Lifeboat Foundation

Moderna has accelerated its manufacturing capacity for its COVID-19 vaccine candidate mRNA-1273 and additional future products through a 10-year agreement with Lonza announced today by the companies.

The companies agreed to establish manufacturing suites for Moderna at Lonza’s facilities in the U.S. and Switzerland for the production of mRNA-1273. Technology transfer is expected to begin in June, with the first batches of mRNA-1273 set to be manufactured at Lonza’s U.S. site in July.

Moderna and Lonza also said they intend to establish additional production suites across Lonza’s worldwide facilities, ultimately allowing for the manufacture of material equivalent to up to 1 billion doses of mRNA-1273 per year for use worldwide, based on the currently expected dose of 50 mcg.

Then there is the COVID-19 Open Research Dataset (CORD-19), a multi-institutional initiative that includes The White House Office of Science and Technology Policy, Allen Institute for AI, Chan Zuckerberg Initiative (CZI), Georgetown University’s Center for Security and Emerging Technology (CSET), Microsoft, and the National Library of Medicine (NLM) at the National Institutes of Health (NIH).

The goal of this initiative is to create new natural language processing and machine learning algorithms to scour scientific and medical literature to help researchers prioritize potential therapies to evaluate for further study. AI is also being used to automate screening at checkpoints by evaluating temperature via thermal cameras, as well as modulations in sweat and skin discoloration. What’s more, AI-powered robots have even been used to monitor and treat patients. In Wuhan, the original epicenter of the pandemic, an entire field hospital was transitioned into a “smart hospital” fully staffed by AI robotics.

Any time of great challenge is a time of great change. The waves of technological innovation that are occurring now will echo throughout eternity. Science, technology, engineering and mathematics are experiencing a call to mobilization that will forever alter the fabric of discovery in the fields of bioengineering, biomimicry and artificial intelligence. The promise of tomorrow will be perpetuated by the pangs of today. It is the symbiosis of all these fields that will power future innovations.

In an effort to create first-of-kind microelectronic devices that connect with biological systems, University of Maryland (UMD) researchers are utilizing CRISPR technology in a novel way to electronically turn “on” and “off” several genes simultaneously. Their technique, published in Nature Communications, has the potential to further bridge the gap between the electronic and biological worlds, paving the way for new wearable and “smart” devices.

“Faced with the COVID-19 pandemic, we now have an even deeper understanding of how ‘smart’ devices could benefit the general population,” said William E. Bentley, professor in UMD’s Fischell Department of Bioengineering and Institute for Bioscience and Biotechnology Research (IBBR), and director of the Robert E. Fischell Institute for Biomedical Devices. “Imagine what the world would be like if we could wear a device and access an app on our smartphone capable of detecting whether the wearer has the active virus, generated immunity, or has not been infected. We don’t have this yet, but it is increasingly clear that a suite of technologies enabling rapid transfer of information between biology and electronics is needed to make this a reality.”

With such a device, this information could be used, for example, to dynamically and autonomously conduct effective contact tracing, Bentley said.

Genetic enhancement could allow humanity to push surprisingly far out into the final frontier.

Colonizing Mars may require humanity to tweak its DNA :

“The number of coronavirus disease 2019 (COVID-19) cases in Austria dropped from 90 to 10 cases per one million people, two weeks after the government required everyone to wear a face mask on April 6.”

Austria managed to slow down the rate of coronavirus cases in the country by 90% after requiring everyone to wear a face mask. Meanwhile, other countries are struggling to keep the number of cases and fatalities low.

A team of researchers with members from Lawrence Livermore National Laboratory, Wright-Patterson Air Force Base and the Barnes Group Advisors found that controlling spatter during laser-powder bed fusion can reduce defects in metal-based 3D printing. In their paper published in the journal Science, the group describes studying the additive manufacturing printing methodology and what they learned about it. Andrew Polonsky and Tresa Pollock with the University of California, Santa Barbara have published a Perspective piece on the work done by the team in the same journal issue.

As additive manufacturing printing methodologies mature, new materials are being tested to find out if they might be used in 3D printers to create new products. In recent years, this has extended to metals. One such technique is called laser-powder bed fusion (L-PBF). It involves the use of a high-powered laser to melt and fuse metallic powders layer by layer to produce a 3D part. It has been hoped that the technique could eventually be used for aerospace and biomedical applications. But thus far, such efforts have fallen short due to the large number of defects that occur with the process. In this new effort, the researchers have discovered a way to reduce such defects, perhaps paving the way for the technique to finally fulfill its promise.

To better understand why the L-PBF process leads to so many defects (such as undesired pores) the researchers conducted X-ray synchrotron experiments and built predictive multi-physics models to gain a better understanding of what occurs during printing. One of their goals was to better understand how energy is absorbed during printing with powder layers that are only a few particles thick.

A Duke University research team has found a small area of the brain in mice that can profoundly control the animals’ sense of pain.

Somewhat unexpectedly, this brain center turns pain off, not on. It’s also located in an area where few people would have thought to look for an anti-pain center, the amygdala, which is often considered the home of negative emotions and responses, like the fight or flight response and general anxiety.

“People do believe there is a central place to relieve pain, that’s why placebos work,” said senior author Fan Wang, the Morris N. Broad Distinguished Professor of neurobiology in the School of Medicine. “The question is where in the brain is the center that can turn off pain.”

As people get older, they often feel less energetic, mobile or active. This may be due in part to a decline in mitochondria, the tiny powerhouses inside of our cells, which provide energy and regulate metabolism. In fact, mitochondria decline with age not only in humans, but in many species. Why they do so is not well understood. Scientists at the Max Planck Institute for Biology of Ageing in Cologne set out to understand how mitochondrial function is diminished with age and to find factors that prevent this process. They found that communication between mitochondria and other parts of the cell plays a key role.

For their studies, the scientists used the simple roundworm, Caenorhabditis elegans, an important model system for aging research. Over half the genes of this animal are similar to those found in humans, and their mitochondria also decline with age. From their research, the scientists found a nuclear protein called NFYB-1 that switches on and off genes affecting mitochondrial activity, and which itself goes down during aging. In mutant worms lacking this protein, mitochondria don’t work as well and worms don’t live as long.

Unexpectedly, the scientists discovered that NFYB-1 steers the activity of mitochondria through another part of the cell called the lysosome, a place where basic molecules are broken down and recycled as nutrients. “We think the lysosome talks with the mitochondria through special fats called cardiolipins and ceramides, which are essential to mitochondrial activity,” says Max Planck Director, Adam Antebi, whose laboratory spearheaded the study. Remarkably, simply feeding the NFYB-1 mutant worms cardiolipin restored mitochondrial function and worm health in these strains.

Patients recovering from severe lung infections develop “immunological scars” that stifle their body’s immune response and heighten their risk of contracting pneumonia, a common killer of COVID-19 sufferers, researchers said Monday.

Studies in both humans and mice showed that the body’s immune response is temporarily switched off after some severe infections, rendering patients more vulnerable to new bacterial or viral diseases.

A team of researchers from the University of Melbourne’s Peter Doherty Institute for Infection and Immunity and the University Hospital of Nantes found that the cells that form the immune system’s first line of defence—macrophages—were “paralysed” after severe infection.