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In a potential game changer for patients with type 2 diabetes, a team of researchers at the Diabetes, Obesity, and Metabolism Institute (DOMI) at the Icahn School of Medicine at Mount Sinai has identified a therapeutic target for the preservation and regeneration of beta cells (β cells) — cells in the pancreas that produce and distribute insulin. The discovery could prevent insulin resistance and thus have significant benefits for millions of people worldwide. The results of the study were published in Nature Communications in July.
All major forms of diabetes are caused by insufficient β-cell mass. When blood glucose levels rise in the body, such as in response to a high-fat diet, β cells respond by producing and releasing more insulin to bring blood glucose levels under control. But prolonged high blood glucose, known as hyperglycemia, can impair the ability of β cells to produce and secrete insulin. This results in a vicious cycle of ever-increasing glucose levels and ever-declining β-cell function, leading to β-cell death — a phenomenon known as glucose toxicity. Thus, preservation and regeneration of β cells is a therapeutic goal for diabetes.
The Mount Sinai research team found a molecular mechanism that appears to be involved in β-cell preservation and regeneration involving carbohydrate response-element binding protein (ChREBP). The researchers showed that production of a hyperactive isoform of this protein, ChREBPβ, is necessary to produce more β cells in response to an increased demand for insulin in the body due to a high-fat diet or significant glucose exposure. However, prolonged, increased glucose metabolism can result in a vicious cycle in which ChREBPβ is overproduced, resulting in glucose toxicity in the β-cells and their subsequent death.
The research team found that it was possible to counteract the effects of ChREBPβ and the β-cell death they observed by increasing expression of an alternate form of the protein, ChREBP⍺, or by activating nuclear factor-erythroid factor 2 (Nrf2) — a protein that protects cells from oxidative damage — in mice and human β cells, thus preserving β-cell mass.
“Traditionally, ChREBP was thought to be a mediator of glucose toxicity, but we noticed one form, ChREBPa, appeared to protect beta cells” said Donald Scott, PhD, a Professor of Medicine (Endocrinology, Diabetes and Bone Disease) at Icahn Mount Sinai, and a member of DOMI and of The Mindich Child Health and Development Institute. “By using tools we developed that enabled us to interrogate these isoforms independently, we found that ChREBPβ plays a key role in the gradual destruction of β cells. Thus, we believe it is a marker of hyperglycemia and glucose toxicity.”
“Moreover, we found that if you remove ChREBPβ or counteract it pharmacologically, you can mitigate the effects of glucose toxicity and protect those cells. This exciting discovery creates an opportunity to develop therapeutic agents that target this molecular mechanism, effectively block ChREBPβ production, and thus preserve β-cell mass. This would not only address the challenge that has driven diabetes research for years but also prevent patients with type 2 diabetes from becoming insulin dependent due to loss of β-cell mass, which would have a significant impact on outcomes and quality of life.”
Based on these findings, the research team is interested in exploring the impact of ChREBPβ overproduction in patients with type 1 diabetes, which differs from type 2 diabetes in that the pancreas does not produce any insulin. The team is also interested in screening for more molecular mechanisms that have the potential to block ChREBPβ production and thus prevent glucose toxicity and the subsequent death of β cells. Furthermore, there are plans to investigate whether the vicious cycle that was observed in this study occurs in other tissues in which ChREBPβ is expressed, such as kidney, liver, and adipose, or body, fat, and thus might contribute to diabetic complications.
“This study was made possible by bringing together the full breadth of DOMI expertise in areas such as RNA sequencing, three-dimensional imaging, and bioinformatics. Our findings provide a foundation for preserving existing β-cell mass and for developing new therapeutic approaches that have the potential to successfully prevent thousands of type 2 diabetes patients from progressing to insulin dependence,” said the study’s lead author Liora S. Katz, PhD, Assistant Professor of Medicine at Icahn Mount Sinai.

One injection of a candidate monoclonal antibody (mAb) known as L9LS was found to be safe and highly protective in U.S. adults exposed to the malaria parasite, according to results from a National Institutes of Health Phase 1 clinical trial published in The New England Journal of Medicine. Additional clinical trials evaluating if L9LS can prevent malaria over six to 12 months against seasonal and perennial transmission are underway in infants and children in Mali and Kenya, where malaria is endemic. The trial was sponsored by the National Institute of Allergy and Infectious Diseases (NIAID), part of NIH.
“These early clinical trial results demonstrating that a monoclonal antibody administered subcutaneously can protect people from malaria are highly encouraging,” said NIAID Director Anthony S. Fauci, M.D. “A one-time intervention that protects against malaria for six months to a year could significantly reduce morbidity and mortality among children in malaria-endemic regions and offer an effective preventive tool for health care workers, military personnel and travelers to these areas.”
Malaria is a mosquito-borne disease caused by Plasmodium parasites. The World Health Organization estimates that in 2020, about 240 million people had malaria and about 627,000 of them died. A disproportionate burden of malarial disease is seen in Sub-Saharan Africa, where children under age 5 account for approximately 80% of all malaria deaths. A vaccine to prevent malaria is now available; however, its variable efficacy underscores the need for new interventions that offer high-level protection against disease.
Scientists from NIH’s Vaccine Research Center (VRC), part of NIAID, developed L9LS and led the Phase 1 clinical trial. L9LS is a laboratory-made version of a naturally occurring antibody called L9, derived from the blood of a volunteer who had received an investigational malaria vaccine. The antibody prevents malaria by neutralizing the parasites in the skin and blood before they can infect liver cells.
L9LS is similar to a candidate anti-malarial antibody known as CIS43LS that the VRC developed and found to be highly protective in a small trial when administered by the intravenous route. However, L9LS is two to three times more potent. Increasing the potency allowed for subcutaneous injection, a more cost-effective and feasible route of administration than intravenous infusion.
The Phase 1 study was conducted from Sept. 13 to Nov. 16, 2021, at the NIH Clinical Center in Bethesda, Maryland, and the Walter Reed Army Institute of Research (WRAIR) in Silver Spring, Maryland. The trial involved 18 volunteer participants receiving various doses of L9LS subcutaneously or intravenously. After tolerating the injection and experiencing no safety concerns, the participants allowed mosquitoes carrying the malaria parasite to bite their forearm five times, starting from two to six weeks after receiving the mAb candidate. This took place in a carefully controlled setting, known as controlled human malaria infection (CHMI). As part of this approach, which has been used for decades in malaria research, medical staffers closely monitor participants and provide proper treatment if they become infected. L9LS fully protected 15 of 17 (88%) participants from malaria infection during the 21-day challenge period. All volunteers in the control group that underwent CHMI, but did not receive L9LS, became infected and were promptly treated without complications. Encouragingly, four of the five participants who received a low, subcutaneous dose of the mAb were protected from malaria.
“This is the first demonstration that a monoclonal antibody can provide protection when given by the subcutaneous route, with important implications for widespread clinical use and reaching the goal of eliminating malaria,” said Robert Seder, M.D., chief of the Cellular Immunology Section in the VRC, who led the development of L9LS. “We look forward to results in larger field studies that will help establish an effective dose.”
Lt. Cmdr. Richard Wu, M.D., staff clinician in the VRC’s Clinical Trials Program, led the Phase 1 trial. Study collaborators included scientists from the U.S. Public Health Service Commissioned Corps; the Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard University; NIAID’S Biostatistics Research Branch; WRAIR; and the University of California at San Diego.

People on a plant-based diet who do strength training as opposed to other forms of exercise such as biking or swimming may have stronger bones than other people on a vegan diet, according to new research published in the Endocrine Society’s Journal of Clinical Endocrinology & Metabolism.
About 6 percent of people in the United States are vegans. Recent research shows a plant-based diet can be associated with lower bone mineral density and increased fracture risk.
“Veganism is a global trend with strongly increasing numbers of people worldwide adhering to a purely plant-based diet,” said Christian Muschitz, M.D., of St. Vincent Hospital Vienna and the Medical University of Vienna in Vienna, Austria. “Our study showed resistance training offsets diminished bone structure in vegan people when compared to omnivores.”
The authors compared data from 43 men and women on a plant-based diet for at least five years and 45 men and women on an omnivore diet for at least five years. Omnivores eat meat as well as plant-based foods.
The researchers found vegan participants who did resistance training exercises such as using machines, free weights, or bodyweight resistance exercises at least once a week had stronger bones than those who did not. They also found vegans and omnivores who engaged in resistance training had similar bone structure.
“People who adhere to a vegan lifestyle should perform resistance training on a regular basis to preserve bone strength,” Muschitz said.
Other authors of this study include: Robert Wakolbinger-Habel of the Vienna Healthcare Group and the Medical University of Vienna in Vienna, Austria; Matthias Reinweber of the Vienna Healthcare Group; Jürgen König, Daniel König and Rochus Pokan of the University of Vienna in Vienna, Austria; and Peter Pietschmann of the Medical University of Vienna.
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Materials provided by The Endocrine Society. Note: Content may be edited for style and length.

Scientists from the Yong Loo Lin School of Medicine, National University of Singapore (NUS Medicine) have created a probiotic to restore bile salt metabolism, found in the gastrointestinal tract, to counter the onset and effects of Clostridium Difficile Infection (CDI).
CDI is the infection of the large intestine or colon that leads to infectious diarrhea, caused by an infectious bacterium known as Clostridium. Most cases of CDI have been observed to occur in those who have been taking antibiotics or just finished their course of antibiotics.
The administration of antibiotics in the treatment of CDI causes an imbalanced gut microbiome, known as dysbiosis, which can disrupt other microbiome processes such as bile salt metabolism. The dysregulation of bile salt metabolism can activate dormant Clostridioides difficile spores, leading to CDI, causing severe diarrhea and colitis — inflammation of the large intestine, or a reinfection of CDI.
A team of researchers, led by Associate Professor Matthew Chang, from the Synthetic Biology Translational Research Programme at NUS Medicine and NUS Synthetic Biology for Clinical and Technological Innovation (SynCTI), engineered a probiotic that can detect the occurrence of antibiotic-induced microbiome imbalance and express an enzyme that can regulate the bile salt metabolism upon detection. This probiotic contains a genetic circuit that comprises a genetically encoded sensor, amplifier and actuator.
The team used an E. coli probiotic strain as the host because of its proven safety record in humans and its gram-negative nature makes it compatible with the current CDI therapy that uses antibiotics targeting gram-positive bacteria. The sensor in this probiotic, detects the presence of sialic acid, a gut metabolite that is indicative of microbiome imbalance. The actuator produces an enzyme that can regulate the bile salt metabolism, activated by the sensor, and it reduces the germination of the Clostridioides difficile spores that causes CDI, when induced by the sialic acid sensor. The team also included an amplifier in the probiotic which amplifies the activation by the sensor and increases the production of the enzyme, reducing the germination of the Clostridioides difficile spores by 98%. Experiments showed that the probiotic significantly reduced CDI in laboratory models, as demonstrated by a 100% survival rate and improved clinical outcomes.
Assoc Prof Chang is encouraged by this advancement that sheds more light on the gut environment and how it can be manipulated to create less invasive treatment strategies. He says, “This scientific innovation gives a better understanding on how we can control the microenvironment in the body, without needing to exert direct lethality to kill the Clostridioides difficile bacterium, give additional drugs, or use invasive methods to rid the infection. Our perspectives have shifted towards studying how we can come up an antimicrobial strategy to complement and assist the natural biological processes in the body to help limit the onset of infection. This is useful when considering the development or improvement of future therapeutics for CDI.”
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Materials provided by National University of Singapore, Yong Loo Lin School of Medicine. Note: Content may be edited for style and length.

A new study in mice has revealed never-before-seen details about how the complicated visual network forms in them. This research could inform future research into the treatment of congenital blindness. But given the parallels between biological neural tissue and digital artificial intelligence, this research could also help software engineers develop better and more general-purpose artificial intelligences.
If you could see the weblike nature of the neurons and structures that make up the brain and sensory systems of animals, you might think it’s just a random complicated mess. But researchers such as neuroscientists are able to look at this chaos and deduce not only discrete structures, but also ascertain their functions. Recently, Professor Kenichi Ohki and Assistant Professor Tomonari Murakami from the University of Tokyo’s Department of Physiology and their team have been studying a particular formation to learn how it forms — the vision system.
“The eyes, certain parts of the brain and the neural network connecting these form the vision system. A crude analogy might be a camera connected by a wire to a screen that your conscious self can watch. But an accurate biological description of this system is extremely complicated,” said Murakami. “There is a large number of visual cortical areas involved and these are arranged in layers which form a sort of hierarchical structure. This idea is not new, but it was not known how connections between the early stages of this network, or primary areas, and areas involved in the processing of visual signals, or higher visual cortical areas, form during development. We set out to find out how this happens.”
The team studied the developing vision systems of mice. In particular they looked at areas the called cortical and thalamic regions. By seeing how networks of neurons in these regions developed in newborn mice, and when these networks became active, the team was able to describe in a more general way the mechanisms governing the growth of the vision system.
“As we recorded the increasingly dense network of connections in time, something jumped out that surprised us,” said Murakami. “We expected the visual network to form a lot of connections among the cortical area first, reflecting the hierarchical structure of the whole system. But in fact, parallel neural pathways from the retinas in the eyes leading up to the cortical areas form earlier than those among cortical areas. This new fact changes what we know about this area of cortical development.”
This study was done not only to satisfy curiosity, but also because fundamental research of this kind can form the foundation of future medical research which can improve peoples’ lives: in this case, the team’s hypothesis that their research in mice can likely explain visual development in primates, including humans. And this in turn could help researchers aiming to treat congenital blindness.
“There is another field of research that can learn from what we have done here as well,” said Ohki. “Artificial intelligence is often based on digital artificial neural networks. These are usually structured in multiple layers, which can give them complex functionality. But now that we’ve shown at least some biological neuronal systems develop parallel structures prior to layered ones, software engineers might gain inspiration from this to experiment with new design methodologies. It is conceivable this might help them in their goal of creating ever more general-purpose intelligences capable of solving a wide variety of problems.”
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Materials provided by University of Tokyo. Note: Content may be edited for style and length.

A specific group of bacteria-killing proteins inside the immune system could hold the key to developing smarter and more effective drugs capable of eliminating certain infectious diseases including meningitis, pneumonia and sepsis, according to scientists from The Australian National University (ANU).
In a new study published in Nature Communications, the ANU researchers demonstrate the potential of these immune proteins, known as guanylate-binding proteins (GBPs), to directly bind to and kill specific types of bacteria.
In addition to laying the foundation for new treatments, these killer proteins can also be used in combination with existing antibiotics to give doctors more options when treating certain types of infectious diseases.
Lead author and PhD scholar Shouya Feng, from The John Curtin School of Medical Research (JCSMR) said this specific type of protein works by “busting open” bacteria — similar to an axe splitting wood in two — destroying the membrane and causing it to die.
“Our immune system is equipped with weapons that can destroy germs. When foreign bodies, such as bacteria, enter our body the immune system triggers a defensive response,” Ms Feng said.
“We believe we can extract and harness the power of these immune system proteins, known as GBP1, and use them to treat a range of infectious diseases, without negatively affecting our body’s cells.”
Co-author Professor Si Ming Man, also from JCSMR, said disease-causing microbes are continually adapting to and outsmarting current drug treatments, and scientists are always looking to uncover new ways to develop more effective solutions.

Commonly used in medicine as an anaesthetic, ketamine is also increasingly prescribed to relieve depressive symptoms. This very fast-acting psychotropic drug is particularly indicated for the treatment of patients resistant to conventional antidepressants. However, its prescription has been the subject of debate: some believe that it presents a strong addictive risk. A team from the University of Geneva (UNIGE) has investigated this by administering the drug to mice. While it triggers an increase in dopamine in their brains — like all drugs — it also inhibits a specific receptor that precludes the progression to addiction. These results can be found in the journal Nature.
Discovered in 1962 by the American chemist Calvin Lee Stevens, ketamine is a synthetic drug derived from phencyclidine with powerful anaesthetic properties. It is commonly used in human and veterinary medicine, particularly for pain relief and brief sedation. It is also used illicitly for recreational purposes, its dissociative effect inducing an altered perception of reality.
For the past ten years or so, ketamine has also been prescribed to treat the depressive symptoms of people who are resistant to conventional treatments. Its action has the advantage of being very rapid: its effect is felt a few hours after the first dose, whereas traditional antidepressants take several weeks to act. Although its prescription is increasing for this type of treatment, this substance is still widely debated within the scientific community.
”Some people believe that ketamine presents a strong addictive risk if taken for a long time, others do not. The whole point of our research was to try to provide some answers,” explains Christian Lüscher, a Full Professor in the Department of Basic Neurosciences at the UNIGE Faculty of Medicine and a specialist in the mechanisms underlying addiction.
Addiction vs. Dependence
Addiction is defined as the compulsive use of a substance despite its negative consequences (behavioural disorder). Dependence, on the other hand, is characterised by the appearance of one or more withdrawal symptoms on abrupt cessation of use (physiological disorder). Dependence — the physical manifestations of which vary greatly depending on the drug — affects everyone. Addiction, on the other hand, affects only a minority of people and is not caused by all drugs.

A research team from the lab of Quing Zhu, the Edwin H. Murty Professor of Engineering in the Department of Biomedical Engineering at the McKelvey School of Engineering at Washington University in St. Louis, has combined optical coherence tomography (OCT) and machine learning to develop a colorectal cancer imaging tool that may one day improve the traditional endoscopy currently used by doctors.
The results were published in the June issue of the Journal of Biophotonics.
Screening for colon cancer now relies on human visual inspection of tissue during a colonoscopy procedure. This technique, however, does not detect and diagnose subsurface lesions.
An endoscopy OCT essentially shines a light in the colon to help a clinician see deeper to visualize and diagnose abnormalities. By collaborating with physicians at Washington University School of Medicine and with Chao Zhou, associate professor of biomedical engineering, the team developed a small OCT catheter, which uses a longer wavelength of light, to penetrate 1-2 mm into the tissue samples.
Hongbo Luo, a PhD student in Zhu’s lab, led the work.
The technique provided more information about an abnormality than surface-level, white-light images currently used by physicians. Shuying Li, a biomedical engineering PhD student, used the imaging data to train a machine learning algorithm to differentiate between “normal” and “cancerous” tissue. The combined system allowed them to detect and classify cancerous tissue samples with a 93% diagnostic accuracy.
Zhu also is a professor of radiology at the School of Medicine. Her team worked with Vladimir Kushnir and Vladimir Lamm at the School of Medicine, Zhu’s team of PhD students, including Tiger Nie, started a trial in patients in July 2022.
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Materials provided by Washington University in St. Louis. Original written by Brandie Jefferson. Note: Content may be edited for style and length.

A high school athlete got desperately sick and needed life support. Years later, she helped discover the cause of her rare illness.The 21-year-old woman gasped as she read the headline: “The 16-Year-Old Girl Who Walks and Eats Tacos While on Life Support.” She scanned the article about a girl who had a mysterious illness that destroyed her lungs and who now needed a machine to breathe for her. “I need to do something,” she told herself once she finished the article. She believed she knew what was killing this young girl, because the story could have been her own, six years earlier. Back then, she was a high school junior on the starting lineup of the girls’ volleyball team. Just days into the new school year, she developed a 103-degree fever and sore throat. Her doctor, in tiny Thief River Falls, Minn., figured she had some type of viral infection and predicted she would feel better after a few days of rest. He was wrong. The fever resolved but was replaced with the most profound fatigue the girl had ever known. Just getting out of bed left her breathless. Her mother took her to the nearest emergency room, 25 miles away. As the nurse checked the young woman’s vital signs, she looked alarmed. The patient’s oxygen saturation, which would normally be well over 90 percent, was in the 60s, dangerously low. The nurse slapped an oxygen mask over her nose and mouth and reached out to the doctor in charge. A chest X-ray showed a gray cloud invading her lungs. Minutes later she was in an ambulance headed for the Sanford Medical Center in Fargo, N.D., the closest hospital with a pediatric intensive-care unit. In Fargo she was started on several broad-spectrum antibiotics. The doctors there didn’t know which bug was causing this pneumonia, but until they did, they figured these antibiotics should protect her. But she continued to worsen, and within days needed to be put on a ventilator. When even that wasn’t enough, the doctors at Sanford contacted the Mayo Clinic in Rochester, Minn. Eight days after she walked into the E.R., the patient’s lungs were hardly working at all. The next step was an artificial-heart-and-lung machine known familiarly as ECMO — short for extracorporeal membrane oxygenation. This device, about the size of a refrigerator, acts as a lung to remove the carbon-dioxide waste product from the blood and replace it with oxygen and then as a heart to recirculate the oxygenated blood back through the body. The ECMO team from the Mayo Clinic flew out to Fargo with their machine, attached the young woman to the device and flew back with her to the Mayo Clinic Hospital. That machine breathed for her for the next 116 days.Months on the Transplant List Like the girl in the article, she, too, had walked while connected to the massive machine. She, too, had eaten while on the machine, though not tacos. The first thing to pass her lips was a communion wafer when she finally felt well enough to walk at least part of the way to the hospital chapel surrounded by a squad of doctors, nurses and technicians. They never figured out why her lungs failed. She spent months on the transplant list, waiting for a new heart and lungs to replace the ones her doctors thought would never recover. But they did. And finally, after seven months in the hospital, she was able to go home. For a few years afterward she returned to Mayo every six months for a checkup. During those visits, she always stopped by the pediatric intensive-care unit to see the nurses who had become a second family to her in the months she hovered near death. At one visit, two years after her own time in the hospital, several nurses told her about a child whose illness seemed remarkably like her own.Hours later she and her parents met with this child’s parents, who told the story of their daughter, just 12 years old, whose lungs had simply stopped working after what looked like a viral illness. The families compared notes to see if there were any similarities between the two children’s lives and exposures. They lived in different environments — one rural, one urban — in different parts of the state. Nothing seemed to match, until finally the child’s parents reported that in the weeks before coming to the hospital, their daughter had been taking an antibiotic: trimethoprim-sulfamethoxazole (TMP-SMX), known under the brand name Bactrim. The young woman gasped. She had been taking this antibiotic (in her case to treat acne) — right up to the day she went to the E.R. Since then, another family contacted her with a familiar story: A healthy, active adolescent gets desperately sick, with lungs so damaged that he needed life support. She asked these parents if their son was taking TMP-SMX when he got sick. Yes, came the amazed reply. That made a total of three cases. Maybe she had found a real connection.And now there was this young woman in the news. Her name was Zei Uwadia. The article named Dr. Jenna Miller as the pediatric I.C.U. specialist at Children’s Mercy Hospital in Kansas City, Mo., who was taking care of Uwadia. The young woman found an email address for the doctor and immediately sent her a note. “I began taking Bactrim for acne about 3-4 weeks prior to [my] acute lung failure,” she wrote. “This happened to at least 3 children between 12-20 years [old]. … The similarities between our cases are uncanny.” She asked if Uwadia had been taking TMP-SMX too. Photo illustration by Ina JangThe Same Unusual PatternMiller was astonished. Indeed, the girl was taking TMP-SMX when she got sick. Could there be a link? Miller reached out to a friend, Dr. Jennifer Goldman, who was a pediatrician trained in infectious disease and clinical pharmacology. She had been doing research on adverse reactions to this drug for years. TMP-SMX is an effective, safe and inexpensive drug and, because of that, is the sixth-most-prescribed antibiotic in the country. It could be a coincidence that these four people, a tiny fraction of the millions on this medicine on any given day, got sick. Still, the doctors agreed that they should investigate. The two pediatricians collected the medical records of the patient who sent the email and the other cases she had found. All were healthy young people who developed a devastating lung injury after a brief flulike illness often with a fever, sore throat or cough. And all had taken TMP-SMX.What convinced the doctors that there was a link were the biopsies of the affected lungs. Each showed the same unusual pattern of focused destruction: The only cells within the lung that were affected were those in which carbon dioxide was taken up and oxygen supplied — the cells that do the most important work of breathing. In two, including the patient who first noted the connection between her illness and the drug, these essential cells eventually grew back, allowing them to once again breathe on their own. Others whose lung tissue did not recover needed a lung transplant. Of those first cases, two died: the 12-year-old that the young woman met at Mayo and Uwadia, the girl in the news story. In the four years since Miller received the patient’s email, she and Goldman have identified a total of 19 patients, most under age 20, who had this reaction after being treated with TMP-SMX. Six died. It is still unclear how the antibiotic triggers this rare but devastating destruction. Goldman thinks it is probably some kind of allergic reaction. But they still cannot predict who is at risk, or why. As an I.C.U. doctor, Miller tells me, she uses this drug frequently. And although these cases are rare, the devastation caused is terrible. “Most of these people,” she says, referring to the 19 cases, “were not getting treated for a life-threatening illness, and yet they were given this ordinary drug — and it ended their life or changed it forever.”This original patient shares Miller’s mixed feelings. She is 26 now and is a nurse who cares for patients who have just had a heart-and-lung transplant. She regularly gives her patients TMP-SMX. And they need it — to treat diseases they have and to prevent diseases they might get. Yet she knows that, because of her reaction to that drug, her lungs will never be the same. She can play a friendly game of volleyball but gets winded after climbing a couple flights of stairs. Still, she has a good life. And she is proud to have made a contribution to the science that she hopes will, one day, prevent this from happening to anyone else.Lisa Sanders, M.D., is a contributing writer for the magazine. Her latest book is “Diagnosis: Solving the Most Baffling Medical Mysteries.” If you have a solved case to share, write her at Lisa.Sandersmdnyt@gmail.com.

A far-reaching review of academic papers and reports evaluated 46 proposed “win-win” solutions for reducing human infectious disease burdens and advancing conservation goals, which now can be explored on a publicly available website. The study highlights diverse and widespread bright spots where there could be opportunities to simultaneously safeguard human and ecosystem health.
Nearly 30 researchers from across the United States and overseas conducted the study, which appears in The Lancet Planetary Health. The interdisciplinary team included academic researchers, practitioners at government and nonprofit organizations, and veterinarians.
Skylar Hopkins, an assistant professor of applied ecology at NC State and corresponding author of the study, said the interdisciplinary group worked on this synthesis for four years. They painstakingly searched the existing academic literature for potential solutions and then developed a new process for determining whether a specific “win-win” solution is safe, feasible and cost-effective. They found that the solutions have varied levels of evidence for success; some have strong support already and others are ripe for further study.
“We like to think of these solutions like options on a bespoke menu. To select and design a solution that meets your needs, you’re going to need a lot of information. So we provide an evidence summary for each solution,” Hopkins said. “We also created a decision process that anyone can follow, so researchers and decision makers can design their own solutions or evaluate whether an existing solution will work in their situation.”
But Hopkins said that it wasn’t easy to evaluate some of the potential solutions.
“Sometimes the evidence for a potential solution conflicted,” Hopkins said. “One study would suggest that an intervention would reduce human disease burdens and another study would suggest that the same intervention would increase human disease burdens. Potential solutions could also have trade-offs or collateral impacts, where the intervention was good for some people but not others.” The team had to develop a method for quantifying evidence diversity, consistency and applicability to deal with these complications.