Lifeboat Foundation

Substantial transmission of SARS-CoV-2 infection occurred in the population of Wuhan in December 2019 with most cases reported in the second half of that month. Many early reported cases were associated with Huanan Market, indicating that it was one of the focus of the transmission. Nevertheless, transmission was also occurring elsewhere in Wuhan at the same time.

It is not possible on the basis of the current epidemiological information to determine how the SARS-CoV-2 was introduced into the Huanan Market. Substantial transmission of SARS-CoV-2 infection occurred among the population of Wuhan in December 2019.

While some of the early cases had an association with the Huanan Seafood Market, others were associated with other markets and other cases have no market association at all. It is likely that Huanan Seafood Market acted as a focus for transmission of the virus, but there are also transmissions appearing to have the occurrence elsewhere in Wuhan at the same time. This is our basic judgment. It is not possible on the basis of the current information to determine how SARS-CoV-2 was introduced into the Huanan Market.

The third part of my introduction will be the research of the animal environment group, the third group of our joint mission. Coronaviruses that phylogenetically relate to SARS-CoV-2 have been identified in different animals, including horseshoe bats and pangolins. Sampling of bats in Hubei Province, however, has failed to identify evidence of SARS-CoV-2-related viruses and sampling of wildlife in different places in China has so far failed to identify the presence of SARS-CoV-2.

Continue reading “COVID-19 Virtual Press conference transcript” »

Summary: A new technique which involves fusing human and chimpanzee skin cells that have been modified to act like stem cells, allowed researchers to identify two novel genetic differences between humans and chimps.

Source: Stanford University.

One of the best ways to study human evolution is by comparing us with nonhuman species that, evolutionarily speaking, are closely related to us. That closeness can help scientists narrow down precisely what makes us human, but that scope is so narrow it can also be extremely hard to define. To address this complication, researchers from Stanford University have developed a new technique for comparing genetic differences.

Today on the Science Talk podcast, Noam Slonim speaks to Scientific American about an impressive feat of computer engineering: an AI-powered autonomous system that can engage in complex debate with humans over issues ranging from subsidizing preschool and the merit of space exploration to the pros and cons of genetic engineering.

In a new Nature paper, Slonim and colleagues show that across 80 debate topics, Project Debater’s computational argument technology has performed very decently—with a human audience being the judge of that. “However, it is still somewhat inferior on average to the results obtained by expert human debaters,” says Slonim.

Continue reading “AI Can Now Debate with Humans and Sometimes Convince Them, Too” »

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Papers referenced in the video:

Continue reading “Carotenoids Are Associated With A Younger Epigenetic Age And Reduced All-Cause Mortality Risk” »

Check out “How Watson Works here.”

Is it possible to live forever by using narrow AI that can perform faster and smarter than humans? Having a doctor give you the correct diagnosis and treatment plan only happens on average, 54% of the time, as the New England Journal of Medicine has pointed out. Having Watson instantly diagnose you with the correct diagnosis and treatment plan 95% of the time will become the new standard. Our crop of new personal medicine products such as continual internal diagnostics, synthetic immune systems, virtual assistants, and regenerative medicine will diagnose and stop sickness from ever occurring while constantly rebuilding and improving body and mind capabilities.

IBM has made a series of Watson computer systems so that any company can raise their industries products and services far beyond our human capability. IBM’s Watson was first featured to the public with its historic Jeopardy win over Ken Jennings and Brad Rutter the best human Jeopardy players. At the time, Watson contained 200 million pages of structured and unstructured content in a ninety server computing system with an analytical software IBM designed called DeepQA. Now, the financial markets, medicine, insurance companies, government, engineering, and customer service call centers are employing (buying) Watson is an artificial intelligence system, that can be specifically tailored to any digitized industry and quickly evolve their industries potential.

Summary: It’s not only our genetics and environment that play a role in aging and longevity, it’s also the random, tiny changes that arise on the cellular level.

Source: USC

A new model of aging takes into account not only genetics and environmental exposures but also the tiny changes that randomly arise at the cellular level.

Most cancers are driven by continuous cell division, the cause of which is largely a mystery. Scientists at Vanderbilt University have discovered a genetic switch that seems to touch off that abnormal proliferation of cells—and they did it with the gene editing system CRISPR.

Using a genomewide CRISPR screen, the Vanderbilt team discovered that deleting a protein made by the gene TRAF3 causes cells to proliferate without stopping, even after they reach a certain density that would normally signal them to stop dividing. Because TRAF3 has not been linked to cancer before, the finding could offer key insights into the development of some cancers, the researchers reported in the journal eLife.

The team started with 40 million epithelial cells, using CRISPR to select cells that kept dividing uncontrollably. They were surprised to discover that a loss of TRAF3 activates signaling that in turn drives cell proliferation. TRAF3 normally activates immunity and had not been linked to uncontrolled cell growth before, they said.

As the world fights the SARS-CoV-2 virus causing the COVID-19 pandemic, another group of dangerous pathogens looms in the background. The threat of antibiotic-resistant bacteria has been growing for years and appears to be getting worse. If COVID-19 taught us one thing, it’s that governments should be prepared for more global public health crises, and that includes finding new ways to combat rogue bacteria that are becoming resistant to commonly used drugs.

In contrast to the current pandemic, viruses may be be the heroes of the next epidemic rather than the villains. Scientists have shown that viruses could be great weapons against bacteria that are resistant to antibiotics.

I am a biotechnology and policy expert focused on understanding how personal genetic and biological information can improve human health. Every person interacts intimately with a unique assortment of viruses and bacteria, and by deciphering these complex relationships we can better treat infectious diseases caused by antibiotic-resistant bacteria.

In the new study, researchers instead aimed to reduce the amount of Nav1.7 that cells make in the first place. Bioengineer Ana Moreno and her colleagues at the University of California, San Diego, modified the “molecular scissors” of the gene editor CRISPR. Changes to the cutting enzyme Cas9 caused it to bind to DNA that makes Nav1.7 without slicing it, effectively preventing the Nav1.7 protein from being made. The researchers enhanced this silencing effect by hitching Cas9 to a repressor, another protein that inhibits gene expression.

The researchers tested the Cas9 approach—and a similar approach using another gene-editing protein known as a zinc finger—in mice given the chemotherapy drug paclitaxel, which can cause chronic nerve pain in cancer patients. The team measured pain by poking the animals’ paws with a thin nylon filament. Paclitaxel prompted mice to withdraw from gentler pokes, indicating that a normally nonpainful stimulus had become painful. But 1 month after an injection of the gene-silencing treatment into their spinal fluid, rodents responded much like mice that had never gotten paclitaxel, whereas untreated rodents remained hypersensitive, the team reports today in.

The approach could also prevent pain when given before paw injections of either the inflammation-causing compound carrageenan or a molecule called BzATP that increases pain sensitivity. And treated mice behaved no differently from untreated ones when their opposite paw—not inflamed by carrageenan—was exposed to a hot surface. That’s an encouraging initial sign that the injection didn’t silence Nav1.7 so completely that it creates a dangerous numbness to all pain, Moreno says. Behavioral tests so far haven’t turned up evidence of potentially concerning side effects; the injections didn’t appear to alter the animals’ movement, cognition, or anxiety levels.