Publisher Health

New findings by UT Southwestern researchers help better understand the how one of the most commonly mutated genetic drivers of cancer passes signals that cause the disease.
The study, published in Nature Structural & Molecular Biology, focuses on a family of proteins called RAS, which is mutated in 20 to 25% of all cancers, especially in lethal cancers such as pancreatic, colorectal and lung cancers.
“A framework to develop RAS inhibitor strategies is badly needed because recently approved RAS inhibitors such as sotorasib only work against one specific mutation, and many other RAS mutations also cause cancer,” said Kenneth Westover, M.D., Ph.D., Associate Professor of Radiation Oncology and Biochemistry, member of the Chemistry and Cancer Research Program in the UT Southwestern Harold C. Simmons Comprehensive Cancer Center, and an author of the study. “This work sets the stage for development of new targeted RAS inhibitors to address major drivers of lethal cancers, such as pancreatic and colon cancer.”
Starting in 2012, Dr. Westover’s lab worked with the Dana-Farber Cancer Institute to develop drugs that bind to a specific RAS mutant where a glycine amino acid at position 12 in the RAS protein is changed to a cysteine, the so-called KRAS G12C.
“Cysteine is a distinctive amino acid that allows us to irreversibly attach drugs using special chemistries. Other major cancer-associated RAS mutations do not give us the same foothold,” Dr. Westover said.
His lab’s work helped propel the field that saw approval of one KRAS G12C inhibitor, sotorasib, in May. Approval of an analogous drug, adagrasib, is widely anticipated.
In the latest study, the Westover lab sought to understand how cancer-causing RAS mutants pass inappropriate signals from the surface of the cell to the cell nucleus. The formation of large protein clusters as part of the mechanism was known, but the clusters’ structure was unknown. Dr. Westover and collaborators used computer simulations to arrive at an atomistic structural model of a RAS assembly and validated the model using biological systems.
“This structural model is now available to the wider RAS research community. We hope it will enable researchers to test new ideas about how RAS works in normal physiology and new strategies for targeting cancer-causing RAS mutations,” said Carlos L. Arteaga, M.D., Director of the Simmons Cancer Center.
Because RAS signaling relies on formation of RAS complexes, Dr. Westover thinks it may be possible to create new generations of RAS-targeted drugs that work by breaking apart such RAS complexes.
Funding for the study came from the National Cancer Institute, the Department of Defense, and the Cancer Prevention and Research Institute of Texas.
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Materials provided by UT Southwestern Medical Center. Note: Content may be edited for style and length.

Many of the processes that keep us alive also put us at risk. The energy-producing chemical reactions in our cells, for example, also produce free radicals — unstable molecules that steal electrons from other molecules. When generated in surplus, free radicals can cause collateral damage, potentially triggering malfunctions such as cancer, neurodegeneration, or cardiovascular disease.
Cells solve this problem by synthesizing antioxidants, compounds that neutralize free radicals. In a new study, Rockefeller scientists identify a key molecule that ferries glutathione, the body’s major antioxidant, into the cell’s mitochondria, where free radicals are produced en masse. The discovery, published in Nature, opens new possibilities for investigating oxidative stress and its damaging effects.
“With the potential transporter identified, we can now control the amount of glutathione that enters mitochondria and study oxidative stress specifically at its source,” says Kivanç Birsoy, Chapman Perelman Assistant Professor at The Rockefeller University.
The shuttle into the mitochondria
To avoid oxidative stress, cells need to properly balance the levels of free radicals and antioxidants within their mitochondria, where energy production happens. Because glutathione is produced outside of mitochondria, in the cell’s cytosol, the scientists wanted to know how it gets transported into these tiny powerhouses in the first place.
To shed light on this process, Birsoy’s team monitored protein expression in cells in response to glutathione’s levels. “We hypothesized that glutathione is shuttled by a transporter protein whose production is regulated by glutathione,” Birsoy says. “So if we lower the levels of glutathione, the cell should compensate by upregulating the transporter protein.”
The analysis pointed to SLC25A39, a protein in the mitochondrial membrane whose function was hitherto unknown. The researchers found that blocking SLC25A39 reduced glutathione inside the mitochondrion, without affecting its levels elsewhere in the cell. Other experiments showed that mice cannot survive without SLC25A39. In animals engineered to lack this protein, red blood cells quickly die by oxidative stress due to their failure to bring glutathione into mitochondria.
The identification of the transporter may lead to a better understanding of a variety of disease pathways linked to oxidative stress, including those involved in aging and neurodegeneration. “These conditions could potentially be treated or prevented by stimulating antioxidant transport into mitochondria,” Birsoy says.
Moreover, the team is now exploring whether SLC25A39 might hold promise as a drug target for cancer, by helping to induce fatal oxidative stress in tumor cells. “In cancer, we would want to prevent antioxidants from getting into mitochondria, and the transporter protein may be our way to do that,” Birsoy says.
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Materials provided by Rockefeller University. Note: Content may be edited for style and length.

Start-up investors have often suspended skepticism while chasing a hot deal. The trial of Ms. Holmes, the founder of Theranos, has put that behavior under the spotlight.SAN JOSE, Calif. — In 2014, Dan Mosley, a lawyer and power broker among wealthy families, asked the entrepreneur Elizabeth Holmes for audited financial statements of Theranos, her blood testing start-up. Theranos never produced any, but Mr. Mosley invested $6 million in the company anyway — and wrote Ms. Holmes a gushing thank-you email for the opportunity.Bryan Tolbert, an investor at Hall Group, said his firm invested $5 million in Theranos in 2013, even though it did not have a detailed grasp of the start-up’s technologies or its work with pharmaceutical companies and the military.And Lisa Peterson, who handles investments for Michigan’s wealthy DeVos family, said she did not visit any of Theranos’s testing centers in Walgreens stores, call any Walgreens executives or hire any outside experts in science, regulations or legal matters to verify the start-up’s claims. In 2014, the DeVos family invested $100 million into the company.The humiliating details of bad investments like Theranos are rarely displayed so prominently to the public. But they have been laid bare in recent weeks at the trial of Ms. Holmes, 37, who faces a dozen counts of wire fraud and conspiracy to commit wire fraud; she has pleaded not guilty. She and Theranos fell from grace — with investor money evaporating and the company shutting down in 2018 — after claims about its blood-testing technology were shown to be false.Now in its ninth week, Ms. Holmes’s trial has offered an especially clear picture of the many ways sophisticated investors can be swept up in the hype of a hot start-up, ignoring red flags that look obvious in hindsight. That behavior still resonates today, as investors compete to pour money into Silicon Valley start-ups, which have been in a frenzied state of record-breaking fund-raising.With so many new investors flocking to start-ups, due diligence is sometimes so minimal that it is used as a punchline, investors said. An overheated market “definitely creates an environment for people to make more inflated claims” and may even tempt them to lie, said Shirish Nadkarni, a longtime entrepreneur, investor and author.During its lifetime, Theranos exemplified that dynamic. The company raised $945 million from famous venture capitalists including Tim Draper, Donald Lucas and Dixon Doll; wealthy heirs to the founders of Amway, Walmart and Cox Communications; and powerful tech and media moguls such as Larry Ellison and Rupert Murdoch..css-1xzcza9{list-style-type:disc;padding-inline-start:1em;}.css-3btd0c{font-family:nyt-franklin,helvetica,arial,sans-serif;font-size:1rem;line-height:1.375rem;color:#333;margin-bottom:0.78125rem;}@media (min-width:740px){.css-3btd0c{font-size:1.0625rem;line-height:1.5rem;margin-bottom:0.9375rem;}}.css-3btd0c strong{font-weight:600;}.css-3btd0c em{font-style:italic;}.css-1kpebx{margin:0 auto;font-family:nyt-franklin,helvetica,arial,sans-serif;font-weight:700;font-size:1.125rem;line-height:1.3125rem;color:#121212;}#NYT_BELOW_MAIN_CONTENT_REGION .css-1kpebx{font-family:nyt-cheltenham,georgia,’times new roman’,times,serif;font-weight:700;font-size:1.375rem;line-height:1.625rem;}@media (min-width:740px){#NYT_BELOW_MAIN_CONTENT_REGION .css-1kpebx{font-size:1.6875rem;line-height:1.875rem;}}@media (min-width:740px){.css-1kpebx{font-size:1.25rem;line-height:1.4375rem;}}.css-1gtxqqv{margin-bottom:0;}.css-1g3vlj0{font-family:nyt-franklin,helvetica,arial,sans-serif;font-size:1rem;line-height:1.375rem;color:#333;margin-bottom:0.78125rem;}@media (min-width:740px){.css-1g3vlj0{font-size:1.0625rem;line-height:1.5rem;margin-bottom:0.9375rem;}}.css-1g3vlj0 strong{font-weight:600;}.css-1g3vlj0 em{font-style:italic;}.css-1g3vlj0{margin-bottom:0;margin-top:0.25rem;}.css-19zsuqr{display:block;margin-bottom:0.9375rem;}.css-12vbvwq{background-color:white;border:1px solid #e2e2e2;width:calc(100% – 40px);max-width:600px;margin:1.5rem auto 1.9rem;padding:15px;box-sizing:border-box;}@media (min-width:740px){.css-12vbvwq{padding:20px;width:100%;}}.css-12vbvwq:focus{outline:1px solid #e2e2e2;}#NYT_BELOW_MAIN_CONTENT_REGION .css-12vbvwq{border:none;padding:10px 0 0;border-top:2px solid #121212;}.css-12vbvwq[data-truncated] .css-rdoyk0{-webkit-transform:rotate(0deg);-ms-transform:rotate(0deg);transform:rotate(0deg);}.css-12vbvwq[data-truncated] .css-eb027h{max-height:300px;overflow:hidden;-webkit-transition:none;transition:none;}.css-12vbvwq[data-truncated] .css-5gimkt:after{content:’See more’;}.css-12vbvwq[data-truncated] .css-6mllg9{opacity:1;}.css-qjk116{margin:0 auto;overflow:hidden;}.css-qjk116 strong{font-weight:700;}.css-qjk116 em{font-style:italic;}.css-qjk116 a{color:#326891;-webkit-text-decoration:underline;text-decoration:underline;text-underline-offset:1px;-webkit-text-decoration-thickness:1px;text-decoration-thickness:1px;-webkit-text-decoration-color:#326891;text-decoration-color:#326891;}.css-qjk116 a:visited{color:#326891;-webkit-text-decoration-color:#326891;text-decoration-color:#326891;}.css-qjk116 a:hover{-webkit-text-decoration:none;text-decoration:none;}And as investors have testified at Ms. Holmes’s trial, a central tension has emerged around due diligence. Could these investors have avoided disaster if they had simply done better research on Theranos? Or were they doomed because their research was based on lies?Prosecutors have presented a growing list of examples supporting the latter argument. For example, Theranos added pharmaceutical company logos to validation reports indicating the pharmaceutical firms had endorsed its technology when they hadn’t, according to evidence and testimony. Theranos also claimed in late 2014 that it would bring in $140 million in revenue that year when it had none, according to evidence and testimony. The start-up also faked demos of its blood-testing machines to investors, witnesses have testified.The Theranos blood-testing machine at the company’s lab before the start-up was shut down.Carlos Chavarria for The New York TimesIn response, Ms. Holmes’s lawyers have needled Theranos’s investors for their oversights, aiming to convince the jury that the investors were the ones at fault for not digging into Ms. Holmes’ claims.Her lawyers recently pushed Wade Miquelon, the former chief financial officer of Walgreens, to admit that he didn’t know if his company had ever gotten one of Theranos’s devices in its offices for testing before entering into a partnership. The lawyers also got Mr. Mosley to concede he never directly asked Ms. Holmes whether a pharmaceutical company had written the validation report.The strategy has sometimes veered into condescension. That was evident last week when Lance Wade, a lawyer for Ms. Holmes, asked Ms. Peterson, an investment professional, if she was familiar with the concept of due diligence.“You understand that’s a typical thing to do in investing?” he said.The investors have pushed back, explaining that they were acting on false information supplied by Ms. Holmes.“You’re trying to measure our sophistication as an investor when we weren’t given complete information,” Ms. Peterson said. Mr. Wade asked the judge to strike the comment from the record.Still, testimony from pharmaceutical company executives who interacted with Theranos showed it was possible to see through at least some of Ms. Holmes’s grandiose claims.Constance Cullen, a former director at Schering Plough, said this week that she was responsible for evaluating Theranos’s technology in 2009. She said she came away “dissatisfied” with Ms. Holmes’s answers to her technical questions, calling them “cagey” and indirect. She said she stopped responding to emails from Ms. Holmes.Shane Weber, a director at Pfizer, looked into Theranos in 2008 and concluded that the company’s responses to his technical questions were “oblique, deflective or evasive,” according to a memo used as evidence. He recommended Pfizer cease working with Theranos.

Using nanopore DNA sequencing technology, researchers from TU Delft and the University of Illinois have managed to scan a single protein: by slowly moving a linearized protein through a tiny nanopore, one amino acid at the time, the researchers were able to read off electric currents that relate to the information content of the protein. The researchers published their proof-of-concept in Science today. The new single-molecule peptide reader marks a breakthrough in protein identification, and opens the way towards single-molecule protein sequencing and cataloguing the proteins inside a single cell.
Proteins are the workhorses of our cells, yet we simply don’t know what proteins we all carry with us. A protein is a long peptide string made of 20 different types of amino acids, comparable to a necklace with different kinds of beads. From the DNA blueprint, we are able to predict of which amino acids a protein consists. However, the final protein can greatly differ from the blueprint, for example due to post-translational modifications. Current methods to measure proteins are expensive, limited to large volumes, and they cannot detect many rare proteins. With nanopore-based technology, one is already able to scan and sequence single DNA molecules. The team led by Cees Dekker (TU Delft) now adapted this technique to instead scan a single protein, one amino acid at a time.
“Over the past 30 years, nanopore-based DNA sequencing has been developed from an idea to an actual working device,” Cees Dekker explains. “This has even led to commercial hand-held nanopore sequencers that serve the billion-dollar genomics market. In our paper, we are expanding this nanopore concept to the reading of single proteins. This may have great impact on basic protein research and medical diagnostics.”
Like beads down the drain
The new technique reveals characteristics of even single amino acids within a peptide, but how? Lead author of the paper Henry Brinkerhoff, who pioneered this work as a postdoc in Dekker’s lab, explains: “Imagine the string of amino acids in one peptide molecule as a necklace with different-sized beads. Then, imagine you turn on the tap as you slowly move that necklace down the drain, which in this case is the nanopore. If a big bead is blocking the drain, the water flowing through will only be a trickle; if you have smaller beads in the necklace right at the drain, more water can flow through. With our technique we can measure the amount of water flow (the ion current actually) very precisely.” Cees Dekker enthusiastically adds: “A cool feature of our technique is that we were able to read a single peptide string again and again: we then average all the reads from that one single molecule, and thus identify the molecule with basically 100% accuracy.”
This results in a unique read-off which is characteristic for a specific protein. When the researchers changed even one single amino acid within the peptide (‘a single bead within the necklace’), they obtained very different signals, indicating the extreme sensitivity of the technique. The group led by Alek Aksimentiev at the University of Illinois performed molecular dynamics simulations that showed how the ion current signals relate to the amino acids in the nanopore.
Scanning the barcode for identification
The new technique is very powerful for identifying single proteins and mapping minute changes between them — much like how a cashier in the supermarket identifies each product by scanning its barcode. It also may provide a new route towards full de novo protein sequencing in the future. Henry Brinkerhoff clarifies: “Our approach might lay a basis for a single-protein sequencer in the future, but de novo sequencing remains a big challenge. For that, we still need to characterize the signals from a huge number of peptides in order to create a ‘map’ connecting ion current signals to protein sequence. Even so, the ability to discriminate of single-amino-acid substitutions in single molecules is a major advance, and there are many immediate applications for the technology as it is now.”
Glimpsing the ‘dark matter’ of biology
Using the current nanopore peptide reader, researchers can start analyzing what proteins float around in our cells. After synthesis in cells, proteins still undergo changes that affect their function, called post-translational modifications. The resulting millions of protein variants are difficult to measure, and could be considered the ‘dark matter of biology’. Cees Dekker: “To continue the metaphor: after a necklace with its beads is made, it will still be changed: some red beads get a phosphoryl attached to it, some blue beads a sugar group, etc. These changes are crucial to protein function, and also a marker for diseases such as cancer. We think that our new approach will allow us to detect such changes, and thus shine some light on the proteins that we carry with us.”
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A new Dartmouth-led study published in Pediatric Research has found a direct and sex-specific association between the composition of infant microbiome and early childhood behavioral health.
Previous studies have established a link between the gut microbiome — the overall communities of microbes that colonize the intestinal tract and play an important role in immune system development and health outcomes — and behaviors like depression, anxiety, and attention-deficit hyperactivity disorder. But until now, there has been little to no human data from which to characterize the role of the microbiome during infancy in relation to these outcomes in children, and how they may differ in boys and girls.
“A lot of the prior research has looked at participants who are already exhibiting depressive or anxious symptoms,” explains Hannah Laue, ScD, a research associate at Dartmouth’s Geisel School of Medicine and first author on the study. “We wanted to look very early on, before these behaviors were expressed, to see if we could establish if the microbiome was influencing the neurobehavior or if it was the other way around.”
Focusing in on infancy also allowed the investigators to study a critical window of time, says Laue, when the microbiome and the brain are going through their most rapid periods of development, and when the brain may be particularly susceptible to changes in the microbiome.
To determine whether differences in the infant microbiome were related to neurobehavior, and whether that behavior varied in boys and girls — the study team leveraged the New Hampshire Birth Cohort Study, which was established in 2009 to investigate the role of environmental factors on pregnancy and newborn outcomes. Through initiatives led by Dartmouth’s Drs. Juliette Madan and Margaret Karagas, the cohort involves longitudinal follow-up of the developing microbiome beginning at birth to understand its influence on the health and well-being of children.
For the study, the researchers analyzed stool samples (collected by the caregivers) from 260 infants at multiple timepoints — six weeks, one year, and two years. This allowed them to characterize the species of microbes present in each participant’s gut and their functions. They then used the Behavioral Assessment System for Children, an instrument that measures a wide range of clinical and adaptive behaviors in children and young adults, to assess their behavioral development.
The study team was able to establish that microbiome changes occur before behavioral changes. They also found that infant and early-childhood microbiomes were related to neurobehaviors such as anxiety, depression, hyperactivity, and social behaviors in a time- and sex-specific manner.
“For example, we found that increased diversity in the gut was better for boys, meaning it was associated with fewer behaviors like anxiety and depression, but not among girls,” says Laue. “We saw differences in social behaviors with microbiomes measured at later stages, where there was evidence that diversity, again, could be beneficial for boys but not for girls. And we found there were differences in certain species of bacteria and the essential functions they perform — such as the synthesis of vitamin B — that were related to these outcomes, as well.”
While their findings don’t identify a microbial species that can immediately be used to help prevent children from developing neurobehaviors such as anxiety or depression, “We think the results do inform future studies that can look a little more deeply at some of our specific findings and clarify whether they could be developed as probiotics or other types of interventions such as the promotion of breastfeeding,” says Laue.
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Materials provided by The Geisel School of Medicine at Dartmouth. Original written by Timothy Dean. Note: Content may be edited for style and length.

Tackling pollution from the emission of nitrogen compounds, particularly ammonia, could reduce many of the 23.3 million years of life that were lost prematurely across the world in 2013 due to nitrogen-related air pollution, an international study led by Chinese scientists has discovered using a modeling framework, including the IIASA GAINS model.
A research team led by scientists from Zhejiang University in China used the IIASA GAINS model, among other tools, to develop a new metric, called the ‘Nitrogen-share’ (N-share), to estimate the contribution of nitrogen compounds to PM2.5 (fine particle) air pollution and the associated health effects.
N-share expresses the contribution of a given compound containing nitrogen to an effect in question.
PM2.5 air pollution is the largest environmental risk factor for human health worldwide. Sulphur dioxide and nitrogen compounds such as nitrogen oxides (NOx), deriving from fossil fuel combustion in power plants, industrial furnaces or boilers, as well as vehicle emissions, and ammonia (NH3) emissions mainly from agricultural and natural sources are important precursors of PM2.5 formation in the atmosphere.
The study, published in Science, revealed, via a cost-benefit analysis, that ammonia mitigation is one of the most cost-effective ways to improve global air quality and public health.
The research team used three atmospheric chemistry transport models to simulate total PM2.5 concentration with and without nitrogen compound emissions and found that NH3 emissions have a larger contribution to PM2.5 than NOx emissions. Using the GAINS model developed by IIASA, the team was able to quantify the potential to reduce emissions, and the financial costs such measures would have.

The drop in estrogen levels that occurs with menopause brings declines in the volumes of “gray matter,” the cellular matter of the brain, in key brain regions that are also affected in Alzheimer’s disease. But a new study from Weill Cornell Medicine researchers, in collaboration with the University of Arizona, suggests that greater cumulative exposure to estrogen in life, for example from having had more children or from having taken menopause hormone therapy, may counter this brain-shrinking effect.
The findings, reported Nov. 3 in Neurology, come from an analysis of personal histories, MRI scans and cognitive tests on 99 women in their late 40s to late 50s. The researchers confirmed an earlier finding linking menopause to lower gray matter volume (GMV) in brain areas that are also vulnerable to Alzheimer’s. But they also linked indicators of higher overall estrogen exposure, such as a longer span of reproductive years (menarche to menopause), more children and the use of menopause hormone therapy and hormonal contraceptives, to higher GMV in some of these brain areas.
The study was an observational study rather than a clinical trial, but it adds to the evidence that estrogen may have a protective effect on the female brain, limiting the loss of gray matter that normally comes with menopause, and thereby potentially reducing Alzheimer’s risk.
“Our findings suggest that while the menopause transition may bring vulnerability for the female brain, other reproductive history events indicating greater estrogen exposure bring resilience instead,” said study senior author Dr. Lisa Mosconi, an associate professor of neuroscience in neurology at Weill Cornell Medicine and director of the Women’s Brain Initiative, and associate director of the Alzheimer’s Prevention Clinic at Weill Cornell Medicine and NewYork-Presbyterian/Weill Cornell Medical Center.
Researchers estimate that nearly two thirds of those living with Alzheimer’s in the United States are women. The higher prevalence of Alzheimer’s in women may be due in part to women’s greater longevity, among other reasons. A leading hypothesis is that that vulnerability relates to estrogen.
Receptors for estrogen molecules are found in cells throughout women’s brains, and the sex hormone has long been known not just to help steer brain development and behavior but also generally to have a nourishing and protecting role in the central nervous system. That protection doesn’t last forever, though. Estrogen levels decline steeply during the transition through menopause, and as recent research from Dr. Mosconi and others has shown, women tend to experience significant GMV loss during this transition.
The volume loss occurs especially in brain regions that are the most heavily affected in Alzheimer’s, and at roughly the same time of life when the long, slow process of late-onset Alzheimer’s is believed to start. Thus, women’s mid-life loss of estrogen may be a key factor behind the higher risk of Alzheimer’s.
The flip side of this hypothesis is that more estrogen, in particular a cumulatively greater estrogen exposure, could serve as a counter to the brain-weakening effect of menopause. That possibility is what Dr. Mosconi and her team sought to investigate in the new study.
The analysis covered 99 women aged 46-58 and a comparison group of 29 similarly aged men. It confirmed that the post-menopausal and peri-menopausal (starting menopause) women, compared with the pre-menopausal women and the men, had significantly lower GMV — adjusted for age and head size — in brain areas such as the hippocampus, entorhinal cortex and temporal lobe regions, which are heavily affected by Alzheimer’s.
By contrast, among the women, having more estrogen exposure as implied by various factors was associated with greater GMV in certain brain areas. Longer reproductive span, for example, was significantly linked to more GMV in a cluster of regions near the top of the brain including the superior parietal lobule and precuneus of the left hemisphere. Having had more children was significantly associated with more GMV in inferior and middle frontal gyri, and middle and inferior temporal gyri. Having used hormone replacement therapy was associated with more GMV in superior frontal gyrus and several other brain regions. All these brain regions are known to be affected by aging and Alzheimer’s.
The results support the idea that estrogen can be protective, the researchers say, and suggest that further investigation of the specific biological pathways underlying this effect could yield medical or lifestyle changes that help women reduce their risk of cognitive decline with aging as well as Alzheimer’s dementia risk.
“We’re hoping now to get further into the details of these links between estrogen and GMV, for example by comparing the effects of surgical menopause and spontaneous menopause, and by focusing specifically on certain types of estrogen exposure, such as menopause hormone therapy,” said study first author Eva Schelbaum, research assistant in Dr. Mosconi’s laboratory. “The goal as always is to understand why Alzheimer’s affects more women than men, and how we can reduce that risk.

Multiple sclerosis (MS) is a chronic neurological disease that affects the body’s central nervous system. It can limit a person’s mobility, impair physical and cognitive functions, and increase the risk of falling, collectively compromising quality of life.
Cognitive impairment has been particularly difficult for researchers to address, with few intervention strategies proven effective in preserving or restoring cognitive functions for people with MS.
Associate Professor Feng Yang worked with Francois Bethoux from the Cleveland Clinic Foundation and Georgia State University faculty members Pey-Shan Wen and Yichuan Zhao to study whether vibration training – an intervention used to improve physical function for people with MS – could also improve cognitive function and overall quality of life.
Vibration training requires individuals to sit or stand on a platform that vibrates at a fast pace but with a small movement for a specific amount of time.
For Yang’s study, believed to be the first of its kind, 18 adults with MS completed assessments to determine their perceived disability status, cognitive function and quality of life. Then, some of the participants attended vibration training three times a week for six weeks.
The study, published in the International Journal of MS Care, found that the vibration training improved not only physical abilities, such as increased walking speeds, but also cognitive functions, such as memory capacity and executive function.
“Despite the limitations – such as a small sample size, narrow MS types and disability levels, etc. – this study suggests that a six-week vibration training course could improve cognitive functions and quality of life among people with MS,” Yang and his colleagues wrote. “The goal of rehabilitation in people with MS is to decrease the impact of MS on personal activity, function and social participation to allow people with MS the highest possible independence and quality of life.”
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Materials provided by Georgia State University. Note: Content may be edited for style and length.

Research has increasingly shown that warming is taking a deadly toll on human health. At the global climate summit in Glasgow, the issue has gained new prominence.For the first time at a major United Nations climate conference, human health is emerging as a leading issue, a reframing that brings climate change’s far-reaching and long-lasting effects to the forefront.Although health has been addressed at conferences going back to the first U.N. environmental summit in 1992, never before has it held such a central role. The 2015 Paris accord, the global agreement among nations to reduce greenhouse gas emissions, was billed foremost as a historic environmental moment.However, “the Paris Agreement is not an environmental treaty,” said Dr. Maria Neira, the director of the World Health Organization’s department on environment, climate change and health. “It is a basic public health treaty.”There is a growing body of research showing that climate change is contributing to a wide range of health risks around the world. It is exacerbating heat waves, intensifying wildfires, heightening flood risks and worsening droughts. These are, in turn, increasing heat-related mortality, pregnancy complications and cardiovascular disease. And as with many things climate-related, the risks and harms are particularly severe in places that are the least able to respond.There is also a cascade of indirect health consequences that threaten to unravel decades of progress on improving water quality and food security. Drier soil can contribute to malnutrition. Warming temperatures and changing humidity levels can expand habitats suitable to dengue- or malaria-carrying mosquitoes, lyme-carrying ticks, and the pathogens that cause diseases like cholera and Valley Fever.At the same time, two years of grappling with the coronavirus pandemic has underscored to politicians the importance of health as a national and global priority.For reasons like these, the health community has strategized that if it can make people the face of climate change — rather than traditional environmental icons, such as polar bears or forests — political leaders may be more inclined to take action.In the months leading up to the Glasgow conference, known as COP26, the world’s leading public health organizations, medical journals and professional organizations released a series of reports and editorials placing health at the heart of the climate issue. One letter signed by organizations representing 47 million global health professionals declared the climate crisis “the single biggest health threat facing humanity.” The World Health Organization estimates that between 2030 and 2050, at least 250,000 additional deaths will occur every year as a result of climate change.In one sign of the emphasis placed on health this year, 15 countries, including Ireland and Mozambique, have already made significant pledges to decarbonize their national health systems.“This year represents a quantum leap in how health is being covered at COP,” said Josh Karliner, the international director of program and strategy at Health Care Without Harm, an organization that has worked to reduce the health care sector’s environmental footprint.Around the world, health care providers have said that they are already seeing the effects of climate change on their patients, as well as on the ability of hospitals to continue providing care during extreme weather. At the same time, there has been a growing awareness of the health care sector’s own contribution to greenhouse gas emissions.Haze in New York City, wafting from wildfires in the West last summer.Bjoern Kils/ReutersDifficulties providing careHospitals around the world have been hit hard by extreme weather and are increasingly grappling with the reality that they weren’t designed for the intensity of storms, heat and other challenges that are becoming more commonplace. Floods killed Covid patients at a hospital in Mexico. Hospitals in India suffered severe flooding. As wildfires burned on the West Coast, hospitals struggled to maintain their indoor air quality. A hurricane ripped the roof of a rural Louisiana hospital.During the Pacific Northwest heat wave this summer, Dr. Jeremy Hess, a professor of emergency medicine at the University of Washington, was working in the emergency department at Harborview Medical Center, the highest-level trauma center for several states. Dr. Hess has worked in emergency departments during mass casualty events, but the heat wave stuck out.“It was more sustained,” he said. “It was an environmental emergency that wasn’t stopping.”For days, patients came in with third-degree burns on their feet from walking on hot asphalt, he said. Many succumbed to heat-related death before even making it to the hospital. Doctors scrambled to have body bags filled with ice on gurneys.Hospitals across the region were stressed in other ways. Providence, a large health care organization in the West, had no spare beds at their emergency departments spanning the northern part of Washington state down to southern Oregon. One hospital closed its psychiatric unit to ensure there was adequate power in more critical parts of the building.That week, more than 1,000 heat-related emergency visits were reported in the Pacific Northwest, compared with fewer than 10 visits during the same period in 2019. Researchers found that such an intensive heat wave would have been virtually impossible without the influence of human-caused climate change.A cooling shelter in Oregon this summer.Maranie Staab/ReutersDoctors say they have also seen the health effects of a changing climate in their day-to-day interactions with patients.For years, Dr. Renee Salas, an emergency medicine doctor at Massachusetts General Hospital, said that she has noticed allergy seasons are lasting longer, stressing her patients with asthma and lung diseases. She thought climate change may be behind it — and science has borne out her suspicions. Studies have found that since 1990 pollen seasons have not only become longer but also contain higher pollen concentrations, and that climate change is a driving factor.“I think about climate change as a secondary diagnosis in my patients,” said Dr. Salas, a co-author of The Lancet Countdown, a report on climate change and health.The health burdens are unlikely to be shared equally.In September, a report from the Environmental Protection Agency found that although all Americans will be affected by climate change, minorities are likely to face more health risks. Black Americans, for instance, are 40 percent more likely to live in areas with the highest increases in mortality due to extreme temperature.“The same vulnerable communities that were disproportionately hurt by Covid-19 are bearing disproportionate harm from climate change,” Dr. John Balbus, the interim director of the U.S. Department of Health and Human Services’ Office of Climate Change and Health Equity, wrote in an email.Hospitals as pollutersMeanwhile, there’s been growing recognition within the health industry of its own contributions to climate change.It is estimated that the health care sector accounts for close to 5 percent of all global carbon dioxide emissions. Some of that comes from powering energy-intensive hospitals and clinics 24 hours a day, but the majority — an estimated 70 percent — is related to its supply chain and the energy required to produce, ship and dispose of the machines, pharmaceuticals and equipment used every day.Over the past decade, 43,000 hospitals and health centers in 72 countries have signed on as members of the Global Green and Healthy Hospitals, a network of organizations aimed at reducing their environmental impact.“It is a trend,” said Alison Santore, the chief advocacy and sustainability officer for Providence, the hospital chain, which is a member of the green-hospital group. “But it’s still the minority of hospitals when we look at the whole.”Last year, in the midst of the pandemic, Providence pledged to go carbon negative by 2030, meaning that the company aims to remove more carbon dioxide from the atmosphere than it adds.Solar panels being installed at the San Juan Children’s Hospital in Puerto Rico.Alvin Baez/ReutersHealth care centers and hospitals are 2.5 times as energy intensive as other buildings. Rooms and hallways are filled with computers and machines. Many items in hospitals are single-use to prevent infection. It is estimated that hospitals produce between 29 and 43 pounds of waste per patient per day.“We are called to heal, and yet we are hurting the environment,” Ms. Santore said.So far, the transition has not been easy. Beth Schenk, a registered nurse and the executive director of environmental stewardship at Providence, said that meeting the company’s goals has required rethinking every aspect of their operations. In addition to adding solar panels to roofs and transitioning to low-flow water, they’ve taken out water-intensive lawns and redesigned surgical kits.Even for the few hospitals that have made progress, significant obstacles remain. Clinica Biblica, a large hospital in San Jose, Costa Rica, achieved carbon neutrality by installing solar panels on its roof, purchasing carbon offsets, and otherwise relying on the country’s electric grid, which is powered by 99 percent renewable energy. But its commitment to becoming carbon neutral along its entire supply chain will be a major challenge when there is little transparency over the greenhouse gas emissions of overseas suppliers and waste disposal.Many health care providers are also learning that greenhouse gases can be found where you least expect them. For instance, the main ingredients in essential medical tools like anesthetic gases and inhalers are actually potent greenhouse gases, like hydrofluorocarbons.Despite their own efforts, though, health care leaders point out that it will be difficult for the industry to achieve carbon neutral goals without changes that are beyond their control, like the wider availability of renewable energy on the power grid.Burning fossil fuels costs society $5 trillion on treating chronic disease, and air pollution results in 7 million premature deaths each year, said Dr. Neira, adding that “society needs to put that in the balance.”

SharecloseShare pageCopy linkAbout sharingImage source, Getty ImagesUniversity of Oxford scientists have uncovered a gene that doubles the risk of lung failure and death from Covid.They say around 60% of people from South Asian backgrounds and 15% of people of European ancestry carry the high-risk version of the gene.Vaccines are key and help significantly reduce these risks, researchers say.The Nature Genetics study sheds light on why some communities in the UK and South Asia are at higher risk from Covid – but does not fully explain it.Building on previous genetic work, researchers used a combination of artificial intelligence and new molecular technology to pinpoint the exact gene – called LZTFL1 – responsible for the increased risks.They estimate the risky version of the gene is present in about 2% of people from African-Caribbean backgrounds and 1.8% of people of East Asian descent. Lead researcher Prof James Davies said the discovery that the risky gene does not affect all populations equally was very important.But he said a complex mix of factors – including age in particular – contributed to each person’s individual risk. South Asian Covid death rates ‘alarming’Black people ‘twice as likely to catch Covid’He added “Socio-economic factors were also likely to be important in explaining why some communities have been particularly badly affected by the pandemic.”Although we cannot change our genetics, our results show that the people with the higher risk gene are likely to particularly benefit from vaccination.”‘Derailing defences’Researchers believe the risky version of the gene makes people’s lungs more susceptible to coronavirus.They hypothesise that the high-risk gene derails a key protective mechanism that cells lining the lungs normally employ to defend themselves from Covid. When cells lining the lung interact with coronavirus, one of their defence strategies is to turn into less specialised cells and become less welcoming to the virus. This despecialisation process reduces the amount on the surface of cells of a key protein called ACE-2, which is key to coronavirus attaching itself to cells.But for people with the risky version of the LZTFL1 gene this process does not work as well, and lung cells are left vulnerable to invasion of the virus.Scientists say it is significant that the gene involved affects the lungs, but does not have an impact on the immune system. This means people at high risk can still get immune protection from the vaccine, they say.And scientists hope the discovery helps lead to new customised drugs that focus on the lungs – current ones focus mostly on the immune system.Nature.websiteCoronavirus (COVID-19) vaccines – NHS.websiteThe BBC is not responsible for the content of external sites.