A new system for growing heart tissue in the lab may make future heart, liver, and lung repair much easier. University of Toronto scientists have developed asymmetrical honeycomb-shaped 2D meshes of protein scaffolding that stick together like Velcro and imitate the environments in which tissue and muscle cells grow in the body.
The meshes are made from a flexible polymer called POMaC (which is short for this mouthful: "poly(octamethylene maleate (anhydride) citrate)"). T-shaped posts bonded onto the top of the mesh act like the tiny hooks on velcro strips – they loop through the holes in a mesh placed above and lock the two together. The researchers tested with both two and three-sheet-thick mesh scaffolds in a variety of configurations (i.e. with them lined up in different ways).
"As soon as you click them together, they start beating," says project lead Milica Radisic, referring to the way the heart muscle cells contract together and bend the polymer meshes. "And when we apply electrical field stimulation, we see that they beat in synchrony."
The way the scaffold bends and stretches as it "beats" helps the heart cells grow tougher and more robust, which makes them more likely to survive the ravages of life in an actual heart. That's the long-term plan – to get these flexible, modular mesh scaffolds producing artificial tissue that can be used to repair damaged hearts.
"If you had these little building blocks, you could build the tissue right at the surgery time to be whatever size that you require," Radisic says. Surgeons could then graft the scaffold onto the patient's heart, and after a few months the patient would be left with a repaired heart (and no scaffold, as that gradually gets absorbed by the body as harmless waste).
Imagine living a healthy, normal life without the ability to re-experience in your mind personal events from your past. You have learned details about past episodes from your life and can recite these to family and friends, but you can’t mentally travel back in time to imagine yourself in any of them.
Cognitive scientists from Baycrest Health Sciences’ Rotman Research Institute in Toronto had a rare opportunity to examine three middle-aged adults (two from the U.S., the other from the U.K.) who essentially live their lives in the “third person” because of a condition known as lifelong severely deficient autobiographical memory (SDAM).
The intriguing findings are posted online in the journal Neuropsychologia, ahead of the print edition.
“Many of us can relate to the idea that people have different abilities when remembering events. What is unique about these individuals is that they have no personal recollection,” said Dr. Brian Levine, senior scientist at Baycrest’s Rotman Research Institute, and senior author on the paper.
“Even though they can learn and recall information normally and hold down professional careers, they cannot re-experience the past with a vivid sense of personal reliving. It’s as if their past was experienced in the third person.”
A French woman has won a court-ordered disability grant after claiming to suffer from a 'gadget allergy' due to electromagnetic radiation.
Marine Richard, who lives in the mountains of southwest France to avoid electronics, said that the ruling was a "breakthrough" for people who claim to suffer from Electromagnetic Hypersensitivity (EHS).
Sufferers say they experience symptoms including headaches, nausea, tiredness and 'tingling' sensations when exposed to electromagnetic radiation from cellphones, WiFi or even just batteries, screens and other elements of technology which give off electromagnetic radiation. In the UK several forums and groups exist to help self-identified sufferers, including ES UK
Richard's disability allowance was granted by the court in Toulouse, though the ruling does not mean that EHS is formally considered an illness.
Scientific studies have not demonstrated a clear link between the type of radiation emitted by household gadgets and health problems in humans. EHS is not a recognised condition in the UK, and Public Health England has said there is no evidence that these low-level fields damage health. The government does recognise the minor health impacts of some very high-level electromagnetic radiation exposure however, such as from power lines.
If there is one health myth that will not die, it is this: You should drink eight glasses of water a day.
It’s just not true. There is no science behind it.
And yet every summer we are inundated with news media reports warning that dehydration is dangerous and also ubiquitous.
These reports work up a fear that otherwise healthy adults and children are walking around dehydrated, even that dehydration has reached epidemic proportions.
Let’s put these claims under scrutiny.
I was a co-author of a paper back in 2007 in the BMJ on medical myths. The first myth was that people should drink at least eight 8-ounce glasses of water a day. This paper got more media attention (even in The Times) than pretty much any other research I’ve ever done.
It made no difference. When, two years later, we published a book on medical myths that once again debunked the idea that we need eight glasses of water a day, I thought it would persuade people to stop worrying. I was wrong again. Many people believe that the source of this myth was a 1945 Food and Nutrition Board recommendation that said people need about 2.5 liters of water a day. But they ignored the sentence that followed closely behind. It read, “Most of this quantity is contained in prepared foods.”
The human brain can be compared to something like a big, bustling city. It has workers, the neurons and glial cells which co-operate with each other to process information; it has offices, the clusters of cells that work together to achieve specific tasks; it has highways, the fibre bundles that transfer information across long distances; and it has centralised hubs, the densely interconnected nodes that integrate information from its distributed networks.
Like any big city, the brain also produces large amounts of waste products, which have to be cleared away so that they do not clog up its delicate moving parts. Until very recently, though, we knew very little about how this happens. The brain’s waste disposal system has now been identified. We now know that it operates while we sleep at night, just like the waste collectors in most big cities, and the latest research suggests that certain sleeping positions might make it more efficient.
Although most people with multiple sexual partners know that being checked for STDs is the responsible thing to do, many don’t do so because of the stigma associated with going to the clinic. That’s why a Silicon Valley-based startup has developed the Hoope ring. It’s worn on the thumb, and can reportedly diagnose diseases such as syphilis, gonorrhoea, chlamydia and trichomoniasis in less than a minute.
Users start by using Hoope’s electric pulse generator to numb their skin. They then press a button on the ring, which causes its single-use retractable needle to come out. That needle is then used to draw a blood sample, which is carried by capillary action to the ring’s lab-on-a-chip.
There, the blood flows through four microfluidic channels, in which it’s exposed to different antigens that have been synthesized to catch antibodies associated with each of the targeted diseases. If any of those antibodies are present and thus captured, an electrochemical reaction occurs which is detected by the onboard electronics.
The Hoope then wirelessly transmits the data to an app on the user’s smartphone, which tells them what disease has been detected, and where in their community they can go for treatment.
THANKS to Caitlyn Jenner, and the military’s changing policies, transgender people are gaining acceptance — and living in a bigger, more understanding spotlight than at any previous time.
We’re learning to be more accepting of transgender individuals. And we’re learning more about gender identity, too.
The prevailing narrative seems to be that gender is a social construct and that people can move between genders to arrive at their true identity.
But if gender were nothing more than a social convention, why was it necessary for Caitlyn Jenner to undergo facial surgeries, take hormones and remove her body hair? The fact that some transgender individuals use hormone treatment and surgery to switch gender speaks to the inescapable biology at the heart of gender identity.
This is not to suggest that gender identity is simply binary — male or female — or that gender identity is inflexible for everyone. Nor does it mean that conventional gender roles always feel right; the sheer number of people who experience varying degrees of mismatch between their preferred gender and their body makes this very clear.
In fact, recent neuroscience research suggests that gender identity may exist on a spectrum and that gender dysphoria fits well within the range of human biological variation. For example, Georg S. Kranz at the Medical University of Vienna and colleagues elsewhere reported in a 2014 study in The Journal of Neuroscience that individuals who identified as transsexuals — those who wanted sex reassignment — had structural differences in their brains that were between their desired gender and their genetic sex.
A fungus that grows on horse dung contains a protein that can kill bacteria.
The substance, known as copsin, has the same effect as traditional antibiotics, but belongs to a different class of biochemical substances. Copsin is a protein, whereas traditional antibiotics are often non-protein organic compounds.
The researchers led by Markus Aebi, a mycology professor at ETH Zurich, discovered the substance in the common inky cap mushroom Coprinopsis cinerea. Aebi and colleagues were interested in understanding how this fungus and various bacteria affect each other’s growth.
This involved cultivating the fungus in a laboratory along with several different types of bacteria. It was found that C. cinerea is able to kill certain bacteria. Further research demonstrated that the copsin produced by the mushroom is responsible for this antibiotic effect.
Copsin belongs to the group of defensins, a class of small proteins produced by many organisms to combat microorganisms that cause disease. The human body also produces defensins to protect itself against infections. They have been found, for example, on the skin and in the mucous membranes.
For Aebi, the main focus of this research project was not primarily on applications for the new substance.
A gene called FTO has been a major blip on the obesity radar since 2007 – but we hadn’t yet figured out how the connection applied. Thanks to a number of lab mice, we now know that FTO directly affects how the body decides to store energy.
More specifically, a defect in this gene causes significantly more energy to be converted into fat rather than being burned as fuel. In effect – two otherwise identical subjects with identical habits would have significantly different levels of weight gain based entirely on this gene.
Intrigued by the implication, MIT scientists used DNA editing technology to switch on and off the gene in lab mice. Mice with the fully activated gene showed much higher metabolism rates and remained lean and fit regardless of diet.
There are several types of fat in the human body – brown fat, white fat, subcutaneous fat and visceral fat for example – and not all of them are harmful to your health.
White fat has two jobs – first to store energy, and second to produce hormones that are passed into the bloodstream. A particularly important hormone produced by white fat cells is adiponectin. Also known as GBP-28 or AdipoQ, adiponectin is a protein hormonethat plays a role in preventing Type 2 Diabetes among other things. Studies have shown however that in overweight people, production of this hormone is reduced.
Brown fat helps you stay warm, and actually burns white fat to produce energy. We have more of it as children than later in life, and there’s far less of it than white fat in general. Even in lean, healthy adults the ratio of white fat to brown fat is likely to be 100 to 1 by weight. If properly stimulated, just 2 ounces of brown fat could burn up to 500 calories in a day.
When your body decides to create new fat cells, the choice of brown or white depends largely on a pair of genes that control thermogenesis (energy burn) – and these genes are directly affected by the FTO gene which acts like a “master switch”.
In essence, defective FTO genes cause your body to produce more white fat – while good ones cause your body to produce more brown fat.
The drug modafinil was developed to treat narcolepsy (excessive sleeping), but it is widely used off-licence as a ‘smart drug’ to promote cognitive enhancement, where qualities such as alertness and concentration are desired to assist someone with, for example, exam preparation. Past studies on sleep-deprived individuals have shown a strong positive effect of modafinil on these functions, but there has been less attention and scientific consensus on the drug’s overall effectiveness as a cognitive enhancer in people that are not sleep-deprived – presumably the majority of people taking it.
Now, a new systematic review, published online in the peer-reviewed journal European Neuropsychopharmacology shows that modafinil does indeed confer significant cognitive benefits in this group, at least on a particular subset of tasks.
Dr Ruairidh Battleday and Dr Anna-Katharine Brem from the University of Oxford and Harvard Medical School evaluated all research papers on cognitive enhancement with modafinil from January 1990 to December 2014. They found 24 studies dealing with different benefits associated with taking modafinil, including planning and decision making, flexibility, learning and memory, and creativity.
Unsurprisingly, they found that the performance-enhancing capacity of modafinil varied according to the task. What emerged was that the longer and more complex the task tested, the more consistently modafinil conferred cognitive benefits.
Modafinil made no difference to working memory, or flexibility of thought, but did improve decision-making and planning. Very encouragingly, the 70% of studies that looked at the effects of modafinil on mood and side effects showed very little overall effect, although a couple reported insomnia, headache, stomach ache or nausea (which were also reported in the placebo group).
Norovirus is a nasty bug that brings about inflammation in the stomach and intestines leading to pain, nausea, diarrhea and sometimes even death. It affects around 20 million people per year in the US, but despite its rampant nature, questions remain over how exactly it is transmitted. To shed further light on how one of the world's most common pathogens spreads between humans, scientists have built a vomiting machine to study its behaviour when projected into the air.
Earlier studies have indicated that norovirus can become aerosolized when a person vomits. This means that particles containing the virus can become airborne post-puke, lingering threateningly in the air or on surfaces ready to infect innocent bystanders. But these have only really been suspicions rather than proven scientific fact, so a team from North Carolina (NC) State University went searching for more concrete answers.
There are many ways to get rid of excess fat, most of them involving diet and exercise. But scientists have identified a gene that may do the trick without all that effort.
A Holy Grail of fat—one that can turn more quickly into energy and melt away without building up in those unwanted bulges—is actually backed by some intriguing evidence. The trouble is, it’s hard to find in most adults. It turns out we have more of the less desirable kind, the white fat that accumulates around the middle and in our tissues, that potentially leads to dangerous health problems.
Now, scientists reporting in the New England Journal of Medicine report that they have connected the dots between the strongest gene associated with obesity and a way to make white fat more active. The idea is to literally give white fat fewer couch potato tendencies and help it more actively burn energy, more like the so-called brown fat that’s in such short supply.
In the May 15, 2014, edition of the journal Nature, Floyd Romesberg’s chemistry lab at San Diego’s Scripps Research Institute published a paper titled “A Semi-Synthetic Organism with an Expanded Genetic Alphabet.” Romesberg and his colleagues had created a bacterium incorporating chemical building blocks that, as far as anybody knows, have never been part of any earthly life form.
There had been previous claims to “creating life.” Genome pioneer Craig Venter led a team that manufactured a genome for a germ that causes pneumonia in cows, but their effort used the familiar chemical bases of DNA, known by the letters A, G, C, and T. Romesberg’s group, on the other hand, added two additional letters, dubbed X and Y. When the bacteria successfully replicated X and Y in succeeding generations, Romesberg’s lab could claim to have made the first living thing with an expanded genetic code.
“People would ask what the big deal is, and I said, ‘Imagine you had a language with only four letters’” Romesberg says. “‘It would be clumsy and would really curtail the kinds of stories you could tell. So imagine two more letters. Now you could write more interesting stories.’”
New drugs are the most obvious story that could be told with the technology. A startup company called Synthorx, created by Romesberg and the venture fund Avalon Ventures, says it has exploited E. coli bacteria containing X and Y to help manufacture a protein, a step the company’s president and CEO Court Turner describes as “our baby unicorn.” The company didn’t identify the protein, except to say it is “well studied” and that they’d added a new function to it, a way for another drug to attach to the protein at a specific site.
TOWARD the end of the Second World War, researchers at the University of Minnesota began a legendary experiment on the psychology and physiology of human starvation — and, thus, on hunger. The subjects were 36 conscientious objectors, some lean, some not. For 24 weeks, these men were semi-starved, fed not quite 1,600 calories a day of foods chosen to represent the fare of European famine areas: “whole-wheat bread, potatoes, cereals and considerable amounts of turnips and cabbage” with “token amounts” of meat and dairy.
As diets go, it was what nutritionists today would consider a low-calorie, and very low-fat diet, with only 17 percent of calories coming from fat.
What happened to these men is a lesson in our ability to deal with caloric deprivation, which means, as well, a lesson in any expectations we might have about most current weight-loss advice, and perhaps particularly the kind that begins with “eat less” and “restrict fat.”
The men lost an average of a pound of body fat a week over the first 12 weeks, but averaged only a quarter-pound per week over the next 12, despite the continued deprivation. And this was not their only physiological reaction. Their extremities swelled; their hair fell out; wounds healed slowly. They felt continually cold; their metabolism slowed.
More troubling were the psychological effects. The men became depressed, lethargic and irritable. They threw tantrums. They lost their libido. They thought obsessively about food, day and night. The Minnesota researchers called this “semi-starvation neurosis.” Four developed “character neurosis.” Two had breakdowns, one with “weeping, talk of suicide and threats of violence.” He was committed to the psychiatric ward. The “personality deterioration” of the other “culminated in two attempts at self-mutilation.” He nearly detached the tip of one finger and later chopped off three with an ax.
People who suffer from neuroticism – a condition characterised by anxiety, fear and negative thoughts – are extremely tuned in to looking for threats. For that reason, you may expect them to perform well in jobs requiring vigilance: stunt pilots, aviators and bomb defusement. Yet, the evidence suggests they are actually more suited to creative jobs.
Exactly what drives neuroticism and the creativity it is associated with is not known. But researchers have now come up with a theory which suggests that it could be down to the fact that people who score highly on neuroticism tests, meaning they are prone to anxiety or depression, tend to do a lot of thinking – often at the expense of concentrating at the task at hand. Past, present and future
The hypothesis, which is yet to be experimentally verified, is an extension of what we already know. People who have neurotic traits typically look for things to worry about (a mechanism dubbed “self-generated thinking”). For example, people who get depressed are consumed by such self-generated negative thoughts that they forget what they are supposed to be doing. In other words, they are not very tuned in to the ”here and now”, which is pretty important if you need somebody to concentrate on defusing a bomb.
What the new research helps to do is explain the underlying brain mechanisms that interfere with “on the job thinking”. A certain amount of brain arousal is great for concentration but too much interferes with clear thinking and that’s what you want when performing stunts, flying planes, and disposing of bombs.
So where does the creativity come in? The authors argue that people who engage in self-generated thinking are creative because they are not rooted in reality – they are away with the fairies. Indeed, they may resist attempts to get them to concentrate on reality whilst they focus on their own thoughts. It is hardly a surprise, then, that their ideas can be new, whacky and original.
So while people scoring high on neuroticism may struggle with a lot of stress, they can still have a successful working life. They may actually be able to find creative solutions to problems that didn’t exist in the first place, and in the process come with some pretty useful and imaginative stuff. Rather like Billy Liar, in his escape from his tedious existence conjuring up some fairly exciting daydreams.
Inspired by the Star Trek tricorder, engineers and physicians at the Johns Hopkins University School of Medicine have developed a hand-held, battery-powered device called MouthLab that quickly picks up vital signs from a patient’s lips and fingertip.
Updated versions of the prototype could replace the bulky, restrictive monitors now used to display patients’ vital signs in hospitals and actually gather more data than is typically collected during a medical assessment in an ambulance, emergency room, doctor’s office, or patient’s home.
The MouthLab prototype’s measurements of heart rate, blood pressure, temperature, breathing rate, and blood oxygen from 52 volunteers compared well with vital signs measured by standard hospital monitors. The device also takes a basic electrocardiogram. The study was published in the September issue of the Annals of Biomedical Engineering.
Early warning for non-doctors
“We see it as a ‘check-engine’ light for humans,” says the device’s lead engineer, Gene Fridman, Ph.D., an assistant professor of biomedical engineering and of otolaryngology–head and neck surgery at Johns Hopkins. “It can be used by people without special training at home or in the field.” He expects the device may be able to detect early signs of medical emergencies, such as heart attacks, or avoid unnecessary ambulance trips and emergency room visits when a patient’s vital signs are good.
Noting that most current methods of diagnosing cognitive diseases can only detect impairment after the disorders have taken hold, researchers at MIT have combined digital pen technology and some custom software to develop an objective model for early detection.
The new system, still in its concept stage, is a development on the Clock Drawing Test (CDT) that doctors use to screen for illnesses such as Alzheimer’s and Parkinson’s. In this test patients are asked to draw a clock face showing the time as 10 minutes past 11, and then asked to copy a pre-drawn clock face showing the same time. The results are then examined for signs of problems by a doctor.
Researchers at MIT’s Computer Science and Artificial Intelligence Laboratory (CSAIL) swapped out the ink pen used in current tests for the Anoto Live Pen, a digitizing ballpoint pen that, with the help of a built-in camera, can measure its position on the paper more than 80 times a second. Rather than only relying on the final drawing for subjective analysis by medical practitioners, the pen can pick up on all the patient's hesitations and movements.
Working at Lahey Hospital and Medical Center, the CSAIL researchers helped produce analysis software for the Live Pen version of the test, resulting in what the team calls the digital Clock Drawing Test.
Nearly half of all Europeans are genetically predisposed to obesity. The condition is a worldwide epidemic affecting more than half a billion people and rising every year in most countries.
Despite this, we know little about the genetic origin of the condition and have no good medical treatment for it other than bariatric surgery. But now a genetic study seems to have cracked the mystery – raising hopes for more efficient treatment.
The global obesity crisis is often blamed on an increasingly sedentary life style and poor eating habits. However, studies have shown that 70-80% of the differences between people in body fat are due to their genes (this is called the heritability).
The first large-scale genetic studies for obesity were launched in 2007, after the initial mapping of the human genome. And one gene, dubbed FTO, made the headlines by popping its head above the other 20,000 genes in the pack. For the past eight years, despite finding nearly 100 other genes linked to obesity, FTO and the area around it have remained the top signals. But scientists around the world have struggled to understand how the gene works and whether it really is behind obesity.
Scientists in the US have found that a feel-good exercise hormone called irisin does indeed exist in humans, putting to bed long-disputed claims that it is a myth.
The research team, led by Bruce Spiegelman from the Dana-Farber Cancer Institute, used mass spectrometry to look for irisin in blood samples of individuals after exercise, finding that these people had released the exercise hormone from their body, which activates fat cells to increase energy turn over.
The research was published today in the journal Cell Metabolism.
“Concentrations are present in sedentary individuals and are significantly increased in individuals undergoing aerobic interval training,” the researchers said in the paper.
“We therefore also confirm our earlier report of irisin being regulated by endurance exercise in humans.” Working out, feeling good
Irisin received a lot of attention recently because of divisions in the scientific community about whether or not it actually existed.
Irisin’s discovery in 2012 was exciting because scientists had potentially found one reason why exercise keeps us healthy.
When irisin levels were increased in mice, their blood and metabolism improved. Results from human studies are still mixed as to what kinds of exercise raise irisin, but data suggest that high-intensity training protocols are particularly effective.
Professor Mark Febbraio, Head of the Cellular and Molecular Metabolism Laboratory and Head of the Diabetes and Metabolism Division at the Garvan Institute for Medical Research, said that the form of mass spectrometry used in the new study was far more accurate and reliable in measuring irisin.
“Using state-of-the-art technology, the researchers have proven beyond doubt that irisin is real. It settles the argument,“ said Professor Febbraio, who was not involved in the research.
Previous studies using commercially available kits called “ELISA” kits detected the presence of irisin, by recognising an antigen, in samples, which could produce inconsistent results with irisin, he said.
Scientists have found antibiotic resistance genes in the bacterial flora of a South American tribe who have never been exposed to antibiotic drugs.
The findings suggest that bacteria in the human body have had the ability to resist antibiotics since long before such drugs were ever used to treat disease.
The research stems from the 2009 discovery of a tribe of Yanomami Amerindians in a remote mountainous area in southern Venezuela. Largely because the tribe had been isolated from other societies for more than 11,000 years, its members were found to have among the most diverse collections of bacteria recorded in humans.
Within that plethora of bacteria, though, the researchers have identified genes wired to resist antibiotics.
Researchers have created unusually intelligent mice by altering a single gene and as a result the mice were also less likely to feel anxiety or recall fear.
The study, led by the University of Leeds and Mount Sinai Hospital in Toronto, is published today in the journal Neuropsychopharmacology.
It sheds light on the molecular underpinnings of learning and memory and could form the basis for research into new treatments for age-related cognitive decline, cognitive disorders such as Alzheimer’s disease and schizophrenia, and other conditions.
The researchers altered a gene in mice to inhibit the activity of an enzyme called phosphodiesterase-4B (PDE4B), which is present in many organs of the vertebrate body, including the brain.
In behavioural tests, the PDE4B-inhibited mice showed enhanced cognitive abilities.
They tended to learn faster, remember events longer and solve complex exercises better than ordinary mice.
For example, the “brainy mice” showed a better ability than ordinary mice to recognise another mouse that they had been introduced to the day before. They were also quicker at learning the location of a hidden escape platform in a test called the Morris water maze.
However, the PDE4B-inhibited mice also showed less recall of a fearful event after several days than ordinary mice.
Genes, like people, have families — lineages that stretch back through time, all the way to a founding member. That ancestor multiplied and spread, morphing a bit with each new iteration.
For most of the last 40 years, scientists thought that this was the primary way new genes were born — they simply arose from copies of existing genes. The old version went on doing its job, and the new copy became free to evolve novel functions.
Certain genes, however, seem to defy that origin story. They have no known relatives, and they bear no resemblance to any other gene. They’re the molecular equivalent of a mysterious beast discovered in the depths of a remote rainforest, a biological enigma seemingly unrelated to anything else on earth.
The mystery of where these orphan genes came from has puzzled scientists for decades. But in the past few years, a once-heretical explanation has quickly gained momentum — that many of these orphans arose out of so-called junk DNA, or non-coding DNA, the mysterious stretches of DNA between genes. “Genetic function somehow springs into existence,” said David Begun, a biologist at the University of California, Davis.
The first ever prescription pill to boost women's libido has won the approval of US regulators. Addyi got the final nod from the Food and Drug Administration (FDA) on Tuesday after three 24-week trials showed it to offer an increase in sexual desire in premenopausal women, though the agency does warn of side effects that include low blood pressure and fainting.
The company behind the drug, North Carolina-based Sprout Pharmaceuticals, has sought to develop a medication to treat acquired, generalized hypoactive sexual desire disorder (HSDD). This condition is defined by an absence of sexual desire that brings about significant stress and interpersonal difficulties. Studies have shown it affects nearly one in 10 US women.
Addyl (aka flibanserin) is a serotonin 1A receptor agonist and a serotonin 2A receptor antagonist, but the FDA says the precise mechanism that gives it libido-enhancing properties is not currently known. While the drug has been tested in more than 11,000 women, the all important FDA approval follows three 24-week studies involving around 2,400 women with HSDD. The women were aged 36 on average and had suffered from the condition for an average of five years.
In the four weeks leading up to treatment, the women were made to record the number of satisfying sexual events experienced, measure their sexual desire on a scale ranging from 1.2 to 6.0 and measure the stress resulting from HSDD on a scale of zero to four.
Thinking about plants and animals, including humans, as autonomous individuals is a serious over-simplification, according to new research.
New studies reveal that what we have always thought of as individuals are actually “biomolecular networks” that consist of visible hosts plus millions of invisible microbes that have a significant effect on how the host develops, the diseases it catches, how it behaves, and possibly even its social interactions.
“It’s a case of the whole being greater than the sum of its parts,” says Seth Bordenstein, associate professor of biological sciences at Vanderbilt University, whose work adds to the scientific knowledge suggesting that symbiotic microbes play a fundamental role in virtually all aspects of plant and animal biology, including the origin of new species.
In this case, the parts are the host and its genome plus the thousands of different species of bacteria living in or on the host, along with all their genomes, collectively known as the microbiome.
(The host is something like the tip of the iceberg while the bacteria are like the part of the iceberg that is underwater: Nine out of every 10 cells in plant and animal bodies are bacterial. But bacterial cells are so much smaller than host cells that they have generally gone unnoticed.)
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