Publisher Health

Getting an annual flu shot may be associated with a lower risk of stroke, according to a study published in the September 7, 2022, online issue of Neurology®, the medical journal of the American Academy of Neurology.
“Studies have shown that getting the flu increases your risk of having a stroke, but research is still being collected on whether getting the flu vaccine can help protect against a stroke,” said study author Francisco J. de Abajo, MD, MPH, PhD, of the University of Alcalá in Madrid, Spain. “This observational study suggests that those who have a flu shot have a lower risk of stroke. To determine whether this is due to a protective effect of the vaccine itself or to other factors, more research is needed.”
The study looked at ischemic stroke, which is caused by a blockage of blood flow to the brain and is the most common type of stroke.
For the study, researchers looked at a health care database in Spain and identified people who were at least 40 years old and had a first stroke over a 14-year period. Each person who had a stroke was compared to five people of the same age and sex. There were 14,322 people who had a stroke and 71,610 people who did not have a stroke.
Then the researchers looked at whether people had received the influenza vaccine at least 14 days before the stroke or before that same date for those who did not have a stroke.
A total of 41.4% of those who had a stroke had received the flu shot, compared to 40.5% of those who did not have a stroke. But the people who got the shot were more likely to be older and to have other conditions such as high blood pressure and high cholesterol that would make them more likely to have a stroke. Once researchers adjusted for those factors, they found that those who received a flu shot were 12% less likely to have a stroke than those who did not.
The researchers also looked at whether the pneumonia vaccine had any effect on the risk of stroke and found no protective effect.
“These results are yet another reason for people to get their yearly flu shot, especially if they are at an increased risk of stroke,” de Abajo said. “To be able to reduce your risk of stroke by taking such a simple action is very compelling.”
Since the study was observational, it does not prove that getting the flu shot reduces the risk of stroke. It only shows an association. There could be other factors that were not measured that could affect the risk of stroke.
The study was supported by the Biomedical Research Foundation of the Prince of Asturias University Hospital in Madrid and the Institute of Health Carlos III in Madrid.
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Neutralizing antibody levels against the original COVID-19 virus and omicron variants in vaccinated adults tend to decline by at least 15% per month after a single booster shot, a new study using serum from human blood samples suggests.
Data from two adults in the same study who had a dramatic loss in antibodies but received a second booster showed that the second dose completely restored antibodies to protective levels.
“The message from our study is clear: If you have a dramatic loss of antibodies from the first booster, you definitely need a second booster to get antibodies back,” said Shan-Lu Liu, senior author the study and a virology professor in the Department of Veterinary Biosciences at The Ohio State University.
“It’s not surprising to us to find that we see this antibody decline — in general, vaccine-induced antibodies decline over time regardless of the virus, and especially if the virus changes over time in the way that SARS-CoV-2 has changed,” said Liu, also a professor in the Department of Microbial Infection and Immunity.
The study is published as a letter to the editor today (Sept. 7, 2022) in the New England Journal of Medicine.
Researchers tested serum from 46 health care professionals who had received the initial two-dose mRNA vaccine course and, later, one booster shot between one and nine months before their antibody levels were tested against the parent SARS-CoV-2 virus and the most dominant omicron variants, including BA.5, among recent and current infections. The team also had access to samples from two vaccinated health care workers who had received the second booster shot.

Electrical signals tell the heart to contract, but when the signals form spiral waves, they can lead to dangerous cardiac events like tachycardia and fibrillation. Researchers at the Georgia Institute of Technology and clinicians at Emory University School of Medicine are bringing a new understanding to these complicated conditions with the first high-resolution visualizations of stable spiral waves in human ventricles.
“Clinicians have known for decades that spiral waves of electrical activity can occur in the heart, and researchers have done experiments in animal and human hearts before,” said School of Physics Professor Flavio Fenton. “However, this is the first time the evolution of relatively stable spiral waves of voltage and calcium in the ventricles of human hearts have been mapped at very high spatial and temporal resolution.”
Studying live hearts from heart transplant patients gives a rare window into the detailed behavior of the heart during conditions that are difficult to treat like fibrillation. As a result, doctors can gain a better understanding of how spiral waves begin and are sustained, which can lead to new therapies.
The present work has been part of a decade-long collaboration between the Georgia Tech School of Physics and the Emory School of Medicine. The researchers published their latest findings, “Direct observation of a stable spiral wave reentry in ventricles of a whole human heart using optical mapping for voltage and calcium” and “Spiral wave breakup: Optical mapping in an explanted human heart shows the transition from ventricular tachycardia to ventricular fibrillation and self-termination,” in the journal Heart Rhythm.
Mapping the Heart
To generate the conditions for spiral waves, the researchers applied timed electric shocks to the heart. Then, to visualize and record the spiral waves, they injected florescent dyes for voltage and calcium into the blood substitute that keeps the heart alive. The changes in light intensity enable them to record signals across the heart tissue, a technique known as optical mapping.

Infections in pregnant women have been linked to an increased risk of neurodevelopmental conditions, such as autism, in the child later in life. But it does not seem to be the infections themselves that cause autism, researchers from Karolinska Institutet in Sweden show in a study published in The Lancet Psychiatry.
“Our results can reassure expectant parents by indicating that infections during pregnancy may not pose as great a risk to the baby’s brain as previously thought,” says Håkan Karlsson, researcher at the Department of Neuroscience at Karolinska Institutet and the study’s senior author.
Previous studies have shown a link between infections in the expectant mother during pregnancy and an increased risk of neurodevelopmental conditions, such as autism or intellectual disability, in the child later in life.
But they have not been able to say whether the mother’s exposure to infection is truly the cause, or whether other factors are behind this link. Researchers from Karolinska Institutet have now studied this in more detail.
The current study is based on data on more than 500,000 children born between 1987 and 2010. The aim was to investigate whether there is a causal relationship between infections in the woman during pregnancy and autism or intellectual disability in the child. Infections were included if they were severe enough to requirespecialist care and they were identified using diagnostic codes from patient and birth records.
Similar to previous studies, the researchers could see that infections that required specialist care during pregnancy were linked to an increased risk of autism and intellectual disability in children.

A potential new treatment combining natural manuka honey with a widely used drug has been developed by scientists at Aston University to treat a potentially lethal lung infection and greatly reduce side effects of one of the current drugs used for its treatment.
The findings, which are published in the journal Microbiology, show that the scientists in the Mycobacterial Research Group in the College of Health and Life Sciences at Aston University were able to combine manuka honey and the drug amikacin in a lab-based nebulisation formulation to treat the harmful bacterial lung infection Mycobacterium abscessus.
Manuka honey is long known to have wide ranging medicinal properties, but more recently has been identified for its broad spectrum antimicrobial activity. Now scientists have found that manuka honey has the potential to kill a number of drug resistant bacterial infections such as Mycobacterium abscessus — which usually affects patients with cystic fibrosis (CF) or bronchiectasis.
According to the Cystic Fibrosis Trust, CF is a genetic condition affecting around 10,800 people — one in every 2,500 babies born in the UK -and there are more than 100,000 people with the condition worldwide. The NHS defines bronchiectasis as a long-term condition where the airways of the lungs become widened, leading to a build-up of excess mucus that can make the lungs more vulnerable to infection..
In the study, the researchers used samples of the bacteria Mycobacterium abscessus taken from 16 infected CF patients. They then tested the antibiotic amikacin, combined with manuka honey, to discover what dosage was required to kill the bacteria.
As part of the study the team used a lab-based lung model and nebuliser — a device that produces a fine spray of liquid often used for inhaling a medicinal drug. By nebulising manuka honey and amikacin together, it was found they could improve bacterial clearance, even when using lower doses of amikacin, which would result in less life-changing side-effects to the patient.

A new University of California, Irvine-led study reveals how mechanical forces and tissue mechanics influence the morphology of the developing brain, and establishes a direct link in neural stem cells between Piezo1, a mechanically-activated ion channel, and intracellular cholesterol levels during neural development.
The study, titled, “Piezo1 regulates cholesterol biosynthesis to influence neural stem cell fate during brain development,” was published today in the Journal of General Physiology. Study findings demonstrate a role for Piezo1 in the neurodevelopmental process that modulates the quantity, quality, and organization of cells by influencing cellular cholesterol metabolism.
“Our surprising discovery linking Piezo1 and cholesterol also motivates investigations for Piezo1 in neurodegenerative diseases linked to cholesterol homeostasis, such as Alzheimer’s Disease,” said Medha Pathak, PhD, an assistant professor in the Department of Physiology & Biophysics at UCI School of Medicine. “By controlling Piezo1 activity through therapeutics we may be able to develop novel treatments for some of these diseases.”
Neural development is a multi-step process that involves the orchestration of many complex events to generate the brain and spinal cord. As the brain develops, cells multiply and organize into structures and connect with other cells. These processes produce mechanical forces that further shape brain patterning, but how cells detect these mechanical signals is not fully understood.
“We previously found that Piezo1 channels are activated in response to both externally applied and cell-generated mechanical forces in human fetal brain-derived neural stem/progenitor cells, and we now show in our current study thatPiezo1 is important for proper brain development,” said Jamison Nourse, PhD, assistant project scientist in the Department of Physiology & Biophysics and first author on the study. “Through our research, we discovered a novel link between Piezo1 and cholesterol biosynthesis, which opens up new lines of investigation into how mechanical forces influence lipid metabolism in the brain.”
Prior research has established the role the Piezo family of mechanically-activated ion channels plays in mechanotransduction in many physiological systems, including vascular development, cardiovascular homeostasis, lymphatic development, red blood cell volume regulation, the baroreceptor response in neurons, cartilage mechanics, bone formation, macrophage polarization responses, keratinocyte migration in wound healing, and neural stem cell fate. In 2021, Dr. Ardem Patapoutian of The Scripps Research Institute, San Diego, was awarded a Nobel Prize in Physiology or Medicine for the groundbreaking discovery of the Piezo channels.
“Improper brain development can cause life-long malformations and functional defects,” said Pathak. “And, while we still do not understand the reason behind many brain developmental defects, our work provides new approaches for understanding how brain defects may arise.”
Pathak and her research team are continuing to explore Piezo1 and its effect on cholesterol metabolisminearly human brain development and in adult-onset neurodegenerative diseases.
This work was funded by the National Institutes of Health.
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The brain mechanisms that cause aggressive behavior have been well studied. Far less understood are the processes that tell the body when it’s time to stop fighting. Now, a new study by Salk scientists identifies a gene and a group of cells in the brain that play a critical role in suppressing aggression in fruit flies.
The findings, published in Science Advances on September 7, 2022, have implications for disorders such as Parkinson’s disease, which can sometimes cause behavioral changes like increased aggression and combativeness.
“We’ve found an important mechanism in the brain that normally prevents us from expressing high levels of aggression,” says senior author Kenta Asahina, assistant professor in Salk’s Molecular Neurobiology Laboratory. “Although our findings are in fruit flies, the same mechanism may be at play in humans, at least at the molecular level, which could help better explain a host of psychiatric diseases.”
De-escalation, or the ability to decide when it’s time to stop fighting, is a vital behavior for survival because it allows animals to adjust their aggressiveness according to the costs and benefits of an encounter with a rival — at a certain point, continuing to fight is no longer worth it. Sensing when it’s time to de-escalate is complex because there isn’t an obvious trigger, such as the way fullness triggers an animal to stop eating.
For the study, scientists compared the behavior of normal fruit flies (Drosophilia) and fruit flies lacking various genes of interest. Specifically, they examined how frequently male flies lunged at other males, a typical aggressive behavior in this species. They found that flies missing a gene called nervy were significantly more aggressive than their normal counterparts.
The nervy gene isn’t actually involved in the animal’s moment-to-moment decision to stop fighting. Rather, it helps give the fly the ability to respond to environmental cues (likely the fly’s past experience with other individuals), the researchers say.

COVID-19 transmission can be more accurately modeled by incorporating meteorological factors, with ultraviolet (UV) radiation as the main driver, according to a new study published this week in the open-access journal PLOS ONE by a team of scientists from the Qatar Environment & Energy Research Institute (QEERI), at Hamad Bin Khalifa University and Transvalor S.A., France.
A growing number of studies suggest that climate may impact the spread of COVID-19 but the extent to which it modifies COVID-19 risk and transmission is not well understood. Studies on the impact of climate have been piecemeal or poorly controlled — limited to single countries, only taking into account a few climatic parameters, or ignoring socioeconomics, for instance.
In the new paper, the researchers studied data on reported COVID-19 cases in 196 countries over a 14-month period, using socioeconomic, environmental, and global health factors as control variables. They developed three different analytic approaches — statistical, machine learning and econometric — which modeled the potential contributions of climate to confirmed case numbers.
The results suggest that while disease susceptibility, lockdown compliance, and increased testing are the most effective strategies for preventing the spread of COVID-19, UV radiation is the climate factor most strongly correlated with the spread of COVID-19, with greater UV radiation associated with reduced transmission. For other meteorological and air quality factors, including temperature, absolute humidity and solar radiation, discrepancies between results in the three analysis methods emphasized the difficulty in understanding the correlations. For instance, humidity was positively correlated with COVID-19 spread in the machine learning analysis and negatively correlated in the econometric analysis. Temperature was moderately negatively associated with COVID-19 in the statistical analysis but positively correlated with COVID-19 transmission in both the machine learning and econometric analyses.
The authors conclude that UV radiation emerges as the most impactful meteorological factor in COVID-19 transmission across all methods. This could help refine transmission predictions based on seasonality or weather forecasts, and help inform future pandemic response measures that limit the economic impact of complete lockdowns. They point out that this is supported by overwhelming evidence that UV light can effectively kill SARS-CoV-2 and other coronaviruses.
The authors add: “The impact of climate on COVID-19 transmission rates has been the subject of many studies, but it is still poorly understood. In our study we demonstrated that meteorological factors play a key role in statistical, machine learning and econometric analyses of COVID-19 risk, with ultraviolet radiation (UV) as the main driver.”
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A new protein, named MAIA after the Greek goddess of motherhood, could be crucial in helping doctors better understand some aspects of infertility and develop novel treatments. Currently, infertility is unexplained in more than half of people who are unable to conceive naturally.
In the first study of its kind, the international team of researchers led by the University of Sheffield created artificial eggs using thousands of beads. Each of these beads had a different piece of protein, known as a peptide, on its surface so that sperm could bond with them.
When sperm were incubated with the beads scientists found only a small number of beads had sperm attached to them. After several painstaking rounds of removing any beads that didn’t have sperm bound to them, researchers were eventually left with beads corresponding to one particular protein — MAIA — and sperm bound to all of these beads.
The gene corresponding to MAIA was then inserted into human culture cells, and these became receptive to sperm in the exact way that it would during the natural fertilisation process.
The findings, published in Science Advances, reveal that during the process, MAIA is responsible for drawing sperm into the egg for fertilisation.
Professor Harry Moore, Lead Investigator of the study from the University of Sheffield’s School of Biosciences, said: “Infertility is unexplained in more than half of those who struggle to conceive naturally. What we know about fertility in humans has been severely limited by ethical concerns and the lack of eggs for research.
“The ingenious artificial fertilisation technique which enabled us to identify the MAIA protein will not only allow scientists to better understand the mechanisms of human fertility, but will pave the way for novel ways to treat infertility and revolutionise the design of future contraceptives.”
The findings could help to confirm the theory that some sperm may not be compatible with some eggs. Researchers now plan to explore whether sperm from different individuals bind to the protein differently.
Professor Allan Pacey, Co-Author of the study and Head of the University of Sheffield’s Departments of Oncology and Metabolism and Infection, Immunity and Cardiovascular Disease, said: “This discovery of the MAIA protein is a major step forward in how we understand the process of human fertilisation. It would have been almost impossible to discover without the use of the artificial beads to replicate the surface of human eggs as we simply wouldn’t have been able to get enough eggs to do the experiment. A classic case of thinking out of the box.”
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Psychological distress, including depression, anxiety, worry, perceived stress, and loneliness, before COVID-19 infection was associated with an increased risk of long COVID, according to researchers at Harvard T.H. Chan School of Public Health. The increased risk was independent of smoking, asthma, and other health behaviors or physical health conditions.
“We were surprised by how strongly psychological distress before a COVID-19 infection was associated with an increased risk of long COVID,” said Siwen Wang, a researcher in the Department of Nutrition at Harvard Chan School who led the study. “Distress was more strongly associated with developing long COVID than physical health risk factors such as obesity, asthma, and hypertension.”
The study will be published online in JAMA Psychiatry on September 7, 2022.
According to the U.S. Centers for Disease Control, about 20% of American adults who have had COVID-19 have developed long COVID, which is defined as experiencing COVID-19-related symptoms, such as fatigue, brain fog, or respiratory, heart, neurological, or digestive symptoms, for longer than four weeks after infection. Severe COVID-19 illness increases the risk of long COVID, although people with milder COVID-19 cases can also develop long COVID. Symptoms, which can be debilitating, could last months or years, and little is known about which traits are linked to developing long COVID.
Mental health is known to affect the outcomes of some diseases. Depression and other mental illnesses have been associated with greater risk of more severe COVID-19 including the risk of hospitalization, which is a risk factor for long COVID. In other acute respiratory tract infections, such as flu or common cold, mental health conditions are associated with greater severity and longer duration of symptoms. Previous studies have also suggested that distress is associated with chronic symptoms following Lyme disease and in chronic fatigue syndrome and fibromyalgia, which have symptoms similar to those of long COVID.
To determine the effects of psychological distress before COVID-19 infection on developing long COVID, Wang and her colleagues enrolled more than 54,000 people in April 2020. At the beginning of the study, the researchers asked the participants about their psychological distress. Over the following year, more than 3,000 participants contracted COVID-19, and the researchers asked participants about their COVID-19 symptoms and symptom duration.
After analyzing the responses and comparing those who developed long COVID to those who did not, the researchers determined that distress before COVID-19 infection, including depression, anxiety, worry, perceived stress, and loneliness, was associated with a 32%-46% increased risk of long COVID. These types of psychological distress were also associated with 15%-51% greater risk of daily life impairment due to long COVID.
“To the best of our knowledge, this is the first prospective study to show that a wide range of social and psychological factors are risk factors for long COVID and daily life impairment due to long COVID,” said Andrea Roberts, senior research scientist in the Department of Environmental Health at Harvard Chan School and senior author of the JAMA Psychiatry paper. “We need to consider psychological health in addition to physical health as risk factors of long COVID-19. These results also reinforce the need to increase public awareness of the importance of mental health and to get mental health care for people who need it, including increasing the supply of mental health clinicians and improving access to care.”
Other Harvard Chan co-authors include Luwei Quan, Jorge Chavarro, Natalie Slopen, Laura Kubzansky, Karestan Koenen, and Marc Weisskopf.
This research was supported by the National Institutes of Health (3R01HD094725-02S1, U01HL145386, R24ES028521, U01 CA176726, R01 CA67262, and R01 HD057368); the Dean’s Fund for Scientific Advancement Acceleration Award from the Harvard T. H. Chan School of Public Health; and the Massachusetts Consortium on Pathogen Readiness Evergrande COVID-19 Response Fund Award, and the Veterans’ Administration (IIR 20-076, INV 20-099, IIR 20-101).