Publisher Health

Hail severity will increase in most regions of the world while Australia and Europe are expected to experience more hailstorms as a result of climate change, an international review led by a UNSW Sydney researcher has found.
The review study, published in Nature Reviews Earth & Environment, examined the effects climate change will have on hail in the future.
It shows a global summary of hail trends from past observations and projected future trends from simulations and models.
The review led to the general expectation that hailstorm frequency will decrease in East Asia and North America, while increasing in Australia and Europe, and that hailstorm severity will increase in most regions.
Researchers from University of Bern, Central Michigan University, Karlsruhe Institute of Technology, University of Illinois, Colorado State University and Peking University took part in the study.
“We came to the conclusion that on balance, the hail threat is likely to increase in Australia, especially in Australia’s south-east including the Sydney area,” lead author and postdoctoral researcher at UNSW Sydney’s Climate Change Research Centre, Tim Raupach said.

A combination of esophageal brushing and extensive genetic sequencing of the sample collected can detect chromosome alterations in people with Barrett’s Esophagus, identifying patients at risk for progressing to esophageal cancer, according to a new study by researchers at the Johns Hopkins Kimmel Cancer Center and Case Western Reserve University.
In Barrett’s Esophagus (BE), chronic acid reflux from the stomach damages the cells lining the lower esophagus, causing them to become more like cells of the lower digestive system. Cells in the lower esophagus progress through several precancerous stages before sometimes developing into esophageal adenocarcinoma, a cancer with a five-year survival rate below 20 percent. BE is the only known precursor to esophageal adenocarcinoma.
Clinicians can detect these progressive states in BE by looking for chromosomal alterations known as aneuploidy — a common feature in most cancer cells — but until now the process has involved multiple biopsies.
A single esophageal brushing paired with the sequencing technique called RealSeqS is sensitive and specific enough to identify aneuploidy at several stages of BE progression, and can even match specific types of aneuploidy with specific stages of the disease, the researchers say.
“Aneuploidy has long been implicated in the development, initiation or progression of esophageal cancer but the assays or experimental methods to detect this have not been as easily achieved or as high throughput as we would have wanted to allow for clinical implementation,” says senior study author Chetan Bettegowda, M.D., Ph.D., Jennison and Novak Families Professor of Neurosurgery at the Kimmel Cancer Center.
The method could help clinicians identify people at higher risk of having BE progress to esophageal adenocarcinoma, “instituting more intensive follow-up for those patients or instituting treatments at earlier stages of the disease,” Bettegowda says.

The coronavirus most likely emerged in bats before spreading to humans through another animal, according to a report to be released by the World Health Organization on Tuesday, offering some clues on a question that has become politically fraught amid accusations of interference from Beijing.According to the report on the origin of the pandemic, which was obtained by The New York Times in advance of its release, a team of experts who recently visited the Chinese city of Wuhan, where the coronavirus was first detected in late 2019, also dismissed the idea that the virus might have leaked accidentally from a Chinese laboratory as “extremely unlikely.”Officials in the United States and elsewhere have expressed concern about China’s efforts to reshape the narrative about the outbreak in Wuhan, which the authorities initially tried to conceal.Critics have assailed the inquiry by the W.H.O. team as insufficient, saying the global health agency has been too deferential to Beijing. Chinese scientists, many of whom are affiliated with the government, helped oversee the inquiry, and the report was repeatedly delayed amid delicate negotiations with Chinese officials. For months, China sought to delay the visit of the investigators in an apparent attempt to avoid scrutiny of its early mistakes in handling the pandemic.The Chinese government has defended its approach, saying it is fully cooperating with the W.H.O.In the 123-page report, the scientists outlined several theories that might explain how the virus first spread to humans. The findings in the document were first reported on Monday by The Associated Press.The report was written jointly by a team of 17 scientists from around the world and 17 Chinese scientists. The experts led a fact-finding visit to Wuhan for 27 days in January and February.During the visit to Wuhan, Chinese officials refused to share raw data about some of the earliest possible virus cases with the W.H.O. team, frustrating some of the visiting scientists.China’s lack of transparency as well as other concerns prompted a small group of scientists not affiliated with the World Health Organization to call this month for a new inquiry into the origin of the pandemic. They said such an inquiry should consider the possibility that the virus escaped from a laboratory in Wuhan or infected someone inside it.The lab leak theory has been promoted by some officials in the Trump administration, including Dr. Robert Redfield, the former director of the Centers for Disease Control and Prevention, in comments to CNN last week. He offered no evidence and emphasized that it was his opinion; the theory has been widely dismissed by scientists and U.S. intelligence officials.Matt Apuzzo contributed reporting.

The coronavirus most likely emerged in bats before spreading to humans through another animal, according to a report to be released by the World Health Organization on Tuesday, offering some clues on a question that has become politically fraught amid accusations of interference from Beijing.According to the report on the origin of the pandemic, which was obtained by The New York Times in advance of its release, a team of experts who recently visited the Chinese city of Wuhan, where the coronavirus was first detected in late 2019, also dismissed the idea that the virus might have leaked accidentally from a Chinese laboratory as “extremely unlikely.”Officials in the United States and elsewhere have expressed concern about China’s efforts to reshape the narrative about the outbreak in Wuhan, which the authorities initially tried to conceal.Critics have assailed the inquiry by the W.H.O. team as insufficient, saying the global health agency has been too deferential to Beijing. Chinese scientists, many of whom are affiliated with the government, helped oversee the inquiry, and the report was repeatedly delayed amid delicate negotiations with Chinese officials. For months, China sought to delay the visit of the investigators in an apparent attempt to avoid scrutiny of its early mistakes in handling the pandemic.The Chinese government has defended its approach, saying it is fully cooperating with the W.H.O.In the 123-page report, the scientists outlined several theories that might explain how the virus first spread to humans. The findings in the document were first reported on Monday by The Associated Press.The report was written jointly by a team of 17 scientists from around the world and 17 Chinese scientists. The experts led a fact-finding visit to Wuhan for 27 days in January and February.During the visit to Wuhan, Chinese officials refused to share raw data about some of the earliest possible virus cases with the W.H.O. team, frustrating some of the visiting scientists.China’s lack of transparency as well as other concerns prompted a small group of scientists not affiliated with the World Health Organization to call this month for a new inquiry into the origin of the pandemic. They said such an inquiry should consider the possibility that the virus escaped from a laboratory in Wuhan or infected someone inside it. The lab leak theory has been promoted by some officials in the Trump administration, including Dr. Robert Redfield, the former director of the Centers for Disease Control and Prevention, in comments to CNN last week. He offered no evidence and emphasized that it was his opinion; the theory has been widely dismissed by scientists and U.S. intelligence officials.Matt Apuzzo contributed reporting.

Bioengineering researchers at Lehigh University have identified a previously unknown interaction between receptors in human cells and the spike, or “S,” protein of SARS-CoV-2, the virus that causes COVID-19. This new information could aid in the development of new strategies to block SARS-CoV-2 entry into human cells.
X. Frank Zhang and Wonpil Im knew from recent studies that the interaction between the SARS-CoV-2 spike protein and angiotensin-converting enzyme 2 (ACE2) receptors in human cells is stronger than the interaction between the structurally identical spike protein of SARS-CoV-1, the virus that caused the 2002-2004 SARS outbreak, and the same receptors.
“Our goal was to characterize SARS-CoV-2 and study the protein-protein interactions during its invasion of human cells to provide more insights into the mechanisms that make this first step in its successful invasion process possible,” says Zhang, an associate professor in Bioengineering and Mechanical Engineering & Mechanics at Lehigh.
Their findings appear in an article called “Biomechanical characterization of SARS-CoV-2 spike RBD and human ACE2 protein-protein interaction” in a special issue of Biophysical Journal, “Biophysicists Address Covid-19 Challenges I,” published in mid-March. Additional authors include, from Lehigh University: Wenpeng Cao, Decheng Hou and Seonghan Kim in bioengineering; Chuqiao Dong in mechanical engineering and mechanics; and, from Lindsley F. Kimball Research Institute, New York Blood Center, Wanbo Tai and Lanying Du.
Using combined single-molecule force spectroscopy and molecular dynamics simulations, Zhang’s and Im’s teams were able to identify a previously unknown interaction between ACE2 glycans (sugar groups attached to the surface of proteins) and the SARS-CoV-2 spike. It is this interaction that appears to be responsible for the strengthening of the virus-cell interaction. This may partially explain the higher infection rate of COVID-19 compared to the similar virus that caused the 2002-2004 SARS outbreak, they say.
“We were surprised to find that the specific interaction between ACE2 glycans and the SARS-CoV-2 spike protein is what makes the separation of the virus from cells so difficult,” says Im, who is a professor of bioengineering, computer science, chemistry and biological sciences, as well as the Presidential Endowed Chair in Health, Science and Engineering at Lehigh.
To arrive at these findings, the team employed Zhang’s innovative single-molecule detection technique, measuring the detachment force of the spike protein-ACE2 receptor interaction. Using the all-atom molecular dynamics simulations of the complex system available in CHARMM-GUI developed by Im, they then identified the detailed structural information in this interaction.
“After we carefully removed all of the ACE2 glycans and measured the force of the interaction, we saw that the strength of the SARS-CoV-2 spike-ACE2 interaction fell back to levels similar to SARS-CoV-1,” says Zhang.
“It is possible that this newly-discovered interaction with ACE2 glycans could be a contributing factor to the higher rates of COVID-19 than the structurally similar SARS-CoV-1, which has a weaker interaction,” says Zhang. “Our hope is that researchers may be able to use this information to develop new strategies to identify, prevent, treat and vaccinate against COVID-19.”
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Materials provided by Lehigh University. Original written by Lori Friedman. Note: Content may be edited for style and length.

Adults with periodontitis, a severe gum infection, may be significantly more likely to have higher blood pressure compared to individuals who had healthy gums, according to new research published today in Hypertension, an American Heart Association journal.
Previous studies have found an association between hypertension and periodontitis, however, research confirming the details of this association is scarce. Periodontitis is an infection of the gum tissues that hold teeth in place that can lead to progressive inflammation, bone or tooth loss. Prevention and treatment of periodontitis is cost effective and can lead to reduction of systemic markers of inflammation as well as improvement in function of the endothelium (thin membrane lining the inside of the heart and blood vessels).
“Patients with gum disease often present with elevated blood pressure, especially when there is active gingival inflammation, or bleeding of the gums,” said lead study author Eva Muñoz Aguilera, D.D.S., M.Clin.Dent., senior researcher at UCL Eastman Dental Institute in London, United Kingdom. “Elevated blood pressure is usually asymptomatic, and many individuals may be unaware that they are at increased risk of cardiovascular complications. We aimed to investigate the association between severe periodontitis and high blood pressure in healthy adults without a confirmed diagnosis of hypertension.”
The study included 250 adults with generalized, severe periodontitis (≥50% of teeth measured with gum infection) and a control group of 250 adults who did not have severe gum disease, all of whom were otherwise healthy and had no other chronic health conditions. The median age of the participants was 35 years, and 52.6% were female. The research was completed in collaboration with the department of dentistry at the Universitat Internacional de Catalunya in Barcelona, Spain.
All participants underwent comprehensive periodontal examinations including detailed measures of gum disease severity, such as full-mouth dental plaque, bleeding of the gums and the depth of the infected gum pockets. Blood pressure assessments were measured three times for each participant to ensure accuracy. Fasting blood samples were also collected and analyzed for high levels of white blood cells and high sensitivity C-reactive protein (hsCRP), as both are markers of increased inflammation in the body. Additional information analyzed as confounders included family history of cardiovascular disease, age, body mass index, gender, ethnicity, smoking and physical activity levels.
The researchers found that a diagnosis of gum disease was associated with higher odds of hypertension, independent of common cardiovascular risk factors. Individuals with gum disease were twice as likely to have high systolic blood pressure values ?140 mm Hg, compared to people with healthy gums (14% and 7%, respectively). Researchers also found: The presence of active gum inflammation (identified by bleeding gums) was associated with higher systolic blood pressure. Participants with periodontitis exhibited increased glucose, LDL (“bad” cholesterol), hsCRP and white blood cell levels, and lower HDL (“good” cholesterol) levels compared to those in the control group. Nearly 50% of participants with gum disease and 42% of the control group had blood pressure values for a diagnosis of hypertension, defined as ?130/80 mmHg.”This evidence indicates that periodontal bacteria cause damage to the gums and also triggers inflammatory responses that can impact the development of systemic diseases including hypertension,” said corresponding author Francesco D’Aiuto, D.M.D., M.Clin.Dent., Ph.D., professor of periodontology and head of the periodontology unit at the UCL Eastman Dental Institute. “This would mean that the link between gum disease and elevated blood pressure occurs well before a patient develops high blood pressure. Our study also confirms that a worryingly high number of individuals are unaware of a possible diagnosis of hypertension.”
D’Aiuto added, “Integration of hypertension screening by dental professionals with referrals to primary care professionals and periodontal disease screening by medical professionals with referrals to periodontists could improve detection and treatment of both conditions to improve oral health and reduce the burden of hypertension and its complications. Oral health strategies such as brushing teeth twice daily are proven to be very effective in managing and preventing the most common oral conditions, and our study’s results indicate they can also be a powerful and affordable tool to help prevent hypertension.”
This study did not account for other factors that may also impact blood pressure, such as abdominal obesity, salt intake, use of anti-inflammatory medications, hormone treatments or stress, or any other oral health conditions.
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Materials provided by American Heart Association. Note: Content may be edited for style and length.

Each human being is made of billions of cells. In order to ensure his survival, cells must coordinate with each other and attach in the right place to perform their tasks. Scientists from the University of Geneva (UNIGE), Switzerland, in collaboration with the University of Tampere in Finland, have highlighted the key role of a protein called paxillin, which enables cells to perceive their environment and anchor at the right place with the help of cellular “crampons.” Indeed, without functional paxillin, the cell is unable to attach properly and slips continuously. These results, to be read in the journal Communications Biology, shed new light on how cells adhere or migrate, mechanisms essential to the good functioning of our organs, but also involved in the development of metastatic tumors.
To ensure our survival, each cell performs specific functions in coordination with their neighbours. In such a dynamic system, the migration of cells and their anchoring at the right place are essential. But how do cells manage to coordinate with each other? Scientists have long believed that cells communicate mainly through chemical signals, such as hormones. However, recent discoveries suggest that mechanical signals play a major role in cell coordination. “This is why we started to study the ability of cells to decipher and respond to their physical environment,” explains Bernhard Wehrle-Haller, Professor at the Department of cell physiology and metabolism at UNIGE Faculty of Medicine. “Especially as it could help us to understand how cancer cells use these mechanisms to invade other organs and form metastases.”
From a mechanical cue to a biological signal
When a cell has to move, it “senses” its environment with the help of proteins on its surface, the integrins. When the cell detects a suitable location, a complex network of proteins, called focal adhesion, is then set up to form cellular crampons that anchor the cell to its environment. “But how is this anchoring mechanism regulated? This is what we wanted to find out,” explains Marta Ripamonti, researcher in the laboratory of Prof. Bernhard Wehrle-Haller and first author of the study.
By studying paxillin, one of the many proteins that make up these crampons, researchers were able to unravel the mystery. “We knew that this protein played a role in the assembly of focal adhesions, but we didn’t expect it to be the key regulator,” says Prof. Bernhard Wehrle-Haller with enthusiasm. Without functional paxillin, cells are unable to anchor, regardless of the suitability of their environment. In addition, paxillin has also the function of informing the cell that anchoring has taken place correctly, thus transforming a mechanical response into a biological signal that the cell can understand.
Disrupting the crampons to prevent metastases?
These in vitro experiments highlight the major role of paxillin in the migration and adhesion of healthy cells, but they could also be a starting point for a better understanding of cancer development. “It is indeed likely that cancer cells use paxillin to find a place that enhance their survival. Would it be possible to block this mechanism in tumor cells and prevent the formation of metastases? Yes, we think so! ” concludes Prof. Bernhard Wehrle-Haller.
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Materials provided by Université de Genève. Note: Content may be edited for style and length.

As NASA seeks to build a lunar outpost, visit Mars and commercialize spaceflight, the long-term effects of weightlessness on the human heart are of critical importance, according to researchers. By analyzing data from astronaut Scott Kelly’s year in space and comparing it to information from extreme long distance, which simulates weightlessness, swimming of Benoît Lecomte, researchers found that low-intensity exercise was not enough to counteract the effects of prolonged weightlessness on the heart, according to new research published today in the American Heart Association’s flagship journal Circulation.
Each time a person sits or stands, gravity draws blood into the legs. The work the heart does to keep blood flowing as it counters Earth’s gravity helps it maintain its size and function. Removing gravitational effects causes the heart to shrink.
Researchers examined data from retired astronaut Scott Kelly’s stint aboard the International Space Station from 2015 to 2016 and elite endurance swimmer Benoît Lecomte’s swim across the Pacific Ocean in 2018.
In this new study, researchers evaluated the effects of long-term weightlessness on the structure of the heart and to help understand whether extensive periods of low-intensity exercise can prevent the effects of weightlessness.
“The heart is remarkably plastic and especially responsive to gravity or its absence. Both the impact of gravity as well as the adaptive response to exercise play a role, and we were surprised that even extremely long periods of low-intensity exercise did not keep the heart muscle from shrinking,” said Benjamin D. Levine, M.D., the study’s senior author and a professor of internal medicine at UT Southwestern Medical Center and director of Texas Health Presbyterian’s Institute for Exercise and Environmental Medicine, both in Dallas.
The research team examined the health data of Kelly’s year in space aboard the International Space Station and Lecomte’s swim across the Pacific Ocean to investigate the impact of long-term weightlessness on the heart. Water immersion is an excellent model for weightlessness since water offsets gravity’s effects, especially in a prone swimmer, a specific swimming technique used by long-distance endurance swimmers.

SharecloseShare pageCopy linkAbout sharingimage copyrightAFPA French drug maker has been found guilty of aggravated fraud and involuntary manslaughter over a weight loss pill at the centre of a major health scandal.The drug Mediator was developed for use in overweight diabetics and was on the market for 33 years.It was eventually withdrawn in 2009 over concerns it could cause serious heart problems.Hundreds of people are believed to have died as a result of the drug.Around five million people were prescribed the medicine over the course of 33 years, despite various warnings over its side effects.French trial on fatal weight-loss drug beginsFrance braced for drug scandal reportFrance pledges drug system reformThousands of plaintiffs were involved in the trial, which began in 2019.Drug maker Servier had denied any knowledge of Mediator’s side effects but a court on Monday issued it with a fine of €2.7m (£2.3m, $3.2m).The company’s former chairman Jean-Philippe Seta was also given a four-year suspended prison sentence.France’s medical regulator, meanwhile, was fined more than €300,000 for its role in the scandal. The judge found the body had “seriously failed” in its duties, according to the AFP news agency.Ahead of Monday’s verdict, French pulmonologist Dr Irène Frachon, who is credited with exposing the drug’s side effects, told AFP that she hoped the ruling would “give us the tools to understand how such deceit could have gone on for so long”.A number of other European countries, including Italy and Spain, banned Mediator in the early 2000s.In France, however, it continued to be offered to diabetics and other patients as an appetite suppressant.One study concluded that 500 deaths could be linked to Mediator between 1976 and 2009. A second one put the figure at 2,000.

New research has linked growth hormone treatment to serious adverse health effects years later.An 8-year-old boy I know is small for his age, shorter and slighter than his friends, even smaller than his 5-year-old sister. Concerned about the increasing use and possible risks of growth hormone, I asked his mother if she’d considered treating him with it. She replied, “Not really. He’s built like his father, who was short and slight as a boy and didn’t shoot up until college.”Their son, she said, has no sign of a hormone deficiency. “He’s in the third percentile for height and has maintained the same growth trajectory for years, so there’s no reason to do something about it,” she said. “He’s very athletic, physically capable and can keep up with his friends in other ways.”His father, at 41, is now 6 feet tall, though still very slender. He recalls being a reasonably athletic child but without the physical power of his friends, making up for what he lacked in mass with speed and agility. “I enjoyed competitive sports and worked on skills others didn’t have,” he told me, and said he encourages his son to recognize and capitalize on the skills he has.If only every parent with a short but healthy child approached the matter as sensibly. Experts estimate that 60 percent to 80 percent of children who are short for their age do not have a growth hormone deficiency or other medical condition that limits growth. But knowing there’s a therapy available to increase height, some parents seek a medical solution for a perceived problem, even when there is no medical abnormality. They should also know, however, that new research has linked growth hormone treatment to serious adverse health effects years later.Undue shortness may have many causes in addition to a deficiency of growth hormone, including malnutrition, Crohn’s disease or celiac disease, and potential medical conditions should be ruled out or, if present, treated. But height is most often related to the child’s genetics. Like father or mother, like son or daughter. Given the height of my parents — a 5-foot-1 mother and a 5-foot-6 father — I was not likely to become a forward for the Knicks at 4 feet 11.Dr. Adda Grimberg, a pediatric endocrinologist at Children’s Hospital of Philadelphia, recalled that “20 years ago, families were focused on health. They came in with a child who was not growing right and wanted to know if there was an underlying disease. Now, more and more, they’re focused on height. They want growth hormone, looking for a specific height. But this is not like Amazon; you can’t just place an order and make a child the height you want.”Originally, growth hormone was used to treat children with an established deficiency, which can result in a host of serious health problems. Cadavers were the initial limited source of the hormone until 1985, when scientists succeeded in producing recombinant human growth hormone in the laboratory, greatly increasing the supply and its use to treat growth hormone deficiency.Estimates of the incidence of this deficiency range from one in 3,000 to one in 10,000 children. According to the Pediatric Endocrine Society, those affected are usually much shorter than their peers — well below the third percentile — and over time fall increasingly behind.In 2003, the Food and Drug Administration approved use of recombinant human growth hormone for the condition known as “idiopathic short stature,” or short stature of unknown cause, which is not a disease. But it has prompted a growing number of parents to consider using the hormone to boost the height of their children. The resulting rush to therapy reflects concerns about a widespread societal bias against shortness, rather than a true medical need, Dr. Grimberg said.Parents considering treatment for this otherwise medically benign condition should know what it entails: daily injections for years until the child’s growth is completed, rotating injection sites in the body to minimize scarring. Although few children experience side effects, which can include severe headaches and hip problems, treatment requires repeated doctor visits, X-rays and blood work and, Dr. Grimberg said, “gives the child a powerful message that there’s something wrong with him that needs fixing.”According to the Pediatric Endocrine Society, the decision to administer growth hormone for idiopathic short stature should be made on a case-by-case basis in which benefits and risks are carefully considered for each child.What, then, are the benefits and risks? Although manufacturers have supported monitoring drug safety beyond the 10 years mandated by the U.S. government, reporting is voluntary and necessarily incomplete. However, a far more reliable assessment is available from Sweden, where population-wide data are routinely collected.In JAMA Pediatrics in December, pediatric endocrinologists from Karolinska University Hospital reported that among 3,408 patients who were treated with recombinant growth hormone as children and adolescents and followed for up to 25 years, the risk of developing a cardiovascular event like a heart attack or stroke was two-thirds higher for men and twice as high for women than among 50,036 untreated but otherwise similar people.The Swedish finding follows a report last June from a research team in Tokyo that growth hormone promotes biomedical pathways that stimulate the development of atherosclerosis, the basis for most cardiovascular events.Not yet known is whether other long-term adverse effects will become apparent in the years ahead. Based on its known action, giving growth hormone when no deficiency exists might raise the risk of cancer, respiratory disease and diabetes. In an editorial in JAMA Pediatrics, Dr. Grimberg wrote that “indirect evidence suggests that the potential for untoward effects of growth hormone treatment is sufficiently plausible” to warrant further study.Equally important for parents to know is how much height their children might gain from years of daily hormone injections. Though impossible to predict in advance for an individual child, the average benefit for children with idiopathic short stature is about two inches in adult height. Dr. Grimberg suggested that if there is no measurable benefit within a year of therapy, parents should consider stopping it.In discussing the psychological aspects of growth hormone therapy when no deficiency exists, experts have noted that the practice perpetuates the notion that short stature is unacceptable, leading to a spiraling demand for therapy. It is far better, one group suggested, to help a short child develop coping skills than to buy inches through pharmacological means.In a report in Hormone Research in Pediatrics, Dr. Talia Hitt and colleagues at Children’s Hospital of Philadelphia and the University of Pennsylvania wrote that parents’ high expectations that growth hormone therapy will improve the quality of life for their children are unlikely to be met if the children are not hormone deficient. They urged clinicians to “support families in other ways that promote positive development in children with short stature.”Dr. Philippa Gordon, a pediatrician in Brooklyn, N.Y., urges parents to make sure their children know “that people can be all different sizes and shapes and that their love for them is unconditional.”