Publisher Health

Researchers have reported findings that add to our knowledge of how human behavior may be shaped by the default mode network, a specific network of brain regions with both resting and task-related states. The article, “Reward enhances connectivity between the ventral striatum and the default mode network,” was epublished on June 18, 2022, in NeuroImage. The authors are Ekaterina Dobryakova, PhD, of Kessler Foundation and David V. Smith, PhD, of Temple University.
The default mode network (DMN), which comprises the posterior medial cortex, medial prefrontal cortex, and lateral temporal-parietal regions, has been shown to be engaged in several task-related behaviors. Studies show that DMN activity increases during inward-directed thought and decreases during externally directed tasks requiring focused attention. Despite evidence for a role for the DMN in shaping behavior, little is known about how task-related changes in the DMN influence connectivity with other brain regions. For example, while some observations indicate an indirect relationship between the DMN and the striatum, how the DMN and striatum interact during tasks remains unclear.
To further explore the functions of the DMN, Drs. Dobryakova and Smith applied a novel analysis to the reward task, using behavioral and neuroimaging data from 495 randomly selected individuals in the Human Connectome Project, an open access database of healthy participants. The goals of this network-based psycho-physiological interaction analysis were twofold, according to Dr. Dobryakova, a senior research scientist in the Foundation’s Center for Traumatic Brain Injury Research. “First, to test the effects of reward on connectivity between the DMN and the striatum; and second, whether such connectivity is associated with behavioral and personality characteristics relevant to reward processing,” she explained.
In line with other studies, during the task, they observed decreased activation of the DMN and relative increased activation of other networks. “Most notably, we found that the experience of reward enhanced connectivity between the DMN and the ventral striatum,” Dr. Dobryakova reported, “an effect specific to the DMN. We were also surprised that the strength of this connectivity correlated with personality characteristics relating to openness,” she added.
Greater understanding of the workings of the healthy brain will influence future research and care for individuals with neuropsychiatric syndromes. “Improving our understanding of the interaction of the DMN with other brain networks has the potential to aid clinical research into better treatments for common syndromes such as depression, substance abuse, and schizophrenia,” Dr. Dobryakova concluded.
This research was supported by grants from the National Institutes of Health grants R21-MH113917 (DVS), R03-DA046733 (DVS), RF1-AG067011 (DVS), R01-NS121107 (ED).
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A genomic test being developed by a Charlottesville, Va., company can predict a patient’s risk of developing severe COVID-19, new research from UVA Health suggests. That information could help doctors identify patients at high risk for poor outcomes and quickly begin tailored treatment.
The approach proved more than 90% accurate at predicting outcomes among more than two dozen patients in the intensive care unit at UVA and 100 patients from publicly available data generated at Duke and Harvard. The test, called CovGENE, analyzes genes expressed in a person’s blood to determine whether they may experience a severe disease course with increased risk of death.
“We have come far in the prevention and treatment of COVID-19 in the past two years. Regardless, we still struggle to identify patients at highest risk for severe disease. Our study uses a gene-analysis approach to identify an immune cell signature, distinct from other respiratory illnesses, that correlates with worse outcomes,” said researcher Alexandra Kadl, MD, of UVA Health’s Division of Pulmonary and Critical Care Medicine. “This knowledge has the potential to help evaluate patients’ immune profile with commonly, readily available assays to identify patients at risk for bad outcomes who would benefit from closer monitoring and advanced therapies to aid their recovery.”
Predicting COVID-19 Severity
Based on the promising results of the UVA research, CovGENE’s developer, AMPEL Biosolutions, is seeking to partner with a diagnostic testing company or pharmaceutical company to bring the approach to market as a simple PCR-based blood test.
“This unique collaboration with our colleagues from the University of Virginia has provided an easy and novel means to assess an individual patient’s response to the SARS-CoV-2 virus and predict the clinical outcome,” said Peter Lipsky, MD, AMPEL’s CEO, chief medical officer and co-founder. “Now that this unique approach has been validated, we look forward to its rapid development as a precision-medicine tool that can improve the outcome of patients with COVID-19 and reduce the number of hospitalizations, especially the most vulnerable.”
AMPEL Biosolutions aims to use genomic data to improve healthcare for patients. The company develops gene expression tests for blood or tissue samples to assist doctors in clinical decision-making.
Company co-founder Amrie Grammer, PhD, is an alumna of UVA, having received both her bachelor’s and master’s degree there.
Findings Published
The researchers have published their findings in the journal Frontiers in Immunology. The team consisted of Andrea R. Daamen, Prathyusha Bachali, Catherine A. Bonham, Lindsay Somerville, Jeffrey M. Sturek, Amrie Grammer, Alexandra Kadl and Peter Lipsky. Daamen, Bachali, Grammer and Lipsky are employed by AMPEL BioSolutions.
The work was supported by the National Institutes of Health’s National Heart Lung Blood Institute, grant K23 HL143135; the National Institute of Allergy and Infectious Diseases, grant 1R21AI160334; the COVID-19 Rapid Response Initiative by UVA’s Global Infectious Disease Institute; and The RILITE Foundation.
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The first study to treat moderate-to-severe eczema in infants and children 6 months to 5 years old with a biologic drug (monoclonal antibody) rather than immune-suppressing medications shows the drug was highly effective in reducing the signs and symptoms of moderate-to-severe eczema, report researchers involved in a new multi-site international phase III study led by Northwestern Medicine.
A 16-week course of dupilumab, a medication that targets a key immune pathway in allergies, resulted in more than half the children having at least a 75% reduction in signs of eczema and highly significant reductions in itch with improved sleep.
This is the first large-scale, randomized, placebo-controlled trial of a monoclonal antibody in any skin disease, including eczema, in children as young as 6 months. The study, which included 31 sites in Europe and North America, will be published Sept. 15 in The Lancet.
“Preschoolers who are constantly scratching, awake multiple times a night with their parents, irritable and markedly curtailed in their ability to do what other children their ages can do improved to the extent that they sleep through the night, change their personalities and have a normal life — as babies and children should,” said lead study author Dr. Amy Paller, chair of dermatology at Northwestern University Feinberg School of Medicine and an attending physician at Ann & Robert H. Lurie Children’s Hospital of Chicago.
Eczema, also known as atopic dermatitis, is a chronic inflammatory skin disorder characterized by red, dry, often oozing skin and itch that can profoundly affect the lives of affected patients and their families.
An estimated 19% or more of all children under 6 years of age have eczema and 85 to 90% of individuals affected overall with eczema have the onset of disease during the first five years of life.

A prospective seroprevalence study in the Catalan population underlines the need to get vaccinated despite having been infected, and confirms that hybrid immunity (vaccination plus infection) is more robust and long-lasting. The study, co-led by the Barcelona Institute for Global supported by the Daniel Bravo Andreu Foundation (FDBA), has been published in BMC Medicine.
Both infection and vaccination against SARS-CoV-2 contribute to building a population’s immunity to the virus — an important factor for deciding when and to whom booster shots should be offered. Although immunity against a pathogen is more than antibodies, the easiest strategy for assessing population immunity is to perform seroepidemiological studies (i.e., quantifying virus-specific antibodies in a given population group).
“Most of the serological studies performed after COVID-19 vaccination focused on specific groups such as healthcare workers, did not distinguish between people with or without previous infection, or did not have clinical and immunological data of the infection,” explains Manolis Kogevinas, ISGlobal researcher and senior co-author of the study together with Carlota Dobaño, also researcher at ISGlobal.
In this study, the research team performed a second measurement in a population-based cohort from Catalonia (COVICAT study — GCAT cohort) six months after the start of the vaccination campaign (the first one was just after the first confinement), to monitor the level and type of antibodies against five viral antigens (the whole Spike (S) protein, the RBD receptor binding domain, the S2 fragment, the full nucleocaspid (N) protein, or the N-terminal fragment). They also used information from a questionnaire and health records to identify potential factors that determine the magnitude and duration of the antibody response in unvaccinated, vaccinated, or vaccinated and infected persons. A total of 1,076 people, aged 43 to 72 years, were included in the analysis.
The results yielded three main conclusions: First, that in 36% of infected but unvaccinated persons, antibodies were no longer detectable almost a year after the infection, particularly in those older than 60 years and smokers.
Second, that vaccination induced significantly higher antibody levels in people who had a prior infection, as compared to those without prior infection; and that these levels were strongly associated with the magnitude of the response during the infection. “Our data underscore the importance of vaccinating people even if they have been previously infected, and confirm that hybrid immunity is superior and more durable. This means that people who have been vaccinated but have not been infected would need a booster earlier than those who have,” points out Marianna Karachaliou, first author of the study together with Gemma Moncunill.
Third, the factor most strongly associated with the level of antibodies is the type of vaccine — Moderna’s Spikevax generated the highest levels of antibodies. Other factors also appear to play a role: people older than 60 or with mental illness had lower antibody levels post-vaccination. “The association between mental health and antibody responses requires further investigation, but it is known that people with disorders such as depression, chronic stress or schizophrenia have a lower response to vaccination in general,” explains Dobaño.
Among those vaccinated, only 2.1% had no antibodies at the time of testing and approximately 1% had a breakthrough infection. “However, it should be noted that this study was done before the Omicron variant became dominant,” warns Kogevinas.

The human gut microbiome is composed of thousands of different bacteria and archaea that vary widely between populations and individuals. Scientists from the Max Planck Institute for Biology in Tübingen have now discovered gut microbes that share a parallel evolutionary history with their human hosts: the microorganisms co-evolved in the human gut environment over hundreds of thousands of years. In addition, some microbes exhibit genomic and functional features making them dependent on their host. Now published in Science, the researchers present the results of their study conducted with data from 1225 individuals out of Africa, Asia and Europe.
Many microbe species in the human gut can be found across populations from all over the world. However, within a microbe species the microbe strains vary remarkably between individuals and populations. Despite their importance for human health, little was known so far about the origins of these strains. Moreover, most of these strains live almost exclusively in the human gut. This raises the question of where the microorganisms in the human gut come from.
The research team conjectured that specific species and strains have been with people as humanity diversified and spread over the globe. To test if microbes evolved and diversified simultaneously with their human hosts, researchers from the Max Planck Institute for Biology, the Institute for Tropical Medicine, and the Cluster of Excellence CMFI at the University of Tübingen systematically compared for the first time the evolutionary histories of humans and of gut microbes. The researchers created phylogenetic trees for 1225 human study participants as well as for 59 microbial species found within their guts, and used statistical tests to investigate how well these trees match.
Over 60 percent of the investigated species matched with the evolutionary history of their human host, meaning that these microbes co-diversified over ~100,000 years in the human gut when people fanned out of Africa across the continents. “We didn`t know that any of our gut microbes followed our evolutionary history this closely,” marvels Ruth Ley, head of the department for Microbiome Science at the Max Planck Institute for Biology, Tübingen, where the study was conducted, and deputy spokesperson of the CMFI.
Gut microbes became dependent on their hosts
“It is also remarkable that the strains that followed our history most closely are now those who rely most on the gut environment,” Ley adds. Indeed, some of the microbe strains that evolved together with humans are heavily dependent on the human gut environment: they possess smaller genomes and are more sensitive to oxygen levels and temperature — traits making it difficult to survive outside the human body. In contrast, microorganisms that showed weaker association with the human history showed more characteristics similar to free living bacteria. “Some of the gut microbes behave like they are part of the human genome,” explains Taichi Suzuki, who shares main authorship of the study with his colleague Liam Fitzstevens. Suzuki adds: “You can imagine that those microbes are on a gradient from ‘free-living’ to reliant on the human body environment. We have seen that some human gut bacteria are further along the gradient towards irreversible host dependence than previously thought.” Ley further states: “This fundamentally changes how we view the human gut microbiome.”
To obtain data from a diverse subset of the global population, the research team analyzed the gut microbes and genomes of 1225 individuals in Europe, Asia, and Africa. The stool and saliva samples were collected with the help of researchers from the Institute for Tropical Medicine at the University of Tübingen and their partners in Vietnam and Gabon. In addition, researchers around the globe supported the study by providing similar datasets from participants recruited in Cameroon, South Korea, and the UK.
The findings of the study help to further understand population-specific microbes that have long been associated with the local human population. With this knowledge, microbiome-based therapies of diseases can be adapted and refined to a population-specific treatment.
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Conventional wisdom holds that low protein intake is essential for kidney disease patients. However, scientists from Osaka Metropolitan University demonstrated that it might not always be the case with their recent study on the relationship between protein intake and skeletal muscle mass in kidney transplant recipients. Their findings were published in Clinical Nutrition.
Chronic kidney disease patients are known to have induced sarcopenia due to chronic inflammation, hypercatabolism, decreased nutrient intake, and decreased physical activity associated with impaired kidney function. Recovery of renal function due to successful kidney transplantation is able to correct or improve many of those physiological and metabolic abnormalities. As a result, kidney transplant recipients increase skeletal muscle mass after kidney transplantation. Since excessive protein intake worsens kidney function, it is commonly believed that patients with chronic kidney disease, including kidney transplant recipients, should limit protein intake to protect their kidneys. On the other hand, it has been suggested that severe protein restriction may worsen sarcopenia and adversely affect prognosis.
Since nutrition and exercise therapy are recommended to improve sarcopenia, protein intake is suspected to relate to recovery of skeletal muscle mass after kidney transplantation. However, few studies have examined the relationship between skeletal muscle mass and protein intake in kidney transplant recipients.
Responding to this gap, the research group led by Dr. Akihiro Kosoku, Dr. Tomoaki Iwai, and Professor Junji Uchida at the Department of Urology, Graduate School of Medicine, Osaka Metropolitan University investigated the relationship between changes in skeletal muscle mass — measured by bioelectrical impedance analysis — and protein intake, which was estimated from the urine collected from 64 kidney transplant recipients 12 months after kidney transplantation. The results showed that changes in skeletal muscle mass during this period were positively correlated with protein intake, and that insufficient protein intake resulted in decreased muscle mass.
Dr. Iwai and Dr. Kosoku commented, “To improve the life expectancy of kidney transplant recipients, further research is needed to clarify the optimal protein intake to prevent either deterioration in kidney function or sarcopenia. We hope that nutritional guidance, including protein intake, will lead to improved life expectancy and prognosis.”
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During development, the cells of an embryo divide until a fully functional organism emerges. One component of the cell is especially important during this process: the cell cortex. This fine network of hair-like filament structures (called actin) just below the cell membrane is the main determinant of cell shape and is involved in almost everything a cell does, such as moving, dividing, or sensing its environment. Yet, the cortex must first be built from single molecules, and if it is not built just right, the cells of an organism would never get to the right place to perform their functions.
An international team of researchers from the Max Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG) in Dresden, the Max Planck Institute for the Physics of Complex Systems (MPI-PKS), and the Cluster of Excellence Physics of Life (PoL) at the TU Dresden studied the formation of this dynamic cell cortex in the roundworm Caenorhabditis elegans. They found that thousands of dynamic and short-lived droplet-like condensates made up of actin filaments control the generation of a first cortex, at the time when an unfertilized egg cell transitions into an embryo after fertilization. The principles uncovered in this study help to understand how the formation of subcellular structures is controlled.
Right after an egg cell is fertilized, the formation of the cell cortex begins, and it takes about ten minutes until it is fully formed. The cortex consists of actin filaments and motor proteins, which are organized into a dense crosslinked network. The dynamics of the cortex stem from motor proteins pulling on actin filaments, generating stresses that result in cortical tension. This cortical tension drives, for example, the shape of cells, their ability to sense their environment and their ability to perform their functions in our bodies. The dynamics of the cell cortex has been intensely studied in the past, but the mechanism by which the cell cortex is first activated right after fertilization is unknown. It is crucial to understand the principles behind the cell cortex formation since it is involved in almost every function of the cell, and improper cortical organization leads to an impairment of key cellular and developmental processes.
Protein condensates have a short life and ensure proper development
To investigate how the cell cortex gets activated, an interdisciplinary team of researchers at MPI-CBG, MPI-PKS, and PoL studied this process in the roundworm C. elegans. “We were able to observe how actin and the actin-nucleating proteins WSP-1 and ARP2/3 came together to assemble into condensates that lasted only seconds, just to disassemble right thereafter. These condensates ensure that there is the right amount of actin filaments and that they are connected in just the right way. To me, the beauty of these structures, made of highly branched actin filaments, like a snowflake, lies in what their dynamics teach us about the unconventional chemistry of living matter,” explains Arjun Narayanan, one of the lead authors of the study and researcher in the group of Stephan Grill, director at MPI-CBG. Victoria Tianjing Yan, the other lead author, continues, “We developed our own imaging and image analysis method, called mass balance imaging, to study how the structure of the short-lived condensates grows and evolves.” During their studies, the researchers found that internal chemical reactions control how fast a condensate grows and when it shrinks away. Thus, cortical condensates robustly organize their own life cycle, largely independent of their external environment.
Stephan Grill summarizes, “We conclude that the condensates in the cell cortex represent a new type of biomolecular condensate driven by specific chemical reactions to assemble and disassemble within seconds.” He adds, “We suggest that these short-lived condensates control the activation of the cell cortex and the delicate precision of its growing architecture after fertilization of the C. elegans oocyte. Frank Jülicher, director at MPI-PKS and another supervising author, adds, “This study is yet another example of bridging physics and biology here in Dresden. Our interactive environment with biologists and theoretical physicists together ensures new interdisciplinary approaches to unravel the physics of biological processes.”

In Germany, about ten per cent of all children are born before the 37th week of pregnancy and are thus considered premature. Many of these premature babies require help with breathing due to their underdeveloped lungs. However, clinical practice shows that mechanical ventilation can cause irreversible damage to the lungs, although the exact causes are not yet known. In an interdisciplinary study, physicists and physicians at Leipzig University have now shown that increased pressure on the lung tissue, as caused by mechanical ventilation, poses the risk of overstretching the tissue, even with small amounts of air, and disrupting cell function during gas exchange.
They have just published the results of their study in the journal Frontiers in Bioengineering and Biotechnology. During normal breathing, the diaphragm descends below the lungs with each breath. This causes the lungs to expand inside the chest, creating a negative pressure, or vacuum, in the lungs. To compensate for this negative pressure, air automatically flows into the lungs and the person breathes in. Mechanical ventilation involves pumping air into the lungs through a tube. The lungs then expand due to this positive pressure. “We assume that this positive pressure causes a slight compression of the lung tissue, whereas during normal breathing the lung is ‘pulled’ from the outside in order to create the expansion,” explains physicist Professor Mareike Zink, who conducted the interdisciplinary study on the physics of the premature lung together with her colleague Dr Mandy Laube from the neonatology research laboratory at the Faculty of Medicine.
“In our experiments, we studied foetal lung tissue under tensile and compressive stress to explore differences in tissue mechanics in the premature lung,” Mareike Zink reports. The experiments showed that the lung tissue deformed completely elastically under tension, as occurs during normal breathing. When subjected to pressure, however — as occurs with mechanical ventilation — viscoelastic deformation of the lungs was observed. This means that although the tissue returns to its original state after deformation, at the molecular level, there are already structural changes that indicate irreversible tissue damage.
“Furthermore, our results show that lung cell function is impaired under pressure. Even low pressure, as is common in mechanical ventilation, can result in structural units on the cell surface, which are important in the transport of molecules and water, for example, no longer being able to perform their function,” explains Mandy Laube.
The two scientists draw the following conclusion: for some premature infants, mechanical ventilation is the only treatment to ensure survival. Nevertheless, there is a risk of complications due to the altered mechanical properties of premature lungs compared to adults. Future therapeutic strategies should therefore consider the influence of physical forces on tissues and cells, and limit pressure increases in the lungs so as to minimise the risk of damage. “Since it has also been observed in ventilated Covid-19 patients that mechanical ventilation may result in further lung damage, we postulate that here, too, the damaged lung can be more easily overstretched by the positive pressure and that lung cell function stops or changes more quickly under increased pressure,” Mareike Zink concludes.
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Materials provided by Universität Leipzig. Original written by Susann Huster. Note: Content may be edited for style and length.

Human beings and fruit flies have very little in common — at first sight. However, studying these flies it is in fact possible to find out more about human nature, particularly when it comes to depressive disorders. It is on this basis that scientists at Johannes Gutenberg University Mainz (JGU) are attempting to gain a better understanding of depression-like states and thus improve means of treating them. The results were published recently in the journal Current Biology.
Natural substances used in traditional Asian medicine could prove beneficial
“We have been looking at the effects of natural substances used in traditional Asian medicine, such as in Ayurveda, in our Drosophila fly model,” explained Professor Roland Strauss of the JGU Institute of Developmental Biology and Neurobiology (IDN). “Some of these could have an anti-depressive potential or prophylactically strengthen resilience to chronic stress, so that a depression-like state might not even develop.” The researchers intend, among other things, to demonstrate the efficacy of these substances, to identify their optimal formulations, and to isolate the actual active substances in pure form from the original plant material. In the long run, these might be marketed as drugs. But there is still a long way to go — after all, this is basic research.
“In the Drosophila model we can pinpoint exactly where these substances are active because we are able to analyze the entire signaling chain,” Strauss pointed out. “Furthermore, every stage in the signaling pathway can also be proven.” The researchers subject the flies to a mild form of recurrent stress, such as irregular phases of vibration of the substrate. This treatment results in the development of a depression-like state (DLS) in the flies, i.e., they move more slowly, do not stop to examine unexpectedly encountered sugar, and — unlike their more relaxed counterparts — are less willing to climb wide gaps. How does their behavior change when the flies receive the various natural substances? The results depend decisively on the preparation of each natural substance — for example, whether it has been extracted with water or alcohol.
Evening rewards can ameliorate depression
The research team has also discovered that if they reward the flies for 30 minutes on the evening of a stressful day, by offering them food with a higher sugar content than usual, or by activating the reward signaling pathway, this can prevent the development of a DLS. But what happens when the flies get a sugar reward? It was already known that the flies have sugar receptors on their tarsi, i.e., the lower part of their legs, and their proboscis, while the end of the signaling pathway at which serotonin is released onto the mushroom body had also been located. The mushroom body is a center for associative learning in flies, equivalent to the human hippocampus.
The researchers’ investigations showed that the pathway was considerably more complex than anticipated. Three different neurotransmitter systems have to be activated until the serotonin deficiency at the mushroom body, which is present in flies in a DLS, is compensated for by reward. One of these three systems is the dopaminergic system, which also signals reward in humans. In view of these findings, however, human beings should not assume that it would be a good idea to consume foods with a high sugar content accordingly. Flies perceive sweetness as a reward, whereas humans can achieve the same effect by other and more healthy means.
Boosting resilience by preventing depression
In addition, the researchers decided to look for resilience factors in the fly genome. Just like humans, Drosophila flies have an individual genetic make-up — no two flies are identical in this respect. For this reason, the team intends to find out whether and how the genomes of flies that are able to better cope with stress differ from those that develop a DLS in response to exposure to recurrent mild stress. The hope is that in the future it will be possible to diagnose genetic susceptibility to depression in humans — and then treat this with the natural substances that are also being investigated during the project.
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Children with certain immunodeficiency diseases carry mutations in genes that regulate the body’s immune system against viral infections and they have a higher mortality rate due to COVID-19. This is according to a study by researchers from Karolinska Institutet in Sweden, published in the Journal of Allergy and Clinical Immunology.
Most children infected with the SARS-CoV-2 coronavirus develop a mild illness or show no symptoms at all. But for a small percentage, serious complications may develop.
“Mortality is much higher among children with primary immunodeficiency diseases infected with SARS-CoV-2. Our results indicate that basic immunological examination and genetic analysis should be conducted in children with severe COVID-19 or multi-inflammatory syndrome (MIS-C). The clinicians will then be able to help these children with more precise therapies based on their genetic changes,”says Qiang Pan-Hammarström, professor at the Department of Biosciences and Nutrition, Karolinska Institutet, who led the study.
How the infection affects patients with primary immunodeficiency diseases, i.e. hereditary and congenital diseases of the immune system, is controversial. Even among these patients, some suffer from severe COVID-19 while others experience mild or no symptoms.
To investigate this more closely, and try to find genetic explanations for severe forms of COVID-19, researchers from Karolinska Institutet have studied young patients with primary immunodeficiency diseases (also called inborn errors of immunity, IEI) who developed severe or critical SARS-CoV-2 infection. Genetic and immunological analyses were performed.
“Our results clarify the molecular mechanism of these immune diseases, which opens up the possibility of developing a more targeted therapy. The knowledge acquired from the study also allows us to develop better strategies for the treatment and prevention of severe COVID-19 disease in these patients,” says Qiang Pan-Hammarström.