Culture

Hartford, CT - Links between obesity and complications of COVID-19 have received increasing attention throughout the ongoing pandemic. But a different aspect of body weight - the social stigma that people face because of their weight - may also have harmful implications for people's health during the pandemic.

New research from the UConn Rudd Center for Food Policy and Obesity and the University of Minnesota shows that young adults who experienced weight stigma before the pandemic have higher levels of depressive symptoms, stress, eating as a coping strategy, and are more likely to binge-eat during COVID-19 compared to those who haven't experienced weight stigma.

Over the last decade, considerable evidence has documented harmful health consequences for people who are teased, bullied, stigmatized, or treated unfairly because of their body weight. Based on this knowledge, researchers wanted to learn whether such weight mistreatment predicts health behaviors during COVID-19 that may worsen health, especially in this time period of increased anxiety and stress for many Americans.

"Understanding whether weight stigma elevates risk for health challenges during the pandemic represents a critical first step for the development of health messaging, responses, and support during outbreaks of COVID-19 and similar public health emergencies," says lead author of the study Rebecca Puhl, professor of Human Development & Family Sciences and Deputy Director at the University of Connecticut's Rudd Center.

The study, published in the Annals of Behavioral Medicine, reports findings from 584 young adults enrolled in the population-based longitudinal EAT (Eating and Activity over Time) 2010-2018 study, who were invited to complete a follow-up survey during the COVID-19 outbreak. Weight stigma reported previously by these participants in 2018 was examined as a predictor of binge eating, eating to cope, physical activity, depressive symptoms, and stress during COVID-19.

Key findings include:

Pre-pandemic experiences of weight stigma in 2018 predicted higher levels of stress, depressive symptoms, eating to cope with stress, and binge eating among young adults during the COVID-19 pandemic.

The likelihood of engaging in binge eating during the pandemic was almost 3 times higher for people who had experienced weight stigma prior to the pandemic compared to those who hadn't.

Weight stigma predicted these health consequences for both males and females, regardless of their body weight.

Weight stigma predicted these worse health outcomes during both time periods of initial stay-at-home restrictions and after such restrictions had been lifted during the COVID-19 outbreak.

"Our findings importantly identify weight stigma, independent of BMI, as a factor that may worsen eating behaviors and psychological distress for young adults during this pandemic. These increased health risks, particularly for binge eating, indicate a need for supportive and educational resources to help lessen the negative impact of stigma on eating behaviors," says Dianne Neumark-Sztainer, professor at the University of Minnesota and principal investigator of the EAT cohort study.

"This research highlights the relevance of weight stigma to the COVID-19 pandemic," adds Puhl. "With additional outbreaks and more cases of COVID-19 expected in the coming months, it is important to support individuals who may be prone to worse health and health behaviors exacerbating their risk during these times of pandemic. Weight stigma warrants attention in research and discourse related to COVID-19 and should be considered in public health messaging."

A recent study that examined the psychological health of pregnant women during the COVID-19 outbreak uncovered fear and depression in many participants. The findings are published in the Journal of Clinical Nursing.

In an online questionnaire completed in February 2020 by 331 pregnant women in China without COVID-19, participants were mostly worried about the following: "potential infected people were unprotected and non-isolated," "self-infection could affect the health of their baby," and "they themselves becoming infected and being isolated" (83.1%, 78.6% and 56.2%, respectively).

Women's psychological responses to the COVID-19 outbreak increased pregnancy stress, whereas their sense of security decreased pregnancy stress.

The authors urged clinicians to promptly evaluate pregnant women's psychological responses and provide them with guidance to enhance their sense of security and alleviate their fears related to COVID-19.

"If a pregnant woman is diagnosed or suspected of COVID-19 infection, it may induce different degrees of psychological stress such as fear and anxiety, which would not be conducive to the mother's or child's health," said co-author Xiu-Min Jiang, RN, of Fujian Maternity and Child Health Hospital, in China. "It is essential for the health staff to build trust with pregnant women and their families, and to communicate accurate information to them during COVID-19 outbreak."

URL Upon Publication: https://onlinelibrary.wiley.com/doi/10.1111/jocn.15460

Emerging evidence suggests that obstructive sleep apnea (OSA) may negatively affect bone health. Results from a new study published in the Journal of Bone and Mineral Research now indicate that women with history of OSA may face a higher risk of spine, or vertebral, fractures.

Using information from the Nurses' Health Study, investigators examined data pertaining to 55,264 women without a prior history of bone fractures. OSA was self-reported in 1.3% of participants in 2002 and increased to 3.3% by 2012. Between 2002 and 2014, 461 vertebral fractures and 921 hip fractures occurred.

Women with a history of OSA had a 2-fold higher risk of vertebral fracture relative to those with no OSA history, with the strongest association observed for OSA associated with daytime sleepiness. No association was observed between OSA history and risk of hip fracture.

"Our study provides important evidence at the population level that obstructive sleep apnea may have an adverse impact on bone health that is particularly relevant to the development of vertebral fracture," said lead author Tianyi Huang, ScD, of Brigham and Women's Hospital. "Given that we used self-reported clinical diagnoses of sleep apnea and fracture in our study, future studies could use more deeply characterized data to further the understanding of the mechanisms linking sleep apnea to bone health and fracture risk."

Results from a new study suggest that lifestyle changes may help to improve cognition in older adults experiencing cognitive decline that precedes dementia.

In the study published in the Journal of the American Geriatrics Society, 119 individuals older than 65 years of age who were experiencing cognitive decline were randomized to a control group or an intervention group for 8 weeks. The control group received online information related to dementia and lifestyle risk factors, Mediterranean diet, physical activity, and cognitive engagement.

Participants were instructed to implement this information into their own lifestyles. The intervention group received the same online information, plus active components to assist with implementing this information into their lifestyles: dietitian sessions, an exercise physiologist session, and online brain training.

Over 6 months of follow-up, investigators noted that participants in the intervention group were able to improve their lifestyle and had higher cognition scores than those in the control group. The results suggest that lifestyle-based changes may modify the course of cognitive decline.

"We've known for some time that lifestyle changes such as these can reduce dementia risk in the general population. What this study adds is that with the right intervention, people experiencing cognitive decline may retain sufficient neuroplasticity for their brain to 'bounce back' from decline," said lead author Mitchell McMaster, a PhD student at The Australian National University.

A recent analysis published in Campbell Systematic Reviews indicates that body cameras worn by police do not have clear or consistent effects on officers' use of force, arrests, or other activities. Nor do they have significant effects on citizens' calls to police or assaults or resistance against officers. Body-worn cameras can reduce the number of citizen complaints against police officers, but it is unclear whether this finding signals an improvement in the quality of police-citizen interactions or a change in reporting.

The analysis summarizes evidence from 30 studies on the effects of body-worn cameras on various officer and citizen behaviors.

"For the police agencies that have already purchased body-worn cameras, researchers should continue testing for ways in which both police and citizens might gain benefits from the cameras' continued use," said lead author Cynthia Lum, PhD, of George Mason University. "These could include limiting the discretion that officers have with body-worn camera use; using body-worn cameras for coaching, training, or evidentiary purposes; and finding ways that body-worn cameras can be used to strengthen police-citizen relationships, internal investigations, or accountability systems."

Children born to mothers who had diabetes during pregnancy may age faster biologically and be at an increased risk for obesity and high blood pressure, according to Rutgers researchers.

The study, published in the journal Epigenetics, explored how more than 1,000 children born to mothers in China aged on a cellular level. Researchers examined their exposure to gestational diabetes in utero and their DNA methylation, or epigenetic age, which indicates how experiences and exposures reflect true biological age even in early childhood.

Accelerated aging, which can be determined by evaluating if a person's estimated DNA methylation age is greater than their chronological age, has been shown to be associated with cardiovascular risks and poor health outcomes later in life.

The researchers measured the epigenetic age of 1,156 children who were ages 3 to 10 in Tianjin, China, to see how it differed from their chronological age. They found that children born to mothers who had diabetes while pregnant had a higher epigenetic age -- or were "older" than their actual age -- and that this epigenetic age is associated with higher weight, body mass index, body fat percentage, upper-arm circumference and blood pressure.

"These findings suggest that gestational diabetes may have long-term effects on epigenetic aging in offspring and lead to poorer cardiometabolic health outcomes," said lead author Stephanie Shiau, an instructor at the Rutgers School of Public Health.

The findings support the need for further studies using longitudinal samples to evaluate the association between epigenetic age and later onset of adult metabolic diseases.

In the United States, between 2 percent to 10 percent of pregnancies are affected by the condition annually, according to the National Institutes of Health.

Researchers at the University of Cambridge and the University of Zurich have discovered that a drug newly approved for cancer improves kidney dysfunction in a mouse model of Dent disease 2 and Lowe syndrome

The study is published today in Kidney International and offers hope for the first disease-modifying treatment. In addition to kidney dysfunction, characteristic of Dent disease 2, boys with Lowe syndrome also require eye cataract surgery as newborns, and suffer seizures and other disabilities. Only supportive treatments are available, such as nutrient supplements and help with learning.

These rare diseases are caused by the lack of an enzyme called OCRL that normally controls the lipid composition of cell membranes. The disruption activates a system of filaments inside the cells, called the actin cytoskeleton, in the wrong place. The actin blockage means that the cells in the kidneys that usually reabsorb filtered proteins and essential nutrients don't work properly, causing a loss of these in the urine.

Dr Jennifer Gallop's group at the Wellcome Trust/ Cancer Research UK Gurdon Institute in Cambridge worked out how the actin system was being activated by the disruption in cell membrane lipids. "By understanding the details of what is happening in cells during Lowe syndrome and Dent disease 2," said Dr Gallop, "we realised that alpelisib, a drug that is already approved for use in patients with cancer, could prevent the actin blockage". This is because alpelisib targets a different step in the pathway, and rebalances the lipid composition.

The Gallop group teamed up with Professor Oliver Devuyst from the Institute of Physiology, University of Zurich to test alpelisib in a humanized mouse model of Lowe syndrome and Dent disease 2. Devuyst said "amazingly, treatment with alpelisib improved the actin cytoskeleton of the kidney cells and rescued the reabsorption of the filtered proteins".

The researchers don't yet know whether the drug will work in patients and if their neurological symptoms will be helped as well. However, because alpelisib has been used before in another rare disease in children, as well as in adults, there is evidence that it is safe. These efforts of repurposing a drug could potentially lead to the cost-effective development of a treatment for these rare disorders.

With life expectancy increasing, age-related diseases are also on the rise, including sarcopenia, the loss of muscle mass due to aging. Researchers from the University of Basel's Biozentrum have demonstrated that a well-known drug can delay the progression of age-related muscle weakness.

Already in our best years, our muscles begin to shrink and their strength dwindles. Unfortunately, this is a natural part of aging. For some people, the decline in muscle mass and function is excessive. This condition, called sarcopenia, affects every second or third person over 80, reducing mobility, autonomy and quality of life.

The causes of sarcopenia are diverse, ranging from altered muscle metabolism to changes in the nerves supplying muscles. Researchers led by Professor Markus Rüegg have now discovered that mTORC1 also contributes to sarcopenia and its suppression with the well-known drug rapamycin slows age-related muscle wasting.

Rapamycin preserves muscle function

"Contrary to our expectations, the long-term mTORC1 suppression with rapamycin is overwhelmingly beneficial for skeletal muscle aging in mice, preserving muscle size and strength," says Daniel Ham, first author of the study. "Neuromuscular junctions, the sites where neurons contact muscle fibers to control their contraction, deteriorate during aging. Stable neuromuscular junctions are paramount to maintaining healthy muscles during aging and rapamycin effectively stabilizes them." The researchers also demonstrate that permanently activating mTORC1 in skeletal muscle accelerates muscle aging.

Molecular signature of sarcopenia

In collaboration with Professor Mihaela Zavolan's team, the scientists identified a molecular ?signature? of sarcopenia, with mTORC1 as the key player. To help the scientific community further investigate how gene expression in skeletal muscle changes during aging or in response to rapamycin treatment, they developed the user-friendly web application, SarcoAtlas, which is supported by sciCORE, the Center for Scientific Computing at the University of Basel.

There is currently no effective pharmacological therapy to treat sarcopenia. This study provides hope that it may be possible to slow down age-related muscle wasting with treatments that suppress mTORC1 and thereby extend the autonomy and life quality of elderly people.

WASHINGTON -- Individuals who can unconsciously predict complex patterns, an ability called implicit pattern learning, are likely to hold stronger beliefs that there is a god who creates patterns of events in the universe, according to neuroscientists at Georgetown University.

Their research, reported in the journal, Nature Communications, is the first to use implicit pattern learning to investigate religious belief. The study spanned two very different cultural and religious groups, one in the U.S. and one in Afghanistan.

The goal was to test whether implicit pattern learning is a basis of belief and, if so, whether that connection holds across different faiths and cultures. The researchers indeed found that implicit pattern learning appears to offer a key to understanding a variety of religions.

"Belief in a god or gods who intervene in the world to create order is a core element of global religions," says the study's senior investigator, Adam Green, an associate professor in the Department of Psychology and Interdisciplinary Program in Neuroscience at Georgetown, and director of the Georgetown Laboratory for Relational Cognition.

"This is not a study about whether God exists, this is a study about why and how brains come to believe in gods. Our hypothesis is that people whose brains are good at subconsciously discerning patterns in their environment may ascribe those patterns to the hand of a higher power," he adds.

"A really interesting observation was what happened between childhood and adulthood," explains Green. The data suggest that if children are unconsciously picking up on patterns in the environment, their belief is more likely to increase as they grow up, even if they are in a nonreligious household. Likewise, if they are not unconsciously picking up on patterns around them, their belief is more likely to decrease as they grow up, even in a religious household.

The study used a well-established cognitive test to measure implicit pattern learning. Participants watched as a sequence of dots appeared and disappeared on a computer screen. They pressed a button for each dot. The dots moved quickly, but some participants - the ones with the strongest implicit learning ability - began to subconsciously learn patterns hidden in the sequence, and even press the correct button for the next dot before that dot actually appeared. However, even the best implicit learners did not know that the dots formed patterns, showing that the learning was happening at an unconscious level.

The U.S. section of the study enrolled a predominantly Christian group of 199 participants from Washington, D.C. The Afghanistan section of the study enrolled a group of 149 Muslim participants in Kabul. The study's lead author was Adam Weinberger, a postdoctoral researcher in Green's lab at Georgetown and at the University of Pennsylvania. Co-authors Zachery Warren and Fathali Moghaddam led a team of local Afghan researchers who collected data in Kabul.

"The most interesting aspect of this study, for me, and also for the Afghan research team, was seeing patterns in cognitive processes and beliefs replicated across these two cultures," says Warren. "Afghans and Americans may be more alike than different, at least in certain cognitive processes involved in religious belief and making meaning of the world around us. Irrespective of one's faith, the findings suggest exciting insights into the nature of belief."

"A brain that is more predisposed to implicit pattern learning may be more inclined to believe in a god no matter where in the world that brain happens to find itself, or in which religious context," Green adds, though he cautions that further research is necessary.

"Optimistically," Green concludes, "this evidence might provide some neuro-cognitive common ground at a basic human level between believers of disparate faiths."

Frontotemporal lobar degeneration (FTLD) is a type of dementia that appears earlier in life than Alzheimer's disease (AD). Both FTLD and AD, along with several other neurodegenerative diseases, are marked by the appearance and clustering of the protein "tau" in nerve cells. However, there is much left to be explored about this mechanism.

Now, a team of researchers from various collaborating universities and hospitals in Japan has uncovered crucial molecular details regarding tau's activity, promising to revolutionize the therapy of tau-induced neurodegenerative diseases. Their findings were recently published in the journal BRAIN.

Tau-induced neurodegenerative diseases include not only FTLD and AD, but also an array of conditions like amyotrophic lateral sclerosis (ALS), progressive supranuclear palsy (PSP), and corticobasal degeneration (CBD). Many people from various age groups are affected by the tau-induced diseases, but the effective therapeutic strategy against tau aggregation is yet to be available. One reason behind this gap is that, despite a lot of effort and resource invested, the exact mechanism of the action of tau inside the cell is still unclear. Knowing this will help us pin down an appropriate treatment strategy.

The aforementioned research team, led by Dr Shinsuke Ishigaki of Nagoya University Graduate School of Medicine, has now discovered new layers of complexities hidden in the cellular activities of tau. The researchers report a novel role of tau that is specific for FTLD spectrum diseases, and as per their findings published in BRAIN, these finer mechanisms specifically contribute to the development of conditions such as FTLD, ALS, PSP, and CBD, but not in AD and Pick's diseases.

However, while this research puts tau in the spotlight, it all started with another related protein. Dr Ishigaki explains the reasons for arriving at their study question: "Earlier, while studying FTLD mouse models, we found two interacting proteins, fused in sarcoma (FUS) and splicing factor, proline- and glutamine-rich (SFPQ), were important for the generation of functional tau. The interaction of FUS and SFPQ inside the nucleus is disrupted due to mutations in FUS results in neurodegeneration by the accumulation of a dysfunctional variant '4-repeat tau', causing FTLD in mouse."

So how did the researchers link their findings of mouse model to the tau-induced pathogenesis in humans? They studied the interaction of SFPQ and FUS in brain autopsy samples of 142 deceased individuals with various neurodegenerative diseases like FUS-related ALS/FTLD, TDP-43-related ALS/FTLD, PSP, AD, or Pick's disease, with the latter disease used as a control to compare the results.

Using their findings, the researchers have proposed a unique model of "imbalanced accumulation of tau" in cells. As per this new model, FUS and SFPQ regulate the processing of MAPT, the gene that "codes" for tau, specifically by removing a genetic region called exon 10. In normal conditions, the balance in the ratio of variants "4-repeat tau" and "3-repeat tau" is maintained by MAPT. In disease conditions, the processing of MAPT is hampered, leading to an unchecked increase in the amount of 4-repeat tau. Interestingly, an increased level of 4-repeat tau causes FTLD spectrum diseases, but not AD or Pick's disease, in humans.

"Now that we know how tau specifically causes FTLD spectrum diseases, we can design a treatment strategy for these diseases that could 'target' the factors involved in the process, like '4-repeat tau' or FUS/SFPQ proteins," concludes Dr Ishigaki, talking about the significance of their discovery.

(LOS ANGELES) - Engineering new tissues can be used to alleviate shortages of organs in transplantation, as well as to develop physiological models for drug discovery applications. One of the emerging approaches to building tissues is through 3D Printing, where cells and materials can be combined to make inks that can generate tissue structures. One of the limitations for making new tissues is that they require oxygen to survive. This oxygen is delivered through blood vessels, which take a few days to develop in a transplanted tissue.

A collaborative team, which includes a group from the Terasaki Institute for Biomedical Innovation (TIBI), has developed a bioink that offers a solution to this problem. This bioink can generate oxygen and deliver it to cells in 3D printed tissues to keep them alive before blood vessels penetrate the tissue. Therefore, when it is used in 3D bioprinting to construct tissue implants, the ability of cells to regenerate new tissue is greatly enhanced.

As discussed in their recent publication in Advanced Healthcare Materials, the TIBI group tested their oxygen-generating bioink extensively to optimize its chemical and physical properties. As a result, oxygen was delivered to the cells in the tissue constructs for the period necessary for blood vessels to develop fully. These blood vessels would then be able to resume their oxygen delivery functions, and the cells would have the additional support needed to grow and regenerate new tissue. The group also conducted separate experiments on tissue constructs using two different types of cells, including cardiac cells and muscle cells, and they demonstrated the positive effects of using the new bioink.

"By delivering oxygen to the implanted cells, we would be able to improve the tissue functionality and integration to the host tissue. A similar approach can be used to make functional tissues with improved survival for drug screening applications and pathophysiological studies within a long period of time," said Samad Ahadian, Ph.D., lead investigator of the Terasaki Institute team.

Such developments can result in a variety of medical applications, including the enhancement of tissue regeneration in patients who have suffered a heart attack. These patients have experienced a period in which their heart is without a sufficient supply of oxygen. Therefore, there may be damage or a higher risk of harm to parts of their cardiac tissue. Tissue implants using the new bioink may help not only to increase the survival of the affected cardiac cells but can also help to support the growth and formation of the cardiac blood vessels.

At a time when much of instruction is performed digitally and university lecture halls are often illuminated by a sea of laptops, it can be difficult to imagine that all instruction was recorded by pen and paper until about 20 years ago.

Digital technology constitutes a significant presence in education, with many advantages - especially during these corona times, when a great number of students have been forced to work from home.

But digital technology in the classroom is not without its drawbacks. A lack of concentration and absence of attention among students became too much for one Danish lecturer to bear.

"The lecturer felt as if their students' use of social media on their laptops and smartphones distracted and prevented them from achieving deeper learning. Eventually, the frustration became so great that he decided to ban all screens in discussion lessons," explains Katrine Lindvig, a postdoc at the University of Copenhagen's Department of Science Education.

Together with researchers Kim Jesper Herrmann and Jesper Aagaard of Aarhus University, she analysed 100 university student evaluations of the the lecturer's screen-free lessons. Their findings resulted in a new study that had this to say about analogue instruction:

"Students felt compelled to be present -- and liked it. When it suddenly became impossible to Google their way to an answer or more knowledge about a particular theorist, they needed to interact and, through shared reflection, develop as a group. It heightened their engagement and presence," explains Katrine Lindvig.

Without distraction, we engage in deeper learning

What explains this deeper engagement and presence when our phones and computers are stashed away?

According to Katrine Lindvig, the answer rests in the structure of our brains:

"A great deal of research suggests that humans can't really multitask. While we are capable of hopping from task to task, doing so usually results in accomplishing tasks more slowly. However, if we create a space where there's only one thing -- in this case, discussing cases and theories with fellow students -- then we do what the brain is best at, and are rewarded by our brains for doing so," she says.

Furthermore, a more analog approach can lead to deeper learning, where one doesn't just memorize things only to see them vanish immediately after an exam. According to Lindvig:

"Learning, and especially deep learning, is about reflecting on what one has read and then comparing it to previously acquired knowledge. In this way, one can develop and think differently, as opposed to simply learning for the sake of passing an exam. When discussing texts with fellow students, one is exposed to a variety of perspectives that contribute to the achievement of deep learning."

We're not going back to the Stone Age

While there are numerous advantages to engaging in lessons where Facebook, Instagram and text messages don't diminish concentration, there are also drawbacks.

Several students weren't so enthusiastic about hand-written note taking explains Katrine Lindvig.

"They got tired of not being able to search through their notes afterwards and readily share notes with students who weren't in attendance," she says.

Therefore, according to Lindvig, it is not a question of 'to screen or not to screen' -- "we're not going back to the Stone Age", as she puts it. Instead, it's about how to integrate screens with instruction in a useful way:

"It's about identifying what form best supports the content and type of instruction. In our case, screens were restricted during lessons where discussion was the goal. This makes sense, because there is no denying that conversation improves when people look into each other's eyes rather than down at a screen," Lindvig says.

Speaking to the value of screens, she adds:

"When it comes to lectures which are primarily one-way in nature, it can be perfectly fine for students to take notes on laptops, to help them feel better prepared for exams. We can also take advantage of students' screens to increase interaction during larger lectures. It's about matching tools with tasks. Just as a hammer works better than a hacksaw to pound in nails."

Perhaps as far back as the history of research and philosophy goes, people have attempted to unearth how life on earth came to be. In the recent decades, with exponential advancement in the fields of genomics, molecular biology, and virology, several scientists on this quest have taken to looking into the evolutionary twists and turns that have resulted in eukaryotic cells, the type of cell that makes up most life forms today.

The most widely accepted theories that have emerged state that the eukaryotic cell is the evolutionary product of the intracellular evolution of proto-eukaryotic cells, which were the first complex cells, and symbiotic relationships between proto-eukaryotic cells and other unicellular and simpler organisms such as bacteria and archaea. But according to Professor Masaharu Takemura of the Tokyo University of Science, Japan, "These hypotheses account for and explain the driving force and evolutionary pressures. But they fail to portray the precise process underlying eukaryotic nucleus evolution."

Prof Takemura cites this as his motivation behind his recent article published in Frontiers in Microbiology, where he looks into the recent theories that, in addition to his own body of research, have built up his current hypothesis on the subject.

In a way, Prof Takemura's hypothesis has its roots in 2001 when, along with PJ Bell, he made the revolutionary proposal that large DNA viruses, like the poxvirus, had something to do with the rise of the eukaryotic cell nucleus. Prof Takemura further explains the reasons for his inquiry into the nucleus of the eukaryotic cell as such: "Although the structure, function, and various biological functions of the cell nucleus have been intensively investigated, the evolutionary origin of the cell nucleus, a milestone of eukaryotic evolution, remains unclear."

The origin of the eukaryotic nucleus must indeed be a milestone in the development of the cell itself, considering that it is the defining factor that sets eukaryotic cells apart from the other broad category of cells--the prokaryotic cell. The eukaryotic cell is neatly compartmentalized into membrane-bound organelles that perform various functions. Among them, the nucleus houses the genetic material. The other organelles float in what is called the cytoplasm. Prokaryotic cells do not contain such compartmentalization. Bacteria and archaea are prokaryotic cells.

The 2001 hypothesis by Prof Takemura and PJ Bell is based on striking similarities between the eukaryotic cell nucleus and poxviruses: in particular, the property of keeping the genome separate in a compartment. Further similarities were uncovered after the discovery and characterization of a type of large DNA virus called "giant virus," which can be up to 2.5 μm in diameter and contain DNA "encoding" information for the production of more than 400 proteins. Independent phylogenetic analyses suggested that genes had been transferred between these viruses and eukaryotic cells as they interacted at various points down the evolutionary road, in a process called "lateral gene transfer."

Viruses are "packets" of DNA or RNA and cannot survive on their own. They must enter a "host" cell and use that cell's machinery to replicate its genetic material, and therefore multiply. As evolution progressed, it appears, viral genetic material became integrated with host genetic material and the properties of both altered.

In 2019, Prof Takemura and his colleagues made another breakthrough discovery: the medusavirus. The medusavirus got its name because, like the mythical monster, it causes encystment in its host; that is, it gives its host cell a "hard" covering.

Via experiments involving the infection of an amoeba, Prof Takemura and his colleagues found that the medusavirus harbors a full set of histones, which resemble histones in eukaryotes. Histones are proteins that keep DNA strands curled up and packed into the cell nucleus. It also holds a DNA polymerase gene and major capsid protein gene very similar to those of the amoeba. Further, unlike other viruses, it does not construct its own enclosed "viral factory" in the cytoplasm of the cell within which to replicate its DNA and contains none of the genes required to carry out the replication process. Instead, it occupies the entirety of the host nucleus and uses the host nuclear machinery to replicate.

These features, Prof Takemura argues, indicate that the ancestral medusavirus and its corresponding host proto-eukaryotic cells were involved in lateral gene transfer; the virus acquired DNA synthesis (DNA polymerase) and condensation (histones) genes from its host and the host acquired structural protein (major capsid protein) genes from the virus. Based on additional research evidence, Prof Takemura extends this new hypothesis to several other giant viruses as well.

Thus, Prof Takemura connects the dots between his findings in 2019 and his original hypothesis in 2001, linking them through his and others' work in the two decades that come in between. All of it taken together, it becomes clear how the medusavirus is prime evidence of the viral origin of the eukaryotic nucleus.

He says: "This new updated hypothesis can profoundly impact the study of eukaryotic cell origins and provide a basis for further discussion on the involvement of viruses in the evolution of the eukaryotic nucleus." Indeed, his work may have unlocked several new possibilities for future research in the field.

Critical Illness Myopathy (CIM) has taken on a new relevance as a result of the Corona virus. CIM is the specialists' term for a muscle weakness which occurs in patients being treated in intensive care for a longer period of time. In a severe case of a Covid19 infection, for example, many patients need artificial ventilation for a long time - sometimes over several weeks. CIM subsequently occurs in up to 30 percent of these patients, and this can entail symptoms of long-term paralysis, making it more difficult to take the patient off the ventilator. A group of researchers headed by Prof. Wolfgang Linke, the Director of the Institute of Physiology II at the University of Münster's Medical Faculty, has now found a potential method of treating Critical Illness Myopathy. The research results have been published in the latest issue of the journal Nature Communications.

As a result of its research, the team was able to describe for the first time what happens in an organism when the production of the muscle protein titin is suppressed in the skeletal muscle. Titin is the largest protein in humans and vertebrates, ensuring both stability and elasticity and functioning as a sensor for muscle power. The researchers deactivated titin in the organisms of mice and were able to demonstrate that after three to four weeks the animals' muscle power declined markedly. These findings can now be used in CIM research. In the case of patients on ventilation, complete immobilization - sometimes lasting weeks - means that there is no longer any incentive in the muscle to produce the muscle protein and thus to enable muscles to grow; the titin spring is defective. As a consequence, the muscle tissue shrinks.

The study now published indicates that Critical Illness Myopathy can be prevented by stretching the patient's peripheral muscles during the ventilation phase. Especially in view of the Corona pandemic and the higher number of patients needing ventilation, the Münster researchers' findings give cause for optimism.

In obese individuals, endurance exercise improves fitness and increases the number of mitochondria * and cellular respiration in skeletal muscles. However, the intervention has no effect on cellular respiration in adipose tissue. This is the result of a study by DZD researchers that has now been published in The Journal of Clinical Endocrinology & Metabolism.

Studies in rodents suggest that exercise not only increases the number of mitochondria and the respiratory capacity of skeletal muscles, but also in adipose tissue. In a study, researchers at the DZD in Tübingen investigated the effects of endurance training on cellular respiration in the human skeletal muscles and abdominal adipose tissue and whether there is a direct connection between increased cellular respiration and improved insulin sensitivity. For this purpose, the researchers carried out an 8-week aerobic endurance training intervention with 25 untrained test subjects (16 women, 9 men aged 29.8 ± 8.4 years) who were overweight or obese. The researchers then analyzed mitochondrial respiration in skeletal muscle fibers and in the subcutaneous adipose tissue of the abdomen.

Based on the change in insulin sensitivity after the intervention, the subjects were grouped into responders (subjects whose insulin sensitivity increased) and low responders (subjects whose insulin sensitivity did not increase significantly). In both groups, fitness, cellular respiration and the amount of mitochondrial enzymes in the skeletal muscles improved equally. The endurance training had no effect on the mitochondria in the abdominal subcutaneous adipose tissue. Another interesting finding of the study is that women exhibited higher cellular respiration in adipose tissue than men.

"Our data show that the increase in the mitochondrial respiratory capacity of the skeletal muscles after endurance training has no predictive power for the improvement of the peripheral insulin sensitivity. Furthermore, the endurance training does not increase cellular respiration in the subcutaneous adipose tissue, with a simultaneous decrease in this fat compartment," said Cora Weigert of the DZD partner Institute for Diabetes Research and Metabolic Diseases of Helmholtz Zentrum München at the University of Tübingen, summarizing the findings.