combination of heroin, and prescription opioids such as morphine and codeine.
“Prescription drug overdoses are the leading cause of accidental death in the United States. Alternatives to opioids for the treatment of pain are necessary to address this issue,” the researchers write.
Although marijuana is far from a perfect solution, there has been no recorded overdoses from marijuana — and this study has shown that the patients themselves rate the drug highly for pain management.
Unfortunately this study leaves some things to be desired – the reporting was all personal, which can sometimes cause biases. It also took its sample from HelloMD, an online community for medical cannabis patients, who were probably more likely to have had success with cannabis for their pain in the past.
However, the study is still interesting, and shows that many people really do prefer using marijuana than opioids for pain management.
Plus, it gives scientists even more of a reason to find out how marijuana affects people over longer periods, and how harm could be minimized in the future.
The research has been published in Cannabis and Cannabinoid Research.
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Verily, the life sciences arm of Google’s parent company, Alphabet, has created a robot that raises about one million mosquitoes every week in an automated lab. It uses them to produce infertile male insects treated with naturally occurring Wolbachia bacteria, and has used its custom-built machines and algorithms to increase its production of mosquitos. The first groups of 20 million sterilized mosquitoes have already been released in Fresno County, California.
Last October, Verily announced its initiative to fight mosquito-borne diseases such as dengue fever and Zika virus. Verily’s effort makes use of an automated sex-sorting procedure to ensure that only males are released, as males do not bite humans. When they mate with females in the wild, the eggs cannot develop or hatch.
The release of the treated male insects in Fresno is the largest such field trial in the U.S. to date. While other release projects have been managed by hand, Verily’s automated system allows for the release of far more mosquitos in a short period of time. This in turn may offer a faster response; a critical factor when serious diseases are potentially being spread.
Verily senior engineer Linus Upson commented to MIT Technology Review, “If we really want to be able to help people globally, we need to be able to produce a lot of mosquitoes, distribute them to where they need to be, and measure the populations at very, very low costs.” Adding that a field trial in Australia is planned for later this year, Upson said, “We want to show this can work in different kinds of environments.”
Modified mosquitoes such as those being released by Verily are regulated by the Environmental Protection Agency (EPA), coming under the heading of “microbial pest control.” A 2016 ecological risk assessment conducted by the EPA concluded that altered mosquitoes like those used in this trial will not harm other organisms.
The post A Branch of Google’s Parent Company is Releasing 20 Million Mosquitos in California to Fight Zika appeared first on Futurism.
Scientists at Monash University in Australia have found another piece of the lab-grown organ puzzle: the team has discovered that a protein called Meox1 is pivotal in promoting the growth of muscles. They came across the protein while studying zebrafish, which are ideal candidates for the research due to their rapid rate of growth and biological similarities with humans. We share 70 percent of our DNA with the species, and they have many of the same internal organs that we do.
Meox1 directs muscle growth by selecting the relevant stem cells for producing the specific tissue (as opposed to the growth being caused by stem cells dividing at random).
Lead researcher on the study, Peter Currie, said in a statement “prior to our work in this field, we didn’t even know that these growth-specific stem cells existed or how they were used […] Just knowing that they exist leads us to the possibility of orchestrating them, controlling them, or reactivating them to regrow damaged tissue.”
This research is pivotal because it doesn’t just show is what the stem cells do — it shows us how. Researchers have known for quite some time that stem cells produce living tissue in the body, but up until this point we haven’t understood the mechanism behind how they do it.
Accruing this piece of knowledge means we have crossed, as the team called it, “one of last frontiers of developmental biology.” It’s also a significant step towards being able to encourage stem cell growth in lab conditions.
When the process is fully developed, the ability to grow organs in laboratories will save thousands of lives. It will allow us to create tailored organs rather than patients waiting for a matching donor to be found. Estimates from the American Transplant Foundation indicate that a new name is added to the organ donor list every 10 minutes, and that 22 people a day die while waiting for a transplant each day.
As well as providing organs that will save lives, stem cells are also increasingly being recognized as an integral tool for treating — and even curing — a number debilitating diseases. Everything from blindness to paralysis to neurological disorders like Alzheimer’s disease and Huntington’s disease have already seen breakthroughs with the help of stem cells.
The post New Discovery Brings Us One Step Closer to Growing Replacement Organs appeared first on Futurism.
For the first time, researchers have shown that a common epilepsy drug can normalise disrupted brain activity in patients with Alzheimer’s disease.
The incurable condition already affects one in ten people over the age of 65, so in the widespread scientific search for new therapies this research result is a highly promising development.
Alzheimer’s patients are known to be at an increased risk of developing epilepsy, but the vast majority don’t experience any seizures with noticeable symptoms.
But research has suggested that, in many such patients, seizure-like brain activity is still going on undetected, possibly even leading to some of the cognitive symptoms that patients experience.
That’s why a team from Beth Israel Deaconess Medical Center (BIDMC) at Harvard Medical School turned to an anti-seizure medication to see whether it might have any effect on the brain activity of patients with mild Alzheimer’s disease.
The drug in question was levetiracetam (LEV for short), commonly used for treating seizures in epilepsy patients. It’s been tested before in mouse models of Alzheimer’s disease, showing benefits for normalising brain activity and even reversing some cognitive deficits.
Previous studies have also shown that low doses of LEV can improve memory in people with ‘amnestic mild cognitive impairment’, a memory deficit that’s known to be a risk factor for Alzheimer’s.
Now researchers have finally tested the drug in actual Alzheimer’s disease patients, and even though this was just a small feasibility study, the results look promising indeed.
The team, led by neurologist Daniel Z. Press from BIDMC, measured the effects of a single dose of LEV in seven patients with diagnosed mild Alzheimer’s disease.
The study was double-blinded, and all patients received a total of three injections – either a low dose of LEV, a higher dose, or a placebo.
Before and after each injection, the patients were given an electroencephalogram (EEG) which can detect disrupted electrical activity in the brain even when there are no obvious symptoms of a seizure.
The patients also took standardised cognitive tests to measure the various abilities affected by Alzheimer’s, such as memory, language abilities and executive function.
The results showed that when patients received the higher dose of LEV, it appeared to reduce abnormalities of brain activity patterns which are typical in Alzheimer’s patients and which the researchers detected before administration of the drug. But there was no improvement in cognitive test scores.
It’s important to note that the team didn’t have a control group without Alzheimer’s, and they say in the study that this “prevents us from determining whether the effects would also be seen in healthy ageing.”
But there is some previous research to indicate that LEV doesn’t change EEG patterns in healthy volunteers. The dosage of the drug will also have to be investigated more thoroughly, to see how patients would fare with smaller doses over longer periods of time.
“Chronic administration would be required to better delineate any potential long-term benefits of the drug,” the team writes in the paper.
But even with the small sample size and other limitations, the effects of the medication look so promising the researchers are now calling for a larger study to further investigate the potential of LEV as an Alzheimer’s treatment.
“It’s worth noting, we did not demonstrate any improvement in cognitive function after a single dose of medication in this study,” says Press.
“It’s too early to use the drug widely, but we’re preparing for a larger, longer study.”
Whether an epilepsy drug could indeed become a treatment option for managing Alzheimer’s symptoms remains to be seen, but over decades of hard work scientists have certainly been making progress in tackling this disease.
Last year another team reported highly promising results in a preliminary trial for a drug that can clear the toxic protein build-up in the brain. This treatment is now being investigated in a large-scale study with results expected in 2020.
And just last week we finally had a close-up look at one of the key proteins involved in Alzheimer’s. Mapping the tau protein’s molecular structure is a significant step towards devising new drugs that can target it.
The study was published in the Journal of Alzheimer’s Disease.
The post A New Drug Can Fix Abnormal Brain Activity in Alzheimer’s Disease appeared first on Futurism.
Today a Food and Drug Administration (FDA) panel unanimously recommended that the agency approve a treatment that genetically alters a patient’s own cells to fight leukemia. If the agency does make the approval, the first-ever such treatment will be the start of the “living drug” era of human medicine, in which we harness technology to boost our natural immune system and improve its ability to master formerly unbeatable diseases.
While this gene therapy treatment for leukemia, known as CTL019, will be the first to reach the market, there are more on the way. Treatments for an aggressive type of brain tumor, as well as myeloma and other varieties of leukemia, are also in development.
This technique is a true example of personalized medicine: a unique version of the treatment must be created for every patient from their own cells. After the cells are removed by medical personnel, they are frozen, shipped to Novartis (the therapy’s maker), processed, refrozen, and shipped back to the medical center.
Assuming this treatment is approved, it will be a first for the FDA. Though the approval wouldn’t necessarily be surprising in light of the results of the trials, which were stunning: patients facing death after all other treatments failed who received just a single dose of the gene therapy experienced long remissions that could, in time, prove curative. The FDA panel therefore recommended approval for treatment of relapsed or treatment-resistant B-cell acute lymphoblastic leukemia in children and young adults ages 3 to 25.
One attendee of the panel’s meeting was the first patient from the trials, Emily Whitehead, age 12. She almost died as a result of leukemia, which was considered fatal until she was treated at age 6. Since that time she has been cancer free. “We believe that when this treatment is approved it will save thousands of children’s lives around the world,” Tom Whitehead, Emily’s father, told the panel, according to The New York Times. “I hope that someday all of you on the advisory committee can tell your families for generations that you were part of the process that ended the use of toxic treatments like chemotherapy and radiation as standard treatment, and turned blood cancers into a treatable disease that even after relapse most people survive.”
Researchers at the University of Pennsylvania developed the treatment, which is now licensed to Novartis. The disease it’s meant to treat, however, is rare — affecting only about 5,000 people annually. Around 60 percent of them are young adults and children. Standard treatments can cure most children, but approximately 15 percent of patients, like Emily, do not respond to treatment or experience relapses.
Novartis will limit the use of CTL019 initially because the treatment process is complex and managing side effects demands expert care. Therefore, only about 30 or 35 medical centers will have access to the treatment upon its release. Furthermore, staff at those centers will receive special training and approval to administer it, according to The New York Times. Although analysts predict that the cost of these unique treatments may exceed $300,000, a Novartis spokesman declined to specify a price when NYT inquired.
The post An FDA Panel Just Approved A Treatment That Genetically Alters Your Own Cells appeared first on Futurism.
The human brain is among the the most sensitive organs in the body — at least in terms of how easily it can be damaged. Traumatic brain injury is usually irreparable, often resulting in cognitive decline and memory loss. To date, there’s no drug or therapy that can reverse this damage when it’s become permanent. Which is why the discovery of a potential treatment by researchers from the University of California, San Francisco (UCSF) is so compelling.
The key to their research is a compound called ISRIB, previously discovered in the lab of UCSF biochemist Peter Walter in 2013. Back then, it was found able to boost the memory of healthy mice. Teaming up with neuroscientist Susanna Rosi, they proceeded to test its effects in mice with brain injuries.
After testing it on two separate groups of mice (who had brain trauma induced under anesthesia) they found that ISRIB improved the performance of the injured mice in two mazes, one in the water and a tabletop version with 40 holes. In the first setup, the injured mice were given ISRIB three days in a row after having rested for four weeks. In the second one, the mice were given ISRIB for four days. In both cases, the mice who had been concussed performed poorly in the initial trials. But after receiving ISRIB, they performed just as well as their healthy counterparts.
The study, published in the journal of the Proceedings of the National Academy of Sciences (PNAS), “offers a glimmer of hope for our traumatic brain injury patients,” neuroscientist Carlos Borlongan from the University of South Florida in Tampa told Science. Borlongan reviewed the research and asserted that it could change motor function rehabilitation for brain trauma patients.
University of Pennsylvania neurologist Ramon Diaz-Arrastia supposed it could also help with cognitive improvement. “Normally you would give up on these mice and say nothing can be done here,” he said. “But ISRIB just magically brings the cognitive ability back.” However, these predictions need to be put to the test, as the research has only proven the effects in mice, not humans. It’s not uncommon for animal trials to fall short when replicated in human test subjects, but the researchers are hopeful.
Before any application could come to fruition, more research is needed to understand the process by which the drug restores memory. Even if no drug was developed, additional research about how ISRIB works would no doubt lend itself to the development of new treatments. There’s lots of work left to do, but if such treatments could give a second chance to over 150 people in the U.S. who die from traumatic brain injuries each day, or the millions around the world who have long term complications from them, it would definitely be worth a shot.
The post “Memory Repair Molecule” Reversed Effects of Traumatic Brain Injury in Mice appeared first on Futurism.
A study published earlier this year warned scientists of potential complications in their work with CRISPR/Cas9, but after review by researchers at another institution, the findings of that study are being brought into question. The original paper was published by a team at Columbia University Medical Center (CUMC) in May of this year in the journal Nature Methods.
In the study’s original press release, co-author Stephen Tsang said: “We feel it’s critical that the scientific community consider the potential hazards of all off-target mutations caused by CRISPR, including single nucleotide mutations and mutations in non-coding regions of the genome.” The researchers had sequenced the genomes of mice whose genes had previously been editing using CRISPR in an attempt to cure their blindness. The genomes revealed there were 1,500 single-nucleotide mutations and over 100 larger deletions,= and/or insertions in two of the mice which had been modified using the gene-editing technique.
In their study, the researchers attributed these genetic anomalies to the use of CRISPR — but a team of researchers from Harvard University and MIT have reviewed the paper and are challenging that attribution. In a paper published in bioRxiv — a pre-print server for biology research which is not a peer reviewed journal — the researchers pointed out the CUMC study had several serious problems. The most glaring of which, the Harvard and MIT researchers argue, is that the mutations found in the mice that were attributed to CRISPR were more likely than not already present in those mice before they were exposed to the gene-editing technique.
The third mouse whose genome had been edited with CRISPR did not demonstrate the mutations, and was also not as genetically similar as the two mice who did. The Harvard and MIT research team argue that this supports the theory that the mutations in the pair of mice were not caused by CRISPR. It should be noted that this criticism comes from a small study that was not peer reviewed.
The team’s goal in refuting the research is to make sure the rest of the scientific community is reminded of the lasting impact claims that are not well supported by data can have. “Given these substantial issues, we urge the authors to revise or re-state the original conclusions of their published work so as to avoid leaving misleading and unsupported statements to persist in the literature,” the team explained in their paper.
The peer review process is essential to scientific disciplines other than biology and genetics, of course. Whether researchers are making claims about climate change, artificial intelligence, or medical treatments, rigorous review of their methods, data, and analysis by other scientists who are doing similar work is essential. This process ensures that the research — and the way it is presented — is accurate, of high quality, and will be useful not only to the scientific community, but to the general public.
For teams who have spent months — if not years — heavily focused on a single study, trial, or data set, it can be very easy to lose sight of the bigger picture. Peer review offers research teams the chance to address inconsistencies, data that doesn’t add up, and conclusions that make assumptions or inferences that aren’t supported by the data.
While there have certainly been instances where teams have intentionally fabricated data in order to mislead their peers and the public, most members of the scientific community do not mislead intentionally. But that’s why the peer review process is so important. It remains to be seen if the team at CUMC plans to revisit, or possible retract, their paper in light of the response.
The post Researchers Refute Study That Claims CRISPR Causes Unexpected Mutations appeared first on Futurism.
A review of the research on combining therapy with the psychoactive component from magic mushrooms has concluded it’s not only a safe and effective way to treat conditions related to anxiety, depression, and addiction, it could be better than many existing forms of treatment.
The findings reinforce the need to explore the full impact of the psychedelic compound called psilocybin, a drug that is showing increasing promise in its ability dramatically improve the lives of those who suffer debilitating psychiatric disorders.
Psychedelics such as lysergic acid diethylamide (LSD) and psilocybin have a reputation more as a party drug than as forms of therapeutic medication.
But their similarity to neurotransmitters such as serotonin and their ability to affect our perception and mess with our state of consciousness has made them attractive candidates for treating various psychiatric conditions.
Studies have found patients with severe depression have improved after taking small amounts of psilocybin alongside supportive therapy sessions, with evidence that their brains have strengthened links across previously disconnected regions.
These kinds of results demand attention, demonstrating great potential for using serotonin agonists such as psilocybin to block problematic networks in the brain while therapy can be used to create more functional ones.
A review by researchers in California has shown such studies aren’t outliers, prompting a need to step forward with testing.
Their analysis of seven clinical trials conducted over the past decade testing the effects of psilocybin-assisted therapy on anxiety, depressive disorders, addiction, and obsessive-compulsive disorder has shown the drug.
“Psilocybin-assisted therapy has been shown to be safe in several studies across a variety of patient populations,” researcher Kelan Thomas of Touro University California explained to Eric W. Dolan of PsyPost.
Compared with other forms of treatment on validated psychiatric rating scales, therapy with psilocybin has resulted in a larger effect, suggesting it could be a better option for many patients, especially those who have failed to respond to other medications or procedures.
“One important distinction from these other session-based treatments would be that the benefits of psilocybin-assisted therapy may only require a few dosing sessions and the effects appear to persist longer than other treatment options,” the researchers write in their report.
This isn’t to say the drug can be beneficial independently as a form of medication – research on the therapeutic impact of psychoactive drugs is pretty thin on the ground due to ethical constraints, but that also means there’s no strong evidence supporting use of psilocybin without the support of therapy sessions.
It is a good reason to now conduct larger trials with more powerful statistical tools to aim for getting the US Food and Drug Administration’s big tick of approval.
Phase 3 trials would establish the drug’s actual effectiveness and comparative value as a bona fide treatment, bringing it one giant step closer to being an option for licensed – and trained – psychiatrists to use with patients.
One advantage of such rigorous testing of pharmaceuticals such as psilocybin is the establishment of evidence challenging decades of negative association as illicit and therefore harmful substances.
3,4-Methylenedioxymethamphetamine (MDMA) is the active component in what’s commonly called ecstasy, a drug that’s come in and out of fashion on the dance club scene since the 1980s.
Studies have also demonstrated its effectiveness in treating conditions associated with everything from autism spectrum disorder to post-traumatic stress, but like psilocybin, there are years of testing and biases to overcome before we’ll be seeing its full potential as a form of medication.
Changing attitudes and laws towards cannabis as a valid treatment could well open the way for other psychoactive substances to be seen in a new light.
This research was published in the Journal of Psychoactive Drugs.
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Cancer comes in all shapes and sizes. It can affect any and every part of the human body in a variety of potentially debilitating — and even life-threatening — ways. So, while the vaccines developed as part of two recent studies published in the journal Nature could lead to a whole new age of groundbreaking cancer therapies and treatments, they are by no means a “cure” for all the different forms of cancer.
Even still, these new vaccines are remarkable. While these vaccines are new, cancer vaccines in general are not. The researchers explored the possibility of creating vaccines personalized to an individual’s unique cancer mutations in order to combat tumors. The two clinical trials run thus far were small: in them, the researchers attempted to design individual vaccines in hopes they would give the patient the ability to fight off tumors in a way optimized for their biology. These studies also briefly noted the potential to combine such vaccines with existing immunotherapies to give the body an increased chance of combatting a cancer’s spread.
In a basic sense, these vaccines are cancer cells combined with immune system stimulating agents. It’s not unlike how flu vaccines combine virus with ingredients designed to ignite a particular immune response. The research team in these trials hoped the vaccines would enable the patient’s immune system to attack the cancer cells.
In the first of two clinical trials, 4 out of the 6 patients hadn’t seen their tumors return. The remaining 2 eventually went into complete remission with additional treatment. In the second trial, 8 out of 13 total patients remained tumor free more than a year after the study. In the remaining 5, their tumors had spread already by the time they received the vaccine — but two of their tumors did shrink. Another 5 went into complete remission after receiving additional treatment.
According to Cornelis Melief, a cancer immunologist at Leiden University Medical Centre in the Netherlands who authored a commentary on the study, “It’s potentially a game changer…The two papers really strongly indicate that the patients experienced clinical benefit.”
As previously stated, only two small clinical trials have been completed so far. These personalized vaccines might seem like our greatest weapon yet in battling tumors, but these studies are just the beginning. While the results seem promising — and certainly very exciting — they are not a direct indicator for success. Additional research and trials will need to be conducted before the idea of cancer vaccines could be implemented on a larger scale.
However, if the direction of these studies continues to trend in this way, cancer treatment could be forever changed. Not only would the vaccine be capable of being personalized and specified for an individual’s biology and specific mutations, it could be tailored for the type of cancer as well. And, the more we can individualize treatment, it seems, the better chance we will have of giving every cancer patient the very best shot at remission.
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This futuristic high-tech vest can see through your chest and into your lungs
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New medicines come to our pharmacies through a rigorous process that begins in the lab and ends with multiple trials in humans. Along the way there can be animal studies, such as trials of type 2 diabetes drugs in mice.
While mice are not people, they do share plenty of biological similarities with us to be valuable trial subjects. But sometimes treatments that work in mice fail without an explanation in humans. And now scientists have finally cracked the case on why that happens.
Researchers from Lund University in Sweden and King’s College London have found that mice and humans have previously unknown differences when it comes to having G protein-coupled receptors (GPCRs) on insulin-producing beta cells in the pancreas.
GPCRs are found on the surfaces of many cells, where they receive chemical messages via various molecules called G proteins. We have nearly 1,000 different GPCRs, each finely tuned to react to a particular molecular signal.
These receptors have a laundry list of jobs in the body, including detection of certain tastes and smells, immune system regulation, transmission of nerve signals, and many more.
That’s why pharmaceuticals can be used to target specific GPCRs. This avenue of delivering drugs is so popular, it is estimated that around 40 percent of all modern prescription meds target this receptor type.
But when it comes to developing GPCR-targeted drugs for type 2 diabetes, we’ve had little success. And that could well be because the receptors in mouse and human beta cells just don’t match up.
Scientists already knew that might be the case, but now they have clearly outlined some of these differences, and also found some promising similarities.
Cells in the pancreas hang out in little clusters known as islets. The team compared islets from two types of laboratory mice, and from non-diabetic human organ donors.
They found that humans don’t actually have some of the GPCRs that we target in mouse islets in order to help with insulin production. Meanwhile other receptors are only found in humans, but not in mice.
“This means that a drug developed to stimulate or inhibit a particular receptor which, in mice, can lead to increased insulin production, might have no effect on humans, or even could cause unbeneficial and diabetes-like symptoms,” says one of the team, Stefan Amisten from King’s College London.
And that’s not even all. The researchers even found receptor differences between the two types of lab mice they used.
“This is well known, and a source of great frustration for researchers and the pharmaceutical industry,” says Lund University’s Albert Salehi.
“Is it then right to continue to develop drugs based on research conducted on mice, when these drugs cannot be used on humans?”
That’s an important question, and it’s exactly the reason why this comparison study will be useful for other scientists who are hunting for new diabetes drugs and thinking of testing them in mice first.
“Overall, the data presented here provide an essential resource for the translation of mouse islet functional data to the human islet context,” the researchers write in the study.
Thankfully, the researchers also mapped a bunch of GPCRs which are similar in both mice and humans, so there’s scope for research there. And now that scientists have a better roadmap of all these differences and similarities, drug testing will hopefully be more precise in the future.
The study was recently published in Scientific Reports.
The post We Now Know Why Some Diabetes Treatments Work on Mice but Not on People appeared first on Futurism.
For the first time, scientists have revealed the chemical structure of one of the key markers of Alzheimer’s disease, capturing high-resolution images of the abnormal tau protein deposits suspected to be behind Alzheimer’s and other neurodegenerative conditions.
The results will now give scientists an unprecedented glimpse at how these harmful deposits function at a molecular level, and could lead to a number of new treatments to prevent them from forming – and in doing so, help to combat Alzheimer’s and dementia.
“This is a tremendous step forward,” says one of the team, Bernardino Ghetti from Indiana University.
“It’s clear that tau is extremely important to the progression of Alzheimer’s disease and certain forms of dementia. In terms of designing therapeutic agents, the possibilities are now enormous.”
In the new study, researchers led by the MRC Laboratory of Molecular Biology (LMB) in the UK extracted tau protein filaments from the brain of a deceased patient with a confirmed diagnosis of Alzheimer’s disease, and imaged them using a technique called cryo-electron microscopy (cryo-EM).
Alzheimer’s disease is linked to the build-up of two kinds of abnormal protein deposits – tau filaments, which form inside nerve cells, and amyloid beta proteins, which builds up outside cells.
In healthy brains, tau acts as a stabiliser, but when the proteins become defective, they can form into bundles of tangled filaments, which are thought to impede communication between brain cells, leading to the neurodegeneration and reduced cognitive ability seen in conditions like Alzheimer’s disease.
Researchers have studied the tau protein’s involvement in Alzheimer’s for decades, but up until now, we’ve never been able to see tau filaments up so close – and the molecular insights afforded by the cryo-EM imaging performed here could mean the opportunities for drug discovery targeting tau is a whole new ball game.
“Drugs that could clear away clumps of protein in the brain are a key goal for researchers, but to directly affect these proteins, molecules that make up a drug need to latch on and bind to their surface,” explains the head of research at Alzheimer’s Research UK, Rosa Sancho.
“Knowing the precise shape of these complex protein structures is enormously valuable in guiding the development of targeted drugs.”
While there’s no shortage of research examining how abnormal tau and amyloid beta proteins function, it’s been unclear just how much artificial samples assembled in the lab differ from the structures that form in the lab.
Thanks to the tau structures obtained from the deceased patient, researchers now have the ability to investigate how abnormal filaments function at an atomic level in the human brain – and studying these tangles won’t only benefit Alzheimer’s research, the team says.
“This is a big step forward as far as tau goes but it is bigger than that,” neuroscientist Michel Goedert from LMB told James Gallagher at BBC News.
“This is the first time anybody has determined the high-resolution structure [from human brain samples] for any of these diseases. The next step is to use this information to study the mechanisms of neurodegeneration.”
We won’t know the full ramifications of this discovery until scientists have a chance to follow up on the new findings presented here, but it’s clear that this could be a major turning point in studying how to counter these harmful protein clumps, with Ghetti describing the result as one of the major discoveries of the last quarter century of Alzheimer’s research.
That said, it may take many more years (or even decades) for new treatments to ultimately come out of this – but at least we’re now a big step closer to that long-hoped-for eventuality, which before now may have been impossible.
“It’s like shooting in the dark – you can still hit something but you are much more likely to hit if you know what the structure is,” explains one of the team, LMB’s Sjors Scheres.
“We are excited – it opens up a whole new era in this field, it really does.”
The findings are reported in Nature.
The post The Atomic Structure of a Key Alzheimer’s Protein Has Been Revealed appeared first on Futurism.
France’s Prime Minister Édouard Philippe has announced that the government will make the 11 vaccines universally recommended by health authorities mandatory from 2018 onward. The announcement comes in response to measles outbreaks across Europe, with 79 cases reported in France in January and February alone. Philippe branded the state of affairs “unacceptable.”
The resurfacing of diseases like measles is believed to be caused by people believing less and less in the power of vaccines. In France, a recent survey found that three in 10 people don’t trust vaccines, with only 52 percent stating they believed that the benefits outweighed the risks.
Italy has also seen a worrying increase in measles infections — the number of cases in April was five times higher than the same month in 2016. Beatrice Lorenzin, the Italian health minister, said that the rapid increase was “an emergency generated by fake news” and cited the Five Star Movement (MS5), a political party that opposes vaccines, as a contributing factor.
The shift in public perception in Italy and France is symptomatic of a Europe-wide trend that has been attributed to the growing anti-vaccine movement. The genesis of the skepticism was Andrew Wakefield, who stated in a 1998 research paper that there was a link between the measles, mumps, and rubella vaccine and the development of autism. The claim has been irrefutably debunked, although dubious science and scare tactics — like those used by MS5 — are perpetuating the findings of the report.
The World Health Organization (WHO) estimates that vaccines saved more than 10 million lives between 2010 and 2015, and thanks to vaccines, we’re on the brink of completely eradicating some diseases, such as polio. Despite this, countries in both the developing and developed world remain doubtful of their effects.
In response, many countries have taken measures to increase the use of vaccines. Italy has made 12 vaccinations obligatory for children, while Australia has introduced a financial incentive by offering parents $129 for every child who meets recommended vaccination levels between the ages of 18 months and 24 months, with the payment being repeated if the same requirements are met between the ages of four and five.
Slovenia, in Eastern Europe, has the world’s strictest vaccination policy, with fines being issued to any parents who fail to provide their children with the nine mandatory vaccines. This has resulted in a compliance rate of 95 percent.
Dr. Farah Jameel told doctors attending the British Medical Association’s annual meeting in June that deaths in Wales from measles in 2013 were a “waste of life.” This is arguably true for all deaths that could have been easily prevented through vaccination, especially given their ever-decreasing price and new delivery methods.
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In April 2017, the winners of the Qualcomm Tricorder XPRIZE were announced: out of more than 300 teams, Final Frontier Medical Devices and Dynamical Biomarkers Group were the two whose devices got us closest to where no one has gone before. The contest was inspired by the medical “tricorder” from the original Star Trek series, a handheld device that could check vitals and diagnose a host of diseases by simply being swept in front of the patient. This vision of the future — with no invasive tests and fast, accurate results — has now ushered in actual technological advances outside the realm of science fiction.
The work of both prizewinning teams focused on integrating multiple technologies into a single device. According to the judges, both devices almost met the contest benchmarks for accurately diagnosing 13 different diseases including anemia, diabetes, lung disease, pneumonia, and urinary tract infections. In fact, these two winners come closest to combining the many functionalities of the original tricorder featured in a single, handheld diagnostic system.
Final Frontier Medical Devices and Basil Leaf Technologies won first prize with their DxtER device. This is actually an AI-equipped iPad that uses non-invasive sensors to collect data about body chemistry, biological functions, and vital signs. The second place prize went to Dynamical Biomarkers Group, who produced three wireless handheld test modules: the Smart Blood-Urine Test Kit, the Smart Vital-Sense Monitor, and the Smart Scope Module. These modules connect to a smartphone and analyze blood, urine, skin appearance, and vital signs.
The post Scientists Want to Make This Medical Device From a Classic Sci-Fi Show a Reality appeared first on Futurism.
Researchers have recently discovered two different types of memory use completely different processes in the same nerves, opening the way for a new pharmaceutical solution for treating anxiety and post-traumatic stress disorder (PTSD).
The find challenges earlier research that had suggested memories of traumatic events used the same nerves in the same ways, making them impossible to physically distinguish.
A team of scientists from Columbia University Medical Center (CUMC) and McGill University analysed neurons from a marine snail called an Aplysia in order to test a hypothesis explaining why memories of incidents surrounding a bad experience can themselves trigger anxiety.
Neurons build long term memories by reinforcing the chemical bridges called synapses that link them together.
An experience that could harm an organism, such as touching a hot surface or experiencing violence, becomes encoded as an associative memory as the connections between neurons strengthens.
Experiences aren’t always quite so cut-and-dried; an organism might touch a hot surface as it hears a bell, or hear a dog bark nearby as they are assaulted. The bell might be related, or might just be incidental – neurons still record the information in case it’s necessary.
Sometimes this incidental memory doesn’t do the individual any favours, triggering anxieties that do little to help prevent them from future harm.
Many people with PTSD re-experience trauma by association with seemingly unrelated stimuli.
“The example I like to give is, if you are walking in a high-crime area and you take a shortcut through a dark alley and get mugged, and then you happen to see a mailbox nearby, you might get really nervous when you want to mail something later on,” says researcher Samuel Schacher from CUMC.
Anxiety caused by the incidental memory of the mail-box can interfere with a person’s life as encounters with similar innocuous mail-boxes produces a stress response, while offering no advantage in avoiding muggings in the future.
The synaptic tagging-and-capture hypothesis alleges a weak stimulus can still create a long-term memory it it’s paired with a stronger stimulation entering the nerve through a different synapse.
The changes in the nerve needed for it to store the memory are sparked by chemicals called plasticity-related proteins, which – according to the hypothesis – are ‘tagged’ in some way at each synapse.
Previous research showed the chemical processes behind the two forms of memory formation have common properties, making it impossible to distinguish the two.
But if those hypothetical tags happened to be different, that would provide a physical property that could be exploited.
“One focus of our current research is to develop strategies to eliminate problematic non-associative memories that may become stamped on the brain during a traumatic experience without harming associative memories, which can help people make informed decisions in the future – like not taking shortcuts through dark alleys in high-crime areas,” says Schacher.
To keep things simple, the researchers took a pair of snail sensory neurons connected to a single motor neuron (dyed red in the image below).
One sensory neuron was stimulated in a way that represented a strong associative memory; the other was stimulated to induce an incidental, non-associative memory.
The researchers found that the strength of the connections at each synapse was the result of a two different types of protein called a kinase, types they called protein kinase M Apl I and protein kinase M Apl III.
Selectively blocking just one of these kinases prevented that particular experience from etching itself onto the neuron, virtually erasing that specific memory from existence.
That’s good news for Mr Aplysia, but what about humans?
Fortunately, vertebrates also have similar versions for these kinases at work in memory formation, suggesting our brains work in rather similar ways.
Far more research would be needed to come even close to developing a pharmaceutical capable of blocking traumatic memories, but the research opens a door that had been considered closed.
“Memory erasure has the potential to alleviate PTSD and anxiety disorders by removing the non-associative memory that causes the maladaptive physiological response,” says Jiangyuan Hu from CUMC.
It could one day be possible to take a pill after a mugging that would let your brain forget mailboxes and barking dogs while still recalling the colour of the assailant’s jacket.
Recent research has also shown forgetting incidental information could have a big payoff in helping our brains retain other key information.
Even without potential therapeutic applications, such a discovery still adds a significant piece to the puzzle on how our brains produce long term memories.
This research was published in Current Biology.
The post Scientists Assert They Will Soon be Able to Edit Human Memories appeared first on Futurism.
A potential cure for Type 1 diabetes looms on the horizon in San Antonio, and the novel approach would also allow Type 2 diabetics to stop insulin shots.
UT Health San Antonio researchers have a goal to reach human clinical trials in three years, but to do so they must first test the strategy in large-animal studies, which will cost an estimated $5 million.
Those studies will precede application to the U.S. Food and Drug Administration for Investigational New Drug (IND) approval, Bruno Doiron, Ph.D., a co-inventor, said.
The scientists received a U.S. patent in January, and UT Health San Antonio is spinning out a company to begin commercialization.
The strategy has cured diabetes in mice.
“It worked perfectly,” Dr. Doiron, assistant professor of medicine at UT Health, said. “We cured mice for one year without any side effects. That’s never been seen. But it’s a mouse model, so caution is needed. We want to bring this to large animals that are closer to humans in physiology of the endocrine system.”
Ralph DeFronzo, M.D., professor of medicine and chief of the Division of Diabetes at UT Health, is co-inventor on the patent. He described the therapy:
“The pancreas has many other cell types besides beta cells, and our approach is to alter these cells so that they start to secrete insulin, but only in response to glucose [sugar],” he said. “This is basically just like beta cells.”
Insulin, which lowers blood sugar, is only made by beta cells. In Type 1 diabetes, beta cells are destroyed by the immune system and the person has no insulin. In Type 2 diabetes, beta cells fail and insulin decreases. At the same time in Type 2, the body doesn’t use insulin efficiently.
The therapy is accomplished by a technique called gene transfer. A virus is used as a vector, or carrier, to introduce selected genes into the pancreas. These genes become incorporated and cause digestive enzymes and other cell types to make insulin.
Gene transfer using a viral vector has been approved nearly 50 times by the U.S. Food & Drug Administration to treat various diseases, Dr. DeFronzo said. It is proven in treating rare childhood diseases, and Good Manufacturing Processes ensure safety.
Unlike beta cells, which the body rejects in Type 1 diabetes, the other cell populations of the pancreas co-exist with the body’s immune defenses.
“If a Type 1 diabetic has been living with these cells for 30, 40 or 50 years, and all we’re getting them to do is secrete insulin, we expect there to be no adverse immune response,” Dr. DeFronzo said.
The therapy precisely regulates blood sugar in mice. This could be a major advance over traditional insulin therapy and some diabetes medications that drop blood sugar too low if not closely monitored.
“A major problem we have in the field of Type 1 diabetes is hypoglycemia (low blood sugar),” Dr. Doiron said. “The gene transfer we propose is remarkable because the altered cells match the characteristics of beta cells. Insulin is only released in response to glucose.”
People don’t have symptoms of diabetes until they have lost at least 80 percent of their beta cells, Dr. Doiron said.
“We don’t need to replicate all of the insulin-making function of beta cells,” he said. “Only 20 percent restoration of this capacity is sufficient for a cure of Type 1.”
This article was provided by University of Texas Health Science Center at San Antonio. Materials may have been edited for clarity and brevity. And make the name of the source a link back to their website.
The post A Team Cured Diabetes in Mice Without Side Effects appeared first on Futurism.
Last week, a bill was put before the House of Representatives that would ban animal testing of industrial chemicals intended solely for use in cosmetics.
The proposed bill would affect a wide variety of products: “cosmetics” are legally defined as any substance used on the body, or in the mouth to change its appearance, cleanse it, perfume it, or protect it. This includes soaps, shampoos, moisturizer, hair dye, perfumes, and deodorants.
It’s difficult to know exactly how many animals will be affected by this ban, as companies do not advertise their use of animal testing and results are often unpublished. It’s likely to be relatively small, but this ban will both improve their lives and be an important international signal.
Cosmetic testing commonly measures the reaction of animals’ skin, eyes, and respiratory tracts to high concentrations of certain chemicals. Other tests determine a product’s potential to cause fetal abnormalities, cancer, or genetic mutations.
As a practice, it has had a turbulent history. It’s increasingly opposed by the public but many governments — including Australia’s — require animal tests to be conducted for some potentially hazardous new cosmetic ingredients.
Most prominent in this arena is the European Union. After animal testing was first banned in Germany in 1986, it was extended to the entire Union in 2004. In 2009 the ban was expanded to include ingredients, not just the finished product. Then imports came under scrutiny, as Japan and the United States are major exporters to the EU, and imports of cosmetic products tested on animals were banned in 2013.
Since that time Israel, India, Norway, New Zealand, South Korea, Turkey, Taiwan, and parts of Brazil have all banned testing of cosmetics on animals. However, the Humane Society International estimates that globally around 100,000-200,000 animals are still used annually for this purpose.
The US is considering a ban, which would drastically diminish the market for any manufacturers still using animal testing. Until recently China required all cosmetics to be tested on animals, although this requirement has now been relaxed for non-specialized cosmetics such as hair, skin and nail care products, perfumes, and make-up.
Until July 2018, animal testing will still be required in Australia for some cosmetic ingredients, as it is considered by the Department of Health to be the best means of testing for potential toxicity. After this time industrial chemicals scheduled for use only in cosmetics may not be tested on animals. Chemicals used for other purposes may still be tested on animals, providing a potential loophole for manufacturers.
However, many ingredients have already been extensively tested on animals, and there is no need to repeat this. For others, alternative means of testing are being developed, such as clinical trials on humans and use of skin samples from cosmetic surgery to test penetration levels.
There have been major advances in alternative testing methods in recent years. As well as clinical studies and skin tests, we can, for example, use hen’s eggs to test if a product is likely to irritate human eyes. In the future differentiated stem cells may be used as well.
Australia already has in place a code of practice for the care and use of animals for scientific purposes. This requires research using animals to be licensed by an authority, usually associated with a university or government services. The committee evaluating applications has to be satisfied that the benefit to humans outweighs the harm to animals.
In the case of cosmetics, the harm to animals is often major and benefit to humans minor. However, my experience is that committees are likely to be persuaded that any government requirement for animal testing should be honored.
The proposed bill will save animals from the suffering often associated with testing. Although Australia’s cosmetic industry is not large by international standards, it is growing rapidly, particularly in body and hair products, cosmeceuticals, sunscreen, and anti-ageing products.
Once this ban passes, it will be noted internationally. This, together with the increasing number of other countries banning all animal testing of cosmetics, suggests an international accord could be possible.
Over the past decade the international World Animal Health Organisation — which primarily promotes animal disease control — has assumed responsibility for animal welfare standards worldwide. With 180 member states, it is in a good position to spearhead movement towards an international agreement. It already has a Code of Practice for Use of Animals in Research and Education, which recognizes that:
Animals should only be used when ethically justified and when no other alternative methods are available.
This Code includes “harm versus benefit” ethical review, similarly to the existing Australian system, but without the government imperative to encourage or require animal testing. This could be used to deny companies the opportunity to conduct animal trials with cosmetics in countries still using them.
Eventually, it is clear, cosmetics will not be tested on animals anywhere in the world. Australia’s new regulations will be a small but valuable step towards this future.
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This scale will take a 3D model of your body to show you incredibly detailed progress
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CRISPR, a gene editing tool, is at the heart of numerous new medical treatments and technologies. Some of the incredible uses of CRISPR we’ve seen in the past year alone include editing phages to kill antibiotic-resistant bacteria; targeting cancer’s “command center” in mice, boosting survival rates from 0 to 100 percent; repairing the gene defects that cause sickle cell disease; and copying the T-cells of naturally HIV-immune individuals.
However, even as CRISPR moves toward clinical trials and practical use, its future remains unclear. This is due to the extreme cost of CRISPR treatments; most people simply cannot afford them, and whether insurance carriers will pay the tab is uncertain. Some insurance companies have already implemented no coverage policies for gene therapies; the American healthcare system is ever-changing, and it’s seeming increasingly likely that these extremely expensive therapies might be out of reach even for people with insurance.
StatNews reports that oncologist and author Dr. Siddhartha Mukherjee, who wrote the bestseller Emperor of All Maladies, told the American Society of Clinical Oncology in spring that the world would soon be divided “into the rich who can afford personalized cancer treatment and the poor who cannot.” The case of Glybera, a gene therapy infamously called “the most expensive drug in the world,” adds more credence to this concern. At a whopping $1.4 million per patient, Glybera was sold only once in Germany, abandoned in the EU, and never came to the US market due to its cost.
Much of the issue arises as we try to treat and cure rare diseases, which the United States defines as diseases that affect fewer than 200,000 people and the European Union defines as one that affects fewer than 1 in 2,000 people. However, cumulatively, rare diseases effect an estimated 25 to 30 million Americans, and there could be up to 7,000 rare diseases.
The tension comes at the nexus between multiple market forces: drug companies who want to invest in research and profit from their investment; insurance companies who must maximize profit for shareholders while insuring as many people as possible; governments and leaders with different policies about intervention into the system; scientists who may have independent interest in conducting research but must find a way to fund it; and patients (some with insurance, some without) who are interested or, in some cases, desperate for treatments and cures. How to relieve the tension and allow science to progress in the best way for the most people is a difficult question, but various experts have ideas.
University of Alberta law and policy expert Tania Bubela suggests to StatNews that insurers should be allowed to reimburse drug companies for gene therapies before they receive FDA approval, requiring them to amass more data before increasing drug costs to full price. Another partial solution might be to grant CRISPR licenses one gene at a time rather than issuing exclusive patents on tools like CRISPR. Other creative intellectual property strategies have been proposed by the Rare Genomics Institute. Pediatric oncologist Stuart Orkin and Phillip Reilly, a Third Rock Ventures partner, along with FDA commissioner Scott Gottlieb, advocate for spreading insurer payments to companies out over years of time contingent upon the drug’s continued performance, a sort of annuities structure; this would recognize the value in paying for even expensive drugs rather than years of care and treatment for expensive diseases.
Some form of government intervention is probably inevitable, according to most experts. The US Orphan Drug Act, for example, facilitates the development of treatments and drugs for rare diseases; Orkin and Reilly argue that funds from the Act could pay for gene therapies. The 2009 Biologics Price Competition and Innovation Act made generic biologics, called biosimilars, possible. However, generic forms of CRISPR are not likely to come for decades. Where does this leave us?
StatNews writer Jim Kozubek frames the ultimate issue, suggesting two possible outcomes. “One of two things will happen: either we will embrace a national health care system with broad access but that severely limits expensive new drugs, gene therapies, and CRISPR-based biologics; or these treatments will be available to only the wealthiest among us who can pay for them, a dystopian vision which is perverse but perhaps more realistic considering the pressures for a return on investment.”
Alzheimer’s disease affects about 5.5 million Americans — a number that’s expected to balloon to 13.8 million by 2050.
As the most common cause of dementia, it’s the sixth leading cause of death in the US, behind conditions like heart disease and cancer.
The growing number of people who have the disease is troubling, because there are only four approved drugs that treat symptoms of the disease, and several hopeful treatments have failed key studies in 2017.
Unexpectedly, it’s something researchers at the top cancer hospital in the US are looking into. While cancer and Alzheimer’s seemingly don’t have that much in common, there is one key link that researchers at MD Anderson think could be useful: People with a history of cancer are less likely to get Alzheimer’s, while people with Alzheimer’s are less likely to get cancer.
“Age is the biggest risk factor for both. But then for some reason, some people go one direction, others go another direction,” Jim Ray, head of research for the Neurodegeneration Consortium at MD Anderson told Business Insider.
In the last decade the researchers have made this observational link between the development of Alzheimer’s and a decreased cancer risk and vice versa. So researchers have been hypothesizing why that happens. At a very simplified level, the cause of the diseases might hold the biggest clue. “Cancer is a disease of cells that cannot die, will not die. Alzheimer’s is a disease of cells that are supposed to live your entire lifetime that you can’t keep alive,” he said.
One of the ways researchers have been getting clues into the link is in cancer patients who have chemotherapy-related cognitive dysfunction. An estimated 75% of cancer patients have some level of cognitive impairment (memory loss, attention problems, etc.). Chemotherapy works by killing cancer cells by targeting fast-dividing cells, and in most cases, kills off some healthy cells along the way, including nerve cells in the brain.
“It’s an understudied area,” Ray said. “And I think a lot of people didn’t fully realize it was a problem.”
It’s something drug researchers have started looking into, to see if there could be a therapy that prevents the neurological damage that happens with chemotherapy. If they can figure out what’s going on and how to prevent the neurological side effects for cancer patients, the same approach could hold some promise in treating Alzheimer’s as well.
The search for new Alzheimer’s treatments hasn’t been going well. The last new drug approved was back in 2003, and a slew of failed trials in the beginning of 2017 has cast a shadow over the field.
Still, more drugs are in late-stage trials that could have an impact on the disease, and researchers are pinning hopes on diagnosing the disease early, before symptoms even show up. If any of those treatments pan out, it could change the way we look at the disease and potentially make the statistics a lot less dire.
Unlike some of the promising treatments that have failed in 2017 that deal with the so-called “amyloid hypothesis” (the treatments target amyloid beta deposits in the brain that accumulate in people with Alzheimer’s disease), approaches that try to prevent nerve cells from dying wouldn’t have any impact on that buildup. Instead of trying to clear the body of the deposits, it would just try to strengthen the nerve cells that are there.
“What we’re trying to do is make your nerve cells more resistant to damage,” Ray said. “It won’t stop the damage, but it’d just make them more resistant longer, be more resilient.
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Mindful meditation is becoming an increasingly popular tool, one that people use to manage both their emotional and mental health. The practice is, in essence, the art of not reacting—the art of finding inner stillness through the use of external stillness. It’s taking the time to close your eyes, turn your focus inward, and put all of your energy into just breathing.
It’s an incredibly simple practice that doesn’t take much time at all, and it is incredibly helpful. In a study published in Clinical Psychology Review, researchers at Boston University and Harvard Medical School found that the technique helps alleviate anxiety and allows individuals to better cope with stressful situations. Similarly, in a study from Frontiers in Psychology, researchers found that individuals who meditate have more gray matter volume in their brains than those that do not.
Yet, only 18 million Americans report their participation. Unfortunately, the reality for many overworked Americans is that relaxation is a luxury. Indeed, 92 % of the country still hasn’t caught onto the trend. It’s a surprising statistic considering the fact that meditation has been proven to increase concentration, decrease anxiety, and even help to preserve the aging brain.
Over the last few years, there have been a variety of apps that have aimed to close the gap between people who make time for meditation and the people who don’t know how to fit it into their lives. And while many of the apps that have hit the market have effective qualities, few are as impressive and progressive as Aura Premium—the app created by meditation teachers and therapists that actually gets to know you, so it can help you better.
The AI-infused app is programmed to take post-session feedback information and use it to become a dynamic tool that assists with your mental health. Each time you use the app, it creates more pathways for you to get better at finding your zen.
And while anyone who’s into mindful meditation will appreciate the app for its relaxation enhancers, it’s most appealing for people who are new to meditation and need guidance. All users need is three minutes a day to practice, though you can also choose 7 and 10-minute meditation durations as well.
The app is mostly geared towards helping its users get into a better headspace through exercises, breathing routines, and key spoken words—though it also has the ability to track user’s moods to help them see patterns and form connections.
Aura is essentially like having a portable guide in your pocket. And it’s been so successful in helping its users find inner peace, it was rated the best new app for February 2017 with thousands of nearly perfect ratings. For $59.99 on StackSocial, you can get a lifetime subscription to the app and start your journey to better mental health.
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Cancer patients are all too familiar with the debilitating effects of chemotherapy, still a mainstay of treatment for many malignancies. But as some researchers work to find new drugs, others are working to create new drug-delivery tools. Some of that work involves hacking things like virus particles and bee venom— even sperm cells.
The goal of the research is to find ways to target the delivery of cancer drugs more effectively in order to boost their effectiveness and alleviate side effects— which in some cases are no less dangerous than the cancer itself.
“Some chemotherapy drugs can destroy patients’ hearts or kidneys,” says Daniel Kohane, a Harvard Medical School professor whose lab conducts research on biomaterials and drug delivery.
Chemotherapy works essentially by killing fast-growing cells. But cancer cells aren’t the only ones in the body that reproduce rapidly. Cells in the intestinal lining turn over quickly. Ditto for hair follicles and blood cells. So as chemo takes on cancer cells, it’s also damaging healthy cells.
“Only about 0.1 percent of the drug molecules actually reach and go into the tumors,” says Haifa Shen, an associate professor of nanomedicine at the Houston Methodist Research Institute who studies drug delivery methods. “Over 99.9 percent of chemo drug molecules stay outside of the tumors, being very toxic to normal tissues.”
Viruses are promising drug-delivery tools because, once inside the body, they’re great at finding their way to specific types of cells while avoiding other types. Cold viruses target cells lining the nose, throat, and lungs, for example, while the Ebola virus attacks cells in the liver and arteries. Once inside their target cells, viruses unload their cargo of genetic material and set the stage for the production of more virus particles.
It would be a major advance in cancer therapy if researchers could find a way to modify viruses so as to retain their targeting capabilities while swapping out their genetic cargo for potent anticancer molecules. And Frank Sainsbury and his team at the University of Queensland in Australia are doing just that. In a series of preliminary experiments, the scientists created “fake” viruses whose outer shells, or capsids, were engineered to attach only to breast cancer cells.
“It’s somewhat similar to how two magnets interact with each other, and we can build the capsid’s surface that way,” Sainsbury says.
Sainsbury started off with Bluetongue, a virus that affects only cows and sheep. Using tobacco plants as incubators, the team created empty Bluetongue capsids and then loosed them on breast cancer cells in a petri dish. The shells did what the scientists hoped they would. They found their targets, and the cancer cells “took them in,” according to Sainsbury.
Bluetongue shells make good drug delivery vehicles because they can carry a lot. “They are big shells with a lot of cargo space that we can fill with drug molecules,” Sainsbury says. He added that the next step for his research will be to load the shells with chemo drugs and get them to unload their cargo to kill tumors.
Cancers vary in lethality, and brain cancer is often a death sentence— in part because few drugs are able to reach the brain.
The brain is separated from the rest of the body by a protective membrane that keeps out microbes, viruses, and other potentially harmful organisms and substances. “Your brain is like a medieval city surrounded by stonewalls with the guards at the gates that select who can go through,” says Ernest Giralt, a professor of organic chemistry at the University of Barcelona in Spain. “So very few chemicals can get into the brain.”
Luckily, some substances are able to sneak in. One is bee venom, or apamin, which bees release when they sting.
In its original form, apamin can’t be used therapeutically because it harms nerve cells. So Giralt’s team chemically modified apamin to take away the molecule’s toxic effects. The team injected mice with the modified apamin and observed no side effects. And the modified apamin crossed the brain membrane even more easily than the original version. “It was pure serendipity,” Giralt says.
The team is now exploring the best way to use apamin to shuttle chemo drugs into the brain. There seem to be two ways to do it, Giralt says. One would be simply to attach a chemo molecule to modified apamin. The other would be to fashion a sort of “bulk shipment”— basically stashing a load of chemo into a virus shell studded with apamin molecules and testing whether it can pass through the membrane.
Hardly anyone would think of sperm as a tool to fight cancer, but a group of researchers at IFW Dresden and Chemnitz University of Technology in Germany did. Their preliminary research suggests that it might be possible to turn sperm into “sperm-hybrid micromotors” able to deliver chemotherapy agents to malignancies of the cervix, ovaries, or uterus.
Sperm, of course, have evolved to navigate the female reproductive tract. They neither damage tissue nor cause toxic side effects. To create the spermbots, the scientists soaked bull sperm cells in the cancer drug doxorubicin and then “dressed” the cells with tiny iron-coated mesh. Then they used magnets to steer the cells toward tumor cells in a petri dish.
Three days later, only 13 percent of tumor cells were still alive–a level of effectiveness far superior to that seen when doxorubicin was delivered without spermbots.
The scientists foresee a day in which patients with gynecological cancers might lie inside a magnetic chamber where an electromagnetic field would direct the sperm cells to their target. “It would be somewhat similar to lying inside an MRI machine,” says Haifeng Xu, lead author of a paper describing the research.
NBC Universal Media, LLC on June 26, 2017 by Lina Zoldovich. Copyright 2017 NBC Universal Media, LLC. All rights reserved.
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Polio is a dangerous viral infection. Most people will never know they were infected and about 5 percent will experience only flu-like symptoms. However, polio attacks spinal nerves and the base of the brain in around one percent of cases, leading to paralysis in a matter of hours or days. The paralysis can be treated, but roughly one of every 200 people affected develops a permanent condition such as muscle weakness, muscle shrinking, tight joints, or deformities, including twisted feet or legs.
Polio used to be fairly common worldwide, but it is now rare thanks to a vaccination that was introduced in the mid-1950s. In 2016, the only countries to have any cases of polio at all were Pakistan, Nigeria, and Afghanistan, and as Bill Gates noted in his remarks at the Rotary International Convention on June 12, those cases were a significant drop off from years past: “We’ve gone from 40 cases an hour back in 1988 to just 40 cases in all of 2016.”
The Rotary Foundation has been pivotal in combatting the spread of polio, traveling to some of the world’s most remote and dangerous places to administer vaccines. Rotary and the Bill & Melinda Gates Foundation have raised a combined total of $1.5 billion in funding to combat polio, and the organization is largely responsible for its rapidly decreasing prevalence in the world today.
In total, infection rates have decreased by 99 percent since 1988, and over that period, 16 million people have been saved from paralysis. However, the disease is potent and highly contagious, which means a single infected person could lead to 200,000 cases a year within ten years if the global effort to eradicate polio does not continue.
The impact of the polio vaccine is a testament to just how successful the method can be in fighting diseases. However, while much of the work toward fighting polio has already been done, other diseases are still rampant, and the potential for vaccines to fight these diseases has been compromised by both fraudulent news stories and cultural beliefs.
In his remarks, Gates provided one such example of cultural superstition and distrust of vaccines, noting how one of Northern Nigeria’s most prominent traditional leaders, His Highness, the Emir of Kano, had to “consume an entire vial of vaccine [in front of a village] to reassure people that it was safe.”
Misinformation has affected how people perceive vaccines as well. Incidents such as Andrew Wakefield falsely claiming that the measles, mumps, and rubella (MMR) vaccine leads to autism, as well as the false claim that too many vaccines can overwhelm a child’s immune system, have impacted the use of vaccinations in the developed world, with measles outbreaks occurring amongst unvaccinated children in the United States.
Vaccines hold the key to eliminating many diseases that cause irreparable harm to individuals and communities. Success stories like polio, the work of individuals such as Bill Gates, and constant development in the sector — which includes a vaccine for malaria and the invention of single-use needles — are all vital to ensuring as many people worldwide as possible are vaccinated.
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South Korea is plagued by both high rates of suicide and social stigmas surrounding mental health treatment, a situation that makes treating depression challenging. Ybrain, a local startup, has developed a product that they’re hoping will help turn the tide: Mindd, a headband that delivers transcranial direct current stimulation (tDCS) to the frontal lobe.
Decreased activity in the brain’s frontal lobe is associated with depression. Therefore, the headband delivers a small stream of electricity to the region, to stimulate the area. The electricity is conducted through a saline-soaked absorbent pad that touches the forehead during treatment. About 20 percent of the electrical waves Mindd generates reach the brain.
Part of the appeal of this device is that it can be used at home, which might help patients avoid the stigma of mental health treatments. However, it does store data from users which is sent automatically to their doctor, including records of when they received the electricity therapy, what hours they slept, and their physical activity levels — all via a smartphone app. Ideally, doctors could use this data to monitor the well-being of their patients and incrementally improve their treatment regimens.
“By objectively recording everyday health markers that were previously reliant on the subjective memory of the patient, we hope to improve the quality of medical treatments,” Ybrain’s founding CEO Lee Ki-won told The Korea Herald.
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Monica A. Perez, P.T., Ph. D. and her colleagues at the University of Miami have produced the first evidence that cortical targets could improve motor function in patients who are paralyzed, specifically by spinal cord injury (SCI). The results of their study have been published in Brain.
In previous treatments and studies, sites within the central nervous system have been targeted to try to improve motor function. However, whether or not cortical targets — areas on the outer layer of the brain’s cerebrum — could improve motor function in patients was unknown.
To explore this potential relationship, the research group noninvasively stimulated the area using magnets. They found that, after this stimulation, the finger muscles of those with SCI exerted more force and produced more electromyographic activity, and the patients’ ability to grasp objects with their hands was significantly improved.
Dr. Jonathan R. Wolpaw, M.D. Director of the National Center for Adaptive Neurotechnologies Albany, New York, sees great promise in Perez’s group’s research.
“This study is a major contribution to the realization of a powerful new class of rehabilitation therapies that can target beneficial plasticity to crucial sites in the nervous system,” he said in a news release from The Miami Project. “By taking advantage of recent scientific and technical advances, Dr. Perez’s group produced beneficial change in the cortical circuitry and spinal connections underlying voluntary movement.”
This study could be a game-changer for those paralyzed or otherwise coping with SCI. Cortical targets are relatively unexplored territory as far as treatment options are concerned, so as further studies are conducted, new ways to improve motor function in paralyzed patients could emerge.
Even beyond that, we could learn new information on how certain cortical targets could be related to motor function in general, and the more we learn about how our brains function, the closer we come to being able to treat all neurological disorders and create advanced brain computer interfaces (BCIs), mind-controlled exoskeletons, and other technologies.
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