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Pfizer Inc said on Tuesday participants were showing mild-to-moderate side effects when given either the company’s experimental coronavirus vaccine or a placebo in an ongoing late-stage study.


(Reuters) — Pfizer Inc PFE.N said on Tuesday participants were showing mostly mild-to-moderate side effects when given either the company’s experimental coronavirus vaccine or a placebo in an ongoing late-stage study.

The company said in a presentation to investors that side effects included fatigue, headache, chills and muscle pain. Some participants in the trial also developed fevers — including a few high fevers. The data is blinded, meaning Pfizer does not know which patients received the vaccine or a placebo.

Kathrin Jansen, Pfizer’s head of vaccine research and development, stressed that the independent data monitoring committee “has access to unblinded data so they would notify us if they have any safety concerns and have not done so to date.”

Myotonic dystrophy type I is the most common type of adult-onset muscular dystrophy. People with the condition inherit repeated DNA segments that lead to the toxic buildup of repetitive RNA, the messenger that carries a gene’s recipe to the cell’s protein-making machinery. As a result, people born with myotonic dystrophy experience progressive muscle wasting and weakness and a wide variety of other debilitating symptoms.

CRISPR-Cas9 is a technique increasingly used in efforts to correct the genetic (DNA) defects that cause a variety of diseases. A few years ago, University of California San Diego School of Medicine researchers redirected the technique to instead modify RNA in a method they call RNA-targeting Cas9 (RCas9).

In a new study, publishing September 14, 2020 in Nature Biomedical Engineering, the team demonstrates that one dose of RCas9 gene therapy can chew up toxic RNA and almost completely reverse symptoms in a mouse model of myotonic dystrophy.

BOSTON, July 27, 2020 /PRNewswire/ — Solid-state batteries keep on attracting tremendous attention and investment with the maturing technologies and closeness to mass production. Even with the influence of COVID-19, the potential market size is expected to grow to over $6 billion by 2030, according to IDTechEx’s report “Solid-State and Polymer Batteries 2020–2030: Technology, Patents, Forecasts, Players.”

A Chinese virologist who has alleged that COVID-19 was human-made in a lab in China released a report on Monday that she says backs up her explosive claim.

Dr. Li-Meng Yan, a former researcher at the Hong Kong School of Public Health, posted a paper on the open-access repository website Zenote, that she claims shows how SARS-CoV-2 could be “conveniently created” in a laboratory setting in six months.

The paper, co-authored with two others, is titled “Unusual Features of the SARS-CoV-2 Genome Suggesting Sophisticated Laboratory Modification Rather Than Natural Evolution and Delineation of Its Probable Synthetic Route.”

Medical Ethics and “Futility” (Note: Listen here function)


We breathe about 12 to 20 times a minute, without having to think. Inhale: and air flows through the mouth and nose, into the trachea. The bronchi stem out like a wishbone, and keep branching, dividing and dividing, and finally feeding out into the tiny air sacs of alveoli. Capillaries – blood vessels thinner than hairs – twine around each alveolus. Both the air sac and the blood vessel are tiny, delicate, one cell thick: portals where blood (the atmosphere of the body) meets air (atmosphere of the world). Oxygen passes from air to blood; carbon dioxide, from blood to air. Then, the exhale pushes that carbon dioxide back out the mouth and nose. Capillaries channel newly oxygenated blood back to the heart. That oxygen fuels the body. That’s why we breathe.

Today, these basics of human respiration and metabolism feel obvious – and ventilators, the machines that breathe for sick people, do, too. We have so many medical devices, so of course we’d need, and have, machines that help us to breathe. But there’s a strange, and deeply human, story behind how we learned to breathe for each other. It starts long ago, when we didn’t understand breathing at all. When the body’s failure to breathe was incomprehensible, incurable, and fatal. When we had no way of knowing how badly we needed ventilators to keep people alive through those moments of vulnerability, lest those moments be their last.

Medical TV shows have accustomed us to the sight of doctors moving quickly to keep the sickest patients alive – but that link between hurry and success hasn’t always existed. Up to 100-odd years ago, for most of human history, when doctors had a dying patient, they rushed to do what they knew, but the patient died anyway. It doesn’t matter if you hurry or move slowly if your ‘cures’ don’t work. Ventilation, the linchpin of critical care medicine, changed that. Doctors could save some of the dying. That new technology helped bring medicine from hopes and crossed fingers to saving lives.

At our first online conference, Ending Age-Related Diseases 2020, Dr. Brian Kennedy of the National University of Singapore discussed the aging population of Singapore, the need for comprehensive healthcare, alpha-ketoglutarate and its effects against frailty in mice, ongoing trials of ketoglutarate in humans, spermidine against obesity, the role of biomarkers, and the importance of keeping people well rather than simply treating them when they are sick.

From the data, the GTEx team could identify the relationship between specific genes and a type of regulatory DNA called expression quantitative trait loci, or eQTL. At least one eQTL regulates almost every human gene, and each eQTL can regulate more than one gene, influencing expression, GTEx member and human geneticist Kristin Ardlie of the Broad Institute tells Science.

Another major takeaway from the analyses was that sex affected gene expression in almost all of the tissue types, from heart to lung to brain cells. “The vast majority of biology is shared by males and females,” yet the gene expression differences are vast and might explain differences in disease progression, GTEx study coauthor Barbara Stranger of Northwestern University’s Feinberg School of Medicine tells Science. “In the future, this knowledge may contribute to personalized medicine, where we consider biological sex as one of the relevant components of an individual’s characteristics,” she says in a statement issued by the Centre for Genome Regulation in Barcelona, where some of the researchers who participated in the GTEx project work.

Another of the studies bolsters the association between telomere length, ancestry, and aging. Telomere length is typically measured in blood cells; GTEx researchers examined it in 23 different tissue types and found blood is indeed a good proxy for overall length in other tissues. The team also showed that, as previously reported, shorter telomeres were associated with aging and longer ones were found in people of African ancestry. But not all earlier results held; the authors didn’t see a pattern of longer telomeres in females or constantly shorter telomeres across the tissues of smokers as previous studies had.

Not everyone is singing the project’s praises. Dan Graur, an evolutionary biologist at the University of Houston who often criticizes big projects like GTEx, tells Science the results are hard to parse and there was little diversity, with 85 percent of the tissue donors being white. He also was critical of the use of deceased donor tissue, questioning if it truly reflects gene activity in living humans. “It’s like studying the mating behaviour of roadkill.”

Other scientists say there’s much work to be done. The gene regulation map leaves many unanswered questions about the exact sequences that cause disease and how gene regulation systems work in tandem. Genomicist Ewan Birney, the deputy director general of EMBL, tells Science, “We shouldn’t pack up our bags and say gene expression is solved.”