Publisher Health

A growing body of evidence has linked the Delta variant of SARS-CoV-2, the virus that causes COVID-19, with an increased risk for pregnancy complications, including stillbirths. Now, for the first time, researchers at Massachusetts General Hospital (MGH) and Brigham and Women’s Hospital (BWH) have detected the Delta variant in the blood and placentas of women who had stillbirths and serious pregnancy complications, which they report in the Journal of Infectious Diseases.
Prior studies have indicated that COVID-19 poses a threat to pregnant women and fetuses. Recently, suspicion has arisen that the Delta variant of SARS-CoV-2 may be particularly dangerous during pregnancy. In late November, the Centers for Disease Control and Prevention (CDC) reported that pregnant women with COVID-19 were four times more likely to have miscarriages than uninfected pregnant women during the period when the Delta variant was causing the majority of SARS-CoV-2 infections in the United States. (Stillbirth describes the death of a fetus after 20 weeks of pregnancy.)
Earlier in the pandemic, before Delta became the dominant strain in the United States, Andrea Edlow, MD, a maternal-fetal medicine specialist at MGH, and several colleagues had studied 64 pregnant women with COVID-19 and found that none had detectable levels of SARS-CoV-2 in their blood or placentas. But as the Delta variant swept across the country in 2021, Edlow began to have her own suspicions. “It seemed like we were seeing even more sick moms and a disproportionate number of stillbirths,” says Edlow.
Edlow and her team received permission to analyze nasal swabs, umbilical cord blood, and placentas of three women who had COVID-19 late in their pregnancies, none of whom had been vaccinated against the coronavirus. Two of the women had stillbirths and a third woman’s fetus experienced distress and was delivered by urgent cesarean birth (C-section). These blood and tissue samples underwent viral sequencing at BWH in the translational virology laboratory directed by Jonathan Li, MD.
The results were striking. “All the moms had detectable virus in the bloodstream. All had high levels of detectable virus in their nasal swabs. All had infected placentas,” says Edlow. And viral sequencing confirmed that each woman was infected with the Delta variant of SARS-CoV-2. “This was definitely different from what we saw with the ancestral strain of SARS-CoV-2 during the first part of the pandemic.”
Li notes that while COVID-19 is widely thought of as a pulmonary disease, studies indicate that when SARS-CoV-2 enters the bloodstream (known as viremia) it can travel throughout the body and cause organ failure and other severe complications. “Our testing showed that the virus was widely disseminated in these three patients,” says Li. That appears to have resulted in severe inflammation of the placenta, which likely caused the stillbirths and complications. “This represents another example of the systemic manifestations of COVID-19.”
Why the Delta variant is a greater threat to pregnancy than earlier strains of SARS-CoV-2 is unknown, as is the potential impact of Omicron, the variant identified shortly after Thanksgiving. However, Edlow hopes these findings can help bolster public health messaging aimed at battling misinformation that leads pregnant women to fear COVID-19 vaccines. She notes that more than 170,000 pregnant women have been vaccinated and, reassuringly, there’s no evidence that the injections increased the risk for birth defects or any form of pregnancy complications. “Yet stillbirth, preterm birth, and poor neonatal outcomes are all associated with getting COVID-19,” says Edlow. “If you want to do the best thing for your baby, get vaccinated.”
Edlow is also an assistant professor of Obstetrics, Gynecology and Reproductive Biology at Harvard Medical School (HMS). Li is an associate professor of Medicine at HMS.
Funding for this work came from the Eunice Kennedy Shriver National Institute of Child Health and Human Development and the March of Dimes.
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Bald eagle populations have slowly recovered from near devastation after the government banned DDT in 1972, but another ongoing issue has weakened that rebound — lead poisoning from gunshot ammunition.
A new study, published in the Journal of Wildlife Management, finds that despite increasing numbers of bald eagles, poisoning from eating dead carcasses or parts contaminated by lead shot has reduced population growth by 4% to 6% annually in the Northeast.
The results could help educate and inform policy on ammunition choices for hunters, as copper-based ammunition exists — though supplies of all ammunitions have been low lately.
“Hopefully, this report will add information that compels hunters, as conservationists, to think about their ammunition choices,” said Krysten Schuler, assistant research professor in the Department of Public and Ecosystem Health at Cornell University and senior author on the study.
The diminished growth rates have the potential to erase cushions that protect populations against unforeseen events.
“Even though the population seems like it’s recovered, some perturbation could come along that could cause eagles to decline again,” Schuler said.

An international metastudy led by researchers at Karolinska Institutet in Sweden has identified a specific gene variant that protects against severe COVID-19 infection. The researchers managed to pinpoint the variant by studying people of different ancestries, a feat they say highlights the importance of conducting clinical trials that include people of diverse descents. The results are published in the journal Nature Genetics.
In addition to old age and certain underlying diseases, genetics can influence whether we become severely affected or only suffer mild illness from COVID-19. Previous studies on mainly people of European ancestry have found that individuals carrying a particular segment of DNA have a 20 percent lower risk of developing a critical COVID-19 infection. This DNA segment encodes genes in the immune system and is inherited from Neanderthals in about half of all people outside Africa.
This region of DNA is, however, packed with numerous genetic variants, which makes it challenging to disentangle the exact protective variant that could potentially serve as a target for medical treatment against severe COVID-19 infection.
To identify this specific gene variant, researchers in the current study looked for individuals carrying only parts of this DNA segment. Since the Neandertal inheritance occurred after the ancient migration out of Africa, the researchers saw a potential in focusing on individuals with African ancestry who lack heritage from the Neanderthals and therefore also the majority of this DNA segment. A small piece of this DNA region is, however, the same in both people of African and European ancestries.
The researchers found that individuals of predominantly African ancestry had the same protection as those of European ancestry, which allowed them to pinpoint a specific gene variant of particular interest.
“The fact that individuals of African descent had the same protection allowed us to identify the unique variant in the DNA that actually protects from COVID-19 infection,” says Jennifer Huffman, the first author of study and a researcher at the VA Boston Healthcare System in the U.S.
The analysis included a total of 2,787 hospitalized COVID-19 patients of African ancestry and 130,997 people in a control group from six cohort studies. Eighty percent of individuals of African ancestry carried the protective variant. The outcome was compared with a previous, larger metastudy of individuals of European heritage.
According to the researchers, the protective gene variant (rs10774671-G) determines the length of the protein encoded by the gene OAS1. Prior studies have shown that the longer variant of the protein is more effective at breaking down SARS-CoV-2, the virus causing the disease COVID-19.
“That we are beginning to understand the genetic risk factors in detail is key to developing new drugs against COVID-19,” says co-author Brent Richards, senior investigator at the Lady Davis Institute of the Jewish General Hospital and professor at McGill University in Canada.
The COVID-19 pandemic has spurred considerable collaboration among researchers in different parts of the world, which has made it possible to study genetic risk factors in a wider diversity of individuals than in many previous studies. Even so, the majority of all clinical research is still being done on individuals of predominantly European descent.
“This study shows how important it is to include individuals of different ancestries. If we had only studied one group, we would not have been successful in identifying the gene variant in this case,” says the study’s corresponding author Hugo Zeberg, assistant professor at the Department of Neuroscience at Karolinska Institutet.
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Heart disease can directly cause brain dysfunction early on which could lead to dementia and can treble the amount of an Alzheimer’s protein in the brain, say scientists.
The new research, published in eLife, has found that heart disease causes a breakdown of a key brain function which links brain activity and blood flow, meaning the brain gets less blood for the same amount of activity.
This is happening in heart disease patients before the build up of fat in the brain’s blood vessels (atherosclerosis) and is a prelude to dementia. Until now it has been unclear how some forms of vascular dementia can happen years before atherosclerosis in the brain.
The researchers also discovered that the combination of heart disease and a genetic predisposition for Alzheimer’s Disease trebles the amount of beta-amyloid, a protein that builds up and triggers Alzheimer’s, and increases the levels of an inflammatory gene (IL1) in the brain.
Dr Osman Shabir, lead author of the study from the University of Sheffield’s Neuroscience and Healthy Lifespan Institutes, said: “Alzheimer’s Disease is the most common form of dementia worldwide and heart disease is a major risk factor for both Alzheimer’s and dementia. The new findings are key to furthering our understanding of the links between heart disease and dementia.
“We’ve discovered that heart disease in midlife causes the breakdown of neurovascular coupling, an important mechanism in our brains which controls the amount of blood supplied to our neurons. This breakdown means the brain doesn’t get enough oxygen when needed and in time this can lead to dementia.”
The team have since been awarded a three year grant by the British Heart Foundation to look at the use of an arthritis drug which targets IL1 to see if it could reverse or reduce the brain dysfunction seen to be caused by heart disease.
The team also found that brain injuries can also worsen brain blood flow regulation, supporting observations that patients’ symptoms often worsen after injuries or falls.
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It is well established that exercise improves health, and recent research has shown that exercise benefits the body in different ways, depending on the time of day. However, scientists still do not know why the timing of exercise produces these different effects. To gain a better understanding, an international team of scientists recently carried out the most comprehensive study to date of exercise performed at different times of the day.
Their research shows how the body produces different health-promoting signaling molecules in an organ-specific manner following exercise depending on the time of day. These signals have a broad impact on health, influencing sleep, memory, exercise performance, and metabolic homeostasis. Their findings were recently published in the journal Cell Metabolism.
“A better understanding of how exercise affects the body at different times of day might help us to maximize the benefits of exercise for people at risk of diseases, such as obesity and type 2 diabetes,” says Professor Juleen R. Zierath from Karolinska Institutet and the Novo Nordisk Foundation Center for Basic Metabolic Research (CBMR) at the University of Copenhagen.
Using exercise to fix a faulty body clock
Almost all cells regulate their biological processes over 24 hours, otherwise called a circadian rhythm. This means that the sensitivity of different tissues to the effects of exercise changes depending on the time of day. Earlier research has confirmed that exercise timing according to our circadian rhythm can optimize the health-promoting effects of exercise.
The team of international scientists wanted a more detailed understanding of this effect, so they carried out a range of experiments on mice that exercised either in the early morning or the late evening. Blood samples and different tissues, including brain, heart, muscle, liver, and fat were collected and analyzed by mass spectrometry. This allowed the scientists to detect hundreds of different metabolites and hormone signaling molecules in each tissue, and to monitor how they were changed by exercising at different times of the day.

Researchers at Karolinska Institutet in Sweden have together with international collaborators completed a comprehensive international validation of artificial intelligence (AI) for diagnosing and grading prostate cancer. The study, published in Nature Medicine, shows that AI systems can identify and grade prostate cancer in tissue samples from different countries equally well as pathologists. The results suggest AI systems are ready to be responsibly introduced as a complementary tool in prostate cancer care, researchers say.
The international validation was performed via a competition called PANDA. The competition lasted for three months and challenged more than 1000 AI experts to develop systems for accurately grading prostate cancer.
Rapid innovation
“Only ten days into the competition, algorithms matching average pathologists were developed. Organising PANDA shows how competitions can accelerate rapid innovation for solving specific problems in healthcare with the help of AI,” says Kimmo Kartasalo, a researcher at the Department of Medical Epidemiology and Biostatistics at Karolinska Institutet and corresponding author of the study.
A problem in today’s prostate cancer diagnostics is that different pathologists can arrive at different conclusions even for the same tissue samples, which means that treatment decisions are based on uncertain information. The researchers believe the use of AI technology holds great potential for improved reproducibility, that is, increased consistency of the assessments of tissue samples irrespective of which pathologist performs the evaluation, leading to more accurate treatment selection.
Accurate diagnostics
The KI researchers have shown in earlier studies that AI systems can indicate if a tissue sample contains cancer or not, estimate the amount of tumour tissue in the biopsy, and grade the severity of prostate cancer, comparably to international experts. However, the main challenge associated with implementing AI in healthcare is that AI systems are often highly sensitive towards data that differ from the data used for training the system, and may consequently not produce reliable and robust results when applied in other hospitals and other countries.

With the Winter Olympics approaching, many people will soon be tuning in to watch events that take place on ice, such as figure skating, speed skating and ice hockey. An ultrathin, super-lubricating layer of water on the ice’s surface is essential for skaters’ graceful glides. Inspired by this surface, researchers reporting in ACS Nano have developed a treatment for osteoarthritis that enhances lubrication and reduces friction and inflammation in a rat model of the disease.
Osteoarthritis, a chronic disease common in middle-aged and older people, is characterized by persistent inflammation and degeneration of cartilage in the joints. Anti-inflammatory drugs can help relieve pain and inflammation, but long-term use can reduce their effectiveness or cause gastrointestinal problems. Corticosteroids injected directly into the joint provide temporary relief, but frequent treatments can sometimes damage the cartilage. Yuanjin Zhao and colleagues wanted to develop drug delivery particles that, when injected into a joint, could safely enhance lubrication and decrease inflammation.
The researchers based their particles on hyaluronic acid (HA), a natural polysaccharide already used as a lubricant to treat osteoarthritis, but this molecule degrades rapidly inside the body. So the researchers used a microfluidic device to make tiny methacrylate anhydride-HA gel particles, which they reasoned might be stronger and persist longer in the body than an HA solution. To enhance the lubrication of the particles, the team coated them with 2-methylacryloyloxyethyl phosphorylcholine (MPC), which has positively and negatively charged chemical groups that attract a thin layer of water, similar to ice. In addition, the particles’ pores were loaded with an anti-inflammatory drug, which could be slowly and continuously released. The researchers then injected drug-loaded HA-MPC particles into the knee joints of rats with early-stage osteoarthritis. The joints of treated rats were more lubricated and had less cartilage destruction, joint friction and inflammation compared with a control group. The treated rats also expressed higher levels of collagen II and aggrecan, two markers of healthy cartilage. The particles have great potential for clinical applications, but first they must undergo additional animal and biosafety tests, the researchers say.
The authors acknowledge funding from the National Key Research and Development Program of China, the National Natural Science Foundation of China, the Natural Science Foundation of Jiangsu and the Shenzhen Fundamental Research Program.
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A green Mediterranean diet, high in polyphenols and low in red and processed meat, seems to slow age-related brain atrophy, according to a new Ben-Gurion University of the Negev-led international study. The DIRECT PLUS 18-month long randomized control trial among approximately 300 participants is one of the longest and largest brain MRI trials in the world.
Their findings were published Tuesday in The American Journal of Clinical Nutrition.
The effect of diet on age-related brain atrophy is largely unproven. Participants were divided into three groups according to diet, and whole brain MRI measurements were taken before, and after the trial. Hippocampal-occupancy (HOC) and lateral-ventricle-volume (LVV) were measured as indicators of brain atrophy and predictors of future dementia. Brain MRI-derived data were quantified and segmented using NeuroQuant, an FDA (Food and Drug Administration) authorized fully automated tool.
Two hundred eighty-four men and women (88% men) aged 31-82 were randomly divided into three groups: A healthy dietary guidelines group, a Mediterranean diet group and a green Mediterranean diet. In the Mediterranean diet group, the participants were further provided walnuts rich in polyphenols. In the green- Mediterranean group the participants were further provided high polyphenol green components: 3-4 daily cups of green tea and a daily green shake of Mankai duckweed, as a substitute for dinner, with minimal consumption of red and processed meat. In addition, all three groups participated in physical activity programs based on aerobic exercise, including free gym memberships.
The trial was performed by Dr. Alon Kaplan and Prof. Iris Shai, professor at Ben-Gurion University, Israel, and adjunct professor at Harvard University, together with several international teams of brain experts. The researchers were surprised to identify dramatic changes in MRI-related brain atrophy within 18-24 months, whereas the rate of brain atrophy markers (i.e., hippocampal occupancy decline and lateral ventricle volume expansion) were significantly accelerated from the age of 50 years and up.
The researchers discovered a significant attenuation in brain atrophy over the 18 months in those who adhered to both Mediterranean diets; with greater magnitude in the green-MED group, specifically among participants over age 50. In addition, the researchers noticed that an improvement in insulin sensitivity was independently associated with attenuated brain atrophy.
Greater Mankai, green tea, and walnuts consumption and less red and processed meat consumption were significantly associated with lower hippocampal occupancy decline.
Participants were initially chosen based on abdominal girth size or dyslipidemia. They were all employees at a remote workplace in Israel (Nuclear Research Center in Dimona) where they did not leave the premises during the workday, and the lunch provided was monitored.
“The beneficial association between the green Mediterranean diet and age-related neurodegeneration might be partially explained by the abundance of polyphenols in plant-based food sources which have antioxidant and anti-inflammatory metabolites. Polyphenols can cross the blood-brain barrier (BBB), reduce neuroinflammation, and induce cell proliferation and adult-onset neurogenesis in the hippocampus,” writes Prof. Shai, the lead author.
“Our findings might suggest a simple, safe, and promising avenue to slow age-related neurodegeneration by adhering to a green-Mediterranean diet,” adds Dr. Alon Kaplan.
This study was funded by grants from the German Research Foundation (DFG), (project number 209933838 — SFB 1052; B11), Israel Ministry of Health grant 87472511; Israel Ministry of Science and Technology grant 3-13604; and the California Walnuts Commission.
None of the funding providers were involved in any stage of the design, conduct, or analysis of the study, and they had no access to the study results before publication.

Scientists have long sought to find out how some diseases can have symptoms restricted to just one tissue when they are caused by a single faulty protein found throughout the body.
Familial Partial Lipodystrophy type 2 (FPLD2) is a rare disorder causing diabetes, loss of fat in the arms and legs and over development of muscles, yet the faulty protein, lamin A, is found in all cells.
University of Edinburgh scientists found that mice lacking the protein Tmem120a, which is mostly found in fat cells, have similar symptoms as FPLD2.
Tmem120a belongs to a group of proteins, known as NETs, that help ensure the cell’s genetic material, found inside the cell’s command centre — the nucleus — is correctly organised and read.
They found that Tmem120a plays a key role in normal development of fat tissue and healthy metabolism by promoting expression of fat genes and shutting off muscle genes in fat tissue.
These effects appear to be due to Tmem120a’s ability to release parts of the genome that control fat metabolism away from the edge of the nucleus while recruiting muscle genes to the edge.

Scientists led by Professor Ana J. Garcia-Saez at the CECAD Cluster of Excellence for Aging Research at the University of Cologne have shown that apoptosis, the programmed cell death, involves a direct physical interplay between the two proteins BAX and DRP1. DRP1 can serve as a direct cell death activator by binding to BAX without the need for other cell death triggers. This finding could lead to the development of new cell death regulators for cancer therapies, for example. The article, ‘DRP1 interacts directly with BAX to induce its activation and apoptosis’ was published in The EMBO Journal.
It is known that the so-called ‘apoptotic enforcer protein’ BAX encounters DRP1 in the cell at the mitochondrial membrane. The latter is a dynamin-like protein that plays a critical role in mitochondrial division. However, the functional implications of their interaction and the contribution of DRP1 to apoptosis have been highly controversial.
BAX is a key protein in the pathway to cell death. Understanding the mechanism of action of BAX is critical for therapeutic regulation of apoptosis. Using super-resolution confocal fluorescence microscopy and biochemical as well as biophysical methods in model membrane systems, the research team was able to demonstrate the direct interaction of the two proteins in dying cells. In addition, using a system that artificially brings the two proteins together, they investigated the functional consequences of the interaction of BAX and DRP1.
“When we artificially force the interaction of the two proteins, they move from the cytoplasm to the mitochondria, where the protein complex triggers a reorganization of the mitochondria. This leads to pores in the membrane. The contents of the mitochondria enter the cell plasma, which ultimately leads to cell death,” said Andreas Jenner, first author of the study.
By combining methods such as the dimerization-dependent fluorescence technique, cross-linked mass spectrometry and the analysis of different protein pieces, the interaction surface could also be identified for the first time. DRP1 binds to the front end (N-terminus) of the amino acid chain of BAX, which is shown to be a regulatory region for BAX activity. ‘It was impressive to see that cells started to die just by forcing the interaction between BAX and DRP1, without the need for another death trigger,’ Garcia-Saez said. ‘It’s great that we now know that DRP1 can act as a direct apoptosis activator, which for the first time gives functional significance to the connection between the two proteins. This could pave the way for the development of new BAX regulators for therapeutic applications.”
Work for this study began at the IFIB (Interfaculty Institute of Biochemistry) in Tübingen, Germany, and was completed at the CECAD Research Center, Institute of Genetics, in Garcia-Saez’s laboratory.
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