Lifeboat Foundation

The last time NASA launched astronauts from the Kennedy Space Center, hundreds of thousands of people showed up to watch the final flight of the space shuttle in July 2011. The expectation, by NASA and others, was that similar crowds would show up when commercial crew flights finally began. The large crowds that showed up for launches like the first Falcon Heavy mission in 2018 or even relatively routine cargo launches appeared to confirm that belief, and NASA was planning for big crowds, not just of the public outside the gates of KSC but also official guests and working media inside, for a historic mission.

Then came the pandemic, and all those plans went out the window.

Now NASA is in the unusual, but understandable, position of telling people not to witness in person one of the agency’s biggest missions in the last decade. “We are asking people to watch from home,” NASA administrator Jim Bridenstine said Friday in a media teleconference about the upcoming SpaceX Demo-2 commercial crew mission.

To trace the trail of the virus worldwide, Lim’s team is using a new technology called next-generation sequencing at ASU’s Genomics Facility, to rapidly read through all 30,000 chemical letters of the SARS-CoV-2 genetic code, called a genome.

Each sequence is deposited into a worldwide gene bank, run by a nonprofit scientific organization called GISAID. To date, over 16,000 SARS-CoV-2 sequences have been deposited GISAID’s EpiCoVTM Database. The sequence data shows that SARS-CoV-2 originated a single source from Wuhan, China, while many of the first Arizona cases analyzed showed travel from Europe as the most likely source.

Now, using a pool of 382 nasal swab samples obtained from possible COVID-19 cases in Arizona, Lim’s team has identified a SARS-CoV-2 mutation that had never been found before—where 81 of the letters have vanished, permanently deleted from the genome.

While COVID-19 has infected millions of people worldwide and killed hundreds of thousands, there is currently no vaccine. In response, researchers have been evaluating the effectiveness of various antiviral drugs as possible COVID-19 treatments.

A new set of recommendations for health care workers on the front lines, to help them make decisions on how to treat the most critical COVID-19 patients, those with severe lung or heart failure, has been published.

Most newly discharged patients who recently recovered from COVID-19 produce virus-specific antibodies and T cells, suggests a study published on May 3rd in the journal Immunity, but the responses of different patients are not all the same. While the 14 patients examined in the study showed wide-ranging immune responses, results from the 6 of them that were assessed at two weeks after discharge suggest that antibodies were maintained for at least that long. Additional results from the study indicate which parts of the virus are most effective at triggering these immune responses and should therefore be targeted by potential vaccines.

It is not clear why immune responses varied widely across the patients. The authors say this variability may be related to the initial quantities of virus that the patients encountered, their physical states, or their microbiota. Other open questions include whether these immune responses protect against COVID-19 upon re-exposure to SARS-CoV-2, as well as which types of T cells are activated by infection with the virus. It is also important to note that the laboratory tests that are used to detect antibodies to SARS-CoV-2 in humans still need further validation to determine their accuracy and reliability.

“These findings suggest both B and T cells participate in immune-mediated protection against the viral infection,” says co-senior study author Chen Dong of Tsinghua University. “Our work has provided a basis for further analysis of protective immunity and for understanding the mechanism underlying the development of COVID-19, especially in severe cases. It also has implications for designing an effective vaccine to protect against infection.”

The breakthrough, which identified the location and function of every human gene, offered the promise of medical care tailored specifically to individual patients, based on their personal genetic makeup.

When researchers identified a gene associated with a 44 per cent risk of breast cancer in women, for example, it seemed that protecting them might be as simple as deactivating that gene.

But the promise of such personalized medicine has not fully materialized, say two McMaster researchers, because the full sophistication of the genetic blueprint has a more complex and far-reaching influence on human health than scientists had first realized.

In the absence of a specific vaccine, there has been much interest in alternative treatments and strategies to help minimise the effects of infection with COVID-19.

One strategy attracting much interest in the media is the importance of achieving sufficient vitamin D levels, and the topic has also been the subject of recent academic articles.1,2 While both articles discuss the potential role of vitamin D in the immune system, they also highlight the lack of direct clinical studies in those with COVID-19. However, a recent research letter3 provides some tentative evidence of the impact of vitamin D status on the severity of COVID-19 symptoms.

The test came out of DARPA, the U.S. military’s research division, and may be granted an accelerated emergency use authorization by the FDA by the end of the week, according to The Guardian.

If the test works as expected, it could play a major role in preventing future outbreaks by letting people know they need to self-isolate well before they start spreading the coronavirus.

“The concept fills a diagnostic gap worldwide,” Dr. Brad Ringeisen, head of DARPA’s biological technologies office, told The Guardian. He added that, should the FDA approve the test for use, it could be “absolutely a gamechanger.”

Electronic devices which mimic the functionality of biological synapses are a large step to replicate the human brain for neuromorphic computing and for numerous medical research investigations. One of the representative synaptic behaviors is paired-pulse facilitation (PPF). It has been widely investigated because it is regarded to be related to biological memory. However, plasticity behavior is only part of the human brain memory behavior.

Here, we present a phenomenon which is opposite to PPF, i.e., paired-pulse inhibition (PPI), in nano oxide devices for the first time. The research here suggests that rather than being enhanced, the phenomena of memory loss would also be possessed by such electronic devices. The device physics mechanism behind memory loss behavior was investigated. This mechanism is sustained by historical memory and degradation manufactured by device trauma to regulate characteristically stimulated origins of artificial transmission behaviors.

Under the trauma of a memory device, both the signal amplitude and signal time stimulated by a pulse are lower than the first signal stimulated by a previous pulse in the PPF, representing a new scenario in the struggle for memory. In this way, more typical human brain behaviors could be simulated, including the effect of age on latency and error generation, cerebellar infarct, trauma and memory loss pharmacological actions (such as those caused by hyoscines and nitrazepam).