Lifeboat Foundation

The robot seen here can work almost 24–7, carrying out experiments by itself. The automated scientist – the first of its kind – can make its own decisions about which chemistry experiments to perform next, and has already discovered a new catalyst.

With humanoid dimensions, and working in a standard laboratory, it uses instruments much like a human does. Unlike a real person, however, this 400 kg robot has infinite patience, and works for 21.5 hours each day, pausing only to recharge its battery.

This new technology – reported in the journal Nature and featured on the front cover – is designed to tackle problems of a scale and complexity that are currently beyond our grasp. New drug formulations could be autonomously discovered, for example, by searching vast and unexplored chemical spaces.

The solution was to split the protein into two harmless halves. Liu’s team, led by graduate student Beverly Mok, used 3D imaging data from the Mougous lab to work out how to divide the protein into two pieces. Each piece did nothing on its own, but when reunited, they reconstituted the protein’s full activity. The team fused each deaminase half to customizable DNA-targeting proteins that did not require guide RNAs. Those proteins bound to specific stretches of DNA, bringing the two halves of the deaminase together. That let the molecule regain its function and work as a precision gene editor—but only once it was correctly positioned.

Liu’s team used the technology to make precise changes to specific mitochondrial genes. Then, Mootha’s lab, which focuses on mitochondrial biology, ran tests to see whether the edits had the intended effect. “You could imagine that if you’re introducing editing machinery into the mitochondria, you might accidentally cause some sort of a catastrophe,” Mootha said. “But it was very clean.” The entire mitochondrion functioned well, except for the one part the scientists intentionally edited, he explained.

This mitochondrial base editor is just the beginning, Mougous suggested. It can change one of the four DNA letters into another. He hopes to find additional deaminases that he and Liu can develop into editors able to make other mitochondrial DNA alterations. Such tools could enable new strategies for treating mitochondrial diseases, as well as help scientists to model diseases and aid in drug testing. “The ability to precisely install or correct pathogenic mutations could accelerate the modeling of diseases caused by mtDNA mutations, facilitate preclinical drug candidate testing, and potentially enable therapeutic approaches that directly correct pathogenic mtDNA mutations,” the authors noted. “Bacterial genomes contain various uncharacterized deaminases, raising the possibility that some may possess unique activities that enable new genome-editing capabilities.”

Scientists at USC Dornsife College of Letters, Arts and Sciences may have found the beginnings of a path toward increasing human lifespan.

The research, published July 10 by the Journal of Gerontology: Biological Sciences, shows the drug mifepristone can extend the lives of two very different species used in laboratory studies, suggesting the findings may apply to other species, including human beings.

Various diseases of the digestive tract, for example severe intestinal inflammation in humans, are closely linked to disturbances in the natural mobility of the intestine. What role the microbiome—i.e. the natural microbial community colonizing the digestive tract—plays in these rhythmic contractions of the intestine, also known as peristalsis, is currently the subject of intensive research. It is particularly unclear how the contractions are controlled and how the cells of the nervous system, that act as pacemakers, function together with the microorganisms.

A research team from the Cell and Developmental Biology group at Kiel University has now succeeded in demonstrating for the first time, using the freshwater polyp Hydra as an example, that phylogenetically old neurons and bacteria actually communicate directly with each other. Surprisingly, they discovered that the nerve cells are able to cross-talk with the microorganisms via immune receptors, i.e., to some extent with the mechanisms of the immune system.

On this basis, the scientists of the Collaborative Research Center (CRC) 1182 “Origin and Function of Metaorganisms” formulated the hypothesis that the nervous system has not only taken over sensory and motor functions from the onset of evolution, but is also responsible for communication with the microbes. The Kiel researchers around Professor Thomas Bosch published their results together with international colleagues today in the journal Proceedings of the National Academy of Sciences (PNAS).

Stem cells can be transformed into lung cells to replace the lung cells infected by COVID-19. These new lung cells will take in oxygen and release carbon dioxide, eliminating the breathing problems.

BALTIMORE (WJZ) — A stem cell therapy trial for the most critically ill coronavirus patients is underway in Maryland.

Researchers at the University of Maryland School of Medicine are trying to save the maximum number of patients who are significantly sickened by the virus and reduce the mortality rate.

Continue reading “Stem Cell Therapy Designed To Treat Severely Ill Coronavirus Patients Being Tested In Maryland” »

According to British neurologists, COVID-19 can cause serious damage to the brain and central nervous system. Such damage can lead to psychosis, paralysis and strokes, which are often detected in their late stages.

The human colon is home to a complex microbial ecosystem (microbiota), composed mostly of anaerobic organisms. Recent data suggest that gut microbes and their metabolites can affect human health through multiple mechanisms including altering the immune response , changing host cell metabolic states , and even affecting the response to immunotherapies.

The potential causative role of gut microbiota in health and disease is one of the most extraordinary findings of the past decade. Yet we are only starting to understand the multitude of mechanisms by which microbes promote changes in intestinal physiology, and how changes in the symbiotic relationship between the host and the resident microbiota contribute to the pathogenesis of both infectious and noninfectious diseases.

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An analysis of more than 17 million people in England — the largest study of its kind, according to its authors — has pinpointed a bevy of factors that can raise a person’s chances of dying from COVID-19, the disease caused by the coronavirus.

The paper, published Wednesday in Nature, echoes reports from other countries that identify older people, men, racial and ethnic minorities, and those with underlying health conditions among the more vulnerable populations.

“This highlights a lot of what we already know about COVID-19,” said Uchechi Mitchell, a public health expert at the University of Illinois at Chicago who was not involved in the study. “But a lot of science is about repetition. The size of the study alone is a strength, and there is a need to continue documenting disparities.”

Most cells in your body come with two genetic libraries; one in the nucleus, and the other inside structures called mitochondria — also known as the ‘powerhouses of the cell’.

Until now, we’ve only had a way to make changes to one.

A combined effort by several research teams in the US has led to a process that could one day allow us to modify the instructions making up the cell’s ‘other’ genome, and potentially treat a range of conditions that affect how we power our bodies.