Publisher Health

From hot volcanic springs where the water is nearly boiling acid, scientists have discovered how lemon-shaped viruses got their form. And that discovery could lead to new and better ways to deliver drugs and vaccines.
While the vast majority of viruses are either rod-like or spherical (such as the coronavirus responsible for COVID-19), scientists have been puzzled by the unusual forms of viruses found in some of the harshest environments on Earth.
The researchers were studying one such virus when they discovered it has strange properties that let it alter its shape. While it normally resembles a lemon or spindle, the virus can grow tails. The structure that lets it do that, the scientists realized, likely explains how ancient rod-like viruses gave rise to all the spindle-shaped viruses seen today.
“We can now understand a new principle in how proteins can form the shell that packages the DNA in a virus,” said lead researcher Edward H. Egelman, PhD, of the University of Virginia School of Medicine. “This has implications for not only understanding how certain viruses evolved but potentially can be used for new ways to deliver everything from drugs to vaccines.”
One Tough Virus
The virus Egelman and his colleagues were studying, Sulfolobus monocaudavirus 1 (SMV1), has a protein shell surrounding the DNA that is spindle- or lemon-shaped. But it has been a puzzle for almost 20 years exactly how that many copies of the same protein can come together to form such a shape.

Gender-affirming facial surgery (GFS) is pursued by transgender individuals who desire facial features that better reflect their gender identity. Until now, there have been few objective guidelines to justify and facilitate effective surgical decision-making for gender-affirming facial surgery.
In order to validate surgical decisions for GFS, researchers from the UC San Francisco and the University of Calgary set out to quantify the effect of sex on adult facial size and shape through an analysis of three-dimensional (3D) facial surface images.
In a study published online Thursday afternoon in Facial Plastic Surgery & Aesthetic Medicine, the investigators undertook a surgically oriented analysis of 3D facial size and shape to quantify and visualize facial sex differences. Their findings reveal significant differences in both shape and size of male and female craniofacial features and provide data-driven anatomic guidance and justification for GFS, particularly for forehead contouring cranioplasty, mandible and chin alterations, rhinoplasty, and cheek modifications.
“Our purpose was to establish an important, definitive, and biologically-based relationship of facial features to sex. This empowers the patient to navigate towards a facial appearance that matches with their gender identity, and thereby reduces mis-gendering and gender dysphoria while improving self-perception,” said senior author Rahul Seth, MD, Associate Professor in the Facial Plastic and Aesthetic Surgery in the UCSF Department of Otolaryngology-Head and Neck Surgery. “We feel that this data provides surgeons, patients, and insurance payors with a life-like and surgically-oriented analysis of 3D facial size and shape to guide patients and surgeons in performing these complex and life-altering surgeries.”
Brow, jaw, nose, cheek show biggest differences by sex
The researchers were able to determine that, on average, male faces are 7.3% larger than female faces. Sex was associated with significant facial shape differences in the entire face as well as in each sub-region considered in the study. The facial regions in which sex has the largest effect on shape are the brow, jaw, nose, and cheek. The authors, therefore, provide supportive evidence and guidelines for the appropriate alterations of these facial areas for GFS, although each individual patient’s goals and face is unique.

While potentially crucial to preventing the spread of COVID-19, lockdowns are associated with increased rates of depression and anxiety as well as food insecurity among women in India and other parts of the developing world, according to a new research.
The study from the University of California San Diego’s School of Global Policy and Strategy finds that women whose social position may make them more vulnerable — those with daughters and those living in female-headed households — experienced even larger declines in mental health as a result of lockdowns.
The paper, to be published in a forthcoming issue of the Journal of Economic Development, surveyed 1,545 households over the phone in various rural regions throughout Northern India. The surveys took place in fall 2019, before the pandemic and in August 2020, near the height of the first COVID-19 wave in India. Certain villages and districts had varying containment policies, which allowed the researchers to compare health outcomes of women who experienced lockdowns for several months to those who experienced zero levels of lockdowns.
The authors took many factors into consideration in their analysis including COVID cases, hospitalizations and deaths from the novel coronavirus.
For surveyed women, moving from zero to average levels of lockdowns is associated with a 38 percent increase in depression, a 44 percent increase in anxiety and a 73 percent increase in exhaustion.
“Not having access to access to work and socialization outside the home can be very detrimental for women’s mental health in developing countries,” said study co-author Gaurav Khanna, assistant professor of economics at the School of Global Policy and Strategy.

A novel angiogenic microRNA drug can be a new option for the treatment of ischemic cardiovascular disease, according to a new study published in PLOS ONE by researchers from the University of Eastern Finland together with international collaborators. In the study, the researchers describe a novel nuclear acting microRNA.
MicroRNAs are small RNA molecules, which regulate gene expression. Their canonical role is gene silencing by targeting messenger RNAs in cell cytoplasm. However, this novel microRNA, miR-466c, has a different mechanism of action. It upregulates the vascular endothelial growth factor A (VEGFA) by targeting the gene promoter in the cell nucleus.
In addition to expanding the academic understanding of microRNA biology, these findings have commercial relevance for the development of novel RNA drugs. Increasing the expression of VEGFA by using small RNAs offers novel options for the treatment of ischemic cardiovascular disease, where the blood supply in the tissue is compromised.
“RNA activation as a phenomenon has been known for 16 years already, but its commercial potential has been recognised only recently,” says Adjunct Professor Mikko Turunen, Chair of the newly founded RNatives company, which will be commercialising the patented microRNA drug.
“Our patented microRNA drug has several advantages over traditional means of increasing gene expression. First of all, by activating the cell’s own therapeutic gene (e.g., VEGFA), all the different spliceforms of the gene are correctly produced. Also, being a small RNA, it is much less immunogenic and more stable than longer RNAs, such as mRNA based drugs,” Turunen says.
In addition to RNA drugs, RNatives is developing engineered exosomes for the delivery of these RNAs into the patients.
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Recent discoveries made by researchers from Charité – Universitätsmedizin Berlin may prove vital in improving the treatment of dystonia, a neurological movement disorder. Published in PNAS, their findings show that very specific networks in the brain must be stimulated in order to relieve the symptoms seen in different types of dystonia.
Dystonia is a rare neurological disorder, which is characterized by involuntary, twisting and distorting movements and postures. People with dystonia may be limited in their ability to perform activities of daily living, such as drinking, walking and speaking. In Germany, approximately 160,000 people have dystonia. The condition is subdivided into generalized dystonia, which affects the entire body, and focal dystonia, which is limited to specific parts of the body. The latter category includes cervical dystonia, which affects the neck. The condition’s underlying causes are not fully understood, but experts assume that symptoms are the result of faulty interactions between specific areas of the brain which lead to abnormal signal transmission. Depending on the form of dystonia involved, genetic defects may also play a role.
One treatment option available to patients with dystonia is a neurosurgical procedure involving the implantation of electrodes into specific areas of the brain. Once implanted, the electrodes emit weak electrical signals which help to restore normal brain function. Known as deep brain stimulation, the procedure involves the implantation of a pacemaker-like device and is often the only treatment capable of providing relief of symptoms.
“The precision with which this stimulation has to be adapted to the symptoms seen in different types of dystonia was not clear until now,” explains study lead Prof. Dr. Andrea Kühn, who is Head of the Department of Neurology and Experimental Neurology’s Movement Disorders and Neuromodulation Section and Spokesperson of the ‘ReTune’ Transregional Collaborative Research Center (SFB/Transregio TRR 295), which helped to support the current study.
Prof. Kühn’s team examined a total of 80 patients who had received treatment for either generalized or cervical dystonia at one of five different hospitals in Germany and Austria. After analyzing the electrodes’ precise positions, the researchers were able to generate computer models showing which brain networks were being activated in each of the patients investigated. By mapping data on symptom improvements to their network models, the researchers were then able to determine which of the identified networks were crucial to treatment success.
One key finding was that the optimal target for stimulation depends on the type of dystonia being treated. This means that optimal treatment outcomes were associated with specific connections between the thalamus (the largest structure in the diencephalon, or ‘interbrain’) and the pallidum (a pale-colored structure at the core of the basal ganglia). The basal ganglia are deep-seated brain structures which play a part in movement control. In patients with cervical dystonia, the determining factor was electrical stimulation of a specific neural network which also activated the head and neck region of the primary motor cortex. As the brain’s motor command center, this area is responsible for planning and initiating movements as well as storing movement memory. In contrast, for patients with generalized dystonia, beneficial effects were elicited through the stimulation of a different network which projected to the entire primary motor cortex.
“Our study shows clear differences in optimal stimulation sites, which correspond to the somatotopic structure of the inner pallidum. This means that neural areas in the brain map to the areas of the body they represent,” says the study’s first author, Dr. Andreas Horn of the Department of Neurology and Experimental Neurology. He adds: “Due to the paucity of alternative treatment options beyond deep brain stimulation, our findings make an important contribution to improving treatment for dystonia. In the future, we will be able to more deliberately treat specific types of the disorder.”
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Infant monkeys conceived while their mothers were naturally exposed to wildfire smoke show behavioral changes compared to animals conceived days later, according to a new study from researchers at the California National Primate Research Center at the University of California, Davis. The work is published April 1 in Nature Communications.
The findings show the importance of timing in effects of smoke exposure on pregnancy and suggest a teratogenic, or developmental mechanism, said senior author Bill Lasley, professor emeritus of population health and reproduction at the UC Davis School of Veterinary Medicine and Center for Health and Environment.
“I think this will have an effect on future studies of exposures in pregnancy, because we’ll know when to look,” Lasley said. Existing studies of environmental exposures during pregnancy in humans are mostly retrospective, and women may not even realize they are pregnant until weeks into the first trimester, he said.
The Camp Fire, which began Nov. 8, 2018, provided a natural experiment in smoke exposure. It blanketed the Davis area, some 100 miles away, with smoke at the peak of breeding season for rhesus macaques housed in outdoor corrals at the California National Primate Research Center.
The 89 animals conceived around that time were born about six months later. They divide between 52 animals conceived on or before Nov. 22, 2018 which were considered as “exposed” to wildfire smoke in their first trimester, and 37 conceived later which were not exposed.
John Capitanio, professor of psychology at UC Davis and a core scientist at the CNPRC, has been conducting standardized assessments on animals born at the Center for two decades. At about 3-4 months old, the young monkeys are assessed on a variety of cognitive and behavioral tests. While the number of animals conceived during the Camp Fire that were assessed was fairly small, they could be compared not only to each other (exposed vs. not exposed), but also to the historical data from hundreds of animals.

Scientists have long queried the causes of immune disorders in only one of two identical twins with identical genes. New research from the Wellcome Sanger Institute, the Josep Carreras Leukaemia Research Institute in Spain and their collaborators, has found the answer lies in both alterations in immune cell-cell communication and the epigenome, the host of biological processes that regulate how our genes function.
The study, published today (1 April 2022) in Nature Communications, is the first cell atlas to categorise common variable immunodeficiency (CVID) at the single-cell resolution. Researchers found that ‘communication problems’ resulting from defects in B cells and other immune cell types impaired immune response, highlighting a number of pathways that are promising targets for epigenetic treatments. In addition, they also identified major defects in the epigenome.
Common variable immunodeficiency (CVID) encompasses a range of immune disorders caused by a reduced ability to produce protective antibodies, which leaves the individual vulnerable to persistent or repeated infection. These individuals usually have low levels of immunoglobulin, more commonly known as antibodies,due to problems with the B cells that create them.
Though identical twins share the same genome, most will be born with a small number of genetic and epigenetic differences and the number of variations will increase over their lifetime. But where one twin experiences a health problem that their sibling does not, in most cases genetic differences alone cannot explain why this has occurred.
Around 20 per cent of CVID cases can be attributed to a defect in a gene associated with the condition. But with four in five cases remaining largely unexplained, scientists have predicted that other factors must be involved. This was confirmed by a recent study, which linked CVID to DNA methylation, an epigenetic process that turns the level of a particular gene up or down1.
In this new study, researchers from the Wellcome Sanger Institute and the Josep Carreras Leukaemia Research Institute generated single-cell data to investigate epigenetic factors involved in CVID. Samples were taken from a pair of identical twins, only one of whom suffered from CVID, as well as a wider group of CVID patients and healthy individuals.

COVID-19 patients commonly report having headaches, confusion and other neurological symptoms, but doctors don’t fully understand how the disease targets the brain during infection.
Now, researchers at Tulane University have shown in detail how COVID-19 affects the central nervous system, according to a new study published in Nature Communications.
The findings are the first comprehensive assessment of neuropathology associated with SARS-CoV-2 infection in a nonhuman primate model.
The team of researchers found severe brain inflammation and injury consistent with reduced blood flow or oxygen to the brain, including neuron damage and death. They also found small bleeds in the brain.
Surprisingly, these findings were present in subjects that did not experience severe respiratory disease from the virus.
Tracy Fischer, PhD, lead investigator and associate professor of microbiology and immunology at the Tulane National Primate Research Center, has been studying brains for decades. Soon after the primate center launched its COVID-19 pilot program in the spring of 2020, she began studying the brain tissue of several subjects that had been infected.
Fischer’s initial findings documenting the extent of damage seen in the brain due to SARS-CoV-2 infection were so striking that she spent the next year further refining the study controls to ensure that the results were clearly attributable to the infection.
“Because the subjects didn’t experience significant respiratory symptoms, no one expected them to have the severity of disease that we found in the brain,” Fischer said. “But the findings were distinct and profound, and undeniably a result of the infection.”
The findings are also consistent with autopsy studies of people who have died of COVID-19, suggesting that nonhuman primates may serve as an appropriate model, or proxy, for how humans experience the disease.
Neurological complications are often among the first symptoms of SARS-CoV-2 infection and can be the most severe and persistent. They also affect people indiscriminately — all ages, with and without comorbidities, and with varying degrees of disease severity.
Fischer hopes that this and future studies that investigate how SARS-CoV-2 affects the brain will contribute to the understanding and treatment of patients suffering from the neurological consequences of COVID-19 and long COVID.
The COVID-19 pilot research program at the Tulane National Primate Research Center was supported by funds made possible by the National Institutes of Health Office of Research Infrastructure Program, Tulane University and Fast Grants.
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Increased levels of blood fats in people with type 2 diabetes and obesity are more harmful than previously thought, a new study has found.
In patients with metabolic diseases, elevated fat levels in the blood create stress in muscle cells — a reaction to changes outside the cell which damage their structure and function.
University of Leeds researchers have discovered that these stressed-out cells give off a signal which can be passed on to other cells.
The signals, known as ceramides, may have a protective benefit in the short-term, because they are part of a mechanism designed to reduce stress in the cell. But in metabolic diseases, which are long term conditions, the signals can kill the cells, make symptoms more severe, and worsen the illness.
Increased fat in the blood has long been known to damage tissues and organs, contributing to the development of cardiovascular and metabolic diseases including type 2 diabetes. The condition can be caused by obesity, rates of which have nearly tripled worldwide since 1975. In 2016, there were more than 650 million adults aged 18 and above with obesity.
Research supervisor Lee Roberts, Professor of Molecular Physiology and Metabolism in the University of Leeds’s School of Medicine, said: “Although this research is at an early stage, our discovery may form the basis of new therapies or therapeutic approaches to prevent the development of cardiovascular and metabolic diseases such as diabetes in people with elevated blood fats in obesity.”
In the lab, the team replicated the blood fat levels observed in humans with metabolic disease by exposing skeletal muscle cells to a fatty acid called palmitate. The cells began to transmit the ceramide signal.

SharecloseShare pageCopy linkAbout sharingImage source, Getty ImagesThe government has been called “disrespectful” for ending a UK-wide scheme that provided financial support to families of deceased health and social care workers in the pandemic. Families of staff who contract Covid at work and then die are no longer entitled to the £60,000 compensation.The Royal College of Nursing (RCN) says it is not the right time to stop. Ministers say the scheme was always intended to be time-limited and there are other death in-service benefits.But the RCN has written to Health Secretary Sajid Javid calling for an extension of life assurance payments.Although vaccines are helping to protect people, including NHS staff, against severe Covid, some deaths are still occurring. Memorial pays tribute to NHS workers who died because of CovidOfficial records for England, Scotland and Wales say 304 NHS staff have died from Covid following workplace exposure, including 10 since the start of December 2021.RCN chief executive Pat Cullen said: “Ending this scheme now is disrespectful to staff continuing to work under pandemic conditions in health and social care.”Her letter to Mr Javid says: “The overriding principle must be that no member of nursing staff who loses their life this year should be afforded any less respect and family support than one who died in 2020 or 2021. “The pandemic is far from over.”I urge you to delay the end of the scheme until a time when nursing staff and all health and care workers are assured that their lives are not at such risk from the pandemic.”Speaking at a Covid death memorial service held last week for NHS frontline workers, Rev Paul Nash, chaplain at Birmingham and Women’s Children Hospital, said staff and carers sacrificed their “mental and physical health”, with many paying the ultimate sacrifice with their lives.”We will never, ever forget and we will be forever grateful,” he said.A Department of Health and Social Care spokesperson said: “Every death from this virus is a tragedy, and our deepest sympathies go out to anyone who has lost a loved one.”The Life Assurance Scheme was introduced to recognise the exceptional risk faced by frontline NHS and social care staff working at peak periods of the pandemic, and was always intended to be time-limited.”NHS staff continue to be eligible for death in-service benefits through the NHS Pension Scheme, including a twice-salary lump sum and pensions for a surviving partner and dependants.”More on this story’He was my soulmate, my everything’Compulsory Covid jabs for care home staff scrappedUK Covid infections climb by a million in a week