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In the last few months, millions of people around the world stopped going into offices and started doing their jobs from home. These workers may be out of sight of managers, but they are not out of mind. The upheaval has been accompanied by a reported spike in the use of surveillance software that lets employers track what their employees are doing and how long they spend doing it.

Companies have asked remote workers to install a whole range of such tools. Hubstaff is software that records users’ keyboard strokes, mouse movements, and the websites that they visit. Time Doctor goes further, taking videos of users’ screens. It can also take a picture via webcam every 10 minutes to check that employees are at their computer. And Isaak, a tool made by UK firm Status Today, monitors interactions between employees to identify who collaborates more, combining this data with information from personnel files to identify individuals who are “change-makers.”

A study by Monash Biomedicine Discovery Institute (BDI) expands the understanding of the molecular pathways that control T cell function and survival and how it relates to declining T cell immunity in the elderly.

The findings, published in Nature Communications, led by Monash BDI’s Professor Nicole La Gruta and Dr. Kylie Quinn (formerly of Monash University BDI, now Vice-Chancellor’s Research Fellow at RMIT University), outline that the of T cells observed with advanced age was an indication that they were working harder merely to survive.

This contradicts previous knowledge, which suggested an increased metabolism was indicative of T cell function, and will have implications for the development of targeted interventions such as vaccines or immunotherapies to treat age-related immune dysfunction.

HOUSTON, June 2, 2020 /PRNewswire/ — Cellenkos Inc., a privately held, clinical stage biotech company announced today that the US Food & Drug Administration (FDA) has cleared the way to initiate a Phase 1 clinical trial of CK0802 (Cryopreserved Cord Blood Derived T-Regulatory Cells) for treatment of COVID-19 associated acute respiratory distress syndrome (ARDS). The trial is designed as a randomized, double-blinded, placebo-controlled study to assess safety and preliminary efficacy in this hospitalized patient population.

“We appreciate FDA’s expedited review of our plans to evaluate CK0802 in critically ill, intubated patients suffering from ARDS, a deadly complication of COVID-19”, said Elizabeth J Read, MD, Chief Technology Officer, Cellenkos Inc. “Preliminary observations in two intubated COVID-19 ARDS patients, who received cryopreserved cord blood T-regulatory cells under FDA Emergency Use Authorization after failing tociluzumab, were promising. In the forthcoming Phase 1 randomized trial, CK0802 will be assessed for both toxicity and 28-day treatment success, as co-primary outcomes.”

“Use of allogeneic, off-the-shelf cord blood-derived T-regulatory cells has emerged as a promising therapeutic strategy for the treatment of inflammatory disorders, specifically in terms of interrupting and arresting the cytokine storm unleashed by COVID-19 infection,” said Dr Siddhartha Mukherjee, MD, PhD, Columbia University, New York, scientific advisor and collaborator on the multi-center clinical trial. “Rather than indiscriminate therapy with a drug such as an inhibitor of single cytokine such as IL-6, the T-regulatory cells can potentially calm inflammation exactly where it is most active, without causing a more general “global” immunosuppression that would be harmful in a virally infected patient. Planned correlative assays during the clinical trial will provide insights into the mechanism of action of CK0802 and its relation to clinical outcomes.”

Chronic stress has long been associated with the pathogenesis of psychological disorders such as depression and anxiety. Recent studies have found chronic stress can cause neuroinflammation: activation of the resident immune cells in the brain, microglia, to produce inflammatory cytokines. Numerous studies have implicated the inflammatory cytokine, interleukin-1 (IL-1), a master regulator of immune cell recruitment and activity in the brain, as the key mediator of psychopathology. However, how IL-1 disrupts neural circuits to cause behavioral and emotional problems seen in psychological disorders has not been determined.

The research team previously detailed how psychosocial stress results in peripheral immune activation, increased levels of circulating monocytes, and robust neuroimmunological responses in the brain. These responses include increases in IL-1 and other inflammatory cytokines, activation of brain glial cells and movements of peripheral immune cells to the brain, along with enhanced activity of specific neuronal pathways. The work makes it clear that inflammatory-related effects of stress are not just global effects, but are associated with increased IL-1 signaling within specific brain circuits.


The study shows for the first time that neuronal IL-1Rs in the hippocampus, a brain structure connected to learning and memory, is necessary and sufficient to mediate some of the behavioral deficits caused by chronic stress, pointing to a critical neuroimmune mechanism for the etiology of these types of disorders. Findings from the study augment the understanding of IL-1R signaling in physiological and behavioral responses to stress and also suggest that it may be possible to develop better medications to treat the consequences of chronic stress by limiting inflammatory signaling not just generally, which may not be beneficial in the long run, but to specific brain circuits.

“We created and validated a unique genetic mouse model to restrict IL-1R1 expression to different cell types to visualize and control IL-1Rs,” said Ning Quan, Ph.D., lead author, a professor of biomedical science in FAU’s Schmidt College of Medicine, and a member of the FAU Brain Institute (I-BRAIN). “We demonstrated that chronic social stress caused the mice to show social withdrawal and working memory deficits. These changes could be prevented if the neuronal IL-1R1 was deleted and restored if IL-1R1 was only allowed to be expressed on hippocampal neurons.”

The discovery of the Dead Sea Scrolls had an incomparable impact on the historical understanding of Judaism and Christianity. ‘Piecing together’ scroll fragments is like solving jigsaw puzzles with an unknown number of missing parts. Because most of the 2,000-year-old scrolls were written on processed animal skin, an international team of researchers used DNA sequencing to ‘fingerprint’ fragments based on their genetic signature.

Scientists have found a new method to strategically add deuterium to benzene, an aromatic compound commonly found in crude oil. When applied to the active ingredient of drugs to incorporate deuterium, it could dramatically improve the drugs’ efficacy and safety and even introduce new medicines.

To validate the method, which was published in Nature, a team led by W. Dean Harman of the University of Virginia worked with Xiaoping Wang at the Oak Ridge National Laboratory’s Spallation Neutron Source. Wang successfully verified the exact position of deuterium atoms that resulted from the selective deuteration of benzene molecules using single crystal neutron diffraction.

“Because the high sensitivity of neutrons to hydrogen and its deuterium isotope, we were able to quantitatively assign not only the positions of the deuterium atoms at the atomic level, but also determine precisely how many were added on each side of the benzene molecule,” Wang said. “This is important in designing new therapeutic drugs.”

An underlying assumption of research on aging holds that dietary restriction (and drugs that mimic its effects) will slow aging to extend both lifespan and healthspan jointly. While eating a Spartan diet has been shown to robustly extend lifespan and delay age-related diseases in many species, a genome-wide analysis of 160 genetically distinct strains of the fruit fly D. melanogaster shows that lifespan and healthspan are not linked under dietary restriction. Results are published in Current Biology.

Though on was extended and healthspan was increased, researchers from the Kapahi lab at the Buck Institute say the devil is in the details. In the study researchers measured nutrient-dependent changes in lifespan and tracked age-related changes in to measure healthspan. While 97 percent of strains showed some lifespan or healthspan extension in response to , only 50 percent of strains showed a significantly positive response to dietary restriction for both. Thirteen percent of the strains were more vigorous, yet died sooner with dietary restriction; 5 percent lived longer, but spent more time in poor health. The remaining 32 percent of the strains showed no benefits or detriments to lifespan or healthspan, or to both.

“Dietary restriction works, but may not be the panacea for those wanting to extend healthspan, delay age-related diseases, and extend lifespan,” said Pankaj Kapahi, Ph.D., Buck professor and senior author on the paper. “Our study is surprising and gives a glimpse into what’s likely going to happen in humans, because we’re all different and will likely respond differently to the effects of dietary restriction. Furthermore, our results question the idea that lifespan extension will always be accompanied by improvement of healthspan.”

A team of scientists from Stanford University is working with researchers at the Molecular Foundry, a nanoscience user facility located at the Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab), to develop a gene-targeting, antiviral agent against COVID-19.

Last year, Stanley Qi, an assistant professor in the departments of bioengineering, and chemical and at Stanford University and his team had begun working on a technique called PAC-MAN—or Prophylactic Antiviral CRISPR in —that uses the gene-editing tool CRISPR to fight influenza.

But that all changed in January, when news of the COVID-19 pandemic emerged. Qi and his team were suddenly confronted with a mysterious new virus for which no one had a clear solution. “So we thought, ‘Why don’t we try using our PAC-MAN technology to fight it?’” said Qi.