Researchers at Mayo Clinic have discovered that senescent cells — cells that no longer divide and accumulate with age — shorten lifespan by as much as 35 percent in normal mice.
Removing these aging cells delays tumor formation, preserves tissue and organ function, and extends lifespan without observed adverse effects, the researchers found, writing Feb. 3 in Nature.
“Cellular senescence is a biological mechanism that functions as an ‘emergency brake’ used by damaged cells to stop dividing,” says Jan van Deursen, Ph.D., Chair of Biochemistry and Molecular biology at Mayo Clinic, and senior author of the paper. “While halting cell division of these cells is important for cancer prevention, it has been theorized that once the ‘emergency brake’ has been pulled, these cells are no longer necessary.”
As the immune system becomes less effective, senescent cells build up and damage adjacent cells, causing chronic inflammation, which is closely associated with frailty and age-related diseases.
Mayo Clinic researchers used a compound called AP20187 to remove senescent cells, which delayed tumor formation and reduced age-related deterioration of several organs, extending mediian lifespan of treated mice by 17 to 35 percent. The mice also had a healthier appearance and less inflammation in fat, muscle and kidney tissue.
The research was supported by the National Institutes of Health, the Paul F. Glenn Foundation, the Ellison Medical Foundation, the Noaber Foundation, and the Mayo Clinic Robert and Arlene Kogod Center on Aging.
Van Deursen is a co-inventor of the technology that has been licensed by Mayo Clinic to Unity Biotechnology. Mayo Clinic and Van Deursen have a financial interest in the technology.
Say someone came up to you selling a dietary supplement—a pill that you take once a day—that could boost your energy, improve your body’s ability to repair its DNA, and keep you healthier as you get older.
It might sound like a scam, or more likely just another in a sea of confusing, undifferentiated claims that make up the $20 billion dollar supplement industry.
But let’s say that someone is MIT’s Lenny Guarente, one of the world’s leading scientists in the field of aging research. And he’s being advised by five Nobel Prize winners and two dozen other top researchers in their fields. You might pay a little more attention.
There is no universally accepted definition of boredom. But whatever it is, researchers argue, it is not simply another name for depression or apathy. It seems to be a specific mental state that people find unpleasant — a lack of stimulation that leaves them craving relief, with a host of behavioural, medical and social consequences.
In studies of binge-eating, for example, boredom is one of the most frequent triggers, along with feelings of depression and anxiety1, 2. In a study of distractibility using a driving simulator, people prone to boredom typically drove at higher speeds than other participants, took longer to respond to unexpected hazards and drifted more frequently over the centre line3. And in a 2003 survey, US teenagers who said that they were often bored were 50% more likely than their less-frequently bored peers to later take up smoking, drinking and illegal drugs4.
Boredom even accounts for about 25% of variation in student achievement, says Jennifer Vogel-Walcutt, a developmental psychologist at the Cognitive Performance Group, a consulting firm in Orlando, Florida. That's about the same percentage as is attributed to innate intelligence. Boredom is “something that requires significant consideration”, she says.
Scientists have uncovered a new enzyme that works to block the adverse effects of sugar on the body. Present in all mammals, the enzyme plays the role of disposing of the unwanted byproducts of heightened glucose levels. In discovering this key step in the metabolism of sugar, the scientists say they have uncovered a new therapeutic target for conditions like type 2 diabetes and obesity, and are now working to develop drugs that boosts its activity.
Dubbed glycerol 3-phosphate phosphatase (G3PP), the newly-discovered enzyme was happened upon by scientists at University of Montreal Hospital Research Centre (CRCHUM). The team was hunting for mechanisms that convert excess glucose in beta cells into glycerol, before diverting them outside the cell wall altogether. The hope is that if this process can be manipulated, then it may be possible to avoid the consequences of high glucose levels which can include obesity, diabetes and heart problems.
"When glucose is abnormally elevated in the body, glucose-derived glycerol-3 phosphate reaches excessive levels in cells, and exaggerated glycerol 3 phosphate metabolism can damage various tissues," explains Marc Prentki, a principal investigator at the CRCHUM and professor at the University of Montreal. "We found that G3PP is able to breakdown a great proportion of this excess glycerol phosphate to glycerol and divert it outside the cell, thus protecting the insulin producing beta cells of pancreas and various organs from toxic effects of high glucose levels."
Could this common painkiller become a future cancer-killer? January 12, 2016
Cancer cells (credit: iStock)
Diclofenac, a common painkiller, has significant anti-cancer properties, researchers from the Repurposing Drugs in Oncology (ReDO) project have found.
ReDO, an international collaboration between the Belgium-based Anticancer Fund and the U.S.- based GlobalCures, has published their investigation into diclofenac in the open-access journal ecancermedicalscience.
Diclofenac is a well-known non-steroidal anti-inflammatory drug (NSAID) widely used to treat pain in conditions such as rheumatoid arthritis, migraine, fever, acute gout, and post-operative pain. Like other drugs examined by the ReDO project, diclofenac is cheap and readily accessible — and it’s already present in many medicine cabinets, so it has been carefully tested, according to ReDO researchers.
NSAIDs for cancer treatment?
NSAIDs have shown promise in cancer prevention, but there is now emerging evidence that such drugs may be useful in actually treating cancer. The ReDO researchers have examined the literature and believe that there is enough evidence to start clinical trials on the use of diclofenac in cancer treatment. For example, diclofenac taken in combination with other treatments, such as chemotherapy and radiotherapy, may improve their effectiveness, the researchers say.
They suggest that cutting down on the risk of post-surgical distant metastases through the use of drugs like diclofenac may represent a huge win in the fight against cancer.
Humans have been trying to cheat death for centuries. But while this may have seemed like an impossible pipe dream, the evolution of technology is making it all the more possible that it’s only a matter of time before humans put their brains — or simply their consciousness — inside a robot body. Essentially, this could mean we’d live forever, and one company believes that time will come sooner than later.
Los Angeles-based startup Humai’s ultimate goal is to “extend and enhance human life,” Humai CEO and founder Josh Bocanegra told Medical Daily in an email. The company plans to do this by using artificial technology and nanotechnology to save data about a person’s “conversational styles, behavioral patterns, thought processes, and information about how [their] body functions from the inside-out,” according to the Humai website. Once it has collected everything it needs to know about who you were as a person, it can then begin building a robot body for your brain to live in after you die, effectively bringing you “back to life.”
“We want to use cryonics to preserve the brain and then use nanotechnology to repair the brain before implanting it to a bionic body,” Bocanegra said. “We have great ideas for how we can accomplish this but the details must be reserved until we conduct the research and run tests needed to come up with a strategy we're confident with. However, we aim to build the technology soon enough to bypass the death process and perform brain transplants before most of us die. ”
Our brains contain billions of neurons linked through trillions of synaptic connections, and although disentangling this wiring may seem like mission impossible, a research team from Baylor College of Medicine took on the task. Researchers worked to decipher the wiring of the mouse neocortex, the outermost part of the brain that is thought to be responsible for cognition and perception.
Their hope was that this complex wiring could be broken down to a set of rules governing the assembly of neocortical networks. Their findings, which appear in the current edition of Science, show that the basic wiring of the local circuitry of the neocortex can indeed be captured using a few connectivity rules that are recycled across the layers of the neocortex.
“To our knowledge this is the most comprehensive study ever attempted to map out the canonical circuit diagram of the mature neocortex,” said Dr. Xiaolong Jiang, assistant professor of neuroscience at Baylor College of Medicine and first author on the study. “We were able to determine the cell types found in the neocortex and create a wiring diagram of its local circuit.”
Using cutting-edge methods for tissue slicing and a novel protocol to recover the morphology of neurons, Jiang, working in Andreas Tolias’ lab at Baylor, and his colleagues identified 15 types of inhibitory neurons (the neurons that inhibit electrical firing in brain circuits). Using simultaneous multiple whole-cell recordings they also characterized their electrophysiological properties and mapped the connectivity diagram between them, and also how they connect with nearby excitatory neurons.
In between anatomy and biochemistry, medical students in the US are learning how to sauté, simmer and season healthy, homemade meals.
Since 2012, first and second year students at Tulane University School of Medicine in Louisiana have been learning how to cook. Since the program launched, Tulane has built the country’s first med school-affiliated teaching kitchen and become the first medical school to count a chef as a full-time instructor.
Sixteen med schools have now licensed the center’s curriculum, as have two non-medical schools, the Children’s Hospital San Antonio-Sky Lakes Residency Program and the Nursing School at Northwest Arkansas Community College. In fact, about 10% of America’s medical schools are teaching their students how to cook with Tulane’s program, Tim Harlan, who leads Tulane’s Goldring Center for Culinary Medicine, told the James Beard Foundation conference last month. It also offers continuing medical education programs with a certification for culinary medicine, for doctors, physicians assistants, nurse practitioners, pharmacists, and registered dietitians.
It’s enough to make your heart beat a little faster. A new study suggests that resting heart rate can be used as a ‘death test’ to predict your chance of keeling over in the next two decades.
Although doctors have known for some time that people with low resting heart rates are usually fitter and more healthy, it is the first time the risk has been quantified.
People who have a resting heart rate of 80 beats per minute (bpm) are 45 per cent more likely to die of any cause in the next 20 years compared to those with the lowest measured heart rate of 45 bpm.
Most people’s resting heart rate is between 60 and 100 bpm but the hearts of professional athletes beat around 40 times per minute.
The researchers found that the risk of dying from any illness or health condition raises by around nine per cent for every 10 bpm over. The chance of suffering a fatal heart attack or stroke rises eight per cent.
"The association of resting heart rate with risk of all-cause and cardiovascular mortality is independent of traditional risk factors of cardiovascular disease, suggesting that resting heart rate is a predictor of mortality in the general population," said Dr Dongfeng Zhang, of the Medical College of Qingdao University, Shandong, China.
There are many ways that men try to impress women - be that with their wallets or their wit.
However, eating massive quantities of food is an unusual way that men innately try to show off to the female sex.
A study of 133 adults (74 males and 59 females) by Cornell University found that men consume a considerable amount more food when they are with women.
It doesn't matter what kind of food it is either - they found that not only did men eat 93% more pizza (1.44 more slices) when dining with a female than when with another man, but they also ate 86% more salad.
“These findings suggest that men tend to overeat to show off,” Kevin Kniffin, visiting assistant professor and lead author of the study, told the LA Times. “Instead of a feat of strength, it’s a feat of eating.”
Apparently, by stuffing their faces, men are showing "that they possess extraordinary skills, advantages, and/or surplus energy in degrees that are superior to other men.”
“Conspicuous consumption of food is a much less dramatic ‘risk’ than, say, going off to the front lines of war, but research on the effects of obesity nonetheless show overeating to constitute risky behavior,” added the study authors.
It also may be to show their physical fitness - which may seem an odd conclusion to draw from a pizza binge.
Juliano Pinto, a 29-year-old paraplegic, kicked off the 2014 World Cup in São Paulo with a robotic exoskeleton suit that he wore and controlled with his mind. The event was broadcast internationally and served as a symbol of the exciting possibilities of brain-controlled machines. Over the last few decades research into brain–computer interfaces (BCIs), which allow direct communication between the brain and an external device such a computer or prosthetic, has skyrocketed. Although these new developments are exciting, there are still major hurdles to overcome before people can easily use these devices as a part of daily life.
Until now such devices have largely been proof-of-concept demonstrations of what BCIs are capable of. Currently, almost all of them require technicians to manage and include external wires that tether individuals to large computers. New research, conducted by members of the BrainGate group, a consortium that includes neuroscientists, engineers and clinicians, has made strides toward overcoming some of these obstacles. “Our team is focused on developing what we hope will be an intuitive, always-available brain–computer interface that can be used 24 hours a day, seven days a week, that works with the same amount of subconscious thought that somebody who is able-bodied might use to pick up a coffee cup or move a mouse,” says Leigh Hochberg, a neuroengineer at Brown University who was involved in the research. Researchers are opting for these devices to also be small, wireless and usable without the help of a caregiver.
Cardiovascular disease kills more people on Earth than anything else—over 17 million a year, and the number keeps going up. Of those deaths, more than 40 percent is due to coronary heart disease. Medicine has drugs that can treat it and practices that can help prevent it, but nobody really knows what causes it or how to cure it. Now, Google and the American Heart Association aim to change that by dropping a $50 million funding bomb on the problem. And as you might expect from a Silicon Valley giant that believes in moving fast and breaking things—an approach that hasn’t always transferred well to basic scientific research—the company isn’t spreading the money around.
In an announcement this month at the American Heart Association meeting in Orlando, Florida, Google Life Sciences and the AHA said the money would go to one team over five years. This isn’t covering the bases. This is, to mix a lot of metaphors, a Manhattan Project. Or as Google likes to call such things: a moonshot.
The announcement that scientists are to be allowed to edit the DNA of human embryos will no doubt provoke an avalanche of warnings from opponents of genetic modification (GM) technology, who will warn that we are “playing God” with our genes.
The opponents are right. We are indeed playing God with our genes. But it is a good thing because God, nature or whatever we want to call the agencies that have made us, often get it wrong and it’s up to us to correct those mistakes.
British researchers get green light to genetically modify human embryos
Sadly, of the half a million or so babies that will be born in the UK this year, about 4% will carry a genetic or major birth defect that could result in an early death, or a debilitating disease that will cause misery for the child and their family. This research will eventually lead to technologies that could edit DNA in the same way that we can edit text – to correct the mistakes before the child’s development goes to its final draft. Its successful implementation could reduce, and eventually eliminate, the birth of babies with severe genetic diseases.
I decided to take a try at the great problem of our time: how to lose weight without any effort. So I did an experiment on myself. I was ripe for it, if truth be told. Here I am eight months later and 50 pounds lighter, so something must have worked. My approach to the problem was different from the usual perspective. I’m a psychologist, not a doctor. From the start I suspected that weight regulation was a matter of psychology, not physiology.
If weight were a matter of calories in and calories out, we’d all be the weight we choose. Everyone’s gotten the memo. We all know the ‘eat less’ principle. Losing weight should be as easy as choosing a shirt colour. And yet, somehow it isn’t, and the Unites States grows heavier. It’s time to consider the problem through an alternative lens.
Whatever else it is, hunger is a motivated state of mind. Psychologists have been studying such states for at least a century. We all feel hungry before dinner and full after a banquet, but those moments are the tip of the iceberg. Hunger is a process that’s always present, always running in the background, only occasionally rising into consciousness. It’s more like a mood. When it slowly rises or eases back down, even when it’s beneath consciousness, it alters our decisions. It warps our priorities and our emotional investment in long-term goals. It even changes our sensory perceptions – often quite profoundly.
“Can I ask you why you’re buying fat-free half-and-half?” I said. Half-and-half is defined by its fat content: about 10 percent, more than milk, less than cream.
“Because it’s fat-free?” she responded.
“Do you know what they replace the fat with?” I asked.
“Hmm,” she said, then lifted the carton and read the second ingredient on the label after skim milk: “Corn syrup.” She frowned at me. Then she set the carton back on the conveyor belt to be scanned along with the rest of her groceries.
The woman apparently hadn’t even thought to ask herself that question but had instead accepted the common belief that fat, an essential part of our diet, should be avoided whenever possible.
Then again, why should she question it, given that we allow food companies, advertisers and food researchers to do our thinking for us? In the 1970s, no one questioned whether eggs really were the heart-attack risk nutritionists warned us about. Now, of course, eggs have become such a cherished food that many people raise their own laying hens. Such examples of food confusion and misinformation abound.
Scientists at University College London (UCL) and Nanion Technologies in Munich have developed synthetic DNA-based pores that control which molecules can pass through a cell’s wall, achieving more precise drug delivery.
Therapeutics, including anti-cancer drugs, are ferried around the body in nanoscale carriers called vesicles, targeted to different tissues using biological markers. The new DNA-based pore design is intended to improve that process.
DNA Lock-and-key drug delivery
In operation, a drug-delivery vesicle (white in diagram above) carries the drug to a target cell for release.
The pore is designed as an open barrel made of six DNA-strand staves (blue and gray). The pore is kept closed by a DNA-strand “lock” (red) until the vesicle is prepared to release a drug. At that time, a “key” DNA-strand key (green) is released to hybridize (combine) with the lock DNA strand (forming the red-green helix on right), causing the pore to open and release the drug.*
The pore’s 2-nm-wide channel allows for selectively releasing small organic molecules, which include many medically important drug compounds.
This design for releasing drugs from vesicles improves on previous designs, in which drug release is triggered by temperature-induced leaky vesicle walls or with inserted peptide channels, both of which are less rigid and predictable than the new DNA mechanism.
The study was published Monday (Jan. 11) in Nature Nanotechnology. According to lead author Stefan Howorka, PhD., of UCL Chemistry, the researchers plan to test the synthetic pores in release of a variety of pharmaceutically active biomolecules, including anti-cancer drugs.
The research was funded by the Biotechnology and Biological Sciences Research Council (BBSRC), Leverhulme Trust and UCL Chemistry.
To most of the scientific community, “anti-aging” is a dirty word.
A medical field historically associated with charlatans and quacks, scientists have strictly restricted the quest for a “longevity pill” to basic research. The paradigm is simple and one-toned: working on model organisms by manipulating different genes and proteins, scientists slowly tease out the molecular mechanisms that lead to — and reverse — signs of aging, with no guarantee that they’ll work in humans.
But it’s been a fruitful search: multiple drug candidates, many already on the market for immune or psychiatric disorders, have consistently delayed age-associated diseases and stretched the lifespan of fruit flies, roundworms and mice. Yet human trials have been far beyond reach — without the FDA acknowledging “aging” as a legitimate target for drug development, researchers have had no way of pitching clinical trials to the regulatory agency.
This year, the FDA green lighted an audacious proposal that seeks to test in 3,000 volunteers a drug that — based on animal studies — could extend human lifespan by up to 40 percent and decrease chances of getting age-related diseases. The double-blind, multi-centered trial, Targeting Aging with Metformin (TAME), is the first that pushes aging as a bona fide disease — one that may eventually be tamed with drugs.
“We think this is a groundbreaking, perhaps paradigm-shifting trial,” said Dr. Steven Austad, scientific director of the American Federation for Aging Research (AFAR).
The notion that the more weight people carry, the more difficulty they'll have slimming down isn't a surprising one, but an element of mystery still surrounds the exact mechanism that makes it increasingly difficult to shed that extra baggage. Scientists are now claiming to have zeroed in on a key factor, identifying a protein that stops fat cells from burning energy, a molecule they say could become a key target in treating obesity and other metabolic conditions.
The human body contains two types of fat. White fat stores excess energy, releasing it if it is needed or resulting in flabby love handles if it is not. The other type, brown fat, mostly performs the role of burning fat to generate heat and keep the body warm, a process known as thermogenesis. As our understanding of this has improved over recent years, research has uncovered proteins that may promote thermogenesis when targeted with diabetes drugs and chemical compounds, potentially creating more "good fat". But little is known about the proteins that inhibit it.
Now an international team of scientists has found a protein called sLR11 that suppresses thermogenesis. It was found that mice lacking the gene for the production of sLR11 were less capable of gaining weight, had higher amounts of energy and burned through calories faster, especially after feasting on high fat foods. A closer look revealed that sLR11 sticks to certain receptors on fat cells, like a key sliding into a keyhole, preventing thermogenesis being triggered.
Scientists know that feeling alone can have a negative effect on health, but now they think they may have uncovered one reason why.
Loneliness can lead to fight-or-flight stress signaling, which can ultimately affect the production of white blood cells.
The findings are from a recent study published in the Proceedings of the National Academy of Sciences that examined loneliness in both humans and rhesus macaques, a highly social primate species. The human subjects were participants in the Chicago Health, Aging, and Social Relations Study, a longitudinal study that began in 2002 with adults aged 50-68.
Previous research identified a link between loneliness and a phenomenon they called “conserved transcriptional response to adversity” or CTRA.
This response is characterized by an increased expression of genes involved in inflammation and a decreased expression of genes involved in antiviral responses. Essentially, lonely people had a less effective immune response and more inflammation than non-lonely people.
For the current study, the researchers from the University of Chicago, UCLA, and UC Davis examined gene expression in leukocytes, cells of the immune system that are involved in protecting the body against bacteria and viruses.
Vocal cords that produce realistic sounds have been grown in the lab from human cells.
The work marks a first step towards better treatments for patients who lose their voices to injury or disease.
Vocal cords are formed by two bands of smooth muscle tissue that are lined with a material called mucosa. When air passes through them, the folds vibrate hundreds of times per second to make sounds.
But diseases such as cancer can destroy the delicate folds and for many patients, the medical treatments are limited. Some patients with damaged vocal cords have viscous materials injected to make the folds more pliable. Others improve with voice coaching.
Researchers in the US took a different approach and grew layers of vocal cord cells onto scaffolds that produced tough elastic tissue similar to those within the natural voice box. When doctors tested the lab-grown tissue in voice boxes taken from dead dogs, they found they produced the same sounds as the natural tissue.
“Voice is a pretty amazing thing, yet we don’t give it much thought until something goes wrong,” said lead researcher Nathan Welham at the University of Wisconsin-Madison. “The ability to vibrate and make sounds is pretty remarkable and unique to this part of the body.”
Vocal cord tissue has been grown in the lab for the first time, paving the way for potentially revolutionary treatments for people who have lost their vocal cords.
Stars such as Adele, Frank Ocean and John Mayer have been afflicted with vocal cord damage -- and have undergone extensive, and expensive, treatment to deal with it. But now researchers have found a solution to outdated ways of dealing with vocal cord damage -- by growing them in a lab.
Previous vocal cord treatment required patients, who had received transplanted cords from cadavers, to be injected with huge doses of immunosuppresants. But a team from the University of Wisconsin Medical School has come up with a new way of transplanting cords. They successfully grew 170 sets of vocal cords in a lab -- cords that don't require the usual round of immunosuppresants.
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