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With around 256 million cases and more than 5 million deaths worldwide, the COVID-19 pandemic has challenged scientists and those in the medical field. Researchers are working to find effective vaccines and therapies, as well as understand the long-term effects of the infection.
While the vaccines have been critical in pandemic control, researchers are still learning how and how well they work. This is especially true with the emergence of new viral variants and the rare vaccine side effects like allergic reactions, heart inflammation (myocarditis) and blood-clotting (thrombosis).
Critical questions about the infection itself also remain. Approximately one in four COVID-19 patients have lingering symptoms, even after recovering from the virus. These symptoms, known as “long COVID,” and the vaccines’ off-target side effects are thought to be due to a patient’s immune response.
In an article published today in The New England Journal of Medicine, the UC Davis Vice Chair of Research and Distinguished Professor of Dermatology and Internal Medicine William Murphy and Professor of Medicine at Harvard Medical School Dan Longo present a possible explanation to the diverse immune responses to the virus and the vaccines.
Antibodies mimicking the virus
Drawing upon classic immunological concepts, Murphy and Longo suggest that the Network Hypothesis by Nobel Laureate Niels Jerne might offer insights.

Certain markers of injury to the brain’s white matter, called white matter hyperintensities, can be seen on brain scans. A new study finds that brain scans taken during the lifetimes of athletes in contact sports, compared to changes in their brains at autopsy, showed that white matter hyperintensities were associated with neuropathological changes. The research is published in the November 24, 2021, online issue of Neurology®, the medical journal of the American Academy of Neurology. The study also found that white matter hyperintensities were more common in athletes who played contact sports longer or had more head impacts during their careers.
White matter hyperintensities are areas that appear bright on magnetic resonance imaging (MRI) scans. They are common in people as they age and with medical conditions like high blood pressure.
“Our results are exciting because they show that white matter hyperintensities might capture long-term harm to the brain in people who have a history of repetitive head impacts,” said study author Michael Alosco, PhD, of the Boston University School of Medicine. “White matter hyperintensities on MRI may indeed be an effective tool to study the effects of repetitive head impacts on the brain’s white matter while the athlete is still alive.”
The study involved 75 people who were exposed to repetitive head impacts and had reported symptoms. This included 67 football players plus eight other athletes in contact sports like soccer and boxing, or military veterans. Of the football players, each of whom played an average of 12 years, 16 athletes played professionally and 11 played semi-professionally.
All donated their brains to research after their death in order to advance research into the long-term effects of repetitive head impacts. Researchers then looked at medical records, including scans which were done while the athletes were still alive. Participants had scans taken of their brains, on average, at age 62. The average age of the athletes at death was 67.
Of the participants, 64% were judged to have had dementia prior to death. This was determined by a discussion with their loved ones. Autopsies showed that 53 people, or 71%, had chronic traumatic encephalopathy (CTE). CTE is a neurodegenerative disease associated with repetitive head impacts, including those from football, that can progress to dementia.
After examining the brain scans, researchers found that for every unit difference in white matter hyperintensity volume, there was about twice the odds of having more severe small vessel disease and other indicators of white matter damage, as well as three times the odds of having more severe tau accumulation in the frontal lobe of the brain. Tau protein accumulation in the brain is a biomarker for progressive brain diseases like Alzheimer’s disease and CTE. Researchers also found that higher amounts of white matter hyperintensities were associated with more years of playing football.
When it came to completing daily tasks, greater amounts of white matter hyperintensities were associated with higher scores on a questionnaire about performing daily tasks that was completed by caregivers of the brain donors.
“There are key limitations to the study, and we need more research to determine the unique risk factors and causes of these brain lesions in people with a history of repetitive head impacts,” Alosco said.
Limitations of the study included the use of MRIs obtained for clinical, not research purposes, and that participants were mostly older, symptomatic, male, former American football players.
The study was supported by National Institute on Aging, National Institute of Neurological Disorders and Stroke, Boston University Alzheimer’s Disease Research Center, Department of Veterans Affairs, the Nick and Lynn Buoniconti Foundation and Boston University’s Clinical & Translational Science Institute.
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Materials provided by American Academy of Neurology. Note: Content may be edited for style and length.

New research from UC San Francisco that tested possible triggers of a common heart condition, including caffeine, sleep deprivation and sleeping on the left side, found that only alcohol use was consistently associated with more episodes of the heart arrhythmia.
The authors conclude that people might be able to reduce their risk of atrial fibrillation (AF) by avoiding certain triggers.
The study is published in JAMA Cardiology and was presented November 14, 2021, at the annual Scientific Sessions of the American Heart Association.
Researchers were surprised to find that although most of the things that participants thought would be related to their AF were not, those in the intervention group still experienced less arrhythmia than the people in a comparison group that was not self-monitoring.
“This suggests that those personalized assessments revealed actionable results,” said lead author Gregory Marcus, MD, professor of medicine in the Division of Cardiology at UCSF. “Although caffeine was the most commonly selected trigger for testing, we found no evidence of a near-term relationship between caffeine consumption and atrial fibrillation. In contrast, alcohol consumption most consistently exhibited heightened risks of atrial fibrillation.”
Atrial fibrillation contributes to more than 150,000 deaths in the United States each year, reports the federal Centers for Disease Control and Prevention, with the death rate on the rise for more than 20 years.
To learn more about what patients felt was especially important to study about the disease, researchers held a brainstorming session in 2014. Patients said researching individual triggers for AF was their top priority, giving rise to the I-STOP-AFib study, which enabled individuals to test any presumed AF trigger. About 450 people participated, more than half of whom (58 percent) were men, and the overwhelming majority of whom were white (92 percent).
Participants in the randomized clinical trial utilized a mobile electrocardiogram recording device along with a phone app to log potential triggers like drinking alcohol and caffeine, sleeping on the left side or not getting enough sleep, eating a large meal, a cold drink, or sticking to a particular diet, engaging in exercise, or anything else they thought was relevant to their AF. Although participants were most likely to select caffeine as a trigger, there was no association with AF. Recent research from UCSF has similarly failed to demonstrate a relationship between caffeine and arrhythmias — on the contrary, investigators found it may have a protective effect.
The new study demonstrated that consumption of alcohol was the only trigger that consistently resulted in significantly more self-reported AF episodes.
The individualized testing method, known as n-of-1, did not validate participant-selected triggers for AF. But trial participants did report fewer AF episodes than those in the control group, and the data suggest that behaviors like avoiding alcohol could lessen the chances of having an AF episode.
“This completely remote, siteless, mobile-app based study will hopefully pave the way for many investigators and patients to conduct similar personalized “n-of-1″ experiments that can provide clinically relevant information specific to the individual,” said Marcus.
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Materials provided by University of California – San Francisco. Original written by Elizabeth Fernandez. Note: Content may be edited for style and length.

Just three minutes of exposure to deep red light once a week, when delivered in the morning, can significantly improve declining eyesight, finds a pioneering new study by UCL researchers.
Published in Scientific Reports, the study builds on the team’s previous work*, which showed daily three-minute exposure to longwave deep red light ‘switched on’ energy producing mitochondria cells in the human retina, helping boost naturally declining vision.
For this latest study, scientists wanted to establish what effect a single three-minute exposure would have, while also using much lower energy levels than their previous studies. Furthermore, building on separate UCL research in flies** that found mitochondria display ‘shifting workloads’ depending on the time of day, the team compared morning exposure to afternoon exposure.
In summary, researchers found there was, on average, a 17% improvement in participants’ colour contrast vision when exposed to three minutes of 670 nanometre (long wavelength) deep red light in the morning and the effects of this single exposure lasted for at least a week. However, when the same test was conducted in the afternoon, no improvement was seen.
Scientists say the benefits of deep red light, highlighted by the findings, mark a breakthrough for eye health and should lead to affordable home-based eye therapies, helping the millions of people globally with naturally declining vision.
Lead author, Professor Glen Jeffery (UCL Institute of Ophthalmology), said: “We demonstrate that one single exposure to long wave deep red light in the morning can significantly improve declining vision, which is a major health and wellbeing issue, affecting millions of people globally.

Bacteria from the digestive system seem to have the potential to cause damage to pancreatic cells, increasing the risk of malignant tumours. Now for the first time, live bacteria from cystic pancreatic lesions that are precursors to pancreatic cancer, have been analysed by researchers at Karolinska Institutet in Sweden. The study, which is published in Gut Microbes, can lead to prophylactic interventions using local antibiotics.
Pancreatic cancer is one of the most aggressive and deadly forms of cancer. Because it can have vague symptoms, if any, in its early stages, it is usually discovered late, by which time it has spread.
Consequently, at the time of diagnosis, the disease has become terminal in the majority of patients. As things look today, pancreatic cancer will soon pass breast cancer as the third most common cause of cancer-related death in the EU.
Cystic lesions, including intraductal papillary mucinous neoplasms (IPMNs), of the pancreas are common. Because they are known as precursors to pancreatic cancer, many patients need regular, lifelong check-ups, and a few can also require surgery. It would be valuable for the individual and for the healthcare to know more about the carcinogenic risk factors.
Reduces the effect of cytostatics
The link between IPMNs and pancreatic cancer is not yet fully known, but earlier studies from Karolinska Institutet and elsewhere indicate that the presence of oral bacteria in the pancreas might be a measure of IPMN lesion severity.

New research from RCSI has demonstrated the significant role that an irregular body clock plays in driving inflammation in the body’s immune cells, with implications for the most serious and prevalent diseases in humans.
Published in Frontiers in Immunology, the research was led by the School of Pharmacy and Biomolecular Sciences at RCSI University of Medicine and Health Sciences.
The circadian body clock generates 24-hour rhythms that keep humans healthy and in time with the day/night cycle. This includes regulating the rhythm of the body’s own (innate) immune cells called macrophages. When these cell rhythms are disrupted (due to things like erratic eating/sleeping patterns or shift work), the cells produce molecules which drive inflammation. This can lead to chronic inflammatory diseases such as heart disease, obesity, arthritis, diabetes and cancer, and also impact our ability to fight infection.
In this study, the researchers looked at these key immune cells called macrophages with and without a body clock under laboratory conditions. They were interested to understand if macrophages without a body clock might use or ‘metabolise’ fuel differently, and if that might be the reason these cells produce more inflammatory products.
The researchers found that macrophages without a body clock took up far more glucose and broke it down more quickly than normal cells. They also found that, in the mitochondria (the cells energy powerhouse), the pathways by which glucose was further broken down to produce energy were very different in macrophages without a clock. This led to the production of reactive oxygen species (ROS) which further fuelled inflammation.
Dr George Timmons, lead author on the study, said: “Our results add to the growing body of work showing why disruption of our body clock leads to inflammatory and infectious disease, and one of the aspects is fuel usage at the level of key immune cells such as macrophages.”
Dr Annie Curtis, Senior Lecturer at RCSI School of Pharmacy and Biomolecular Sciences and senior author on the paper, added: “This study also shows that anything which negatively impacts on our body clocks, such as insufficient sleep and not enough daylight, can impact on the ability of our immune system to work effectively.”
RCSI conducted the study in collaboration with researchers from Swansea University, Trinity College Dublin and University of Bristol.
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Materials provided by RCSI. Note: Content may be edited for style and length.

New research from The University of Texas MD Anderson Cancer Center found that treatment with antihistamines, a commonly used allergy medication, was associated with improved responses to immune checkpoint inhibitors. The preclinical study demonstrated that the histamine receptor H1 (HRH1) acts in tumor-associated macrophages (TAMs) to suppress T cell activation in the tumor microenvironment. The findings were published today in Cancer Cell.
If replicated in prospective clinical trials, the data suggest that targeting HRH1 may be useful as a treatment approach in combination with checkpoint blockade to overcome immunotherapy resistance and improve outcomes, particularly for patients with pre-existing allergies or high plasma histamine levels.
“In searching for factors that might influence responses to immunotherapy, we were surprised to discover that antihistamines, a mediator of the allergy response, were associated with significantly improved outcomes in patients,” said study co-lead Yi Xiao, Ph.D., instructor of Molecular & Cellular Oncology. “Looking closer at this relationship, we discovered that histamine, through its receptor HRH1, can promote cancer cell immune evasion and resistance to immunotherapy.”
Antihistamines associated with improved immunotherapy outcomes
Immune checkpoint inhibitors, a type of immunotherapy, work by blocking certain checkpoint proteins that regulate the activity of T cells, unleashing the T cells to mount an anti-tumor response and eliminate cancer cells. Checkpoint blockade provides long-lasting responses for many patients, but not all benefit equally. Therefore, there is a desire to better understand factors that contribute to immunotherapy sensitivity or resistance.
This study began with the researchers investigating if other commonly used medications might influence responses to checkpoint inhibitors. They performed a retrospective analysis of clinical data from MD Anderson patients undergoing treatment with immune checkpoint inhibitors.

Researchers at the University of Toronto have discovered that an overlooked gene plays a major role in the development of antibodies, which help the immune system recognize and fight viruses including SARS-CoV-2, bacteria and other causes of infectious disease.
The gene — FAM72A — facilitates production of high-quality antibodies by enabling the effect of an enzyme called AID (for Activation-Induced Deaminase), the researchers showed. Immunologists have known for two decades that AID is essential to produce antibodies capable of clearing infections, but the full mechanism of its effect had remained unknown.
“Our findings answer the long-standing question of how AID does its work,” says Alberto Martin, a professor of immunology in U of T’s Temerty Faculty of Medicine. “FAM72A helps AID to promote mutations in antibody genes that are essential for the development of effective antibodies.”
The journal Nature published the findings today, back-to-back with similar results from a research group in France.
Genetic mutations that lead to lasting changes in DNA occur through a process called mutagenesis. In the context of antibody development, mutagenesis unfolds largely through the AID-driven mechanisms called somatic hypermutation and class switch recombination — both of which help antibodies gain the diversity and potency they need to counter a wide range of pathogens.
The results from the Martin lab should help researchers better understand antibody development broadly, but they also have implications for cancer. Uncontrolled mutagenesis in B cells that produce antibodies is linked to B cell lymphoma, and FAM72A is present at very high levels in other cancers such as gastrointestinal, breast, lung, liver and ovarian cancers.

Most human diseases can be traced to malfunctioning parts of a cell — a tumor is able to grow because a gene wasn’t accurately translated into a particular protein or a metabolic disease arises because mitochondria aren’t firing properly, for example. But to understand what parts of a cell can go wrong in a disease, scientists first need to have a complete list of parts.
By combining microscopy, biochemistry techniques and artificial intelligence, researchers at University of California San Diego School of Medicine and collaborators have taken what they think may turn out to be a significant leap forward in the understanding of human cells.
The technique, known as Multi-Scale Integrated Cell (MuSIC), is described November 24, 2021 in Nature.
“If you imagine a cell, you probably picture the colorful diagram in your cell biology textbook, with mitochondria, endoplasmic reticulum and nucleus. But is that the whole story? Definitely not,” said Trey Ideker, PhD, professor at UC San Diego School of Medicine and Moores Cancer Center. “Scientists have long realized there’s more that we don’t know than we know, but now we finally have a way to look deeper.”
Ideker led the study with Emma Lundberg, PhD, of KTH Royal Institute of Technology in Stockholm, Sweden and Stanford University.
In the pilot study, MuSIC revealed approximately 70 components contained within a human kidney cell line, half of which had never been seen before. In one example, the researchers spotted a group of proteins forming an unfamiliar structure. Working with UC San Diego colleague Gene Yeo, PhD, they eventually determined the structure to be a new complex of proteins that binds RNA. The complex is likely involved in splicing, an important cellular event that enables the translation of genes to proteins, and helps determine which genes are activated at which times.

A new study led by researchers at UCLA Health has found that cognitive behavioral therapy (CBT-I) prevented major depression, decreasing the likelihood of depression by over 50% as compared to sleep education therapy in adults over the age of 60 with insomnia.
Their findings, reported today in JAMA Psychiatry, could advance public health efforts to effectively treat insomnia and prevent major depression disorder (MDD) in older adults — a growing population that is projected to rise from about 54 million Americans aged 65 and older today to about 86 million in 2050.
More than 10% of community dwelling adults older than 60 years will experience a major depression later in life in any given year. Late-life depression increases the risk of health conditions such as heart disease and high blood pressure, cognitive decline, and suicide particularly in men. Despite its prevalence in older adults, depression often goes undiagnosed and untreated. And, even among those who receive treatment, only about one-third get better or achieve remission.
“Given that older adults account for nearly 20% of the U.S. population and are the most vulnerable for health risks associated with depression, effective depression prevention is urgently needed,” said Dr. Michael Irwin, lead author of the study and the director of the Cousins Center for Psychoneuroimmunology at the Semel Institute for Neuroscience, and a Professor of Psychiatry and Biobehavioral Sciences at the David Geffen School of Medicine at UCLA. “Insomnia more than doubles the risk for major depression. By targeting insomnia and effectively treating it with CBT-I, depression can be effectively prevented by over 50% in community dwelling older adults with insomnia.”
Insomnia, a condition where people have difficulty falling and staying asleep, occurs in nearly 50% of adults 60 years of age or older and when it occurs, the risk of depression is more than doubled. Although various types of sleep medications are often used to treat insomnia, they provide only temporary relief and pose a risk for daytime side effects such as prolonged drowsiness or headache, and dependency.
Accordingly, CBT-I is recommended as the first line of treatment for people with insomnia and has been highly effective in its treatment. This type of therapy typically centers around working with a therapist to help identify and change inaccurate or?distorted thinking patterns, emotional responses, and behaviors.