Lifeboat Foundation

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.”

Highly energetic, “hot” electrons have the potential to help solar panels more efficiently harvest light energy.

But scientists haven’t been able to measure the energies of those electrons, limiting their use. Researchers at Purdue University and the University of Michigan built a way to analyze those energies.

“There have been many theoretical models of hot electrons but no direct experiments or measurements of what they look like,” said Vladimir “Vlad” Shalaev (shal-AYV), Purdue University’s Bob and Anne Burnett Distinguished Professor of Electrical and Computer Engineering, who led the Purdue team in this collaborative work.

The mole instrument on NASA’s Mars InSight lander has made some progress burrowing into the Red Planet.

Although tidal energy is still in its infancy, it could help to reduce Australia’s dependence on fossil fuels.

“The majority of the energy in the national grid is from coal,” explained Jenny Hayward, a research scientist at Australia’s national science agency, CSIRO. “We also have wind and solar PV [photovoltaic].”

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 increased metabolism 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.

UC Santa Barbara researchers continue to push the boundaries of LED design a little further with a new method that could pave the way toward more efficient and versatile LED display and lighting technology.

In a paper published in Nature Photonics, UCSB electrical and computer engineering professor Jonathan Schuller and collaborators describe this new approach, which could allow a wide variety of LED devices—from virtual reality headsets to automotive lighting—to become more sophisticated and sleeker at the same time.

“What we showed is a new kind of photonic architecture that not only allows you to extract more photons, but also to direct them where you want,” said Schuller. This improved performance, he explained, is achieved without the external packaging components that are often used to manipulate the light emitted by LEDs.

Changing Course

The Air Force announced an AI initiative called “Skyborg” last March with the goal of flying fighter jets without anyone at the controls. Now, Shanahan says that the Air Force may be more interested in swarm drones and other uses for AI than necessarily taking the pilot out of a fighter plane’s cockpit.

“Maybe I shouldn’t be thinking about a 65ft-wingspan, maybe it is a small autonomous swarming capability,” Shanahan told BBC News. “The last thing I would claim is that carriers and fighters and satellites are going away in the next couple of years.”

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.

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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.

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