Scientists at the Walter Reed Army Institute for Research demonstrated that biomarkers associated with traumatic brain injury were elevated among law enforcement and military personnel, particularly in active duty participants with longer duration of service. Most notably, these elevated biomarker levels were observed in individuals without a diagnosed brain injury or concussion.
Some law enforcement and military personnel are regularly exposed to low levels of blast, particularly during training, due to the use of explosive charges and high caliber weapons. Understanding effects from these occupational exposures is a military health care priority to improve diagnosis and mitigation of ill effects.
While repeated exposure to low level blast is not known to result in clinically diagnosed traumatic brain injury, exposures have been linked to a series of reported symptoms such as headaches, fatigue, dizziness, memory difficulties, and tinnitus (ringing in the ears) — collectively referred to as “breacher’s brain” among members of affected communities.
This study, published in the Journal of the American Medical Association, measured neurotrauma biomarker concentrations in blood samples from 106 military and law enforcement personnel who were not actively engaged in training or physical activity at the time of blood collection and compared those concentrations with commercially available samples from individuals who were similar in sex and age but unlikely to have been exposed to blast.
“We found that five biomarkers previously associated with TBI and brain diseases were elevated among personnel when compared to controls,” said Dr. Angela Boutte, lead author on the paper and a researcher at the WRAIR Brain Trauma Neuroprotection branch. “Given the difficulty of identifying and evaluating injury associated with repeated low level blast exposure, we hope these data are the first step in our collective goal to identify objective biomarkers as clinically relevant diagnostic tools.”
Dr. Bharani Thangavelu and Dr. Walter Carr, WRAIR brain health researchers and co-authors, emphasized the potential impact of blast exposure experienced by military personnel stating, “Low level blast exposure in routine military training should not be expected to result in acute, gross behavioral deficits for the majority of personnel. However, repeated exposure across years does correlate with symptomology, especially when a history of chronic exposure is exacerbated by new, large magnitude exposures.”
Efforts to identify and quantify the impact of blast and traumatic brain injury on Service Members have increased dramatically in recent years, including initiatives in response to Congressional mandates. Biomarkers of blast effects on brain health will be a useful tool in this effort, especially as tools that augment decision-making based on symptoms reported by personnel.
Story Source:
Materials provided by Walter Reed Army Institute of Research. Note: Content may be edited for style and length.

Swansea University scientists have uncovered potentially dangerous chemical pollutants that are released from disposable face masks when submerged in water.
The research reveals high levels of pollutants, including lead, antimony, and copper, within the silicon-based and plastic fibres of common disposable face masks.
The work is supported by the Institute for Innovative Materials, Processing and Numerical Technologies (IMPACT) and the SPECIFIC Innovation & Knowledge Centre
Project lead Dr Sarper Sarp of Swansea University College of Engineering said: “All of us need to keep wearing masks as they are essential in ending the pandemic. But we also urgently need more research and regulation on mask production, so we can reduce any risks to the environment and human health.”
Outlined in a recent paper, the tests carried out by the research team used a variety of masks — from standard plain face masks to novelty and festive masks for children with many currently being sold in UK retail outlets.
The rise in single-use masks, and the associated waste, due to the COVID-19 pandemic has been documented as a new cause of pollution. The study aimed to explore this direct link — with investigations to identify the level of toxic substances present.

When COVID-19 patients began filling up ICUs throughout the country in 2020, health care providers faced difficult decisions. Health care workers had to decide which patients were most likely to recover with care and which were not so resources could be prioritized.
But a new paper from the University of Georgia suggests that unconscious biases in the health care system may have influenced how individuals with intellectual disabilities were categorized in emergency triage protocols.
The state-level protocols, while crucial for prioritizing care during disasters, frequently allocated resources to able-bodied patients over ones with disabilities, the researchers found.
The study, published in Disaster Medicine and Public Health Preparedness, found that some states had emergency protocols saying that individuals with brain injuries, cognitive disorders or other intellectual disabilities may be poor candidates for ventilator support. Others had vague guidelines that instructed providers to focus resources on patients who are most likely to survive. Adults with disabilities are significantly more likely to have comorbidities, such as heart disease and diabetes. In the case of COVID-19, those conditions were considered risk factors for poor outcomes, relegating these patients to the bottom of care hierarchy.
To compound the problem, COVID-19 hospital protocols that banned visitors often shut out advocates and family members who might have been able to advocate for these individuals. For patients unable to communicate their needs, the situation could easily turn deadly.
“I think when you leave people out of the conversations making these decisions, you see an issue like structural discrimination and bias,” said Brooke Felt, lead author of the paper who graduated from UGA in 2020 with Master of Social Work and Master of Public Health degrees.

Researchers at Massachusetts General Hospital (MGH) have identified the protein “signature” of severe COVID-19, which they describe in a new study published in Cell Reports Medicine. “We were interested in asking whether we could identify mechanisms that might be contributing to death in COVID-19,” says MGH infectious disease expert Marcia Goldberg, MD, who studies interactions between microbial pathogens and their hosts, and is senior author of the study. “In other words, why do some patients die from this disease, while others — who appear to be just as ill — survive?”
In March 2020, when the first patients with symptoms of COVID-19 began arriving at MGH’s emergency department (ED), Goldberg was contacted by her colleague, Michael Filbin, MD, MS, an attending physician and director of Clinical Research at MGH’s ED, and lead author of the study. Filbin and Goldberg had earlier begun collaborating with MGH immunologist Nir Hacohen, PhD, to develop methods for studying human immune responses to infections, which they had applied to the condition known as bacterial sepsis. The three agreed to tackle this new problem with the goal of understanding how the human immune system responds to SARS-CoV-2, the novel pathogen that causes COVID-19.
To undertake this study, the MGH team used proteomics, which is the analysis of the entire protein composition (or proteome) of a cell, tissue or organism. In this case, proteomic analysis was used to study blood specimens taken from patients arriving at the hospital’s ED with respiratory symptoms consistent with COVID-19. Collecting these specimens required a large team of collaborators from many departments, which worked overtime for five weeks to amass blood samples from 306 patients who tested positive for COVID-19, as well as from 78 patients with similar symptoms who tested negative for the coronavirus.
Next, Arnav Mehta, MD, PhD, a postdoctoral researcher at the Broad Institute of MIT and Harvard, was brought on board to oversee interpretation of the complex data produced by the proteomic analysis. Mehta also works in Hacohen’s lab, and the two had long been interested in using proteomic analysis of blood as an alternative to biopsies (which are invasive and painful). “We have been asking, What can we learn about what’s happening in the body just by looking at protein signatures in the blood?” says Mehta.
The study found that most patients with COVID-19 have a consistent protein signature, regardless of disease severity; as would be expected, their bodies mount an immune response by producing proteins that attack the virus. “But we also found a small subset of patients with the disease who did not demonstrate the pro-inflammatory response that is typical of other COVID-19 patients,” says Filbin, yet these patients were just as likely as others to have severe disease. Filbin notes that patients in this subset tended to be older people with chronic diseases, who likely had weakened immune systems.
The next step was to compare the protein signatures of patients with severe disease (defined as those who required intubation or who died within 28 days of hospital admission) with patients with less-severe cases of COVID-19. The comparison allowed the researchers to identify more than 250 “severity associated” proteins. Importantly, notes Mehta, blood was drawn from patients three times (on enrollment, then three and seven days later). “That allowed us to look at the trajectory of the disease,” says Mehta. Among other revelations, this showed that the most prevalent severity-associated protein, a pro-inflammatory protein called interleukin-6, or IL-6, rose steadily in patients who died, while it rose and then dropped in those with severe disease who survived. Early attempts by other groups to treat COVID-19 patients experiencing acute respiratory distress with drugs that block IL-6 were disappointing, though more recent studies show promise in combining these medications with the steroid dexamethasone.
However, Hacohen notes that many of the other severity-associated proteins the analysis identified are likely important for understanding why only a portion of COVID-19 develop severe cases. Learning how the disease affects the lungs, heart and other organs is essential, he says, and proteomic analysis of the blood is a relatively easy method for getting that information. “You can ask which of the many thousands of proteins that are circulating in your blood are associated with the actual outcome,” says Hacohen, “and whether there is a set of proteins that tell us something.”
Goldberg believes that the proteomic signatures identified in this study will do just that. “They are highly likely to be useful in figuring out some of the underlying mechanisms that lead to severe disease and death in COVID-19,” says Goldberg, noting her gratitude to the patients involved in the study. Their samples are already being used to study other aspects of COVID-19, such as identifying the qualities of antibodies that patients form against the virus.
Goldberg directs the Goldberg Laboratory at MGH, is a professor of Emergency Medicine at Harvard Medical School (HMS) and is an associate member of the Broad Institute. Filbin is an assistant professor of Emergency Medicine at HMS and an associate member of the Broad Institute. Hacohen directs the Hacohen Lab at MGH and is a professor of Medicine at HMS and a member of the Broad Institute. Mehta is a fellow in hematology and oncology at Dana-Farber Cancer Institute and MGH.
The study was supported by the Cystic Fibrosis Foundation Postdoctoral Fellowship; a gift from Sandra, Sarah and Arthur Irving; the American Lung Association (COVID-19 Action Initiative); the Executive Committee on Research at MGH; the Chan-Zuckerberg Initiative; and the Harvard Catalyst/Harvard Clinical and Translational Science Center (National Center for Advancing Translational Sciences, National Institutes of Health Awards).

Researchers from Massachusetts General Hospital (MGH) appear to have solved the 120-year-old mystery surrounding the failing health of famed Antarctic explorer Sir Ernest Shackleton over the course of his daring expeditions to Antarctica in the early part of the twentieth century. In a paper published online in the Journal of Medical Biography, the team moved beyond past theories of congenital heart defect and scurvy advanced by physicians and historians to conclude that the British explorer suffered from beriberi, a serious and potentially life-threatening condition caused by a deficiency of the nutrient thiamine.
“Historians have traditionally looked at Shackleton’s symptoms in isolation and speculated about their cause,” says lead author Paul Gerard Firth, MD, head of the Division of Community and Global Health in the Department of Anesthesia, Critical Care and Pain Medicine at MGH. “We looked at other explorers on the expedition, as well as members of other early expeditions, and found that some had symptoms — such as breathlessness, neuropathy and effort intolerance — similar to Shackleton’s that could be attributed to beriberi. With the benefit of what we now know about nutritional diseases, we believe that beriberi-induced cardiomyopathy — a disease of the heart muscle that makes it difficult for the heart to pump blood — is the correct diagnosis for Ernest Shackleton’s deteriorating health.”
The researchers learned that Edward Wilson, one of two physicians on Shackleton’s first voyage to Antarctica beginning in 1901 — when the explorer fell seriously ill and had to return home after voyaging closer to the South Pole than any previous human — may have suspected beriberi after consulting his medical textbooks, but didn’t settle on that diagnosis at a time when so little was known about the condition. Instead, the prolonged bouts of extreme shortness of breath and physical weakness Shackleton experienced on the British “Discovery” expedition of 1901 to 1903 were ascribed by his contemporaries and subsequent historians to scurvy or underlying heart disease.
“While Wilson concluded that Shackleton’s condition was the result of scurvy — a vitamin C deficiency — that appeared to us to be an incomplete explanation for his labored breathing,” says Firth. “Shackleton, after all, had very slight symptoms of scurvy when his breathing difficulties began, and mild scurvy does not cause heart problems.”
This careful parsing of the historical evidence led Firth and his colleagues to an alternative nutritional cause of Shackleton’s health struggles. “Many of the signs and symptoms of beriberi seen in early explorers developed after three months of thiamine deficiency,” explains co-author Lauren Fiechtner, MD, director of the Center for Pediatric Nutrition at MGH. “And that would be consistent with a thiamine-deficient diet they experienced during the grueling months of winter explorations. Fortunately, replacement of thiamine with vitamin B1 supplements can resolve the deficiency within days or hours, although that was not known at the time.”
Even severe health challenges were not enough to prevent Shackleton from setting out on a third attempt to reach the South Pole in 1914, a fateful voyage since recounted in books and movies of how his ship Endurance became trapped in packed ice and broke apart, with all 28 crewmen reaching safety after two years and two heroic rescue efforts engineered by Shackleton. In late 1921, the intrepid explorer embarked on his fourth expedition, but suffered a heart attack on January 5, 1922, and died on his ship at age 47.
“The exact nature of Ernest Shackleton’s faltering health has puzzled historians and the public for years,” says Firth, “and almost 100 years after the start of his fourth and final expedition we’re satisfied that we have finally uncovered a medically and scientifically valid explanation.”
Story Source:
Materials provided by Massachusetts General Hospital. Note: Content may be edited for style and length.

Studying protein changes in the kidneys as we age, as well as the transcription of genes into proteins, helps provide a full picture of the age-related processes that take place in these organs, says a study in mice published today in eLife.
Aging causes many changes in the body and in essential organs such as the kidneys, which function less efficiently later in life. Age-related changes in the kidneys have mostly been reported by looking at the transcription of genes — the process by which a segment of DNA is copied into RNA. The current study suggests that this approach, combined with studying changes in proteins, gives us a better understanding of age-related changes in the kidney and may point to new approaches for treating age-related kidney dysfunction.
“Physiological changes in kidney function during aging are well documented, but little is known about the underlying molecular processes that drive this loss of function,” explains first author Yuka Takemon, who was a research assistant at the Jackson Laboratory in Bar Harbor, Maine, US, when the study was carried out, and is now a PhD student at the Michael Smith Genome Sciences Centre, University of British Columbia, Canada. “Many previous studies of these physiological changes have looked at the transcription of genes into proteins by measuring messenger RNA (mRNA), but we wanted to see if we could gather more insights by combining this approach with studying protein levels in the kidney.”
In their study, Takemon and colleagues looked at age-related changes in kidney function in about 600 genetically diverse mice. They also measured changes in mRNA and proteins in kidney samples from about one-third of the animals.
They discovered an age-related pattern of changes in both mRNA and proteins in the mice that suggests the animals have increasing numbers of immune cells and inflammation in their kidneys, as well as decreased function in their mitochondria, which produce energy for the cells.
However, not all of the changes in proteins corresponded with changes in the mRNA, suggesting that some of the protein changes occur after the transcription of genes into RNA. This could mean that older kidneys become less efficient at building new proteins, or that proteins are broken down more quickly in older kidneys. If further studies confirm this, it could mean that therapies or interventions that promote protein building or slow protein breakdown may be beneficial for treating kidney diseases associated with aging.
“Our study suggests that mRNA measurements alone provide an incomplete picture of molecular changes caused by aging in the kidney,” concludes senior author Ron Korstanje, Associate Professor at the Jackson Laboratory. “Studying changes in proteins is also essential to understanding these aging-related processes, and for designing possible new approaches for treating age-related diseases.”
Story Source:
Materials provided by eLife. Note: Content may be edited for style and length.

Scientists have revealed how an antibiotic of ‘last resort’ kills bacteria.
The findings, from Imperial College London and the University of Texas, may also reveal a potential way to make the antibiotic more powerful.
The antibiotic colistin has become a last resort treatment for infections caused by some of the world’s nastiest superbugs. However, despite being discovered over 70 years ago, the process by which this antibiotic kills bacteria has, until now, been something of a mystery.
Now, researchers have revealed that colistin punches holes in bacteria, causing them to pop like balloons. The work, funded by the Medical Research Council and Wellcome Trust, and published in the journal eLife, also identified a way of making the antibiotic more effective at killing bacteria.
Colistin was first described in 1947, and is one of the very few antibiotics that is active against many of the most deadly superbugs, including E. coli, which causes potentially lethal infections of the bloodstream, and Pseudomonas aeruginosa and Acinetobacter baumannii, which frequently infect the lungs of people receiving mechanical ventilation in intensive care units.
These superbugs have two ‘skins’, called membranes. Colistin punctures both membranes, killing the bacteria. However, whilst it was known that colistin damaged the outer membrane by targeting a chemical called lipopolysaccharide (LPS), it was unclear how the inner membrane was pierced.
Now, a team led by Dr Andrew Edwards from Imperial’s Department of Infectious Disease, has shown that colistin also targets LPS in the inner membrane, even though there’s very little of it present.
Dr Edwards said: “It sounds obvious that colistin would damage both membranes in the same way, but it was always assumed colistin damaged the two membranes in different ways. There’s so little LPS in the inner membrane that it just didn’t seem possible, and we were very sceptical at first. However, by changing the amount of LPS in the inner membrane in the laboratory, and also by chemically modifying it, we were able to show that colistin really does puncture both bacterial skins in the same way — and that this kills the superbug. ”
Next, the team decided to see if they could use this new information to find ways of making colistin more effective at killing bacteria.
They focussed on a bacterium called Pseudomonas aeruginosa, which also causes serious lung infections in people with cystic fibrosis. They found that a new experimental antibiotic, called murepavadin, caused a build up of LPS in the bacterium’s inner skin, making it much easier for colistin to puncture it and kill the bacteria.
The team say that as murepavadin is an experimental antibiotic, it can’t be used routinely in patients yet, but clinical trials are due to begin shortly. If these trials are successful, it may be possible to combine murepavadin with colistin to make a potent treatment for a vast range of bacterial infections.
Akshay Sabnis, lead author of the work also from the Department of Infectious Disease, said: “As the global crisis of antibiotic resistance continues to accelerate, colistin is becoming more and more important as the very last option to save the lives of patients infected with superbugs. By revealing how this old antibiotic works, we could come up with new ways to make it kill bacteria even more effectively, boosting our arsenal of weapons against the world’s superbugs.”
Story Source:
Materials provided by Imperial College London. Original written by Kate Wighton. Note: Content may be edited for style and length.

University of South Australia researchers have identified an enzyme that may help to curb chronic kidney disease, which affects approximately 700 million people worldwide.
This enzyme, NEDD4-2, is critical for kidney health, says UniSA Centre for Cancer Biology scientist Dr Jantina Manning in a new paper published this month in Cell Death & Disease.
The early career researcher and her colleagues, including 2020 SA Scientist of the Year Professor Sharad Kumar, have shown in an animal study the correlation between a high salt diet, low levels of NEDD4-2 and advanced kidney disease.
While a high salt diet can exacerbate some forms of kidney disease, until now, researchers did not realise that NEDD4-2 plays a role in promoting this salt-induced kidney damage.
“We now know that both a high sodium diet and low NEDD4-2 levels promote renal disease progression, even in the absence of high blood pressure, which normally goes hand in hand with increased sodium,” says Dr Manning.
NEDD4-2 regulates the pathway required for sodium reabsorption in the kidneys to ensure correct levels of salt are maintained. If the NEDD4-2 protein is reduced or inhibited, increased salt absorption can result in kidney damage.

New Edith Cowan University (ECU) research has found that by eating just one cup of nitrate-rich vegetables each day people can significantly reduce their risk of heart disease.
The study investigated whether people who regularly ate higher quantities of nitrate-rich vegetables, such as leafy greens and beetroot, had lower blood pressure, and it also examined whether these same people were less likely to be diagnosed with heart disease many years later.
Cardiovascular diseases are the number one cause of death globally, taking around 17.9 million lives each year.
Researchers examined data from over 50,000 people residing in Denmark taking part in the Danish Diet, Cancer, and Health Study over a 23-year period. They found that people who consumed the most nitrate-rich vegetables had about a 2.5 mmHg lower systolic blood pressure and between 12 to 26 percent lower risk of heart disease.
Lead researcher Dr Catherine Bondonno from ECU’s Institute for Nutrition Research said identifying diets to prevent heart disease was a priority.
“Our results have shown that by simply eating one cup of raw (or half a cup of cooked) nitrate-rich vegetables each day, people may be able to significantly reduce their risk of cardiovascular disease,” Dr Bondonno said.

If a respiratory droplet from a person infected with COVID-19 lands on a surface, it becomes a possible source of disease spread. This is known as the fomite route of disease spread, in which the aqueous phase of the respiratory droplet serves as a medium for virus survival.
The lifespan of the respiratory droplet dictates how likely a surface is to spread a virus. While 99.9% of the droplet’s liquid content evaporates within a few minutes, a residual thin film that allows the virus to survive can be left behind.
This raises the question: Is it possible to design surfaces to reduce the survival time of viruses, including the coronavirus that causes COVID-19? In Physics of Fluids, from AIP Publishing, IIT Bombay researchers present their work exploring how the evaporation rate of residual thin films can be accelerated by tuning surfaces’ wettability and creating geometric microtextures on them.
An optimally designed surface will make a viral load decay rapidly, rendering it less likely to contribute to the spread of viruses.
“In terms of physics, the solid-liquid interfacial energy is enhanced by a combination of our proposed surface engineering and augmenting the disjoining pressure within the residual thin film, which will speed drying of the thin film,” said Sanghamitro Chatterjee, lead author and a postdoctoral fellow in the mechanical engineering department.
The researchers were surprised to discover that the combination of a surface’s wettability and its physical texture determine its antiviral properties.
“Continuously tailoring any one of these parameters wouldn’t achieve the best results,” said Amit Agrawal, a co-author. “The most conductive antiviral effect lies within an optimized range of both wettability and texture.”
While previous studies reported antibacterial effects by designing superhydrophobic (repels water) surfaces, their work indicates antiviral surface design can be achieved by surface hydrophilicity (attracts water).
“Our present work demonstrates that designing anti-COVID-19 surfaces is possible,” said Janini Murallidharan, a co-author. “We also propose a design methodology and provide parameters needed to engineer surfaces with the shortest virus survival times.”
The researchers discovered that surfaces with taller and closely packed pillars, with a contact angle of around 60 degrees, show the strongest antiviral effect or shortest drying time.
This work paves the way for fabricating antiviral surfaces that will be useful in designing hospital equipment, medical or pathology equipment, as well as frequently touched surfaces, like door handles, smartphone screens, or surfaces within areas prone to outbreaks.
“In the future, our model can readily be extended to respiratory diseases like influenza A, which spread through fomite transmission,” said Rajneesh Bhardwaj, a co-author. “Since we analyzed antiviral effects by a generic model independent of the specific geometry of texture, it’s possible to fabricate any geometric structures based on different fabrication techniques — focused ion beams or chemical etching — to achieve the same outcome.”
Story Source:
Materials provided by American Institute of Physics. Note: Content may be edited for style and length.