Lifeboat Foundation: Safeguarding Humanity
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Category: biotech/medical – Page 1,814

Why do we age? What exactly is happening in our bodies? And can we do anything about it? Mankind has sought answers to these questions since time immemorial. While the pharmaceutical scientists Alexandra K. Kiemer and Jessica Hoppstädter from Saarland University are not claiming to have solved this ancient problem, they have uncovered processes within our immune system that contribute to aging. Kiemer and Hoppstädter have shown that low levels of the hormone cortisol and the protein known as GILZ can trigger chronic inflammatory responses in the body. The results have been published in the journal Aging Cell.

The phenomenon of human aging is the result of a complex interaction between numerous factors, with our own immune system playing a critical role. As we get older, our body’s own defense mechanisms age, too. The adaptive or specific immune system that each of us acquires over the course of our lives and that protects us from the pathogens that we came into contact with gradually deteriorates as we age. In contrast, however, our innate or non-specific immune system, which is the first line of defense towards a wide variety of pathogens, becomes overactive. The result is .

A persistent state of inflammation can cause serious damage to our bodies. One consequence is that chronic inflammatory diseases, such as atherosclerosis or arthritis, are far more prevalent in older patients. “This has been well-known for a long time. In fact, the refers to this phenomenon as ‘inflamm-aging’—a portmanteau word that combines the two inseparably linked processes of inflammation and aging,” explains Alexandra K. Kiemer, Professor of Pharmaceutical Biology at Saarland University.

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The Kingsley team pored over genetic data repositories, searching for places in the genetic code near the KITLG gene that tell the gene what to do. They found a location in the DNA where proteins known as transcription factors bind to the sequence and carry out the instructions specified in the code.

They discovered that if the nucleotide guanine holds that spot, the transcription factor cannot bind as tightly to the DNA as when another nucleotide (adenine) is in the same position. This simple alteration – replacing A with G in the DNA sequence – reduces the expression of the gene and, ultimately, changes the colour of the hair.

Guenther’s blue-flecked mice prove that the Kingsley group found the spot on the genome that informs hair follicles how much melanin to incorporate into hair.

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With every droplet that we can’t see, touch, or feel dispersed into the air, the threat of spreading COVID-19 persists. It’s become increasingly critical to keep these heavy droplets from lingering—especially on surfaces, which are welcoming and generous hosts.

Thankfully, our chemical cleaning products are effective, but using them to disinfect larger settings can be expensive, dangerous, and time-consuming. Across the globe there are thousands of warehouses, , schools, and other spaces where cleaning workers are at risk.

With that in mind, a team from MIT’s Computer Science and Artificial Intelligence Laboratory (CSAIL), in collaboration with Ava Robotics and the Greater Boston Food Bank (GBFB), designed a new robotic system that powerfully disinfects surfaces and neutralizes aerosolized forms of the coronavirus.

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Pigs are intermediate hosts for the generation of pandemic influenza virus. Thus, systematic surveillance of influenza viruses in pigs is a key measure for prewarning the emergence of the next pandemic influenza. Here, we identified a reassortant EA H1N1 virus possessing pdm/09 and TR-derived internal genes, termed as G4 genotype, which has become predominant in swine populations since 2016. Similar to pdm/09 virus, G4 viruses have all the essential hallmarks of a candidate pandemic virus. Of concern is that swine workers show elevated seroprevalence for G4 virus. Controlling the prevailing G4 EA H1N1 viruses in pigs and close monitoring in human populations, especially the workers in swine industry, should be urgently implemented.

Pigs are considered as important hosts or “mixing vessels” for the generation of pandemic influenza viruses. Systematic surveillance of influenza viruses in pigs is essential for early warning and preparedness for the next potential pandemic. Here, we report on an influenza virus surveillance of pigs from 2011 to 2018 in China, and identify a recently emerged genotype 4 (G4) reassortant Eurasian avian-like (EA) H1N1 virus, which bears 2009 pandemic (pdm/09) and triple-reassortant (TR)-derived internal genes and has been predominant in swine populations since 2016. Similar to pdm/09 virus, G4 viruses bind to human-type receptors, produce much higher progeny virus in human airway epithelial cells, and show efficient infectivity and aerosol transmission in ferrets. Moreover, low antigenic cross-reactivity of human influenza vaccine strains with G4 reassortant EA H1N1 virus indicates that preexisting population immunity does not provide protection against G4 viruses.

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In an interview with Nature, Elizabeth Maruma Mrema, the new head of the United Nations Convention on Biodiversity, acknowledged that it would be difficult to set a single target because biodiversity is multifaceted. But, if the community succeeds in making it work, she adds: “that will be the best result possible because then it becomes a song everyone will sing, and that everybody can align with to deliver that one key message.”

Elizabeth Mrema has a mighty task ahead of her, leading countries as they negotiate new biodiversity targets.

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In molecular biology, chaperones are a class of proteins that help regulate how other proteins fold. Folding is an important step in the manufacturing process for proteins. When they don’t fold the way they’re supposed to, it can lead to the development of diseases such as cancer.

Researchers at the Sloan Kettering Institute have uncovered important findings about what causes chaperones to malfunction as well as a way to fix them when they go awry. The discovery points the way to a new approach for developing targeted drugs for cancer and other diseases, including Alzheimer’s disease.

“Our earlier work showed that defects in chaperones could lead to widespread changes in cells, but no one knew exactly how it happened,” says SKI scientist Gabriela Chiosis, senior author of a study published June 30 in Cell Reports. “This paper finally gets into the nuts and bolts of that biochemical mechanism. I think it’s a pretty big leap forward.”

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Coronavirus was first detected in China. Over 10 million people have so far infected with the virus across the world while more than five lakh people have died of the disease.

Over 100 research institutions around the world are trying to develop a vaccine to deal with the virus. It was reported that the Oxford vaccine is now at the final stage.

But above all, China has now given final approval to the corona vaccine, according to a report of Yahoo News.

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Two documents dating back to 2015 shed further light on the role the federal government played in discovering remdesivir and its use in treating coronaviruses — work that has taken on new meaning as the Gilead Sciences (GILD) drug has gained global attention and an emergency use authorization from federal regulators to treat patients with Covid-19.

Reporting from the frontiers of health and medicine.

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