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Man Bitten by Stray Cat Contracts Infection Unknown to Science

The bite of a fluffy cat on the street can be more dangerous than you might think.

In the United Kingdom, a 48-year-old who was bit by a stray feline ended up contracting a species of bacterium that scientists have never seen before. His immune response to the foreign microorganism was a doozy. Just eight hours after receiving multiple bites, the man's hands had swollen to such a great extent that he took himself to the emergency department. His puncture wounds were cleaned and dressed and he was given a tetanus shot before being sent on his way with antibiotics. A day later, he was back at the hospital. His pinky and middle fingers on his left hand were painfully enlarged and both his forearms were red and swollen. Doctors had to surgically remove the damaged tissue around his wounds. He was also given three different antibiotics intravenously and was sent home with oral antibiotics. This time, thankfully, the treatment worked and he made a full recovery. Back at the hospital, however, doctors were busy trying to figure out what had happened. When they analyzed the microorganisms present in samples from his wounds, they found an unrecognizable Streptococcus-like organism.

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a very, VERY important post. spread everywhere and screen record the video to your phone. or message me and ill happily send you the video. give to every woman and girl you know.

bc as they both said / demonstrated, its not only super easy to do, but super easy to miss.

Your body deserves to feel safe. Your soul deserves to feel safe. I hope you find environments and invest in healing steps to accomplish this, because you and your body are good and deserving.

Metastatic embolus from breast adenocarcinoma in the lungs

cancer cells are usually very metamorphic, which you can tell by the different shapes of the nuclei in this embolus. i love how you can see the metastasis inside a vessel perfectly in this picture!

Quand on pense qu’il ni a plus rien… y’a encore un peu de vie!

Follow her on Instagram: Tardibabe / Chloé Savard

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How SARS-CoV-2 Hijacks Human Cells to Evade Immune System

Researchers at University of California San Diego School of Medicine have discovered one way in which SARS-CoV-2, the coronavirus that causes COVID-19, hijacks human cell machinery to blunt the immune response, allowing it to establish infection, replicate and cause disease.

In short, the virus’ genome gets tagged with a special marker by a human enzyme that tells the immune system to stand down, while at the same time ramping up production of the surface proteins that SARS-CoV-2 uses as a “doorknob” to enter cells.

The study, published April 22, 2021 in Cell Reports, helps lay the groundwork for new anti-viral immunotherapies — treatments that work by boosting a patient’s immune system, rather than directly killing the virus.

“It’s very smart of this virus to use host machinery to simultaneously go into stealth mode and get inside more cells,” said Tariq Rana, PhD, professor and chief of the Division of Genetics in the Department of Pediatrics at UC San Diego School of Medicine and Moores Cancer Center. “The more we know about how the virus establishes itself in the body, the better equipped we are to disrupt it.”

In human cells, genes (DNA) are transcribed into RNA, which is then translated into proteins, the molecules that make up the majority of cells. But it’s not always so straightforward. Cells can chemically modify RNA to influence protein production. One of these modifications is the addition of methyl groups to adenosine, one of the building blocks that make up RNA. Known as N6-methyladenosine (m6A), this modification is common in humans and other organisms, including viruses.

In contrast to humans, the entire genomes of some viruses, including SARS-CoV-2, are made up of RNA instead of DNA. And rather than carry around the machinery to translate that into proteins, the coronavirus gets human cells to do the work.

Rana and his team previously discovered that m6A plays an important role in HIV and Zika virus infections. In their latest study, the researchers discovered that the human enzyme METTL3 adds methyl groups to introduce m6A in SARS-CoV-2’s RNA. That modification prevents the virus’ RNA from triggering inflammatory molecules known as cytokines. To the team’s surprise, METTL3’s activity also led to increased expression of pro-viral genes — those that encode proteins needed for SARS-CoV-2 replication and survival, such as ACE2, the cell surface receptor that the virus uses to enter human cells.

“It remains to be seen why our cells help the virus out like this,” Rana said.

“How SARS-CoV-2 Hijacks Human Cells to Evade Immune System“