Publisher Health

Mitochondria are known as energy suppliers for our cells, but they also play an important role in the defense against pathogens. They can initiate immune responses, and deprive pathogens of the nutrients they need to grow. A research team led by Lena Pernas of the Max Planck Institute for Biology of Ageing in Cologne, Germany, has now shown that pathogens can turn off mitochondrial defense mechanisms by hijacking a normal cellular response to stress.
To survive, pathogens need to acquire nutrients from their host and counter host defenses. One such defense comes from host mitochondria, which can deprive them of nutrients they need and thus restrict their growth. “We wanted to know how else mitochondrial behaviour changes when mitochondria and pathogens meet in cells. Because the outer membrane of these organelles is the first point of contact with the pathogens, we took a closer look at it,” explains Lena Pernas, research group leader at the Max Planck Institute for Biology of Ageing.
Mitochondria shed their ´skin`
The researchers infected cells with the human parasite Toxoplasma gondii and observed live under the microscope what happens to the outer compartment of mitochondria. “We saw that mitochondria in contact with the parasite started shedding large structures from their outer membrane. This was so puzzling to us. Why would mitochondria shed what is essentially the gateway between them and the rest of the cell?” says Xianhe Li, first author of the study.
Hostile takeover
But how does the parasite get the mitochondria to do it? The research team was able to show that the pathogen has a protein that functionally mimics a host mitochondrial protein. It binds to a receptor on the outer membrane of mitochondria, to gain access to the machinery that ensures proteins are transported inside the mitochondria. “In doing so, the parasite hijacks a normal host response to mitochondrial stress that, in the context of infection, effectively disarms the mitochondria” Pernas said. “Other researchers have shown that a SARS-CoV-2 virus protein also binds to this transport receptor. This suggests the receptor plays an important role in the host-pathogen interaction. But further investigation is needed to better understand its role during different infections.”
Lena Pernas is also a group leader at the CECAD Cluster of Excellence in Aging Research at the University of Cologne.
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Concussion can be frustratingly hard to diagnose and track. The injury doesn’t show up on routine brain scans, and there is no definitive diagnostic test. It’s usually diagnosed based on symptoms, and, in athletes, comparison with baseline testing if it was done. But concussion symptoms are non-specific, unreliable, and easily influenced by emotions.
“Athletes usually want to go back to their sport, so lots of times they say, ‘I feel great, doc,’ putting themselves at risk should they sustain a second brain injury,” says William Meehan, MD, a physician in the Division of Sports Medicine at Boston Children’s Hospital and director of The Micheli Center for Sports Injury Prevention. “But we’ve also had a lot of kids coming in worried, saying, ‘I’m not doing so well in school and I play soccer. Could it be a concussion?’ It would be great if a test could just tell us yes or no.”
Rebekah Mannix, MD, MPH, in Boston Children’s Division of Emergency Medicine, says 40 to 60 percent of concussions are missed in the acute setting, where more visible injuries tend to get the attention. “Concussion can be very subtle. But there are lots of reasons to want to diagnose concussion acutely — it can facilitate recovery, prevent kids from going back to sports too quickly, and avoid second-impact syndrome. We are always looking for objective markers of injury.”
New research in the January 11 issue of Neurology could lead to just that: protein “biomarkers” in urine that could be used to diagnose concussion and monitor recovery.
A chance encounter
In 2015, David Howell, PhD, a postdoctoral fellow with Meehan, gave a talk at Boston Children’s describing a study of concussion they were just beginning in collegiate athletes. Marsha Moses, PhD, director of the Vascular Biology Program at Boston Children’s approached Howell afterward. “My lab works in the urinary biomarker space,” she said. “We should talk.”
Moses’s work, going back more than 20 years, began as a way to detect and monitor a variety of cancers. Several of her team’s non-invasive urine tests are now in clinical trials. Over time, the team has also validated urinary biomarkers for chronic pelvic pain, benign prostatic hyperplasia, endometriosis, and more. Moses’s renowned urine biorepository contains thousands of samples.

People who contracted COVID-19 while pregnant were more likely to have poor birth outcomes including preterm birth, small for gestational age, low birth weight, and stillbirth. The poor outcomes of preterm birth and stillbirth were observed primarily with those infected with SARS-CoV-2 during the first or second trimester, whereas increased rates of small for gestational age were driven largely by third trimester infection.
An Institute for Systems Biology-led study examined the electronic health records of more than 18,000 people with SARS-CoV-2 tests during pregnancy. Researchers compared outcomes of unvaccinated people with a positive test during pregnancy — 882 in total — to those who tested negative.
“We found that SARS-CoV-2 infection indicated increased rates of preterm delivery and stillbirth, largely driven by first and second trimester infections,” said Samantha Piekos, PhD, first author of the study. She added: “The single greatest predictor of gestational age at delivery is gestational age at infection, with earlier age at infection associated with earlier age at delivery.”
The people in the study had mild or moderate SARS-CoV-2 infections. Severity of maternal COVID-19 infection was not correlated with gestational age at delivery. Additionally, poor birth outcomes were present even if maternal COVID-19 didn’t result in severe respiratory problems during infection.
The findings were published today in the journal The Lancet Digital Health and are among the first that account for the trimester of SARS-CoV-2 infection on birth outcomes.
People in the SARS-CoV-2-positive cohort were more likely to have Hispanic ethnicity, race other than Asian or White, Medicaid insurance, lower age, higher BMI, lower education attainment, and other factors known to be associated with negative birth outcomes. To account for this and to make a true apples-to-apples comparison, researchers used a statistical matching technique that controlled for the confounding variables.
“Pregnant people are at an increased risk of adverse outcomes following SARS-CoV-2 infection, even when maternal COVID-19 is less severe, and they may benefit from increased monitoring following infection,” said Jennifer Hadlock, MD, corresponding author of the paper and assistant professor at ISB. “Both maternal and fetal health are at increased risk with COVID-19. Therefore, this reinforces the importance of protecting pregnant women,” she added.
The study was conducted before COVID-19 vaccines were widely available in the United States. There is an opportunity for future studies to examine whether vaccination helps to prevent negative birth outcomes in breakthrough cases.
This research project was a collaboration between ISB and Providence.
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One in 10 people may have clinically relevant levels of potentially infectious SARS-CoV-2 past the 10 day quarantine period, according to new research.
The study, led by the University of Exeter and funded by Animal Free Research UK, used a newly adapted test which can detect whether the virus was potentially still active. It was applied to samples from 176 people in Exeter who had tested positive on standard PCR tests.
The study, published in the international Journal of Infectious Diseases found that 13 per cent of people still exhibited clinically-relevant levels of virus after 10 days, meaning they could potentially still be infectious. Some people retained these levels for up to 68 days. The authors believe this new test should be applied in settings where people are vulnerable, to stop the spread of COVID-19.
Professor Lorna Harries, of the University of Exeter Medical School, oversaw the study. She said: “While this is a relatively small study, our results suggest that potentially active virus may sometimes persist beyond a 10 day period, and could pose a potential risk of onward transmission. Furthermore, there was nothing clinically remarkable about these people, which means we wouldn’t be able to predict who they are.”
Conventional PCR tests work by testing for the presence of viral fragments. While they can tell if someone has recently had the virus, they cannot detect whether it is still active, and the person is infectious. The test used in the latest study however gives a positive result only when the virus is active and potentially capable of onward transmission.
Lead author Merlin Davies, of the University of Exeter Medical School, said: “In some settings, such as people returning to care homes after illness, People continuing to be infectious after ten days could pose a serious public health risk. We may need to ensure people in those setting have a negative active virus test to ensure people are no longer infectious. We now want to conduct larger trials to investigate this further.”
Animal Free Research UK CEO, Carla Owen, said: “The University of Exeter team’s discovery is exciting and potentially very important. Once more, it shows how focusing exclusively on human biology during medical research can produce results that are more reliable and more likely to benefit humans and animals.
“Pioneering animal free work is providing the best chance of not only defeating Covid 19 but also finding better treatments for all human diseases.
“The results also send a loud and clear message to the Government to better fund modern medical research and make the UK a world leader in cutting edge, kinder science.”
The research is a collaboration between the University of Exeter Medical School, the Royal Devon & Exeter NHS Foundation Trust, and the NIHR Exeter Clinical Research Facility.
The paper is entitled ‘Persistence of clinically-relevant levels of SARS-CoV2 envelope gene subgenomic RNAs in non-immunocompromised individuals’, and is published in the international Journal of Infectious Diseases.
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A molecule of RNA called CARMN has been found in abundance in the healthy smooth muscle cells that help give our blood vessels strength and flexibility, and distinctly decreased in vascular diseases like atherosclerosis, a major cause of heart attack and stroke, scientists report.
Their findings in human tissue and confirmed in rodent models of vascular disease, provide new insight into how smooth muscle cells in our blood vessel walls go from enabling a sound passageway for blood flow to instead enabling plaque development in places like our coronary arteries and/or reclosure of those arteries following common treatments including angioplasty and stent placement.
They also potentially point to a new approach to avoiding both, that could one day include adding CARMN to drug-eluting stents, which are currently coated with antiproliferative drugs to help deter the unhealthy cell proliferation and scar formation that may result from their placement.
“If you have a low level of CARMN, it mostly likely predisposes you to a higher susceptibility to get atherosclerosis or angioplasty- induced restenosis,” says Dr. Jiliang Zhou, vascular biologist in the Department of Pharmacology and Toxicology at the Medical College of Georgia at Augusta University. “If CARMN is downregulated, it will induce or trigger those smooth muscle cells to become unhealthy or diseased.”
When the scientists restored healthy CARMN levels in models of common vascular disease, unhealthy cell proliferation and scar formation inside blood vessels were dramatically diminished, and when they removed CARMN from smooth muscle cells, the damage response was exaggerated, leaving little room for blood to flow, they report in the journal Circulation. Many of us likely think about RNA making proteins, and which proteins the RNA makes determine a gene’s function. Less-studied noncoding RNAs don’t make proteins but do help regulate cells, and have been shown to have a role in many different normal body functions as well as disease states like cancer. So the scientists decided to look at what was happening with long noncoding RNA in vascular disease and that’s where CARMN stood out.
Senior postdoctoral fellow Dr. Kunzhe Dong, the study’s first author, led analysis of large-scale human datasets of RNA sequencing of multiple tissue and cell types to find the long-noncoding RNAs — literally the longest of the noncoding RNAs — that were abundant in smooth muscle cells and might have a role in their activity. The datasets enabled them to compare expression in healthy and changed, or modulated, cells in a single individual.

Fibrodysplasia ossificans progressiva (FOP) is a rare disease characterized by extensive bone growth outside of the normal skeleton that pre-empts the body’s normal responses to even minor injuries. It results in what some term a “second skeleton,” which locks up joint movement and could make it hard to breathe. However, new research in mice by a team at the Perelman School of Medicine at the University of Pennsylvania shows that forming extra-skeletal bone might not be the only driver of the disease. Impaired and inefficient muscle tissue regeneration appears to open the door for unwanted bone to form in areas where new muscle should occur after injuries. This discovery opens up the possibility of pursuing new therapies for FOP and was published today in NPJ Regenerative Medicine.
“While we have made great strides toward better understanding this disease, this work shows how basic biology can provide great insights into appropriate regenerative medicine therapies,” said the study’s lead author, Foteini Mourkioti, PhD, an assistant professor of Orthopaedic Surgery and Cell and Developmental Biology, as well as the co-director of the Penn Institute for Regenerative Medicine, Musculoskeletal Program. “From the lab, we’re now able to show that there is potential for a whole new realm of therapies for patients with this devastating condition.”
About 15 years ago, researchers at Penn — including this study’s co-author, Eileen Shore, PhD, a professor in Orthopaedic Surgery and Genetics and the co-director of the Center for Research in FOP and Related Disorders — discovered that a mutation in the ACVR1 gene was responsible for FOP. In that study, the team found that the mutation changed cells within muscles and connective tissues, misdirecting cells within the tissue to behave like bone cells, resulting in new and unnecessary extra-skeletal bone within the body.
“However, while investigations of how the FOP mutation alters the regulation of cell fate decisions have been extensively pursued in recent years, little attention has been paid to the effects of the genetic mutation on muscle and its impact on the cells that repair muscle injuries,” Shore said. “We were convinced that pursuing research in this area could provide clues not only for preventing extra bone formation but also for improving muscle function and regeneration, bringing new clarity to FOP as a whole.”
The researchers studied muscle from mice with the same mutation in the ACVR1 gene that people with FOP have. They focused on two specific types of muscle tissue stem cells: fibro-adipogenetic progenitors (FAPs) and muscle stem cells (MuSCs). Typically, muscle injury repair requires a careful balance of these two cell types. Injured tissue responds by an expansion of FAP cells, which are assigned to recruit muscle stem cells that will regenerate the damaged muscle tissue. After about three days, FAPs die off, their job done. At the same time, MuSCs transition toward a more mature, differentiated state, called muscle fiber, essential to organized movement of our muscles.
In the mice with the ACVR1 mutation that Mourkioti, Shore, and their co-authors studied, apoptosis — the process through which FAP cells die as a part of proper muscle regeneration — had slowed significantly, leading to a high presence of FAPs past their usual lifespan. This altered their balance with the MuSCs. The injured tissue also showed a diminished capacity for muscle stem cell maturation and, as a result, muscle fibers were considerably smaller in mice carrying the ACVR1 mutation compared to muscle fibers in mice without the mutation.
“The prolonged persistence of diseased FAPs within the regenerating muscle contributes to the altered muscle environment in FOP, which reduces muscle regeneration and allows the over-abundant FAPs to contribute to the formation of extra-skeletal bone,” Mourkioti said. “This provides a completely new perspective on how excess extra-skeletal bone is formed — and how it could be prevented.”
The current targets for treating FOP focus on slowing extra-skeletal bone growth. This research may provide a pivotal new direction. “We propose that therapeutic interventions should consider promoting the regenerating potential of muscles together with the reduction of ectopic bone formation,” Shore and Mourkioti wrote. “By addressing both stem cell populations and their roles in the origin of FOP, there is the possibility of greatly enhanced therapies.”
This study was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01?AR041916?15S1, F31-AR069982), the National Institutes of Health (R01?AR071399, NIH P30-AR069619), and the International Fibrodysplasia Ossificans Progressiva Association (IFOPA).
Other authors in the study include Alexandra Stanley, Elisia Tichy, Jacob Kocan and Douglas Roberts.

Scientists from Cardiff University have discovered new links between the breakdown in brain cell development and the risk of schizophrenia and other psychiatric disorders.
Genetic risk factors are known to disrupt brain development in a number of these disorders, but little is known about which aspects of this process are affected.
This research is the first time that genetic disruption of specific cell processes crucial to brain development has been linked to disease risk in a wide range of psychiatric disorders.
The findings are published today in the journal Nature Communications.
The study was jointly led by Dr Andrew Pocklington from the Division of Psychological Medicine and Clinical Neurosciences at Cardiff University and Dr Eunju Jenny Shin from the Neuroscience and Mental Health Research Institute at Cardiff University and now at Keele University.
Dr Pocklington said: “Genetic factors play a significant role in determining a person’s risk of developing psychiatric disorders. Uncovering biological processes impacted by these genetic risk factors is a major step towards understanding the causes of disease.”
Dr Shin said: “To truly understand the root causes of psychiatric disorders, we focused on studying the development of brain cells. The knowledge gained through this approach may ultimately help guide the development of novel therapies or help explain why some individuals respond to some treatments but not others.”

As states legalize cannabis, a growing number of children are inadvertently consuming marijuana-infused foods.Mouthwatering chocolate, soft and chewy cookies, lollipops and fruity gummies: Marijuana edibles often look just like regular foods. Some candies even mimic familiar brands like Skittles or Starburst.And for a young child — or anyone, really — that’s incredibly tempting.Foods and beverages laced with cannabis have exploded in popularity. To protect children from accidentally ingesting marijuana edibles, some states have passed laws governing how these foods can be packaged and presented. Colorado, for example, requires the cannabis edibles to be contained in child-resistant packaging and include the letters “THC” (the main mind-altering chemical in cannabis). In addition, the state has banned the sale of edibles that look like people, animals or fruit.But despite these measures, unintentional marijuana exposures have continued to climb in Colorado and elsewhere, especially in states where recreational cannabis has been legalized. In Washington state, unintentional cannabis exposures among children under 6 nearly tripled in the five years after retail cannabis stores opened. Nationally, in 2016 there were 187 exposures to marijuana edibles among kids 12 and under in the United States, according to data from the American Association of Poison Control Centers. By 2020 that number had risen to more than 3,100 — a majority of the children were 5 years old and under.“That’s just the tip of the iceberg,” said Dr. Sharon Levy, the director of the Adolescent Substance Use and Addiction Program at Boston Children’s Hospital. Not everyone will call Poison Control to report an exposure, she added.Of those who did call Poison Control, edibles were responsible for nearly half of the 4,172 marijuana exposures among children 9 and under between 2017 and 2019, according to a study published in the journal Pediatrics in April. (The other exposures were from things like concentrated extracts or dried marijuana plants.) Exposures were more common among children ages 3 to 5 and were more frequent in states where cannabis use is legal. While there were no deaths, 15 percent of children who were exposed experienced moderate symptoms — for example, they might have been very difficult to wake up or had a seizure. A small proportion — about 1.4 percent — experienced major effects that would be considered life-threatening, such as multiple seizures, sedation to the point where they were no longer responsive or difficulty breathing.It has been nearly a decade since Washington and Colorado became the first states to legalize the recreational use of cannabis. Eventually, 16 other states and Washington, D.C., followed suit.“The trend will likely continue upward as more states legalize cannabis and markets expand,” Jennifer M. Whitehill, the lead author of the Pediatrics study, said in an email.Elizabeth Perry, a mother in Maryland, spoke to WRC-TV, the NBC News station in Washington, D.C., last year about the cannabis overdose that landed her toddler, Oliver, in the emergency room. Initially, when Oliver started displaying signs of lethargy, she didn’t know what was wrong. Then he started crying, shaking and seizing. She rushed him to the hospital where doctors intubated him and ran toxicology tests that revealed Oliver had THC in his system.“I told them that wasn’t possible, we don’t smoke, we don’t have drugs in the house,” Ms. Perry told NBC News. “And then, two minutes later, my jaw dropped.” She suddenly realized that he had most likely eaten the cannabis gummies she bought to help her sleep.The doctors told NBC News that Oliver, who wasn’t yet 2 years old, had eaten about 15 gummies, or about 75 milligrams of THC. That’s more than seven times the typical adult dose. (The amount of THC in one serving varies. Oregon permits a maximum of 5 milligrams per serving size, for example, while Colorado allows no more than 10 milligrams of THC per serving.)A similar phenomenon has been happening in Canada. A study published in JAMA Network Open examined all cannabis-related emergency department visits and hospitalizations in Ontario among children 9 and under between January 2016 and March 2021. The researchers found that after marijuana edibles became available in early 2020, a greater proportion of kids were hospitalized. Overall, 19 of the children, or 3.6 percent, were admitted to intensive care.Many adults and teenagers alike generally assume that edible marijuana products are harmless, said Dr. Levy, who specializes in treating adolescents with substance use disorders.But that’s not the case.“THC is addictive, associated with mental health disorders and interferes with brain development during adolescence,” Dr. Levy said. “People who use edibles are also at risk of using too much and having a bad side effect because it takes longer to feel the effect of edibles than smoking or vaping.”She added: “We are seeing a whole lot more psychosis and cannabinoid hyperemesis syndrome,” a condition that leads to severe vomiting and dehydration.What happens to a child who eats marijuana?Dr. Sam Wang, an associate professor of pediatrics at Children’s Hospital Colorado, said young children who ingest a little cannabis typically become sleepy. They might walk unsteadily and “they look a little high,” he said. But children who consume a larger quantity of marijuana have persistent vomiting or show up in the emergency room comatose, with slowed breathing. In rare cases, they need a mechanical ventilator to help them breathe.The children generally become better over the course of one to two days, he added — and aside from one debatable case involving an infant in 2017, there are no known cases of a child dying from cannabis exposure.“The children I’ve cared for and heard about at our hospital all recovered,” said Dr. Lois Lee, an associate professor of pediatrics and emergency medicine at Harvard Medical School. “But some had to be hospitalized for treatment and monitoring. And others were in the emergency department for hours, while their parents waited for them to improve enough so they could be safely discharged home.”What should you do if your child has eaten cannabis?If you believe that your child might have ingested cannabis, call Poison Control to speak with someone right away, Dr. Lee said.Poison Control can also advise you as to when it is necessary to seek medical care.If your child has more severe symptoms — for example, he or she is vomiting, seizing, having trouble breathing or not waking up — it is best to go straight to the emergency room, where the doctors can run toxicology tests and provide oxygen and other treatments if needed, Dr. Lee added.“Many children don’t require any substantial treatment, just observation until they wake up,” she said.How can you protect children from accidental ingestion?First, don’t assume that child-resistant packaging alone will prevent a determined child from eating your edibles.“Parents and caregivers should always store cannabis products, especially edibles, safely out of reach of children,” Dr. Whitehill said. “Kids are really clever and some kids just get into everything, so actually locking it away — the way one would do with certain medications — is a good idea.”“Locked is best, if possible,” agreed Kaitlyn Brown, the clinical managing director of the American Association of Poison Control Centers. “Parents think they have something up on top of the fridge, completely out of reach, out of sight, and the next thing they know their 2-year-old is a climber and is scaling the counter.”Finally, the Children’s Hospital Colorado website says that if your child will be spending time at a friend’s house, it is important to ask their parents whether they keep marijuana in their home and whether they are storing it safely. Likewise, if you have guests staying at your home who use marijuana edibles, make sure they understand the house rules about keeping cannabis out of sight and out of reach.If you or someone you know may have ingested a dangerous substance, please contact Poison Control immediately at 1-800-222-1222 or go to poisonhelp.org for assistance.

SharecloseShare pageCopy linkAbout sharingImage source, Getty ImagesThe US Supreme Court has blocked President Joe Biden’s rule requiring workers at large companies to be vaccinated or masked and tested weekly.The justices at the nation’s highest court said the mandate exceeded the Biden administration’s authority.Separately they ruled that a more limited vaccine mandate could stand for staff at government-funded healthcare facilities.The administration said the mandates would help fight the pandemic.President Biden, whose approval rating has been sagging, expressed disappointment with the decision “to block common-sense life-saving requirements for employees”.He added: “I call on business leaders to immediately join those who have already stepped up – including one third of Fortune 100 companies – and institute vaccination requirements to protect their workers, customers, and communities.”The puzzle of America’s record Covid hospital rateFormer President Donald Trump cheered the court’s decision, and said vaccine mandates “would have further destroyed the economy”. “We are proud of the Supreme Court for not backing down,” he said in a statement. “No mandates!” The administration’s workplace vaccine mandate would have required workers to receive a Covid-19 shot, or be masked and tested weekly at their own expense.It would have applied to workplaces with at least 100 employees and affected some 84 million workers. It was designed to be enforced by employers. Opponents, including several Republican states and some business groups, said the administration was over-stepping its power with the requirements, which were introduced in November and immediately drew legal challenges.A bridge too farIn the end, Joe Biden’s vaccine mandates stood or fell based on judicial interpretations of federal statute, not principles of individual liberty or appeals to the greater good.According to a majority of the Supreme Court, Mr Biden had the law on his side when ordering healthcare workers to get vaccinated, but using a 51-year-old workplace safety statute to implement a vaccine-or-test requirement on all large employers was a bridge too far.Once again, the current balance of the Supreme Court comes into sharp relief, with four reliably conservative justices, three reliable liberal ones and two – Chief Justice John Roberts and Justice Brett Kavanaugh – at the ideological fulcrum.This mixed judicial bag is just the latest setback for a presidential Covid-response plan that frequently has seemed a step behind the latest twists in the pandemic. The administration was slow to encourage boosters and caught flat-footed by the Omicron-induced surge in demand for testing.Now Mr Biden will either have to convince Congress to act on mandates – an unlikely prospect given the brick wall the rest of his agenda keeps hitting in the Senate – or figure out new ways to shepherd the nation out of the pandemic gloom.In a 6-3 decision, the justices agreed with that argument, saying that the workplace safety rule for large employers was too broad to fall under the authority of the Department of Labor’s Occupational Health and Safety Administration to regulate workplace safety. “Covid-19 can and does spread at home, in schools, during sporting events, and everywhere else that people gather,” the court’s majority wrote. “That kind of universal risk is no different from the day-to-day dangers that all face from crime, air pollution, or any number of communicable diseases.””This is no ‘everyday exercise of federal power,'” they added. “It is instead a significant encroachment on the lives – and health – of a vast number of employees.”The more limited rule concerning more than 10 million staff at healthcare facilities that receive government funding did not pose the same concern, they decided, by 5-4.That said imposing conditions on recipients of public money fit “neatly” into the authority of the Secretary of Health and Human Services.The rulings come as some parts of the policies were due to go into effect this week. The court heard arguments in the case on Friday. The rulings reflected the political make-up of the court, which now has a majority of justices appointed by Republican presidents. The court’s three liberal justices opposed blocking the vaccine mandate, saying such a decision “stymies the federal government’s ability to counter the unparalleled threat that Covid-19 poses to our nation’s workers.”Chief Justice John Roberts and Justice Brett Kavanaugh, seen as moderates in the conservative majority, joined the liberals in allowing the healthcare rule to stand. The decision comes as the US experiences another wave of Covid-19 infections, with the Omicron variant spurring record cases and hospitalisation rates. The Biden administration had estimated that instituting a vaccine requirement at big employers would save 6,500 lives and prevent 250,000 hospital admissions over six months.More than 60% of Americans are fully vaccinated already. Independent of the government’s regulations, some companies, including Google, Citibank and IBM, have started to move forward with their own requirements.But the National Federation of Independent Businesses, a lobby group that was one of the lead plaintiffs challenging the government’s workplace vaccine rule, had charged that it would burden small-business owners with new compliance costs, make it harder to fill positions and lead to lost profits and lost sales.”Today’s decision is welcome relief for America’s small businesses, who are still trying to get their business back on track since the beginning of the pandemic,” said Karen Harned, executive director of the group’s legal arm.You may be interested to watch: This video can not be playedTo play this video you need to enable JavaScript in your browser.

Fourteen percent of Aspergillus fumigatus isolates cultured from garden soils were resistant to an agricultural triazole antifungal drug, tebuconazole. Tebuconazole resistance confers resistance to medical triazoles that are used to treat aspergillosis, a lung infection that can be serious, which results from inhalation of A. fumigatus spores. The research is published in Applied and Environmental Microbiology, a journal of the American Society for Microbiology.
In the study, which was lead author Jennifer Shelton’s Ph.D. thesis, she and her collaborators found that compost and compost-enriched soils contain high concentrations of A. fumigatus spores.
“The research suggests that handling compost presents a public health risk when individuals are exposed to large numbers of aerosolized spores and raises questions of whether compost bags should carry additional health warnings, whether compost should be sterilized before shipping, and whether individuals should be advised to wear face masks when handling compost,” said Shelton.
A novel aspect of this study is that the soil samples — 509 of them — were collected from their gardens by 249 citizen scientists whom Shelton enlisted in this effort via social media and through the Aspergillosis Trust, a charity raising awareness of the problem. The samples were all collected on the same day, June 21, 2019. From these, the investigators cultured 5,174 isolates of A. fumigatus. Many of these A. fumigatus isolates contained polymorphisms in the cyp51A gene, which is frequently associated with triazole-resistance. Soil samples containing compost were significantly more likely to grow tebuconazole-resistant A. fumigatus strains than those that did not, and compost samples grew significantly higher numbers of A. fumigatus than other soil samples.
The study was motivated by a growing number of cases caused by triazole resistant A. fumigatus spores in the UK, said Shelton, who conducted the research at Imperial College London and UK Centre for Ecology and Hydrology. “An estimated 185,000-plus people in the UK live with aspergillosis, with conditions ranging from severe hypersensitization, “fungal asthma,” and chronic colonization or invasion of the lungs that can disseminate to other organs including the brain,” said Shelton. “Chronic forms of aspergillosis are life-limiting and difficult to treat, and invasive infections have mortality rates of between 40 and 70 percent, and higher if infected with triazole resistant A. fumigatus.”
People normally inhale spores from the environment, including those of A. fumigatus. Those with weak immunity, due to immune-suppressing drugs, conditions such as diabetes or rheumatoid arthritis, or lung damage from infection by tuberculosis, COVID-19, severe influenza or smoking, are especially vulnerable, but even those without predisposing conditions can develop aspergillosis if they inhale sufficient numbers of spores.
“Our research suggests that handling compost and compost-enriched soils exposes individuals to large numbers of spores and that behavioral changes on their part, and action taken by the composting industry could reduce these exposures,” said Shelton.
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