By Libby Richards/Professor of Nursing, Purdue University
You’ve probably heard “Don’t go outside in the winter with your hair wet or without a coat; you’ll catch a cold.”
Infectious or chronic diseases such as long COVID, Alzheimer’s disease and traumatic brain injury can cause inflammation in the brain, or neuroinflammation, that weakens muscles. While scientists are aware of this link between inflammation and muscle weakness, the molecules and processes involved have been unclear.
In our research, our team of neuroscientists and biologists uncovered the hidden conversation between the brain and muscles that triggers muscle fatigue, and potential ways to treat it.
Neuroinflammation results when your central nervous system – the brain and spine – activates its own immune system to protect itself against infection, toxins, neurodegeneration and traumatic injury. Neuroinflammatory reactions primarily occur in the brain. But for unknown reasons, patients also experience many symptoms outside the central nervous system, such as debilitating fatigue and muscle pain.
To solve this puzzle, we studied brain inflammation in the context of three different diseases: bacterial infection in E. coli-induced meningitis; viral infection in COVID-19; and neurodegeneration in Alzheimer’s disease. Then, we analyzed how these immune changes affect muscle performance.
We measured immune changes in the brains of fruit flies and mice infected with live bacteria, viral proteins or neurotoxic proteins. After the initial accumulation of toxic molecules in the brain that commonly increase in response to stresses such as infection, the brain produces high levels of cytokines – chemicals that activate the immune system – that are released into the body. When these cytokines travel to muscles, they activate a series of chemical reactions that disrupts the ability of the powerhouse of cells – mitochondria – to produce energy.
Microglia are cells that play a key role in the brain’s immune response. National Institute of Allergy and Infectious Diseases/NIH via Flickr
Though the result of these immune changes doesn’t seem to damage muscle fibers, it does cause fatigue. When we measured the muscle performance of these animals after giving them treatments to offset the effects of immune activation, we found that both flies and mice moved significantly less in response to manual or mechanical stimuli compared with those that were not infected. This indicated that the animals had reduced endurance.
Our findings suggest that the muscle fatigue that results from infection or chronic illness is caused by a brain-to-muscle communication pathway that depletes energy in muscles without disrupting their structure or integrity. Unlike traditional explanations for muscle dysfunction that focus on causes outside the brain, such as damage to the muscle fibers, this pathway directly causes fatigue.
Since the key cytokine involved in brain-to-muscle communication has been preserved throughout evolution across different species, we believe this signaling pathway could represent a universal mechanism the brain uses to claim and reallocate energy to fight against infection.
Cytokines are signaling proteins that help cells communicate with each other.
Since we studied the brain-muscle axis only in the context of simplified models, we don’t know whether it applies to more complex conditions such as fibromyalgia or chronic fatigue syndrome. We also don’t know how impaired energy production in muscles correlates with impaired energy production in the brain.
Furthermore, the brain-muscle axis works through a series of interconnected steps. But the precise mechanism of this communication and the potential involvement of other cytokines are unknown.
Muscle weakness and fatigue are common symptoms in multiple diseases, ranging from bacterial and viral infections to chronic disorders and neurodegenerative conditions. These symptoms are distressing and reduce the quality of life of millions of people worldwide.
For instance, most of the 65 million people around the world struggling with long COVID experience disabling fatigue lasting from months to years.
Similarly, reduced muscle strength is a common symptom of early stage Alzheimer’s disease, a condition that affects at least 50 million people globally.
Better understanding of how neuroinflammation causes muscle fatigue can lead to potential treatments that improve muscle function.
Our work suggests that targeting the brain-muscle axis could offer new treatment strategies for muscle fatigue.
Currently, we are testing neutralizing antibodies – proteins that bind to and inhibit the function of cytokines – in mice with neuroinflammation. These FDA-approved treatments specifically target cytokines secreted by the brain and prevent signaling to muscle. We are interested in identifying which neutralizing antibodies, or combinations of antibodies, prevent muscle fatigue in mice.
We are also planning a long COVID clinical trial to profile cytokine levels in patients. It is unclear whether other COVID-19 proteins can also trigger neuroinflammation and muscle fatigue. Recent evidence suggests that long COVID may be linked to lingering viral particles in several organs, including the brain, even months after infection. However, it is uncertain whether and how this might be connected with the high levels of cytokines seen in long COVID.
With further development, targeting the brain-muscle axis could be a useful treatment for people suffering with long COVID and other diseases that cause brain inflammation.
Diego E. Rincon-Limas, Associate Professor of Neurology, University of Florida and Aaron N. Johnson, Associate Professor of Developmental Biology, Arts & Sciences at Washington University in St. Louis
This article is republished from The Conversation under a Creative Commons license. Read the original article.
In 2017, NASA discovered and later confirmed the first interstellar object to enter our Solar System.
It wasn’t aliens. But artist impressions of the object (called ‘Oumuamua, the Hawaiian word for “scout”) do resemble an alien spaceship out of a sci-fi novel. This strange depiction is because astronomers don’t quite know how to classify the interstellar visitor.
Its speed and path around the Sun don’t match a typical asteroid, but it also has no bright tail or nucleus (icy core) we normally associate with comets. However, 'Oumuamua has erratic motions that are consistent with gas escaping from its surface. This “dark comet” has had astronomers scratching their heads ever since.
An artist’s impression of the dark comet ‘Oumuamua. European Southern Observatory / M. Kornmesser
Flash forward to today, and more of these mysterious objects have been discovered, with another ten announced just last week. While their nature and origins remain elusive, astronomers recently confirmed dark comets fall into two main categories: smaller objects that reside in our inner Solar System, and larger objects (100 metres or more) that remain beyond the orbit of Jupiter.
In fact, 3200 Phaethon – the parent body of the famous Geminid meteor shower – may be one of these objects.
Comets, often described as the Solar System’s “dirty snowballs”, are icy bodies made of rock, dust and ices. These relics of the early Solar System are critical to unlocking key mysteries around our planet’s formation, the origins of Earth’s water, and even the ingredients for life.
Astronomers are able to study comets as they make their close approach to our Sun. Their brilliant tails form as sunlight vaporises their icy surfaces. But not all comets put on such a dazzling display.
The newly discovered dark comets challenge our typical understanding of these celestial wanderers.
Image of comet C/2023 A3 Tsuchinshan-ATLAS taken by astronauts aboard the International Space Station. NASA
Dark comets are more elusive than their bright siblings. They lack the glowing tails and instead resemble asteroids, appearing as a faint point of light against the vast darkness of space.
However, their orbits set them apart. Like bright comets, dark comets follow elongated, elliptical paths that bring them close to the Sun before sweeping back out to the farthest reaches of the Solar System.
They go beyond Pluto, some even making it out to the Oort Cloud, a vast bubble of tiny objects at the fringe of our Solar System. Their speed and paths are what allow astronomers to determine their origins.
A comparison of dark comets and bright comets set against the Milky Way. On the left, a small, rocky, dark comet represents their typical size of one meter to a few hundred meters wide. On the right is a larger, icy, bright comet with a glowing tail, whose size ranges from 750 meters to 20 kilometres wide. The stark difference in size explains why dark comets lack the bright, visible tails of their larger, more iconic counterparts. Composition: Dr Kirsten Banks; Background image: R. Wesson/ESO; Dark comet: Nicole Smith/University of Michigan, made with Midjourney; Bright comet: Linda Davison
But what makes these comets so dark? There are three main reasons: size, spin and composition or age.
Dark comets are often small, just a few metres to a few hundred metres wide. This leaves less surface area for material to escape and form into the beautiful tails we see on typical comets. They often spin quite rapidly and disperse escaping gas and dust in all directions, making them less visible.
Lastly, their composition and age may result in weaker or no gas loss, as the materials that go into the tails of bright comets are depleted over time.
These hidden travellers may be just as important for astronomical studies, and they may even be related to their bright counterparts. Now, the challenge is to find more dark comets.
How do we even find these mysterious dark comets in the first place? As they get closer to the Sun, we don’t see spectacular tails of debris.
Instead, we rely on the light they reflect from our Sun.
Several astronomical images are combined to capture the faint, fast moving object ‘Oumuamua in the centre. The white streaks are stars. ESO/K. Meech et al.
These little guys might be stealthy for our eyes, but they are often no match for our large telescopes around the world. The discovery of ten new dark comets revealed last week was all thanks to one amazing instrument, the Dark Energy Camera (DECam) on a large telescope in Chile.
This camera can’t “see” dark energy directly, but it was designed to take massive photos of our universe – for us to see distant stars, galaxies and even hidden Solar System objects.
In their recent study, astronomers pieced together that some of these nightly images contained likely dark comets.
A) The Dark Energy Camera (DECam), mounted on the Victor M. Blanco four-metre telescope at the Cerro Tololo Inter-American Observatory in the Chilean Andes (Credit: Dark Energy Survey). B) Two examples of newly discovered dark comets within the DECam data, from Seligman et al. (2024).
The good news is, we are starting to focus more attention on these objects and on how to find them.
In even better news, in 2025, we’ll have a brand new mega camera in Chile ready to find them. This will be the Vera C. Rubin Observatory, with the largest digital camera ever built.
It will allow us to take more images of our night sky more quickly, and see objects that are even fainter. It’s likely that in the next ten years we could double or even triple the amount of known dark comets, and start to understand their interesting origin stories.
There could be more 'Oumuamua-like objects out there, just waiting for us to find them.
Rebecca Allen, Co-Director Space Technology and Industry Institute, Swinburne University of Technology; Kirsten Banks, Lecturer, School of Science, Computing and Engineering Technologies, Swinburne University of Technology, and Sara Webb, Lecturer, Centre for Astrophysics and Supercomputing, Swinburne University of Technology
This article is republished from The Conversation under a Creative Commons license. Read the original article.
Three years ago, Andrea Vanek was studying to be an arts and crafts teacher when spells of dizziness and heart palpitations suddenly started to make it impossible for her to even take short walks.
After seeing a succession of doctors she was diagnosed with long COVID and even now spends most of her days in the small living room of her third-floor Vienna apartment, sitting on the windowsill to observe the world outside.
"I can't plan anything because I just don't know how long this illness will last," the 33-year-old Austrian told AFP.
The first cases of COVID-19 were detected in China in December 2019, sparking a global pandemic and more than seven million reported deaths to date, according to the World Health Organization.
But millions more have been affected by long COVID, in which some people struggle to recover from the acute phase of COVID-19, suffering symptoms including tiredness, brain fog and shortness of breath.
Vanek tries to be careful not to exert herself to avoid another "crash", which for her is marked by debilitating muscle weakness and can last for months, making it hard to even open a bottle of water.
"We know that long COVID is a big problem," said Anita Jain, from the WHO's Health Emergencies Programme.
About six percent of people infected by coronavirus develop long COVID, according to the global health body, which has recorded some 777 million Covid cases to date.
Whereas the rates of long Covid after an initial infection are declining, reinfection increases the risk, Jain added.
- 'Everything hurts' -
Chantal Britt, who lives in Bern, Switzerland, contracted Covid in March 2020. Long COVID, she said, has turned her "life upside down" and forced her to "reinvent" herself.
"I was really an early bird.... Now I take two hours to get up in the morning at least because everything hurts," the 56-year-old former marathon runner explained.
"I'm not even hoping anymore that I'm well in the morning but I'm still kind of surprised how old and how broken I feel."
About 15 percent of those who have long COVID have persistent symptoms for more than one year, according to the WHO, while women tend to have a higher risk than men of developing the condition.
Britt, who says she used to be a "workaholic", now works part-time as a university researcher on long COVID and other topics.
She lost her job in communications in 2022 after she asked to reduce her work hours.
She misses doing sports, which used to be like "therapy" for her, and now has to plan her daily activities more, such as thinking of places where she can sit down and rest when she goes shopping.
A lack of understanding by those around her also make it more difficult.
"It's an invisible disease.... which connects to all the stigma surrounding it," she said.
"Even the people who are really severely affected, who are at home, in a dark room, who can't be touched anymore, any noise will drive them into a crash, they don't look sick," she said.
- Fall 'through the cracks' -
The WHO's Jain said it can be difficult for healthcare providers to give a diagnosis and wider recognition of the condition is crucial.
More than 200 symptoms have been listed alongside common ones such as fatigue, shortness of breath and cognitive dysfunction.
"Now a lot of the focus is on helping patients, helping clinicians with the tools to accurately diagnose long COVID, detect it early," she said.
Patients like Vanek also struggle financially. She has filed two court cases to get more support but both are yet to be heard.
She said the less than 800 euros ($840) she gets in support cannot cover her expenses, which include high medical bills for the host of pills she needs to keep her symptoms in check.
"It's very difficult for students who get long COVID. We fall right through the cracks" of the social system, unable to start working, she said.
Britt also wants more targeted research into post-infectious conditions like long COVID.
"We have to understand them better because there will be another pandemic and we will be as clueless as ever," she said.
An MSNBC panel was left confused and uncomfortably laughing Friday afternoon during a discussion over Robert F. Kennedy Jr.'s curious questionnaire he's using to vet candidates to work under him at the Department of Health and Human Services.
Last week, Puck News reported on Kennedy's “Make America Healthy Again” website, where people who want to work for him can respond to questions with odd pre-written responses.
MSNBC Host Nicolle Wallace reading some of the responses:
ALSO READ: Doctors in Congress brace for Dr. Oz and RFK Jr.'s 'crazy ideas'
"I don't have much interest in having sexual experiences with another person."
"I believe in things many others don't like having a sixth sense, clairvoyance, and telepathy."
"I used my physical appearance to draw attention to myself."
The Trump transition team has confirmed the questions.
"I'm asking a serious question," Wallace said. "Is the answer designed to bring people in or push people out of HHS?"
Reporter Vaughn Hillyard confessed he didn't have much of an answer.
"I think when they're looking at who's going to fill the roles of these political appointees on down, of which there are hundreds within the HHS, I think that that is where these questions become pertinent," he said.
Wallace asked critical care physician Dr. Michael Anderson whether he had any interest in "having sexual experiences with another person." She was curious if it was a medical question or a management question.
"You know that it's rare that I'm at a loss for words," Dr. Anderson said, causing Wallace to burst into hysterics.
"I'm just kind of coming up with other things [for] the checklist like: Do you have experience in taking care of patients or in public health or in making sure that kids are safe and well-cared for?" he suggested. "So, I have no idea what that one means, but I would sort of like to add a couple of others that I think maybe weigh a little bit more."
At the end of the discussion, Wallace asked Hillyard if RFK Jr. would make it through confirmation, and Hillyard said, "Yes."
"I think so, too," Wallace said. "I think they all do."
See the video below or at the link here.
- YouTube youtu.be
To hear Donald Trump tell it, his first administration was on a roll and doing well until the 2020 pandemic hit the country and shut down the global economy. Now conspiracy theorists think that President Joe Biden will try to sabotage a new incoming administration by starting another plague or even a civil war.
Mother Jones reported Friday that the right fears the spread of avian flu will take hold in the U.S. and that Trump will be forced to put aside his agenda to deal with it. In addition to avian flu, "last week, a mysterious flu-like outbreak was identified after killing dozens of people in Congo, where it is circulating alongside a new strain of pox that is also spreading elsewhere in eastern and southern Africa," the report said.
The details of how this will lead to a pandemic are a bit muddled, according to the report, which says the ideas are "slightly too vague" and lack "the urgency of a good and salable conspiracy theory."
ALSO READ: The one belief that predicted Trump voters with scary accuracy
It hinges on comments from Dr. Peter Hotez, co-director of the Center for Vaccine Development at Texas Children’s Hospital.
When he spoke to MSNBC on Dec. 4, he commented, “We have some big picture stuff coming down the pipe." He was talking about the avian flu and new strains of COVID.
"All that’s going to come crashing down on January 21 on the Trump administration. We need a really really good team to be able to handle this," said Hotez.
He was talking about Trump's incoming administration being forced to face large-scale problems, and then saying they may not be prepared for it.
Alex Jones, a pro-Trump conspiracy theorist, called the comments “an attempt to terrorize" the American public as well as to promote “forced shots, lockdowns, tyranny, further global collapse.”
One post sharing Hotez's comments has been viewed three million times, the report said.
Critics swarmed, launching fresh attacks on Hotez, who faced harassment during the COVID pandemic. The anti-vaccine website Natural News showed a roundup of attacks on Hotez, citing one person saying he should be arrested and jailed so he can be forced to “explain how he knows this.”
Hotez reviewed the threats the global health community already faces. His comments did not contain new information.
Another pandemic, however, gives conspiracy theorists another opportunity to sell their snake oil, the report said.
"All of this fear-mongering and scapegoating ultimately serves multiple purposes: ginning up skepticism about the next pandemic—whatever it may be before it even appears—as well as preemptively creating hostility against any vaccine that might be developed to fight it in order to peddle fake cures," the report closed.
A new study suggests dogs can learn to express themselves by pressing buttons to create two or more word combinations.
Researchers have been following several thousand dogs since 2022 whose button presses are logged through an app designed by Fluent Pet, which makes soundboards, and they then selected 152 dogs who were pressing two or more buttons in a sequence and found they frequently selected their own name, followed by "want" and then topics like "food" or "outside," reported the Washington Post.
“If we know that they are using the buttons intentionally, they can use them in ways that seem smart, like a young child, “said Federico Rossano, an associate professor of cognitive science at the University of California at San Diego. “This should lead owners to a renewed appreciation of the intelligence of their pets and help them provide for their dogs.”
ALSO READ: The reckoning: Plenty of hurts coming for the people who didn't care about their country
The data was self-reported by dog owners, but those selected for the multi-word combination study were not informed about it to avoid bias, and the researchers conducted computer simulations on probability to determine whether the combinations were random.
“This is how we know that most dogs in this pool were doing multi-button combinations in nonrandom ways,” Rossano said. “Note that nonrandomness can be caused by many things, including imitating the training they received, though the first analysis comparing button presses by owner and their dogs suggests that this is unlikely to be the main explanation.”
However, he said some of the dogs were pressing the buttons at random, which he said bolstered the credibility of their findings.
"If the data lined up as if they were all extremely systematic," Rossano said, "it would seem very hard to believe."
"The dogs understand the meaning of the more frequently used words on these soundboards and suggest that dogs are capable of using these soundboards to communicate with humans about their needs and wants,” Rossano added. “It further raises the possibility that they might be communicating the way a 2-year-old human might, which is more sophisticated than previously believed.”
Amritha Mallikarjun, a researcher at the Penn Vet Working Dog Center who was not involved in the study, said the dogs' first button press might have been random but led to more button presses through reinforcement.
“Dogs trained on buttons will often like to try things and will take a guess at what we want by performing a random behavior,” she said. “The button-trained dog presses ‘want outside’ one time just to try it. There is no real knowledge of what the concept of the verb ‘want’ is. ‘Outside’ usually means the dog’s person lets you in the backyard, and sometimes you hear your owner press ‘want food,’ so the dog associates the ‘want’ button with good things.”
by Issam AHMED
The common murre, a large black-and-white seabird native to northern waters, has become far less common in Alaska over the past decade due to the impacts of climate change.
A study published Thursday in Science reveals that a record-breaking marine heat wave in the northeast Pacific from 2014 to 2016 triggered a catastrophic population collapse, wiping out four million birds -- about half the species in the region.
Strikingly, they have shown little signs of rebounding, suggesting long-term shifts in the food web that have locked the ecosystem into a troubling new equilibrium.
"There's a lot of talk about declines of species that are tied to changes in temperature, but in this case, it was not a long term result," lead author Heather Renner of the Alaska Maritime National Wildlife Refuge told AFP.
"To our knowledge, this is the largest mortality event of any wildlife species reported during the modern era," she and her colleagues emphasized in their paper.
The finding triggers "alarm bells," Renner said in an interview, as human-caused climate change makes heat waves more frequent, intense, and longer-lasting.
With their dapper, tuxedoed look, common murres are sometimes called the "penguins of the north."
Their slender wings power them across vast distances in search of food and make them expert divers. But even these hardy seabirds were no match for an unprecedented environmental catastrophe.
The largest marine heat wave ever recorded began in the late fall of 2014, spanning a massive swath of the northeast Pacific Ocean from California to Alaska.
It persisted for over two years, leaving devastation in its wake. During this time, some 62,000 emaciated murres washed ashore along the North American Pacific coastline -- dead or dying from starvation.
Experts point to two key reasons for the bird deaths: elevated ocean temperatures reduced both the quality and quantity of phytoplankton, impacting fish like herring, sardines, and anchovies -- the mainstay of the murre diet.
At the same time, warmer waters increased the energy demands of larger fish, such as salmon and Pacific cod, which compete with murres for the same prey.
"We knew then it was a big deal, but unfortunately, we couldn't really quantify the effects," explained Renner.
For years after the event, breeding colonies failed to produce chicks, complicating efforts to assess the full impact.
Earlier estimates pegged the number of deaths at around a million, but a more robust analysis -- drawing on data from 13 murre colonies -- revealed the toll was four times higher.
"It is just so much worse than we thought it was," Renner said of the new findings.
The marine heat wave didn't just impact common murres. Pacific cod stocks collapsed, king salmon populations dwindled, and as many as 7,000 humpback whales perished.
Yet the crisis created an uneven playing field: some species emerged unscathed, while others even thrived.
Thick-billed murres, which often share nesting cliffs with common murres, were largely unaffected, possibly due to their more adaptable diet, Renner noted.
For common murres, however, the fallout lingers. Despite nearly a decade since the heat wave, their numbers show no sign of bouncing back -- and the losses may well be permanent.
Part of the reason lies in the long-term decline of some of their prey.
Another factor is murres' survival strategy relies on numbers: they aggregate in massive colonies to protect their eggs from opportunistic predators like eagles and gulls.
With their populations slashed, these birds have lost their critical safety buffer.
Still, Renner offered a glimmer of hope.
While addressing global warming is essential for curbing long-term climate change, conservation efforts can make a difference in the short term, she said.
Removing invasive species like foxes and rats from murre nesting islands could also provide the beleaguered birds with a fighting chance.
© Agence France-Presse
Most of what we know about humans living to very old age is based on faulty data, including the science behind the "blue zones" famous for having a high proportion of people over 100, according to one researcher.
The desire to live as long as possible has driven a booming lifestyle industry selling supplements, books, tech and tips to those wanting to learn the secrets of the world's oldest people.
But Saul Justin Newman, a researcher at University College London's Centre for Longitudinal Studies, told AFP that most extreme old age data "is junk to a really shocking degree".
Newman's research, which is currently being peer-reviewed, looked at data about centenarians and supercentenarians -- people who live to 100 and 110 -- in the United States, Italy, England, France and Japan.
Contrary to what one might expect, he found that supercentenarians tended to come from areas with poor health, high levels of poverty -- and bad record-keeping.
The true secret to extreme longevity seems to be to "move where birth certificates are rare, teach your kids pension fraud and start lying", Newman said as he accepted an Ig Nobel prize, a humorous version of the Nobel, in September.
Just one of many examples is Sogen Kato, who was thought to be Japan's oldest living person until his mummified remains were discovered in 2010.
AFP Supercentenarians tend to come from areas with poor health, high poverty and bad record-keeping, Newman's research found
It turned out he had been dead since 1978. His family was arrested for collecting three decades of pensions payments.The government then launched a review which found that 82 percent of Japan's centenarians -- 230,000 people -- were missing or dead.
"Their paperwork is in order, they're just dead," Newman said.
This illustrates the problem Newman has sought to shine a light on -- that confirming ages in this field involves triple-checking very old documents that could have been wrong from the start.
The industry that has popped up around blue zones is one "symptom" of this problem, he said.
Blue zones are regions around the world where people are said to live disproportionately longer and healthier lives.
The term was first used in 2004 by researchers referring to the Italian island of Sardinia.
The following year, National Geographic reporter Dan Buettner wrote a story that added the Japanese islands of Okinawa and the Californian city of Loma Linda.
AFP Costa Rica's Nicoya Peninsula is one of the blue zones where people are said to live disproportionately longer
Buettner admitted to the New York Times in October that he only included Loma Linda because his editor told him: "you need to find America's blue zone".The reporter teamed up with some demographers to create the Blue Zones lifestyle brand, and they added Costa Rica's Nicoya Peninsula and the Greek island of Ikaria to the list.
However, as seen in Japan, later government records have cast doubt on old age data in these regions.
In Costa Rica, 2008 research showed that 42 percent of centenarians had "lied about their age" in an earlier census, Newman said.
For Greece, he found 2012 data suggesting that 72 percent of the country's centenarians were dead or imaginary.
"They're only alive on pension day," Newman said.
Several prominent blue zone researchers wrote a rebuttal earlier this year, calling Newman's work "ethically and academically irresponsible".
They accused Newman of referring to broader regions of Japan and Sardinia when the blue zones were smaller areas.
The demographers also emphasized they had "meticulously validated" the ages of supercentenarians in blue zones, double-checking historical records and registries dating back to the 1800s.
Newman said this argument illustrated his point.
"If you start with a birth certificate that's wrong, that gets copied to everything, and you get perfectly consistent, perfectly wrong records," he said.
The only "way out of this quagmire" is to physically measure people's ages, Newman said.
AFP Japan's Okinawa prefecture, where poverty rates are double the national average, is listed as a blue zone
Steve Horvath, an aging researcher at the University of California, told AFP he had created a new technique called a methylation clock "for the express purpose of validating claims of exceptional longevity".The clock can "reliably detect instances of severe fraud", such as when a child assumes their parent's identity, but cannot yet tell the difference between a 115- and 120-year-old, he said.
Horvath has offered to test a DNA sample of France's Jeanne Calment, who died at 122 in 1997 and holds the record for the oldest confirmed age.
Newman's analysis "appears to be both rigorous and convincing", Horvath said, adding that several blue zones are overseen by rigorous scientists.
"I suspect both opinions hold some truth," he said.
So what can people at home take away from this debate?
"If you want to live a long time, step number one: don't buy anything," Newman said.
"Listen your GP (doctor), do some exercise, don't drink, don't smoke -- that's it."
© Agence France-Presse
by Tomohiro OSAKI
People with missing teeth may be able to grow new ones, say Japanese dentists testing a pioneering drug they hope will offer an alternative to dentures and implants.
Unlike reptiles and fish, which usually replace their fangs on a regular basis, it is widely accepted that humans and most other mammals only grow two sets of teeth.
But hidden underneath our gums are the dormant buds of a third generation, according to Katsu Takahashi, head of oral surgery at the Medical Research Institute Kitano Hospital in Osaka.
His team launched clinical trials at Kyoto University Hospital in October, administering an experimental medicine to adult test subjects that they say has the potential to jumpstart the growth of these concealed teeth.
It's a technology "completely new" to the world, Takahashi told AFP.
Prosthetic treatments used for teeth lost to decay, disease or injury are often seen as costly and invasive.
So "restoring natural teeth definitely has its advantages", said Takahashi, the project's lead researcher.
Tests on mice and ferrets suggest that blocking a protein called USAG-1 can awaken the third set, and the researchers have published lab photographs of regrown animal teeth.
In a study published last year, the team said their "antibody treatment in mice is effective for tooth regeneration and can be a breakthrough in treating tooth anomalies in humans".
For now, the dentists are prioritising the "dire" needs of patients with six or more permanent teeth missing from birth.
The hereditary condition is said to affect around 0.1 percent of people, who can have severe trouble chewing, and in Japan often spend most of their adolescence wearing a face mask to hide the wide gaps in their mouth, Takahashi said.
"This drug could be a game-changer for them," he added.
The drug is therefore aimed primarily at children, and the researchers want to make it available as early as 2030.
Angray Kang, a dentistry professor at Queen Mary University of London, only knows of one other team pursuing a similar objective of using antibodies to regrow or repair teeth.
"I would say that the Takahashi group is leading the way," the immunotechnology expert, who is not connected to the Japanese research, told AFP.
Takahashi's work is "exciting and worth pursuing", Kang said, in part because an antibody drug that targets a protein nearly identical to USAG-1 is already being used to treat osteoporosis.
"The race to regenerate human teeth is not a short sprint, but by analogy a set of back-to-back consecutive ultra-marathons," he said.
"This is only the beginning."
Chengfei Zhang, a clinical professor in endodontics at the University of Hong Kong, said Takahashi's method is "innovative and holds potential".
"The assertion that humans possess latent tooth buds capable of producing a third set of teeth is both revolutionary and controversial," he told AFP.
He also cautioned that "outcomes observed in animals do not always directly translate to humans".
The results of the animal experiments raise "questions about whether regenerated teeth could functionally and aesthetically replace missing teeth", Zhang added.
A confident Takahashi argues that the location of a new tooth in a mouth can be controlled, if not pinpointed, by the drug injection site.
And if it grows in the wrong place, it can be moved through orthodontics or transplantation, he said.
No young patients with the congenital disorder are taking part in the first clinical trial, as the main objective is to test the drug's safety, rather than its effectiveness.
So for now, the participants are healthy adults who have lost at least one existing tooth.
And while tooth regeneration is not the express goal of the trial this time around, there is a slim chance that it could happen to subjects anyway, Takahashi said.
If so, the researchers will have confirmed that the drug can be effective for those with acquired toothlessness -- which would be a medical triumph.
"I would be over the moon if that happens," Takahashi said.
This could be particularly welcome news in Japan, which has the second-oldest population in the world.
Health ministry data shows more than 90 percent of people aged 75 or older in Japan have at least one tooth missing.
"Expectations are high that our technology can directly extend their healthy life expectancy," Takahashi said.
© Agence France-Presse
Shortly after he was elected, Donald Trump announced an economic gambit that was aggressive even by his standards. He vowed that, on the first day of his second term, he would slap 25 percent tariffs on imports from Canada and Mexico, and boost those already placed on Chinese products by another 10 percent.
The move set off a frenzy of pushback. Canadian Prime Minister Justin Trudeau even flew to the president-elect’s Florida resort to make his case. Economists say the potential levies threaten to upend global trade — including on green technologies, many of which are manufactured in China. The moves would cause price spikes for everything from electric vehicles and heat pumps to solar panels.
“Typically, with tariffs, we’ve seen [companies] pass them along to the consumer,” said Corey Cantor, electric vehicles analyst at Bloomberg NEF. Ansgar Baums, a senior fellow at the nonpartisan foreign policy think-tank Stimson Center, said retaliatory moves from the three targeted countries would only make things worse. “It will drive up consumer costs and hurt those who cannot afford it.”
Trump acknowledges that possibility. But he has argued that tariffs are necessary to force Canada and Mexico to crack down on drugs, particularly fentanyl, and migrants crossing the border into the U.S.
It’s not the first time Trump has turned to tariffs as a foreign policy tool. In 2018 and 2019, he imposed them on a litany of goods, from steel and aluminum to photovoltaic solar panels and washing machines. While the Biden administration eased some of those duties, it kept many in place, especially those targeting China, and recently raised tariffs on Chinese items including electric vehicles, solar cells, and electrical vehicle batteries. Experts say these efforts have done little more than raise prices.
“The consensus on the first round of Trump tariffs is that [they] generally did not improve American productivity,” said Alex Muresianu, a senior policy analyst at the Tax Foundation, a right-leaning think tank. The nonprofit calculated that, in the long run, Trump’s first round of tariffs will hurt gross domestic product and cost the United States some 142,000 jobs. Baums was even more blunt about their impact: “They were a big failure. They didn’t achieve much.”
The recently threatened tariffs would ratchet prices even higher on things like solar panels, but are also much more far reaching because of their broad application to North American trading partners. One sweeping impact would be on gasoline prices because, although the U.S. is world’s largest oil producer, older domestic refineries can only process the type of heavier crude that comes from Canada. GasBuddy projects that tariffs could add 35 to 75 cents to a gallon of gas.
Automakers will also be hard hit, as $97 billion in parts and some four million vehicles come from Canada and, especially, Mexico. That’s where some of the more affordable electric vehicles, such as Ford’s Mustang Mach-E and the Chevrolet Equinox, are manufactured. Wolfe Research said that “given the magnitude, we’d expect most investors to assume Trump ultimately does not follow through with these threats” but that, if they were put in place, tariffs would add $3,000 to the price of the average car, regardless of whether it’s powered by gasoline or a battery.
Cantor, at Bloomberg NEF, says adding even a few thousand dollars to the price can drastically expand or contract the potential market of buyers for a vehicle. For example, about 70 percent of consumers consider a $35,000 car, a number that jumps to about 87 percent when a car is $30,000.
“People adjust their behavior,” he said. That could further harm an EV sector that will also likely be reeling from Trump’s rollback of federal tax-credits for electrified vehicles.
Baums doesn’t believe that more tariffs will meaningfully shift industries to the US and the Trump administration “underestimates” how complicated that process would be. Others say some relocation could occur. Michelle Davis, director and head of global solar for research firm Wood Mackenzie, wrote that the levies “would undoubtedly increase domestic manufacturing activity to meet market needs.” But even then, she adds, that “this would result in a more expensive market for domestic buyers.”
In addition to prices, Muresianu also worries that the type of protectionism that Trump favors could stymie innovation. He points to the U.S. shipbuilding industry as an example: it once supplied most of the world’s ships but, in large part due to policies meant to shield domestic shipyards from competition, American vessels have since become drastically more expensive than those made overseas and now account for less than 1 percent of the global total. Tariffs could impose similar stagnancy on other U.S. industries, Muresianu says.
Baums’ concerns are more existential. Trump, he says, is geo-politicizing issues like climate change in ways that will ultimately make it more difficult to share technology, lower costs, and combat greenhouse gas emissions. He would like countries to instead come together and agree that some industries — including cleantech — are too important to put at the center of a trade war.
“The planet is burning,” said Baums. “If there’s anything we should try to cooperate on, it’s stuff that makes a clean transition happen.”
A concerningly high number of endangered false killer whales are being injured when they get hooked by fishing gear in waters off the main Hawaiian islands, according to a new research paper released Thursday.
Published in the scientific journal Endangered Species Research, the research concludes there should be closer monitoring of that unique but dwindling local population and how the creatures — actually dolphins, not whales, and not killers — interact with the small-scale commercial and recreational boats that fish in those waters.
That could include installing cameras to record encounters with the false killer whales, which feed on the same large fish those boats catch and often go after what is already on the hook, said Robin Baird, a research biologist with the nonprofit Cascadia Research Collective, which led the study.
“We have an idea of where these interactions are likely occurring, but we donʻt know when theyʻre occurring or with what type of gear,” Baird said Wednesday. “Being able to come up with solutions requires (this) information.”
Cascadia, along with two Hawaii-based wildlife foundations and federal fisheries officials, analyzed photographs taken between 1999 and 2021 of three false killer whale populations found near or around the Hawaii archipelago, including the endangered group that inhabits the waters off the main islands.
The researchers flagged the photos that showed clear fishing-related injuries to the animalsʻ mouths and dorsal fins. The endangered group had the most documented injuries by far, the study showed.
Researchers were able to find photos of both the dorsal fin and the mouth for 153 individual dolphins for that group. Out of those 153, some 44 dolphins had been injured by fishing gear, the study found — nearly one in every three.
The rate of injury was drastically lower for the other two Hawaii populations, which arenʻt endangered. One of them is a pelagic, roaming group of several thousand dolphins. The other, which inhabits the Northwestern Hawaiian Islands, has nearly 500 individuals, according to the study.
The endangered group near the main islands is down to an estimated 138 dolphins, according to the study. Itʻs the only endangered population of false killer whales in the world, according to Baird. Theyʻre found anywhere from just off the beach to tens of miles offshore.
That swath of ocean generally coincides with Hawaiiʻs federally mandated “exclusion zone” — a region up to 70 miles offshore where the local longliner fleet is prohibited from fishing.
Thus, the dolphins are getting hooked by smaller-scale boats that fish closer to the islands, not the longliners, Baird said.
Thereʻs already a federally organized False Killer Whale Take Reduction Team thatʻs been working since 2010 to try and reduce the number of species deaths, but the fishers represented in that group are all from Hawaiiʻs longline fishing industry.
Baird on Wednesday recommended forming a new, similar hui (group) that would include the nearshore fisherman to address the plight of the endangered false killer whales.
False killer whales typically hunt and feed on ahi, mahimahi and other fish often sought by human fishers in nearby ocean waters. There have even been unique, documented instances in which the marine mammals have attempted to share their catch with people they encounter in the water, according to Baird.
By Libby Richards/Professor of Nursing, Purdue University
You’ve probably heard “Don’t go outside in the winter with your hair wet or without a coat; you’ll catch a cold.”
That’s not exactly true. As with many things, the reality is more complicated. Here’s the distinction: Being cold isn’t why you get a cold. But it is true that cold weather makes it easier to catch respiratory viruses such as the cold and flu.
Research also shows that lower temperatures are associated with higher COVID-19 rates.
As a professor of nursing with a background in public health, I’m often asked about infectious disease spread, including the relationship between cold and catching a cold. So here’s a look at what actually happens.
Many viruses, including rhinovirus – the usual culprit for the common cold – influenza, and SARS-CoV-2, the virus that causes COVID-19, remain infectious longer and replicate faster in colder temperatures and at lower humidity levels. This, coupled with the fact that people spend more time indoors and in close contact with others during cold weather, are common reasons that germs are more likely to spread.
The flu and respiratory syncytial virus, or RSV, tend to have a defined fall and winter seasonality. However, because of the emergence of new COVID-19 variants and immunity from previous infections and vaccinations decreasing over time, COVID-19 is not the typical cold-weather respiratory virus. As a case in point, COVID-19 infection rates have surged every summer since 2020.
More specifically, cold weather can change the outer membrane of the influenza virus, making it more solid and rubbery. Scientists believe that the rubbery coating makes person-to-person transmission of the virus easier.
It’s not just cold winter air that causes a problem. Air that is dry in addition to cold has been linked to flu outbreaks. That’s because dry winter air further helps the influenza virus to remain infectious longer. Dry air, which is common in the winter, causes the water found in respiratory droplets to evaporate more quickly. This results in smaller particles, which are capable of lasting longer and traveling farther after you cough or sneeze.
How your immune system responds during cold weather also matters a great deal. Inhaling cold air may adversely affect the immune response in your respiratory tract, which makes it easier for viruses to take hold. That’s why wearing a scarf over your nose and mouth may help prevent a cold because it warms the air that you inhale.
Cold weather can affect nasal immunity.Also, most people get less sunlight in the winter. That is a problem because the sun is a major source of vitamin D, which is essential for immune system health. Physical activity, another factor, also tends to drop during the winter. People are three times more likely to delay exercise in snowy or icy conditions.
Instead, people spend more time indoors. That usually means more close contact with others, which leads to disease spread. Respiratory viruses generally spread within a 6-foot radius of an infected person.
In addition, cold temperatures and low humidity dry out your eyes and the mucous membranes in your nose and throat. Because viruses that cause colds, flu and COVID-19 are typically inhaled, the virus can attach more easily to these impaired, dried-out passages.
The bottom line is that being wet and cold doesn’t make you sick. That being said, there are strategies to help prevent illness all year long:
Following these tips can ensure you have a healthy winter season.
This is an updated version of an article originally published on Dec. 15, 2020.
Libby Richards, Professor of Nursing, Purdue University
This article is republished from The Conversation under a Creative Commons license. Read the original article.
The recently updated South African Ethics in Health Research Guidelines have been a recent cause of concern, with some researchers and bioethicists interpreting them as allowing what’s known as heritable human genome editing.
Heritable human genome editing involves editing the DNA of sex cells (eggs, sperm) or early embryos in a manner that may be inherited by offspring. Because the impacts on future offspring and society are unknown, there is vigorous and active ongoing debate on the ethics of such interventions.
Rather than allowing heritable human genome editing, the guidelines acknowledge the reality that South African law already allows human genome editing. The only change lies in how the guidelines provide a framework on oversight into heritable human genome editing. This guidance should not be interpreted as a green light for heritable human genome editing.
From this perspective, the guidelines provide much-needed clarity on how research ethics committees can go about ensuring that research and clinical applications of genome editing in humans are carried out safely.
Human genome editing involves changing the DNA of sex or embryo cells. (Shutterstock)
The current controversy relates to one particular statutory provision: Section 57(1) of the South African National Health Act. The provision reads as follows:
A person may not —
(a) manipulate any genetic material, including genetic material of human gametes, zygotes or embryos; or
(b) engage in any activity, including nuclear transfer or embryo splitting,
for the purpose of the reproductive cloning of a human being.
What stands out from this provision is that it prohibits a number of acts, including the manipulation of genetic material, zygotes and embryos. One might interpret this provision as including heritable human genome editing. Viewed in this way, the guidelines are problematic in that they allow something the law prohibits.
However, such an interpretation of Section 57(1) conflicts with the rules of statutory interpretation in South Africa.
Statutes in South Africa must be interpreted purposively. How to interpret Section 57(1) does not depend on whether the text can be read as applying to heritable human genome editing, but rather whether the apparent purpose of the provision was to prohibit heritable human genome editing, considering the context within which the words appear.
There is no mystery around why Section 57(1) exists, which is to prohibit human reproductive cloning. That this was the purpose is evidenced by the language of the provision itself, which prohibits “manipulation of genetic material” only “for the purposes of the reproductive cloning of a human being.”
Other principles of statutory in South African law point to the conclusion that Section 57(1) does not apply to heritable human genome editing. Where a provision in a statute features the word “include,” the words after it define the general class of things that fall within the scope of that provision.
Section 57(1) prohibits “reproductive cloning,” which it defines as “the manipulation of genetic material in order to achieve the reproduction of a human being and includes nuclear transfer or embryo splitting for such purpose.” The general class of things this section applies to are clarified to be “nuclear transfer or embryo splitting,” which are both cloning techniques.
Therefore, the rules of statutory interpretation require that the definition of what Section 57(1) prohibits (reproductive cloning) not be read as including heritable human genome editing.
Another feature of statutory interpretation in South Africa that is relevant here is the presumption that where a provision is linked with a criminal sanction — as is the case with Section 57(1) — the narrowest possible interpretation of that statutory provision is to be preferred. So if Section 57(1) can reasonably be interpreted as limited only to human reproductive cloning and not heritable human genome editing, such an interpretation is the one our law gives effect to.
The guidelines reflect an accurate understanding of South African law by its drafters. South African law may prohibit genetic manipulation, but this only applies for the purposes of human reproductive cloning.
Genetic manipulation for other purposes, including heritable human genome editing, is not prohibited; there is nothing in the law preventing heritable human genome editing.
Research into genetic manipulation aims to prevent genetic health conditions or provide immunity against tuberculosis and HIV/AIDS. (Shutterstock)
It is important to note that the guidelines should not be taken as endorsing the use of heritable human genome editing technology. South Africa’s health research ethics guidelines serve as a “minimum benchmark of norms and standards for conducting responsible and ethical research in South Africa.” They are a tool meant to inform, guide and empower research ethics committees (RECs).
RECs ultimately decide whether or not to approve research. The guidelines simply provide guidance on how RECs should analyze research protocols including heritable human genome editing, but ultimately such research will not occur unless the relevant committee is convinced that doing so is safe and effective.
The inclusion of a form of research in the guidelines should not be understood as a green light for that kind of research or its clinical applications. There is no reason to believe that South African RECs will permit heritable human genome editing in South Africa before there is compelling evidence that doing so is safe.
Concerns have been expressed about the extent to which South Africa may be pushing the envelope with the new guidelines, given that other countries have not explicitly permitted heritable human genome editing. It is worth noting, however, that research on policies relating to heritable human genome editing reveals that most of the countries with restrictive policies are in the West, and are predominantly in Europe.
An important factor to consider in why South Africa — or any other country — may seek to plot a path forward when it comes to heritable human genome editing has to do with how those countries perceive the ethical considerations in question.
There is hardly consensus on the ethics of heritable human genome editing, and we have relatively little insight into non-western perspectives on editing the human genome editing. What research does exist suggests there may be material differences on what aspects, if any, of heritable human genome editing people consider ethically problematic and a cause for concern.
In the context of South Africa, a deliberative public engagement study found that an overwhelming majority of participants supported allowing the use of heritable human genome editing to prevent genetic health conditions or provide immunity against tuberculosis and HIV/AIDS, provided it was conducted in a safe and effective manner.
The guidelines do well to adopt an open-ended approach to the future of heritable human genome editing, by remaining open to the possibility that there may come a time where at least some applications are found to be both safe and ethically acceptable in South Africa.
Bonginkosi Shozi, Fellow, Center for Law and the Biosciences, Stanford University
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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