Lifeboat Foundation: Safeguarding Humanity
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Category: biotech/medical – Page 2,705

Brushing your teeth has never been so important.

It is conceived that specific combinations of periodontal bacteria are associated with risk for the various forms of periodontitis. We hypothesized that such specificity is also related to human cause-specific death rates. We tested this hypothesis in a representative sample of the US population followed for a mean duration of 11 years and found that two specific patterns of 21 serum antibodies against periodontal bacteria were significantly associated with increased all-cause and/or diabetes-related mortalities. These data suggested that specific combinations of periodontal bacteria, even without inducing clinically significant periodontitis, may have a significant impact on human cause-specific death rates. Our findings implied that increased disease and mortality risk could be transmittable via the transfer of oral microbiota, and that developing personalized strategies and maintaining healthy oral microbiota beyond protection against periodontitis would be important to manage the risk.

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The idea of storing digital data in DNA seems like science fiction. At first glance, it might not seem obvious that a molecule can store data. The term “data storage” conjures up images of physical artifacts like CDs and data centers, not a microscopic molecule like DNA. But there are a number of reasons why DNA is an exciting option for information storage.

The status quo

We’re in the midst of a data explosion. We create vast amounts of information via our estimated 17 billion internet-connected devices: smartphones, cars, health trackers, and all other devices. As we continue to add sensors and network connectivity to physical devices we will produce more and more data. Similarly, as we bring online the 4.2 billion people who are currently offline, we will produce more and more data.

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Rebooting the immune system just got a bit easier. This could potentially be used to treat autoimmune diseases and just as exciting some of the aging processes.

A dietary approach to depleting blood stem cells may make it possible to conduct bone marrow transplantations without the use of chemotherapy or radiation therapy, according to researchers at the Stanford University School of Medicine.

The discovery, made in collaboration with researchers at the University of Tokyo, may also become a new way to treat certain cancers without chemo or radiation, which can cause severe side effects.

The researchers showed that a diet deficient in the essential amino acid valine could effectively deplete the population of in mice and allow them to be successfully transplanted with blood stem cells from other mice. The researchers also showed that human blood stem cells in the laboratory were affected by a lack of access to valine, suggesting that the same therapeutic approach may work in humans.

Continue reading “Withholding amino acid depletes blood stem cells, researchers say” | >

Earlier this year, former Braintree founder Bryan Johnson publicly announced his plans to forge Kernel, a company with the sole purpose of building hardware and software to augment human intelligence. Today, Johnson is investing $100 million of his own money into the concept, looking to rapidly double the size of his team, shore up a portfolio of intellectual property and prepare for animal and human testing trials for a forthcoming device aimed at reducing cognitive deficiencies for sufferers of conditions like Alzheimer’s and dementia.

Kernel is still very much in the planning stages, but the idea is rooted in the research of Theodore Berger, the company’s chief science officer. The futuristic device, which Johnson says might actually not need to be implanted beneath the skull at all, is designed to facilitate communication between brain cells by hacking the “neural code” that enables our brain to store and recall key information. With proper implementation, such a device could correct faulty signals to mend a cognitive impairment.

“We have done this before with biology and genomics,” said Johnson in an interview. “We can program yeast to do a specific function. We can expect the same path with neural code.”

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Studies of different animal species suggest a link between eating less and living longer, but the molecular mechanisms by which caloric restriction affords protection against disease and extends longevity are not well understood.

New clues to help solve the mystery are presented in an article published in the September issue of Aging Cell by scientists at the Center for Research on Redox Processes in Biomedicine (Redoxoma), one of the Research, Innovation and Dissemination Centers (RIDCs) funded by FAPESP.

The results of in vitro and in vivo experiments performed by the Redoxoma team included the finding that a 40% reduction in dietary caloric intake increases mitochondrial calcium retention in situations where intracellular calcium levels are pathologically high. In the brain, this can help avoid the death of neurons that is associated with Alzheimer’s disease, Parkinson’s disease, epilepsy and stroke, among other neurodegenerative conditions.

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Traditional lithium-ion batteries may be on the way out, as scientists continue to overcome the obstacles holding back the longer-lasting lithium-oxygen batteries. The main issue is lack of efficiency and the build-up of lithium peroxide, which reduces the electrodes’ effectiveness. But now a team at Yale has used a molecule found in blood as a catalyst that not only improved the lithium-oxygen function, but may help reduce biowaste.

Lithium-oxygen, or lithium-air batteries, have the potential to hold a charge for much longer than traditional lithium-ion batteries and extend the life of devices like phones to several weeks before they’d need to be recharged. But before those dreams can become a reality, the problems of efficiency and lithium peroxide build-up need to be solved.

Previous studies have tried to fight lithium peroxide by keeping the oxygen in the cell as a solid, and by modifying the electrode to produce lithium superoxide instead. In this case, the Yale researchers were looking for a new catalyst that allowed lithium oxide in the cell to decompose back into lithium ions and gaseous oxygen, and they found one in an unexpected place: animal blood.

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Japanese scientists have successfully grown healthy eggs from mouse skin cells – all within the perimeters of a lab dish. Led by Professor Katsuhiko Hayashi of Kyushu University, this achievement marks the first time the entire process has taken place outside a mouse and raises a tantalizing question for the reproductive science community: What if you could do the same with human cells?

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CRISPR Therapeutics—a Swiss startup hoping to harness the gene-editing technology it’s named after to develop treatments for genetic illnesses like sickle-cell anemia and cystic fibrosis— went public today (Oct. 19), raising $56 million in its initial public offering. It’s the third CRISPR-related biotech to IPO this year despite a pitched battle over who owns the patent to the breakthrough technique.

The market for CRISPR (short for “clustered regularly interspaced short palindromic sequences”) is projected to be worth more than $5.5 billion by 2021, nearly double its current value, according to research firm MarketsandMarkets. The potential of the cheap, easy-to-use technology—which could do everything from creating a mushroom that doesn’t brown to curing cancer by cutting and pasting snippets of DNA—has companies rushing to develop new applications even though no one knows who will ultimately control it.

“It’s a race,” says Fabien Palazzoli, head of biotech intellectual property (IP) analytics for the consulting firm IPStudies. “It’s a race for the IPO, for the scientific results, for the FDA recommendation, for the IP.”

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PCG-1α therapy shows promise in treating age-related decline.

It is always a good idea to look closely at the biochemistry involved in any potential Alzheimer’s disease therapy that shows promise in mouse models. There is perhaps more uncertainty for Alzheimer’s than most other age-related conditions when it comes to the degree to which the models are a useful representation of the disease state in humans — which might go some way towards explaining the promising failures that litter the field. In the research here, the authors are aiming to suppress a step in the generation of amyloid-β, one of the proteins that aggregates in growing amounts and is associated with brain cell death in Alzheimer’s disease. They achieve this goal using gene therapy to increase the level of PGC-1α, which in turn reduces the level of an enzyme involved in the production of amyloid-β. Interestingly, increased levels of PGC-1α have in the past been shown to produce modest life extension in mice, along with some of the beneficial effects to health associated with calorie restriction.

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