Publisher Health

A new study in mice by UCLA scientists reveals how exposure to traffic-related air pollutants causes cellular changes in the placenta that can lead to pregnancy complications and affect the health of both mother and offspring.
The researchers found that the cellular changes caused by chronic exposure to air pollutants were related to immune activation by foreign substances entering the blood from the lungs. This immune response attacks some of the placental cells that are required to maintain the placenta structurally, and most importantly, the blood flow from mother to developing baby.
Although previous research has analyzed the effect of air pollution on pregnancy, those studies did not utilize cell-specific methods or focus on molecular signatures of the placenta. This study is the first to assess how such exposure can negatively affect the placenta, leading to adverse outcomes in pregnancy.
One group of female mice was exposed to environmental air pollutants nasally starting two months before conception and during pregnancy, while the control group of mice was exposed to saline. By the end of the study, tissue samples indicated that inhaled air pollutants had compromised the composition of the placental cells and molecular signatures. Researchers also identified inflammation in the mucosal lining of the uterus triggered by pollution.
The placenta is essential for a successful pregnancy and for maintaining the health of both the mother and the baby. These study findings suggest that maternal cells of immunity may be responsible for destruction of vital vascular cells in the placenta. This auto-destruction of placental structures can disrupt the maintenance of a healthy pregnancy or at least affect nutrient supply from the mother to the baby, with the potential for adverse pregnancy consequences or outcomes such as preterm labor or uteroplacental insufficiency as encountered in pre-eclampsia.
“The cellular changes we have observed could provide the missing link between exposure to air pollutants and adverse pregnancy outcomes, thereby helping to focus development of preventive strategies for at-risk pregnancies,” said Dr. Sherin Devaskar, lead author of the study and physician-in-chief of UCLA Mattel Children’s Hospital and distinguished professor of pediatrics at the David Geffen School of Medicine at UCLA.
The research also underscores the need to examine the timing of exposure and whether acute v. chronic exposures have different effects. The authors also plan to study dietary interventions to alleviate distress on placental molecular signatures, nutrient supply and development.
The collaborative study also involved Dr. Suhas G. Kallapur, chief of neonatology and developmental biology; Amit Ganguly, staff research associate; Shubhamoy Ghosh, PhD, assistant project scientist; Monica Cappelletti, PhD, adjunct assistant professor of pathology and laboratory medicine, all four in the department of Pediatrics-Neonatology at UCLA; Matteo Pellegrini, a professor of molecular, cell and developmental biology at UCLA and Anela Tosevska, PhD, bioinformatics scientist in the division of rheumatology, internal medicine at Medical University of Vienna, Austria.
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Maya Cohen’s entree into the world of obesity medicine came as a shock.In despair over her weight, she saw Dr. Caroline Apovian, an obesity specialist at Brigham and Women’s Hospital, who prescribed Saxenda, a recently approved weight-loss drug. Ms. Cohen, who is 55 and lives in Cape Elizabeth, Maine, hastened to get it filled.Then she saw the price her pharmacy was charging: $1,500 a month. Her insurer classified it as a “vanity drug” and would not cover it.“I’m being treated for obesity,” she complained to her insurer, but to no avail.While Ms. Cohen was stunned by her insurer’s denial, Dr. Apovian was not. She says it is an all too common response from insurers when she prescribes weight-loss drugs and the universal response from Medicare drug plans.Obesity specialists despair but hope that with the advent of highly effective drugs, the situation will change.Novo-Nordisk, the maker of the medicine Dr. Apovian prescribed, and patient advocacy groups have been aggressively lobbying insurers to pay for weight-loss drugs. They also have been lobbying Congress to pass a bill that has languished through three administrations that would require Medicare to pay for the drugs.But for now, the status quo has not budged.No one disputes the problem — more than 40 percent of Americans have obesity, and most have tried repeatedly to lose weight and keep it off, only to fail. Many suffer from medical conditions that are linked to obesity, including diabetes, joint and back pain and heart disease, and those conditions often improve with weight loss.“The evidence is now overwhelming that there are physical changes in weight regulating pathways that make it difficult for people to lose weight and maintain their weight loss,” said Dr. Louis Aronne, an obesity medicine specialist who directs of the comprehensive weight control center at Weill Cornell Medicine. “It’s not that they don’t have willpower. Something physical is holding them back.”Ms. Cohen in 2016.via Maya CohenDr. Aronne and other obesity medicine specialists emphasize that obesity is a chronic disease that should be treated as intensively as heart disease, diabetes, high blood pressure or any other chronic illness are. But, they say, that rarely happens.“Access to medicines for the treatment of obesity is dismal in this country,” said Dr. Fatima Cody Stanford, an obesity medicine specialist at Massachusetts General Hospital and Harvard Medical School.But even if a patient’s insurer will cover weight loss drugs, most doctors do not suggest the drugs and most patients do not ask for them, as they fail to realize there are good treatment options, said Dr. Scott Kahan, an obesity medicine specialist in Washington, D.C. And, he added, even if doctors and patients know there are F.D.A. approved drugs, many think they are “unsafe or not well studied and that everyone regains their weight.”The medical system bears much of the blame, Dr. Stanford said. Just 1 percent of doctors in the United States are trained in obesity medicine. “It’s the biggest chronic disease of our time, and no one is learning anything about it,” she said.Data on medication use by patients predate the newer, more effective and safe drugs made by Novo Nordisk and Eli Lilly. Still, obesity medicine doctors say, they doubt that the number has changed much from the earlier studies that found that less than 1 percent who are eligible obtained one of these drugs. That is the about the same percentage as those who get bariatric surgery which most insurers, including Medicare, pay for.“The perception is, ‘If you are heavy, pull yourself up from your bootstraps and try harder,’” Dr. Kahan said.And that, he adds, is a perception many patients, as well as doctors, share, making them reluctant to seek medical help or prescription medications.Then there is the problem Ms. Cohen ran into: Insurers that do not cover weight-loss drugs.But some obesity specialists have found a strange workaround to get an effective but expensive Novo Nordisk drug for patients with obesity whose insurers will not pay.Ozempic, or semaglutide, is often covered by insurance companies as a diabetes drug.Ryan David Brown for The New York TimesMs. Cohen took a mix of prescription weight-loss pills.Ryan David Brown for The New York TimesThe workaround exploits quirks in the way Novo Nordisk markets its drugs. The company sells a drug, semaglutide, for both diabetes and for obesity. As a diabetes drug, it is called Ozempic and has a list price of $892 for four weeks. It is easily available at pharmacies, and insurance companies cover it for people with diabetes.Novo Nordisk sells two weight loss drugs that are of the same class in two doses — liraglutide as Saxenda, and semaglutide at a higher and more effective dose as Wegovy. The list price — the suggested retail price — for both is about $1,350 a month. That means the same drug costs 51 percent more if it is used to treat obesity than if it is used for diabetes.But as an obesity drug, it is hard to get.Not only do most U.S. insurers decline to pay for Saxenda or Wegovy because they are weight-loss drugs, but Wegovy supplies are so limited that the company has asked doctors not to start new patients on it.Eli Lilly has a similar and seemingly more powerful weight-loss drug, tirzepatide, which it hopes to get approved for people with obesity. It was recently approved to treat diabetes under the name Mounjaro. As a diabetes drug, its retail price is $974 a month.Douglas Langa, an executive vice president at Novo Nordisk, said the Wegovy supply problem was caused by a manufacturing issue that should be resolved later this year.He also said that diabetes and obesity were “separate categories, separate marketplaces” to explain the difference in price between the companies’ two drugs that were based on the same medicine, semaglutide. He said Wegovy’s price “reflects efficacy and clinical value in this area of unmet need.”Dr. Stanford was appalled.“It’s unbelievable,” she said, adding that it was a gross inequity to charge people more for the same drug because of their obesity. She finds herself in an untenable situation: getting excited when her patients with obesity also have diabetes because their insurers pay for the drug.Dr. Apovian says she too finds herself rejoicing when patients have high blood sugar levels — and that was what ultimately resolved Ms. Cohen’s problem.Her insurance company would cover Ozempic, but it would not cover Saxenda. So she started taking Ozempic, with a $70 a month copay.Ms. Cohen — who measured at five feet fall and weighed 192 pounds when she saw Dr. Apovian — had a dramatic response to Saxenda. She has lost 54 pounds and now weighs 138 pounds. Her waist size, which was 46 inches, is now 33 inches. She has more energy and her joints do not hurt.“It has absolutely changed my life,” Ms. Cohen said.

After Kim Gyoo-sik was named an artist of the year in a national contest, he learned he had late-stage cancer. But even now, he’s thinking of ideas for a new project.This piece is one of 10 winners of our 2022 Profile Contest. You can find more here. Nathan Ko, the author, is 17 and goes to the The Loomis Chaffee School in Windsor, Conn.Told He Had Six Months to Live, He Opened an Art ExhibitBy Nathan KoIn 2019, the South Korean photographer Kim Gyoo-sik was recognized as an artist of the year by the Korean company KT&G. He modestly describes his popularity prior to this recognition as a “small group of committed fans.”During his rising fame, doctors diagnosed him with late-stage gastric cancer. After they told him he had six months to live, he claimed his life insurance policy and set out to live the rest of his life to the fullest. He opened his art exhibit in 2021 not only to explore abstract images through photography but also to find meaning during a time of hardship.The following interview has been translated from Korean and edited for clarity.Mr. Kim with his work “nonpicture series n-3.”Nathan KoTell me about yourself.I’m a photographer who uses gelatin silver print, basically black-and-white photography. Most contemporary artists no longer use this medium.The complicated, slow and restricted process of black-and-white photography is inconvenient. I was curious about the contemporary changes occurring in the photo production process. Thus, in my latest series, I focused on each production stage, highlighting the role of black-and-white photography in contemporary art. My work is considered relatively unconventional, which has allowed me to receive positive attention.At the highest point of your career, you were diagnosed with cancer. Your suffering worsened due to the pandemic. I can only imagine the range of emotions you felt.When I was given six months to live, I was miserable. I’ve had many fevers during my battle with cancer. At the beginning of the pandemic, concerns about Covid-19 symptoms, such as fevers, meant that I missed out on chances for desperately needed treatment.I initially thought that preparing for my solo exhibition would be more fruitful than continuing chemotherapy, as the treatment felt painful and insufficient. Then, a friend of mine who is a surgeon convinced me to undergo surgery that many hospitals didn’t endorse at that time. The operation was incredible, and at the end of the seven-hour procedure, all of the doctors in the room applauded. Thanks to the surgery, I’m still here.New Developments in Cancer ResearchCard 1 of 6Progress in the field.

The study of autophagy — the recycling and repair process within cells — has huge potential to aid in fighting the ageing process, bacterial and viral infections and diseases including cancer, Alzheimer’s and Parkinson’s.
A team of researchers led by Professor Ioannis Nezis from the School of Life Sciences at the University of Warwick, has identified the molecular and cellular mechanisms that regulate selective autophagy in the fruit fly Drosophila melanogaster.
While the function of these processes is increasingly understood in mammals this is one of the first studies in insects.
The study opens new avenues in our understanding of the regulation of Golgi complex turnover by selective autophagy.The Golgi complex is a stack of flat sacs formed by membranes inside the cell. It prepares proteins and fat molecules for transportation and use in other places inside and outside the cell.
Professor Nezis and his team used gene editing, confocal and electron microscopy to identify a novel type of selective autophagy, termed Golgiphagy, meaning how cells degrade a cell organelle called Golgi complex by autophagy.
In the paper, ‘GMAP is an Atg8a-inteacting protein that regulates Golgi turnover in Drosophila’ published today in the journal Cell Reports, PhD students Ashrafur Rahman, Raksha Gohel and colleagues describe how gene editing was used to create fruit flies unable to process specific proteins by autophagy.
Comparison of the gene edited flies with their wild type counterparts showed:- That Atg8a’s LDS docking site is important in the execution of selective autophagy That selective autophagy regulates the size and morphology of the Golgi apparatus That the GMAP (Golgi microtubule-associated protein) protein interacts with Atg8a and the LIR motif at position 320-325 is important for this interaction That GMAP’s LIR motif is important GolgiphagyLead author of the research Professor Ioannis Nezis from the School of Life Sciences at the University of Warwick, said:
“Understanding the molecular mechanisms of selective autophagy of Golgi complex in cells will help open new avenues of research that will assist elucidating the underlying cellular mechanisms of diseases.”
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People with both Type 1 and Type 2 diabetes are prone to tooth decay, and a new study from Rutgers may explain why: reduced strength and durability of enamel and dentin, the hard substance under enamel that gives structure to teeth.
Researchers induced Type 1 diabetes in 35 mice and used a Vickers microhardness tester to compare their teeth with those of 35 healthy controls over 28 weeks. Although the two groups started with comparable teeth, enamel grew significantly softer in the diabetic mice after 12 weeks, and the gap continued to widen throughout the study. Significant differences in dentin microhardness arose by week 28.
“We’ve long seen elevated rates of cavity formation and tooth loss in patients with diabetes, and we’ve long known that treatments such as fillings do not last as long in such patients, but we did not know exactly why,” said Mohammad Ali Saghiri, an assistant professor of restorative dentistry at the Rutgers School of Dental Medicine.
The study advances a multiyear effort by Saghiri and other researchers to understand how diabetes affects dental health and to develop treatments that counter its negative impact. Previous studies have established that people with both types of diabetes have significantly elevated rates of most oral health issues, both in the teeth and the soft tissues that surround them. Saghiri and other researchers also have demonstrated that diabetes can interfere with the ongoing process of adding minerals to teeth as they wear away from normal usage.
“This is a particular focus of mine because the population of people with diabetes continues to grow rapidly,” Saghiri said. “There is a great need for treatments that will allow patients to keep their teeth healthy, but it has not been a major area for research.”
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Materials provided by Rutgers University. Original written by Andrew Smith. Note: Content may be edited for style and length.

A new University of California, Irvine-led study identifies sex-specific circuits of muscle signaling to other tissues and that the organs and processes muscle impacts are markedly different between males and females. This new discovery provides insight into how muscle functions, such as exercise, promote healthy longevity, metabolism and improve cognition.
The study, titled, “Genetic variation of putative myokine signaling is dominated by biologic sex and sex hormones,” published in eLife, is the first to evaluate how genetic architecture influences muscle signaling to other tissues, highlighting that sex and estrogens are critical determinants of these processes.
“Muscle is critical for maintaining metabolic state and disruption of muscle function is a hallmark of diseases such as obesity, type 2 diabetes and cardiovascular disease,” said senior author Marcus M. Seldin, PhD, assistant professor of biological chemistry at UCI School of Medicine.
Muscles secrete proteins called myokines, which play roles in a variety of processes by interacting with other tissues. Essentially, myokines allow skeletal muscles to communicate with organs such as the kidneys, the liver or the brain, which is essential for the body to keep its metabolic balance. Some of the process myokines are involved include inflammation, cancer, the changes brought about by exercise, and even cognition. Despite the clear relevance of myokines to so many physiological outcomes, the way these proteins are regulated and their effects are not well understood.
For this study, the research team performed a survey of genetic correlations focused on myokine gene regulation, muscle cell composition, cross-tissue signaling and interactions with genetic sex in humans. While expression levels of a majority of myokines and cell proportions within skeletal muscle showed little relative differences between males and females, nearly all significant cross-tissue enrichments operated in a sex-specific or hormone-dependent fashion; in particular, with estradiol. These sex- and hormone-specific effects were consistent across key metabolic tissues: liver, pancreas, hypothalamus, intestine, heart, visceral and subcutaneous adipose tissue. This study highlighted a few examples such as that muscle signals more to the pancreas in females, compared to males where liver is dominant.
“We already know that skeletal muscle plays an integral role in coordinating physiologic homeostasis. In this study, we sought to understand how muscle interacts with metabolic tissues and illustrate the importance of considering the effects of genetic sex and sexual hormones when studying metabolism,” said Seldin.
Moving forward, the research team plans to generate cell-based systems to evaluate some of the new hormones uncovered as part of this study and investigate why they signal differently between sexes.
This work was supported by the National Institutes of Health.
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Scientists have shed new light on the effects that high-intensity interval training (HIIT) has on human skeletal muscle, according to a study in men published today in eLife.
The findings suggest that HIIT boosts the amount of proteins in skeletal muscle that are essential for energy metabolism and muscle contraction, and chemically alters key metabolic proteins. These results may explain the beneficial effects of HIIT on metabolism and pave the way for additional studies exploring how exercise impacts these processes.
“Exercising has many beneficial effects that can help prevent and treat metabolic diseases, and this is likely the result of changes in energy use by skeletal muscles. We wanted to understand how exercise alters the muscles’ protein content and how it regulates the activity of these proteins through a chemical reaction called acetylation,” says first and co-corresponding author Morten Hostrup, Associate Professor at the Department of Nutrition, Exercise, and Sports at the University of Copenhagen, Denmark. Acetylation occurs when a member of the small molecule group, acetyl, combines with other molecules, and can affect the behaviour of proteins.
For their study, the team recruited eight healthy, untrained male volunteers to complete five weeks of high-intensity cycling training. The men worked out three times per week, finishing four minutes of cycling at a target rate of more than 90% of their maximum heart rate followed by a two-minute rest. They repeated this pattern four to five times per workout.
Using a technique called mass spectrometry, the team analysed changes to the composition of 3,168 proteins in tissue samples collected from the participants’ thighs before the study and after they completed the training. They also examined changes relating to 1,263 lysine acetyl-sites on 464 acetylated proteins.
Their analyses showed an increase in the production of proteins used to build mitochondria, which produce energy in cells, and in proteins related to muscle contractions. The team also identified increased acetylation of mitochondrial proteins and enzymes that are involved in the production of cellular energy. Additionally, they observed changes in the amount of proteins that reduce the skeletal muscle’s calcium sensitivity, which is essential for muscle contractions.
The results confirm some well-known changes to skeletal muscle proteins that occur after exercise, as well as identify new ones. For example, the reduced calcium sensitivity may explain why it can be harder for muscle contraction to occur after an athlete becomes fatigued. The work also suggests that exercise-induced changes in the regulation of proteins through acetylation may contribute to boosting metabolism.
“Using state-of-the-art proteomics technology, our study provides new information about how skeletal muscle adapts to exercise training, including the identification of novel exercise-regulated proteins and acetyl-sites,” concludes co-corresponding author Atul Deshmukh, Associate Professor at the Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen. “We hope our work will stimulate further research into how exercise helps improve metabolic health in humans.”
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The mental workload of intensive care unit nurses can successfully be evaluated using eye-movement tracking glasses.
In research recently published in Human Factors: The Journal of the Human Factors and Ergonomics Society, Nima Ahmadi, a lecturer in the Department of Industrial and Systems Engineering at Rensselaer Polytechnic Institute, and researchers at the Center for Outcomes Research at Houston Methodist employed eyetracking and physiological monitoring technologies to investigate cognitive load and visual search of stressed nurses. The collected data — ocular and physiological responses — from entire 12-hour nursing shifts were analyzed to evaluate the cognitive loads between day and night shifts as well as to compare the beginning with the middle and the end of shifts. Furthermore, the impact of stress on nurses’ visual search was assessed.
His research detected no significant difference in the cognitive levels of the nurses who worked the day shift compared to those working overnight. However, Dr. Ahmadi found that the start of working shifts is more cognitively demanding than the middle and end of ICU shifts, and stressed nurses had shortened fixation, which was accompanied by more sporadic gaze behavior
“This is the first naturalistic study that employs an eye-tracking technology in behavior assessment of critical care nurses,” Dr. Ahmadi said. “Analyzing this rich dataset may shed light on major contributors to nurses’ high-stress and demanding episodes and will pave the way for effective interventions to address providers’ mental health. We believe this research will provide foundational knowledge that could inform the design of real-time stress monitoring and burnout mitigation systems.”
Nurses who work in intensive care units have particularly high workloads that could lead to cognitive overload and medical errors. To support nurses and enhance patients’ outcomes, continuous unintrusive measurements of mental workload and stress are necessary. Previous nursing studies have measured cognitive/mental stress namely through self-reported instruments or by using metrics such as patient-nurse ratios or patients’ acuity scores; these methods fail to capture fluctuation in workload or stress and do not address the general gap in real-time monitoring.
Dr. Ahmadi’s study is the first naturalistic study that attempted to investigate workload and stress in the ICU using ocular metrics and physiological responses including pupil diameter, gaze entropy, fixational, and saccadic eye movements. “Outcomes from this and the follow-up studies will elucidate the complexity of care in ICU and its potential impact on patient safety, and provide much-needed support for providers’ mental health,” Dr. Ahmadi said. Next steps for this research would be to use machine learning tools to pinpoint moments of stress and communicate them in real-time to nurse leaders to address complex care delivery needs for critically ill patients.
The principal investigator for this research was Farzan Sasangohar from Texas A&M University and Houston Methodist. The study received a grant from the Dyer Foundation. Dr. Ahmadi was joined in the paper, “Quantifying Workload and Stress in Intensive Care Unit Nurses Using Naturalistic Evaluation of Clinical Care Delivery,” by Jing Yang and Denny Yu Ph.D. from Purdue University, Valerie Danesh from the University of Texas at Austin, Faisal Masud MD, FCCP, FCCM and Steven Klahn from Houston Methodist.
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We hear a lot about how climate change will change the land, sea, and ice. But how will it affect clouds?
“Low clouds could dry up and shrink like the ice sheets,” says Michael Pritchard, professor of Earth System science at UC Irvine. “Or they could thicken and become more reflective.”
These two scenarios would result in very different future climates. And that, Pritchard says, is part of the problem.
“If you ask two different climate models what the future will be like when we add a lot more CO2, you get two very different answers. And the key reason for this is the way clouds are included in climate models.”
No one denies that clouds and aerosols — bits of soot and dust that nucleate cloud droplets — are an important part of the climate equation. The problem is these phenomena occur on a length- and time-scale that today’s models can’t come close to reproducing. They are therefore included in models through a variety of approximations.
Analyses of global climate models consistently show that clouds constitute the biggest source of uncertainty and instability.

The F.D.A. said the likely source of the outbreak was fresh organic strawberries that were sold under the FreshKampo and H-E-B brands in March and April.Public health officials said they were investigating an outbreak of hepatitis A in the United States and Canada that is potentially linked to organic strawberries.American health officials said the outbreak most likely came from fresh organic strawberries branded as FreshKampo and H-E-B that were bought between March 5 and April 25.The strawberries were sold at stores including Aldi, H-E-B, Kroger, Safeway, Sprouts Farmers Market, Trader Joe’s, Walmart and Weis Markets, the Food and Drug Administration said.The strawberries are now past their shelf life, and people who bought them between March 5 and April 25 should throw them out, even if they froze them to eat later, health officials said.In the United States, the F.D.A. said it had identified 17 cases of hepatitis A linked to the strawberries — 15 in California and one each in Minnesota and North Dakota. Twelve people have been hospitalized, the agency said.In Canada, health officials said they had confirmed 10 cases — four in Alberta and six in Saskatchewan. Four people have been hospitalized in that country.No deaths linked to the strawberries have been reported in the United States or Canada, according to officials in both countries.Hepatitis A is a contagious virus that may cause liver disease. It can be transmitted when food is consumed after it was handled by someone who did not follow proper hand-washing hygiene, the F.D.A. said.Symptoms usually develop 15 to 20 days after eating the contaminated food and can include fatigue, nausea, vomiting, abdominal pain, jaundice, dark urine and pale stool, the F.D.A. said.People who believe they may be infected or may have eaten the tainted strawberries in the last two weeks should talk to their health care provider, the F.D.A. said.In a statement, H-E-B, which is based in Texas, said that it had not received or sold organic strawberries from the supplier under investigation since April 16.“All strawberries sold at H-E-B are safe,” the company said. “No illnesses from strawberries related to the F.D.A. investigation have been reported at H-E-B or in Texas.”FreshKampo said it was no longer shipping fresh organic strawberries linked to the outbreak. Those that were sold between March 5 and April 25 came in a plastic clamshell package with a label that read, “Distributed by Meridian Fruits,” the company said in a statement.“FreshKampo wants consumers to know that it will continue to work with health officials and supply chain partners to determine where a problem may have occurred along the supply chain and take necessary measures to prevent it from happening again,” the statement said.