Publisher Health

Thermo Fisher Scientific’s new air sampler can help monitor for airborne pathogens, and signals renewed interest in bioaerosol surveillance.A decade ago, when the firefighter John Burke earned his master’s degree in health care emergency management, he wrote his thesis on pandemic planning. So when the coronavirus hit last spring, Mr. Burke, now the fire chief in Sandwich, Mass., was ready.“I had my playbook ready to go,” Mr. Burke said.Testing for the virus was a top priority, so he connected with a private laboratory to ensure that his firefighters, who were transporting coronavirus patients to hospitals, could be regularly tested.And then he heard that Thermo Fisher Scientific, a Massachusetts company that makes laboratory equipment and materials, was beta testing an air sampler that could help him detect airborne coronavirus particlesBy December, he had installed one in a fire station hallway. The device, about the size of a toaster oven, sucked in ambient air and trapped airborne virus particles — if there were any to be found — in a specialized cartridge. Each afternoon, an employee would remove the cartridge and walk it to the UPS drop box across the street, sending it off for laboratory analysis.Before the month was out, the air sampler had turned up traces of the virus. Officials ultimately traced it back to a town employee who had been working in the station, without a mask, during a quiet holiday period.It was proof of concept for Thermo Fisher Scientific’s AerosolSense Sampler, which the company was making publicly available on Wednesday. The device, the company says, can be used to detect a variety of airborne pathogens, including the coronavirus. It could be deployed in hospitals, offices, schools and other buildings to monitor for signs of the virus as society begins to reopen.The AerosolSense, which will sell for $4,995, is not the first air sampler capable of capturing the coronavirus; scientists have used several other models to study the pathogen over the past year. But the new device appears to be simpler and more accessible, experts said.“I’m not sure that there’s anything else on the market that’s as easy to use,” said Linsey Marr, an expert in airborne viruses at Virginia Tech. “This will enable collection of air samples by almost anyone.”Thermo Fisher Scientific is likely to face competition. The pandemic has galvanized interest in a once-niche area of disease surveillance — pulling pathogens out of thin air. Experts in the field say they have been inundated with calls and emails from companies, organizations and other laboratories interested in developing or using coronavirus-collecting air samplers. (Dr. Marr is consulting with one company, whose name she could not disclose, to develop an air sampler that would monitor for the virus in public places.)And in November, the Defense Advanced Research Projects Agency began soliciting proposals for research to develop a coronavirus-detecting air sensor.“There’s a tremendous amount of interest,” said John Lednicky, a virologist at the University of Florida.The approach has real potential, experts say. But it also raises a thicket of logistical questions, they add, and must be deployed carefully, with a clear understanding of what the technology can and cannot do.Air samplers are already widely used to detect a variety of pollutants. But capturing airborne viruses is considerably more difficult. Viral aerosols are tiny and compose just a small fraction of the detritus that floats around in the air.“You’re looking for a needle in a haystack in a field of haystacks,” Dr. Marr said.That means that most air samplers need to inhale a lot of air to capture bits of virus, and even then they may not capture viruses present at low levels.The technology is improving, experts said, but remains complicated and labor-intensive. “There are very few places that have the knowledge, the equipment and the virology capability to do this properly,” Dr. Lednicky said.The AerosolSense sampler was designed to be easy to use. The device draws air into a collection pipe and directs it toward a replaceable, cylindrical cartridge. The cartridge, which is about the size of a 10-milliliter syringe, contains a proprietary foamlike substance that traps viral particles.After a few hours, or longer, the cartridge can be pulled out of the machine and sent to a lab for analysis. Technicians can use P.C.R., the polymerase chain reaction technique that underlies the gold-standard test for Covid-19, to determine whether genetic material from the coronavirus is present.It can take a day or two to receive results if the cartridge needs to be shipped to a third-party laboratory, but hospitals, universities and nursing homes that have labs on site can process the cartridges within a few hours, Thermo Fisher Scientific says.The company has also conducted “initial feasibility testing” with a rapid P.C.R. test that returns results in 30 minutes. (The test is made by Mesa Biotech, which Thermo Fisher Scientific recently acquired.)An air sampler at the University of Massachusetts Memorial Medical Center. Though the device shows promise, it can’t be seen as a silver bullet, Chief Burke said.Thermo Fisher ScientificA series of studies — performed in an enclosed box, a 9-by-14-foot room and the hospital rooms of Covid-19 patients — suggested that the AerosolSense sampler could capture the coronavirus even when present at low levels, said Kevin Van Den Wymelenberg, who conducted the research and directs the Biology and the Built Environment Center at the University of Oregon.“We’re confident that this is sensitive enough to use in real-world environments with Covid-positive individuals,” he said.(The research, which has not yet been published in a scientific journal, was funded by Thermo Fisher Scientific.)Thermo Fisher Scientific also piloted the samplers in a Covid-19 field hospital in Worcester, Mass. The hospital deployed the devices in patient care areas, where the virus was expected to be found, and in staff break rooms, where it was not.“Our cold zones were indeed cold,” said Dr. John Broach, an emergency physician at UMass Memorial Medical Center and the medical director of the field hospital. “And our hot zone had heavy contamination, which was expected.”Thermo Fisher Scientific, which will focus on hospitals in the first phase of its rollout, says other health care facilities could use the samplers to make sure that their Covid protocols are working — and that the virus is not making its way out of patient rooms.“We see the facilities asking, are their scheduling and pre-screening activities effective?” said Mark Stevenson, the executive vice president and chief operating officer of Thermo Fisher Scientific. “Are their cleaning and ventilation procedures adequate? And consequently, can I give my patients confidence in their visit to the facility?”Of course, detecting the virus in the hospital room of a Covid-19 patient is one thing, said Alex Huffman, an aerosol scientist at the University of Denver: “It’s another step to go into an environment that likely has much lower concentrations still, surveilling a classroom or a medical clinic where you have no idea if there’s going to be somebody positive or not.”And an air sampler is not a silver bullet, said Mr. Burke, who made sure that his firefighters continued to wear masks, socially distance and get regular Covid tests even after he installed the air sampler.“It can’t be like a smoke detector in your house where you’re, like, ‘I’m just going to have the machine, I’m not going to do anything else, it will let me know when there’s a problem,’” he said.There are not yet any truly autonomous viral samplers, which still require humans to remove and analyze the samples. That takes time — and means that the results provided by these samplers are not real-time snapshots but composite portraits of a building over the previous two or 12 or 24 hours.And although P.C.R. analysis can reveal whether genetic material from the coronavirus is present, it cannot distinguish between intact, infectious virus and viral fragments that pose no risk.None of these drawbacks are dealbreakers, said Dr. Marr, who noted that it was still useful to know whether airborne coronavirus particles were in a space recently.“If they’ve detected it in air, then it’s probably fairly freshly emitted,” she said. “And I’d be willing to bet that there is some infectious virus in there.”But the results need to be interpreted with care. A negative result does not mean that there is no virus present — simply that the air sampler did not collect any.“There’s a high chance for false negatives, because viruses are in notoriously low concentrations in the air,” said Kristen Coleman, an expert in bioaerosols at Duke-NUS Medical School in Singapore.Figuring out how to respond to a positive sample might prove even trickier. “I don’t think the answer is just evacuate the building,” Dr. Van Den Wymelenberg said.Instead, he imagined a suite of more measured responses — from increasing ventilation rates to strategic testing and tracing — that organizations could adopt when they found signs of the virus.But convincing office workers that a temporary ventilation boost makes it safe to come into an office where the virus has been found could be a hard sell. And even these modest measures could prompt concerns about privacy and legal liability.“I have been talking with several large building owners about indoor environmental surveillance throughout this pandemic, and the question of how is this information going to be used and who holds liability for any misapplication of the information always comes up,” Dr. Van Den Wymelenberg said.(Mr. Burke made sure to clear use of the air sampler with the local unions, which were, he said, “100 percent supportive.”)Another approach might be to use air sampling for larger-scale surveillance. If public health authorities see a spike in viral levels in a certain region or neighborhood, this could be an early warning sign that a surge of new Covid-19 cases is coming — and that officials need to step up their testing and contact tracing.Easily available, user-friendly air samplers could also make it possible for more scientists to conduct research on viral aerosols, Dr. Huffman said.“In the medium and long term, I think technology like this has a tremendous role to play in continuing to push forward the state of knowledge about these things such that we can make better decisions that help with other viral aerosols, like influenza and the next pandemic that comes along,” he said. “That’s not to say it can’t help now, but I think its real influence may be even greater as we go further and further into the future.”

A new study hints that excessive HIIT may harm your mitochondria, the energy generators found in every cell of your body.If high-intensity exercise is good for us, is more necessarily better?Maybe not, according to an admonitory new study of the molecular effects of high-intensity interval training, also known as HIIT. In the study, people who began working out strenuously almost every day developed sudden and severe declines in the function of their mitochondria, which are the energy powerhouses inside of cells, along with incipient signs of blood sugar dysfunction.Their metabolic issues started to reverse when they dialed back on their workouts but did not disappear, suggesting that the benefits of extremely vigorous exercise may depend on just how much we do.At this point, almost anyone with an interest in fitness is familiar with the concept and appeal of high-intensity interval training. Consisting of repeated, brief spurts of hard exercise interspersed with a few minutes of rest, HIIT workouts can be quite short but are still able to improve substantially our aerobic fitness and many other aspects of our health. Studies show, for example, that intense bursts of exercise increase the number of mitochondria in our muscle cells, and more mitochondria are thought to contribute to better cellular and metabolic health.But recent research has begun to hint that HIIT also may have unexpected downsides. In a study I wrote about in January, people who worked out with HIIT routines three times a week for six weeks did not improve their blood pressure or body fat as much as people who exercised far more moderately five times a week.The authors of that study speculated that, by being sedentary for four days each week, the intense exercisers in the study may have undermined the otherwise potent effects of their HIIT sessions. On a weekly basis, they were not exercising enough.But whether it would be advisable to do more HIIT sessions in a single week has not been clear. Most past studies and formal recommendations about intense workouts top out at three sessions a week, and few researchers have looked into how HIIT-ing harder or more often might affect health.So, for the new study, which was published recently in the journal Cell Metabolism, researchers at the Swedish School of Sport and Health Sciences and the Karolinska Institute, both in Stockholm, set out, like Goldilocks, to sample different amounts of weekly hard exercise and see if any might be just right.They began by recruiting 11 healthy men and women who exercised but were not competitive athletes. These volunteers visited the researchers’ lab for tests of their current fitness and metabolic health, including blood-sugar levels over the course of a day.Then the volunteers began an ambitious exercise program. During the first week, they performed two sessions of HIIT, repeating four-minute-long intervals five times on a stationary bicycle, with three minutes of rest in between. The riders pedaled as hard as they could during each four-minute surge, while researchers monitored their power output. Afterward, the researchers biopsied leg muscles and rechecked the riders’ fitness and 24-hour blood-sugar control.During week two, the riders added a third HIIT session and ramped up the length of some of their intervals to a draining eight minutes. In week three, they worked out five times, with a mix of four-minute and eight-minute spurts of all-out pedaling. Finally, in week four, for recovery, they effectively halved the amount and intensity of their exercise. Each week, the researchers repeated all testing.Then they compared how people’s bodies had changed week over week.At first, the findings were encouraging. By the end of week two, the riders were pedaling harder and appeared to be getting fitter, with better daily blood-sugar control and more total mitochondria in their muscle cells. Each of these mitochondria was also more efficient now, producing greater amounts of energy than at the start.But something began to go wrong during week three. The volunteers’ ability to generate power while cycling flattened, and their subsequent muscle biopsies showed sputtering mitochondria, each of which was now producing only about 60 percent as much energy as during the previous week. The riders’ blood-sugar control also slipped, with seesawing spikes and dips throughout the day.After a week of lower-intensity riding, their mitochondria started to bounce back, producing more energy, but still 25 percent less than during week two. Their blood-sugar levels also stabilized, but again, not to the same extent as before. The riders could pedal, however, with the same — or even greater — vigor as in week two.Taken as a whole, the monthlong experiment suggests that “HIIT exercise should not be excessive if increased health is a desired outcome,” says Mikael Flockhart, a doctoral student at the Swedish School of Sport and Health Sciences, who conducted the study with his adviser, Filip Larsen, and others.The study was not focused on athletic performance, but even for serious athletes, he says, piling on multiple, intense, interval workouts each week, with little rest between them, is likely to lead to a tipping point, after which performance, as well as indicators of metabolic health, slip.The researchers are not sure precisely what changes within their volunteers’ bodies and muscles precipitated the negative results in week three. They tested multiple potential molecular causes, Mr. Flockhart says, but did not isolate an obvious, single instigator. He and his colleagues suspect that a cascade of biochemical changes within people’s muscles during the hardest week of exercise overwhelmed the mitochondria then, and the weakened mitochondria contributed to the disruptions in people’s blood-sugar control.This study was small, though, and quite short-term, with barely a week of each exercise routine. It also featured healthy volunteers, so does not show whether results would be the same, better or worse in people with existing metabolic problems.Even so, the findings strongly suggest that anyone interested in high-intensity interval training start small, Mr. Flockhart says. Train a few times a week and on the remaining days, maybe take a walk.

For a year we have all lived under Covid-19 restrictions. But how have hospital staff dealt with fighting the pandemic at work and living under lockdown at home?Four staff from University Hospital Southampton tell the BBC about the impact of the last year on their home and work lives. Filmed/edited by Rachel PriceProduced by Alexander Littlewood

A University of Birmingham-led study of top-flight UK rugby players — carried out in collaboration with the Rugby Football Union (RFU), Premiership Rugby, and Marker Diagnostics — has identified a method of accurately diagnosing concussion using saliva, paving the way for the first non-invasive clinical test for concussion for use in sport and other settings.
Following the team’s previous research, which identified that the concentration of specific molecules in saliva changes rapidly after a traumatic brain injury, the researchers embarked on a three-year study in elite rugby to establish if these ‘biomarkers’ could be used as a diagnostic test for sport-related concussion.
Using DNA sequencing technology in the laboratory at the University of Birmingham, the research team tested these biomarkers in saliva samples from 1,028 professional men’s rugby players competing in English rugby’s top two leagues — the Premiership and Championship.
The results of SCRUM (Study of Concussion in Rugby Union through MicroRNAs), published today (March 23) in the British Journal of Sports Medicine, has for the first time shown that specific salivary biomarkers can be used to indicate if a player has been concussed. Additionally, the research has found these biomarkers provide further insights into the body’s response to injury as it evolves from immediately after trauma, to several hours and even days later.
The scientific breakthrough provides a new laboratory-based non-invasive salivary biological concussion test, which could have wide-reaching use and potential to reduce the risk of missing concussions not only in sport — from grassroots to professional levels — but also in wider settings such as military and healthcare.
In community sport, these biomarkers may provide a diagnostic test that is comparable in accuracy to the level of assessment available in a professional sport setting. While, at an elite level of rugby, the concussion test may be used in addition to the existing World Rugby Head Injury Assessment (HIA) protocol.

Scientists have found new, unexpected behaviors when SARS-CoV-2 — the virus that causes COVID-19 — encounters drugs known as inhibitors, which bind to certain components of the virus and block its ability to reproduce.
Published in the Journal of Medicinal Chemistry, the research provides key insights for advancing drug design and drug repurposing efforts to treat COVID-19.
Researchers at the Department of Energy’s Oak Ridge National Laboratory used neutron scattering to investigate interactions between telaprevir, a drug used to treat hepatitis C viral infection, and the SARS-CoV-2 main protease, the enzyme responsible for enabling the virus to reproduce.
They discovered unforeseen changes in the electric charges in the drug binding site of the protease enzyme that were not predicted by prevailing computer simulations.
“We found this particular protein — the SARS-CoV-2 main protease — which a lot of researchers are studying by computational methods, is behaving in a surprising way,” said lead author Daniel Kneller. “Our findings provide critical experimental data needed to improve computer modeling so that simulations more closely match reality.”
The virus reproduces by assembling long chains of proteins, or polyproteins, made from almost 2,000 amino acids that must be cut into smaller chains by the main protease. Finding a drug that effectively blocks or inhibits the protease function is paramount to preventing the virus from replicating and spreading to other healthy cells in the body.

When the human immunodeficiency virus infects cells, it can either exploit the cells to start making more copies of itself or remain dormant — a phenomenon called latency. Keeping these reservoirs latent is a challenge. A new paper, published in the Proceedings of the National Academy of Sciences, has found a way to look for chemicals that can keep the virus suppressed into its dormant state.
“The current drug treatments block healthy cells from becoming infected by the virus,” said Yiyang Lu, a PhD student in the Dar lab at the University of Illinois Urbana-Champaign. “The latent reservoir poses a bigger problem because it can start producing the virus at any time. Consequently, patients have to remain on antiretroviral therapy all their lives to prevent a viral rebound.”
So far, there are two types of drug treatment strategies: shock-and-kill, where reactivated cells are killed due to HIV, and a second drug cocktail prevents other cells from being infected, or block-and-lock, which forces the virus into a deep latent state so that it does not reactivate again. The problem with the first approach is that there are always some leftover reservoirs that do not get activated. The problem with the second approach, which the researchers are trying to solve, is that there aren’t many drugs that have been discovered.
Since the transition from latency occurs randomly, measuring the fluctuations in gene expression can provide more coverage than the average gene expression. “Commercial drug screens usually look at mean gene expression. Instead, we used a drug screen that looks at fluctuations in gene expression. Our screen allowed us to therefore find more compounds that could have been overlooked,” Lu said.
“We implemented a time-series drug screening approach that are less commonly used in other labs,” said Roy Dar, an assistant professor of bioengineering at Illinois and faculty member of the Carl R. Woese Institute for Genomic Biology. The researchers used a T- cell population, which is a reservoir for HIV, that had been infected by the virus. They imaged the cells in 15-minute intervals for 48 hours and tested over 1800 compounds. They looked at noise maps to identify which drugs can modulate the gene expression.
Using the screen, they were able to find five new latency-promoting chemicals, raising the possibility that similar screens can be successfully adapted to study other systems that exhibit variability in gene expression, such as cancer. They are currently working on understanding how the five novel drugs suppress viral reactivation. “We want to test if these drugs have off-target effects in terms of how many other genes they affect in the host cells,” Dar said. “We also want to test these drugs in patient samples to see whether these drugs suppress HIV in them.”
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Materials provided by Carl R. Woese Institute for Genomic Biology, University of Illinois at Urbana-Champaign. Original written by Ananya Sen. Note: Content may be edited for style and length.

People who received a flu shot last flu season were significantly less likely to test positive for a COVID-19 infection when the pandemic hit, according to a new study. And those who did test positive for COVID-19 had fewer complications if they received their flu shot.
These new findings mean senior author Marion Hofmann Bowman, M.D., is continuing to recommend the flu shot to her patients even as the flu season may be winding down.
“It’s particularly relevant for vaccine hesitance, and maybe taking the flu shot this year can ease some angst about the new COVID-19 vaccine,” says Hofmann, an associate professor of internal medicine and a cardiologist at the Michigan Medicine Frankel Cardiovascular Center. Michigan Medicine is the academic medical center of the University of Michigan.
Researchers reviewed medical charts for more than 27,000 patients who were tested for a COVID-19 infection at Michigan Medicine between March and mid-July of 2020. Of the nearly 13,000 who got a flu shot in the previous year, 4% tested positive for COVID-19. Of the 14,000 who hadn’t gotten a flu shot, nearly 5% tested positive for COVID-19. The association remained significant after controlling for other variables including ethnicity, race, gender, age, BMI, smoking status and many comorbid conditions, Hofmann says.
People who received their flu shot were also significantly less likely to require hospitalization, although the researchers didn’t find a significant difference in mortality between the two groups. No one in the study tested positive for both infections at the same time.
The underlying mechanism behind the association isn’t yet clear, Hofmann says.

Scientists are examining a possible link to tinnitus. A businessman’s suicide has lent urgency to the research.The suicide of Kent Taylor, the founder and chief executive of the Texas Roadhouse restaurant chain, has drawn attention to a possible link between Covid-19 and tinnitus, the medical term for a constant ringing in the ears.Mr. Taylor suffered from a variety of symptoms following his illness, including severe tinnitus, his family said in a statement, adding that his suffering had become “unbearable.”Whether tinnitus is linked to Covid-19 — and if so, how often it occurs — is an unanswered question. Neither the World Health Organization nor the Centers for Disease Control and Prevention describes tinnitus as a symptom, although auditory problems are common in other viral infections.But tinnitus is on the list of symptoms of long Covid published by the United Kingdom’s National Health Service, along with fatigue, shortness of breath, dizziness and more. And a few recent case reports and studies have hinted at a potential link.A study published on Monday in the Journal of International Audiology that looked at nearly 60 case reports and studies found that 15 percent of adults with Covid-19 reported symptoms of tinnitus. The authors believe that the respondents were describing either a new condition or a worsening one, though they are following up with the 60 or so researchers to be certain about how the surveys were worded.“In the 24 hours since we published, I’ve received about 100 emails,” said Kevin Munro, a professor of audiology at the University of Manchester and a co-author of the study. “Almost of all of them were people saying, ‘I was so happy to read about this, because my doctor thought I was crazy when I mentioned tinnitus and now I know I’m not the only one.’”There is also some evidence that Covid-19 can aggravate symptoms among people who had tinnitus before they contracted the disease. A study published late last year in the journal Frontiers in Public Health surveyed 3,100 people with tinnitus and found that 40 percent of the 237 respondents who had contracted Covid-19 reported that their symptoms were “significantly exacerbated” following the infection.“There are a lot of viruses that have an impact on the ears, including measles, mumps and rubella,” said Dr. Eldre Beukes, the audiologist at Anglia Ruskin University in England who led the study. “It could also be the case that medication taken to combat Covid is making tinnitus worse. And there is a well-known link between tinnitus and stress.”Kent Taylor, founder and chief executive of the Texas Roadhouse restaurant chain.Ron Bath/Texas Roadhouse, via Associated PressThe study cited a variety of factors that have increased stress for nearly everyone in the pandemic, including fear of catching the coronavirus, and social distancing rules that have increased isolation and loneliness.Home-schooling has also raised stress levels, as has greater consumption of coffee and alcohol, Dr. Beukes added.Covid-19 has complicated life for tinnitus sufferers even if they have not contracted the virus, said Kim Weller, an I.T. specialist who lives in Houston and is part of a tinnitus support group based there.“There’s a gentleman in Ohio who I text and talk on the phone with and I’d describe him as being at the end of his rope,” she said. “He’s not working, trouble sleeping, living alone. His situation is definitely worse because of Covid, because he’s just so isolated.”Exactly why tinnitus affects certain people is a bit of a mystery. There are roughly 200 causes of the condition, including exposure to loud noises, stress, hearing loss and perforated eardrums. There is currently no cure. Patients are often treated with cognitive behavioral therapy — essentially, talk therapy designed to rewire thoughts and behaviors — or coached on how to habituate themselves to the condition.The C.D.C. found in a 2011-2012 survey — the most recent data available — that 15 percent of respondents said they had suffered some kind of tinnitus. Of them, 26 percent said it was constant or near constant ringing, and 30 percent described the condition as a “moderate” or “very big” problem in their lives.A very small group of people in Dr. Beukes’s study — seven — reported that Covid-19 brought on tinnitus for the first time. Just over half of people with tinnitus said the illness had left their symptoms unchanged.Curiously, 6 percent said they were less bothered by tinnitus after contracting the disease. Dr. Beukes speculates that for these people, a life-threatening condition had the effect of reframing the noise in their head.“Contracting Covid meant that in some cases they were struggling to survive, and that left them with a very different perspective,” she said.The roughly 40 percent of respondents who said that Covid-19 made their tinnitus worse includes people like Aisling Starrs of Derry, in Northern Ireland. She’d coped with hearing loss in her right ear her entire life. Two years ago, she gave birth to a daughter and within minutes noticed a buzzing in both ears that did not abate.“Then in September I got Covid, and it went straight for my ears,” said Ms. Starrs, who is an occupational therapist. “On a scale of one to 10, it was a three before Covid. Since then, it’s been a seven.”She had no idea that exacerbated tinnitus might be a Covid-related problem until she learned otherwise on the website of the British Tinnitus Association, a co-sponsor of the Anglia Ruskin study.“I thought, ‘Thank God’ when I realized I wasn’t the only one out there,” she said. “I’ve met people through my work who don’t realize that there’s a medical term for the ringing in their ears. Just knowing that other people have the same condition is an enormous relief.”

Vaccinating health care workers resulted in an immediate and notable reduction of positive COVID-19 cases among employees, reducing the number of required isolations and quarantines by more than 90 percent, according to data at UT Southwestern Medical Center published in the New England Journal of Medicine.
Health care workers were among the first groups to be eligible for vaccination.
“Real-world experience with SARS-CoV-2 vaccination at UT Southwestern demonstrated a marked reduction in the incidence of infections among our employees, preserving the workforce when it was most needed,” notes Daniel K. Podolsky, M.D., president of UT Southwestern and senior author.
During the first 31 days of vaccinations becoming available, UT Southwestern provided a first dose to 59 percent of roughly 23,000 employees, while 30 percent were able to be fully vaccinated in that time frame. Among the findings: 1.5 percent became infected. Infection rates were highest — 2.6 percent — among nonvaccinated employees. Infection rates were lowest — .05 percent — among those fully vaccinated.”Our ability to quickly vaccinate a majority of our workforce in the midst of what became the largest surge to date in the region made a critical difference in ensuring we were able to continue providing top-flight care while health systems were strained,” says John Warner, M.D., executive vice president for health system affairs at UT Southwestern.
Researchers also saw advantages among partially vaccinated individuals, and from Jan. 9, the actual number of positive tests among all UT Southwestern employees was consistently lower than the number projected.
The data also show continued need to address vaccine hesitancy, with UT Southwestern now approaching 70 percent immunization among its workforce.
“In light of this real-world experience clearly demonstrating the effectiveness of immunization, further understanding of the reticence of some individuals to take advantage of vaccination bears even greater importance,” says first author William Daniel, M.D., vice president and chief quality officer at UT Southwestern.
UT Southwestern has provided educational outreach to community groups and businesses, developed extensive online resources including Q&As and blogs, and is preparing to launch a multilingual public service announcement campaign to help educate diverse communities about vaccination and address issues of hesitancy.
“It is important to reach out across multiple platforms to effectively address people’s questions so that we can continue to make progress on vaccine hesitancy,” says Marc Nivet, Ed.D., executive vice president for institutional advancement at UT Southwestern.
Dr. Daniel, professor of internal medicine, holds the William T. Solomon Professorship in Clinical Quality Improvement at UT Southwestern Medical Center. Dr. Nivet is associate professor of family and community medicine. Dr. Podolsky, professor of internal medicine, holds the Philip O’Bryan Montgomery, Jr., M.D. Distinguished Presidential Chair in Academic Administration and the Doris and Bryan Wildenthal Distinguished Chair in Medical Science. Dr. Warner, professor of internal medicine, holds the Nancy and Jeremy Halbreich, Susan and Theodore Strauss Professorship in Cardiology and the Jim and Norma Smith Distinguished Chair for Interventional Cardiology.
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Materials provided by UT Southwestern Medical Center. Note: Content may be edited for style and length.

Another step towards understanding Alzheimer’s disease has been taken at the Maisonneuve-Rosemont Hospital Research Centre. Molecular biologist Gilbert Bernier, and professor of neurosciences at Université de Montréal, has discovered a new function for the BMI1 gene, which is known to inhibit brain aging. The results of his work have just been published in Nature Communications.
In his laboratory, Bernier was able to establish that BMI1 was required to prevent the DNA of neurons from disorganizing in a particular way called G4 structures. This phenomenon occurs in the brains of people with Alzheimer’s disease, but not in healthy elderly people. Thus, BMI1 would protect against Alzheimer’s by preventing, among other things, the excessive formation of G4s that disrupt the functioning of neurons.
“This discovery adds to our knowledge of the fundamental mechanisms leading to Alzheimer’s,” said Bernier. “There is still no cure for this disease, which now affects nearly one million Canadians. Any advance in the field brings hope to all these people and their families.”
In previous articles published in the journals Cell Reports and Scientific Reports, Bernier demonstrated that the expression of the BMI1 gene is specifically reduced in the brains of people with Alzheimer’s disease. He also showed that inactivation of BMI1 in cultured human neurons or in mice was sufficient to recapitulate all the pathological markers associated with Alzheimer’s disease.
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Materials provided by University of Montreal. Note: Content may be edited for style and length.