Anthropologists have been curious about the evolution of human intelligence for many decades. The main lines of research have involved archaeological finds concerning the use of fire, tools and so on. The Conversation
But what about looking for evidence in fossil skulls, the place where the brain resided?
The volume of the human brain increased to be about three and a half times larger than our Australopithecus ancestors 3 million years ago.
It is generally assumed that intelligence is correlated with brain size, and the reason for this is that the number of nerve cells in mammalian brains seems to be directly related to brain size.
Our research focused on the rate of blood flow to the brain, which relates closely to metabolic rate because the blood supplies the essential oxygen. If blood flow to your brain is stopped, you will pass out within seconds.
Normally you have about 7 millilitres of blood flowing to your brain each second. Remarkably, this rate changes little, regardless of whether you are awake, asleep or solving mathematical problems.
The brain's plumbing
The blood flow to the cognitive part of the brain, the cerebrum, comes through two internal carotid arteries, one on the right and one on the left. The size of these arteries is related to the rate of blood flow through them.
Almost two-thirds of cancer mutations are caused by random DNA-copying errors during cell division and are impossible for us to avoid, regardless of lifestyle and the genes we inherit from our parents, according to new research.
The findings – which estimate that 66 percent of cancer mutations are effectively bad luck that we can't do anything about – support the conclusions of a controversial paper released in 2015 by the same researchers, which came under fire for appearing to suggest that there was nothing we could do to prevent various cancers.
This time around, the team from Johns Hopkins University are at pains to emphasise that their findings don't contradict what we know about cancer prevention – nor detract from the importance of environment and heredity in terms of causing cancer.
"It is well-known that we must avoid environmental factors such as smoking to decrease our risk of getting cancer. But it is not as well-known that each time a normal cell divides and copies its DNA to produce two new cells, it makes multiple mistakes," says biostatistician Cristian Tomasetti.
"These copying mistakes are a potent source of cancer mutations that historically have been scientifically undervalued, and this new work provides the first estimate of the fraction of mutations caused by these mistakes."
Working on getting a better night’s sleep can lead to optimal physical and mental well-being over time—but quality of sleep is more important than quantity.
For a new study, researchers analyzed the sleep patterns of more than 30,500 people in UK households over four years and discovered that better sleep leads to levels of mental and physical health comparable to those of somebody who’s won a jackpot of around £200,000.
Positive changes in sleep over time—improved quality and quantity, and using less sleep medication—are linked with improved scores on the General Health Questionnaire (GHQ), which is used by mental health professionals to monitor psychological well-being in patients.
People surveyed who reported positive improved sleep scored a 2-point change in the GHQ—a result comparable to those recorded from patients completing an eight-week program of mindfulness-based cognitive therapy designed to improve psychological well-being.
As we get older, we start to think a little bit more slowly, we are less able to multitask and our ability to remember things gets a little wobblier. This cognitive transformation is linked to a steady, widespread thinning of the cortex, the brain's outermost layer. Yet the change is not inevitable. So-called super agers retain their good memory and thicker cortex as they age, a recent study suggests.
Researchers believe that studying what makes super agers different could help unlock the secrets to healthy brain aging and improve our understanding of what happens when that process goes awry. “Looking at successful aging could provide us with biomarkers for predicting resilience and for things that might go wrong in people with age-related diseases like Alzheimer's and dementia,” says study co-author Alexandra Touroutoglou, a neuroscientist at Harvard Medical School.
Touroutoglou and her team gave standard recall tests to a group of 40 participants between the ages of 60 and 80 and 41 participants aged 18 to 35. Among the older participants, 17 performed as well as or better than adults four to five decades younger. When the researchers looked at MRI scans of the super agers' brains, they found that their brains not only functioned more like young brains, they also looked very similar.
As a couple finishes its business, millions of sperm begin theirs: rushing toward an egg to fertilize it. But these days, scientists say, an increasing proportion of sperm — now about 90 percent in a typical young man — are misshapen, sometimes with two heads or two tails.
Even when properly shaped, today’s sperm are often pathetic swimmers, veering like drunks or paddling crazily in circles. Sperm counts also appear to have dropped sharply in the last 75 years, in ways that affect our ability to reproduce.
“There’s been a decrease not only in sperm numbers, but also in their quality and swimming capacity, their ability to deliver the goods,” said Shanna Swan, an epidemiologist at the Icahn School of Medicine at Mount Sinai, who notes that researchers have also linked semen problems to shorter life expectancy.
Perhaps you were expecting another column about political missteps in Washington, and instead you’ve been walloped with talk of bad swimmers. Yet this isn’t just a puzzling curiosity, but is rather an urgent concern that affects reproduction, possibly even our species’ future. Continue reading the main story
Andrea Gore, a professor of pharmacology at the University of Texas at Austin and the editor of the journal Endocrinology, put it to me this way: “Semen quality and fertility in men have decreased. Not everyone who wants to reproduce will be able to. And the costs of male disorders to quality of life, and the economic burden to society, are inestimable.”
Penicillin has been around since 1928, which means the bugs it's meant to fight have had almost 100 years to develop strategies to survive its effects. As more and more bacterial infections become impervious to penicillin and the other antibiotics that belong to the penicillin group, finding alternative ways to beat down deadly infections is becoming more critical than ever. Now researchers have found what all good combat specialists have long known – getting each other's back in a fight can be a winning strategy.
The bacteria that are immune to penicillins like amoxicillin and ampicillin release enzymes called beta-lactamases that shred the antibiotics, rendering them useless. Some bacteria can defeat even newly developed penicillins by putting out a group of bacterial beta-lactamases called metallo-beta-lactamases (MBLs). One such group of bacteria are those called carbapenem-resistant enterobacteriaceae or CRE, which cause infections that, according to the CDC can kill up to half of their victims.
In a study led by Robert A. Bonomo from Case Western Reserve University School of Medicine in Cleveland, Ohio, it was discovered that combining two antibiotics eliminated 81 percent of CRE specimens tested.
When we talk about animal instinct, we're often talking about pheromones - chemicals that affect the behaviour of other animals, and make individuals irresistible to the opposite sex during mating season.
For decades, debate has raged over whether humans might also release and be susceptible to our own unique pheromones. But a new study has just provided evidence that the two leading 'human sex pheromone' candidates aren't actually pheromones at all.
Until now, researchers had narrowed down the hunt for human pheromones to two chemicals - androstadienone (AND), which is found in male sweat and semen, and estratetraenol (EST), found in women's urine.
The jury has remained out on whether or not they're true human pheromones, but that hasn't stopped the media and perfume makers from running with the idea, leading many people to believe to some extent that, as a species, we're responding to each other's subtle pheromone cues.
But in a new double-blind study, researchers from the University of Western Australia tested the effect on 94 healthy humans, and found that these so-called pheromones had no measurable impact on their behaviour whatsoever.
"Much of the research currently promoted focuses on studies that back AND and EST being pheromones in humans, because of the human fascination on how we can improve our attractiveness to the opposite sex," said lead researcher Leigh Simmons.
"This contributes to a skew in public perception on whether humans do have pheromones with many people believing we do, because research suggesting the opposite tends not to be as published, and if it is published it does not get the same degree of attention."
Researchers have found yet another reason to think the symptoms of Parkinson's disease could be a consequence of the type of bacteria living in our gut.
Such discoveries could help us use changes in our gut bacteria to not only diagnose the debilitating disorder earlier, but potentially create better targeted treatments.
Once referred to as 'the shaking palsy', Parkinson's disease is mostly characterised by tremors and a loss of fine motor control, later progressing into dementia, difficulty walking, and sometimes chronic depression.
In most studies on the condition the brain has been the focus, with the blame for the disease primarily falling on the death of cells in a part of the brain called the substantia nigra – a lump of tissue responsible for movement and reward.
In recent years, however, scientists studying the root cause of Parkinson's disease have shifted their attention from the nervous system onto the denizens of our gut, identifying significant differences in the types of bacteria living in the guts of those with the condition and those who don't.
Now a team of scientists at the University of Alabama at Birmingham in the US have contributed yet another piece of evidence tying Parkinson's disease with our personal community of microorganisms – or microbiota.
The idea that organisms can live longer, healthier lives by sharply reducing their calorie intake is not exactly new. Laboratory research has repeatedly demonstrated the anti-aging value of calorie restriction, often called CR, in animals from nematodes to rats—with the implication that the same might be true for humans.
In practice though, permanently reducing calorie intake by 25 to 50 percent or more sounds to many like a way to extend life by making it not worth living. Researchers have also warned that what works for nematodes or rats may not work—and could even prove dangerous—in humans, by causing muscle or bone density loss, for example.
But now two new studies appear to move calorie restriction from the realm of wishful thinking to the brink of practical, and perhaps even tolerable, reality. Writing in Nature Communications, researchers at the University of Wisconsin–Madison and the National Institute on Aging reported last month chronic calorie restriction produces significant health benefits in rhesus monkeys—a primate with humanlike aging patterns—indicating “that CR mechanisms are likely translatable to human health.” The researchers describe one monkey they started on a 30 percent calorie restriction diet when he was 16 years old, late middle age for this type of animal. He is now 43, a longevity record for the species, according to the study, and the equivalent of a human living to 130.
Between the mid-1990s and the mid-2000s alone, the likelihood of having a classmate with a food allergy increased by 20 per cent in the United States. In fact, over the past five decades, the incidence of all allergies and autoimmune diseases – caused by your body attacking itself – has skyrocketed. What could explain our sudden hypersensitivity to our surroundings and ourselves? Since evolution operates on the timescale of millennia, the culprits lie not in our genes but somewhere within our environment.
One thing that has changed in public health is our awareness of germs and how they spread. In response to that insight, over the past half-century our implementation of hygiene practices has spared us from debilitating infections and enormous human misery. But the new vigilance might have altered the development of our immune system, the collection of organs that fight infections and internal threats to our health.
The idea that too clean an environment might be harmful has been dubbed ‘the hygiene hypothesis’. The concept has been perverted by some to suggest that the less clean the environment, the better. But its meaning is different: it is not dirt that we are missing but exposure to certain microbes that normally contribute to the development of our immune system. ‘It’s not that we aren’t exposed enough to microbes but that we’re not exposed to the right types of microbes,’ says the immunobiologist Ruslan Medzhitov at the Yale School of Medicine, also head of the Food Allergy Science Initiative at the Broad Institute. So what has changed? In short, it’s the standard for what constitutes a good microbe versus a bad one. ‘Take bacterial species that increase nutrient absorption from food,’ Medzhitov says. These were immensely beneficial at a time where you had to go days without eating. Today in the parts of the world with an overabundance of food, having such bacteria in your intestine contributes to obesity. ‘Microbes that cause intestinal inflammation are another example of what we call bad microbes because they induce [detrimental immune] responses. But in the past, these microbes could have protected you from intestinal pathogens,’ he adds.
The option of receiving a skin-cancer diagnosis by smartphone could save lives, say researchers.
It’s scary enough making a doctor’s appointment to see if a strange mole could be cancerous. Imagine, for example, that you were in that situation while also living far away from the nearest doctor, unable to take time off work, and not sure if you had the money to cover the cost of the visit.
Universal access to health care was on the minds of computer scientists when they set out to create an artificially intelligent diagnosis algorithm for skin cancer, making a database of nearly 130,000 skin disease images and training their algorithm to visually diagnose potential cancer. From the very first test, it performed with inspiring accuracy. “We realized it was feasible, not just to do something well, but as well as a human dermatologist,” says Sebastian Thrun, an adjunct professor in the Stanford Artificial Intelligence Laboratory. “That’s when our thinking changed. That’s when we said, ‘Look, this is not just a class project for students, this is an opportunity to do something great for humanity.'”
Being overweight can raise your blood pressure, cholesterol and risk for developing diabetes. It could be bad for your brain, too.
A diet high in saturated fats and sugars, the so-called Western diet, actually affects the parts of the brain that are important to memory and make people more likely to crave the unhealthful food, says psychologist Terry Davidson, director of the Center for Behavioral Neuroscience at American University in Washington, D.C.
He didn't start out studying what people ate. Instead, he was interested in learning more about the hippocampus, a part of the brain that's heavily involved in memory.
He was trying to figure out which parts of the hippocampus do what. He did that by studying rats that had very specific types of hippocampal damage and seeing what happened to them.
In the process, Davidson noticed something strange. The rats with the hippocampal damage would go to pick up food more often than the other rats, but they would eat a little bit, then drop it.
Davidson realized these rats didn't know they were full. He says something similar may happen in human brains when people eat a diet high in fat and sugar. Davidson says there's a vicious cycle of bad diets and brain changes. He points to a 2015 study in the Journal of Pediatrics that found obese children performed more poorly on memory tasks that test the hippocampus compared with kids who weren't overweight.
He says if our brain system is impaired by that kind of diet, "that makes it more difficult for us to stop eating that diet. ... I think the evidence is fairly substantial that you have an effect of these diets and obesity on brain function and cognitive function."
The evidence is growing. Research from the Cambridge Centre for Ageing and Neuroscience published in July found that obese people have less white matter in their brains than their lean peers — as if their brains were 10 years older. A more recent study from researchers at the University of Arizona supports one of the leading theories, that high body mass is linked to inflammation, which affects the brain.
Researchers have identified a cellular mechanism that allows them to reverse ageing in mouse DNA and protect it from future damage.
They've shown that by giving a particular compound to older mice, they can activate the DNA repair process and not only protect against future damage, but repair the existing effects of ageing. And they're ready to start testing in humans within six months.
"The cells of the old mice were indistinguishable from the young mice, after just one week of treatment," said lead researcher David Sinclair from the University of New South Wales (UNSW) in Australia and the Harvard Medical School in Boston.
"This is the closest we are to a safe and effective anti-ageing drug that's perhaps only three to five years away from being on the market if the trials go well."
Sinclair and his team made headlines back in 2013 when they found that the cells of younger mice contained more of a compound called nicotinaminde adenine dinucleotide, or NAD+, than their older counterparts.
Not only that, but when they gave the older mice more NAD+, they started to look younger, too.
It was a big deal at the time, but one of the tricky things about medicine is that in order to show that something could work as a potential treatment, you need to first understand how it's acting in the body.
And although the researchers knew NAD+ was having an impressive effect, they couldn't say for sure how it was doing it.
Now, Sinclair and his team have released a new study, where they outline in detail the mechanism through which NAD+ protects DNA from the damage of ageing and radiation in mice.
Our bodies still hold plenty of secrets, and scientists have just uncovered a doozy: the lungs play a key role in producing blood. Until now, this task was ascribed solely to bone marrow, but studies on mice at the University of California San Francisco (UCSF) have found that, surprisingly, the majority of the body's platelets are produced in the lungs, as is a backup reservoir of blood stem cells that can step in when those in the bone marrow run dry.
Science has long believed that most of the cells that make up blood reside in bone marrow, where a process called haematopoiesis gives us the oxygen-carrying red blood cells, the white blood cells that fight off infection, and components like platelets, whose role is to form clots to stop bleeding. Megakaryocytes – the cells that produce platelets – have been spotted in lung tissue before, but were usually thought to live and work mainly in bone marrow
It’s a comforting message, in a sour-grapes sort of way. It sounds wise and mature, suggesting that we put aside childish dreams and accept once and for all that there can be no vital Veg-O-Matic that slices mortality and dices infirmity. Gerontologists like it, being particularly eager to put on a respectable front and escape the whiff of snake oil that clings to the field of life extension.
In 1946 the newly founded Gerontological Society of America cited, in the first article of the first issue of its Journal of Gerontology, the need to concern ourselves to add “not more years to life, but more life to years.” The dictum was famously sharpened 15 years later by Robert Kennedy when he told the delegates at the first White House Conference on Aging “We have added years to life; it is time to think about how we add life to years.” Political theorist and futurist Francis Fukuyama was particularly eloquent but hardly alone when he warned two decades ago that if we maintain our obsession with extending life at all costs, society may “increasingly come to resemble a giant nursing home.”
Our brains are basically electrochemical computers, so using electricity to manipulate their function is a well-proven technique. From deep-brain stimulation that controls the symptoms of depression to zapping our grey matter to improve our vision, electrical current applied to our brains holds a lot of promise. Now researchers at Imperial College London have shown that a low-voltage stream of electricity can be used to bring different brain regions in sync with each other, leading to improved memory ability and the hope of treating neurological disorders.
In the study, the researchers used what's known as transcranial alternating current stimulation (tACS) to affect the way in which the electric current in two brain regions was oscillating. The weak electric current applied to the forehead from tACS brought the middle frontal gyrus and the inferior parietal lobule into sync with each other. Both of these areas are known to be involved in working memory, which is our extreme short-term memory that helps us function in the here-and-now. An example of working memory would be the way in which we'd be able to recall what we needed when we go out to our cars to retrieve a forgotten item.
Gluten-free diets have exploded in popularity in recent years, but many have questioned whether this new food trend is actually medically helpful for those without a diagnosed celiac disease. A new study released by the American Heart Foundation points to a possible relationship between low-gluten diets and a higher risk of Type 2 diabetes.
A Consumer Reports National Research Centre survey from 2014 revealed that up to a third of American adults polled were trying to cut gluten out of their diets. Yet the prevalence of celiac disease in the United States has been relatively stable at about 1 percent of the population. So many people seem to believe that reducing or eliminating gluten from their diet is an inherently healthy act, but is there actually any science to back up that belief?
Researchers at Harvard University set out to determine what health effects avoiding gluten had on those people with no specific medical reason to avoid the substance. They accumulated data previously recorded from three separate long-term health studies comprising nearly 200,000 participants.
The separate studies involved participants logging their food habits in questionnaires completed every two to four years. The Harvard team estimated the daily gluten intake from this data and found that those who ate the most gluten had a lower risk of developing Type 2 diabetes during the 30 years of follow-up.
Researchers may have uncovered a link between religiosity—a disposition for spiritual experience and religious activity—and epilepsy.
This connection between epilepsy and heightened religious experience has been recognized since at least the 19th century.
“Past research has indicated that humans might have a distinctive neurological tendency toward being spiritually oriented,” says Brick Johnstone, a neuropsychologist and professor of health psychology at the University of Missouri. “This research supports the notion that the human propensity for religious or spiritual experiences may be neurologically based.”
“The end goal of this research is to understand if some type of connection exists between the brain and spiritual experience,” says Daniel Cohen, coauthor and assistant professor of religious studies. “If a connection exists, what does it mean for humans and their relationship with religion?”
The first study to both show and measure the effects of cognitive-enhancing drugs such as modafinil, methylphenidate (best known under the trade name Ritalin), and caffeine, on chess play is being published in the March edition of the peer-reviewed journal European Neuropsychopharmacology. This shows significant cognitive improvements for modafinil and methylphenidate, and may have influence how these drugs are used off-label in a range of activities.
The study shows how certain drugs can alter and even improve the way in which the brain processes complex information. As applied to chess (and other fields), this supports the possibility pharmaceutical enhancement giving a player a competitive advantage. The World Chess Federation, FIDE, recognised this by introducing an anti-doping code in 20141.
Now a new double-blind randomised controlled trial by scientists from German and Swedish universities has shown that the cognitive enhancing drugs, modafinil, methylphenidate, and caffeine can improve chess play. Previous research had shown that the drugs could improve cognitive performance when a subject was tired or was performing below his or her optimal performance, but this is the first work to show improvement of cognitive performance even if the subject is performing at a very high level.
The team, led by Professor Klaus Lieb (University of Mainz, Germany) gave 39 male chess players controlled doses of one of the drugs modafinil, methylphenidate, caffeine, or a placebo. They then played a series of rapid, time-limited (15 minutes) games against a chess programme (the popular Fritz 12 programme) which had been matched to the strength of each individual player. This was a 4-day "crossover" study, meaning that the player had who taken modafinil on day 1 would receive a different drug (or placebo) on each subsequent day, and so on. In total the researchers gathered data from over 3000 chess games.
Researchers at Yale University have discovered that the brain is capable of making fructose – a simple sugar, usually found in fruit, vegetables and honey.
Not all sugars are equal. Glucose is a simple sugar that provides energy for the cells in your body. Fructose has a less important physiological role and has been repeatedly linked to the development of obesity and type 2 diabetes. When there is excess glucose the processes that break it down can become saturated, so the body converts glucose into fructose instead, using a process known as the “polyol pathway”, a chemical reaction involved in diabetic complications. The researchers at Yale reported in the journal, JCI Insight, that the brain uses the polyol pathway to produce fructose in the brain.
Unlike glucose, which can be metabolised throughout the body, fructose is normally metabolised almost completely in the liver and also in semen where it produces energy for sperm. Most fructose produced by this pathway is thought to stay inside the cells that make it, as fructose levels in the blood are usually extremely low. These low circulating levels make it unlikely that fructose made in this way reaches the brain in significant amounts, and yet some studies have previously identified very high levels of fructose in the central nervous system (the brain and spinal cord).
Importantly, research has shown that exposure to fructose can significantly alter the expression of hundreds of genes in the brain, including genes that control metabolism, cell communication, inflammation and brain function. This suggests that fructose is likely to alter brain function.
South Korean women will be the first in the world to have an average life expectancy above 90, a study suggests.
Imperial College London and the World Health Organization analysed lifespans in 35 industrialised countries.
It predicted all would see people living longer in 2030 and the gap between men and women would start to close in most countries.
The researchers said the findings posed big challenges for pensions and care for elderly people.
"South Korea has gotten a lot of things right," Prof Majid Ezzati told the BBC News website.
"They seem to have been a more equal place and things that have benefited people - education, nutrition - have benefited most people.
"And so far, they are better at dealing with hypertension and have some of the lowest obesity rates in the world."
The data also forecasts that Japan, once the picture of longevity, will tumble down the global rankings.
It currently has the highest life expectancy for women, but will be overtaken by both South Korea and France, the study suggests. Meanwhile, male life expectancy will go from the fourth highest to eleventh out of the countries studied.
Self-proclaimed “weight loss hypnosis master” Steve Miller has announced a campaign to see all overweight NHS staff wearing badges that read “I’m fat, but I’m losing it”. He also wants all restaurant menus to carry the warning that “if you’re fat, think before ordering”.
It would be easy to discount Miller’s campaign as a publicity stunt, but doing so would ignore the damaging consequences it is likely to have. Scientific evidence overwhelmingly demonstrates that this sort of obesity stigma is an ineffective way to reduce the incidence of obesity, and in fact perpetuates it. If this strategy supported losing weight, the obesity “epidemic” would already be over, because obese people are frequently framed as lazy, gluttonous and targets for ridicule as it is. Body shaming
Obesity stigma, guilt, and shame reinforce high body weights and can even promote weight gain. Experiencing obesity stigma often leads people to adopt coping strategies that undermine physical health – such as comfort eating, or avoiding exercise in case they are made to feel embarrassed about their bodies. Obesity stigma has also been strongly linked with depression and compromised mental health .
Whether it’s from a surgical procedure, clumsy shaving, or that traumatic biking incident that happened when you were five, just about everyone has a scar they wish would just fade away.
And while there’s not a whole lot that can be done for scars that are already there, researchers have figured out how to make fresh wounds heal as normal, regenerated skin, instead of the usual scar tissue - something that was previously thought to be impossible in mammals.
"Essentially, we can manipulate wound healing so that it leads to skin regeneration rather than scarring," said one of the team, George Cotsarelis, chair of the Department of Dermatology at the University of Pennsylvania.
"The secret is to regenerate hair follicles first. After that, the fat will regenerate in response to the signals from those follicles."
If you've ever wondered why scar tissue looks so different from regular skin, it's because scar tissue doesn't contain any fat cells or hair follicles.
The type of skin that regenerates over a small, superficial cut is filled with fat cells called adipocytes, just like the skin you were born with, which means the two will eventually blend into each other once the wound has healed.
But scar tissue is made up almost entirely of cells called myofibroblasts, and doesn't contain any fat cells at all. So instead of blending into the surrounding skin once the wound has fully healed, it looks completely different - permanently.
The same goes for ageing skin - as we age, we lose our adipocytes, which leads to discolouration and deep, irreversible wrinkles.
But scientists have discovered that existing myofibroblasts can actually be converted into adipocytes, which suggests that as a wound is healing, scar tissue could be converted to regenerated skin instead - something that scientists thought could only be possible in fish and amphibians.
A new study increases and strengthens the links that have led scientists to propose the “transposon theory of aging.”
Transposons are rogue elements of DNA that break free in aging cells and rewrite themselves elsewhere in the genome, potentially creating lifespan-shortening chaos in the genetic makeups of tissues.
As cells get older, prior studies have shown, tightly wound heterochromatin wrapping that typically imprisons transposons becomes looser, allowing them to slip out of their positions in chromosomes and move to new ones, disrupting normal cell function. Meanwhile, scientists have shown that potentially related interventions, such as restricting calories or manipulating certain genes, can demonstrably lengthen lifespans in laboratory animals.
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