Creature

not to be that guy but evolve or repeat those are your only options

Plz reblog, I need to know I'm not alone in this.

VACCINATE YA KIDS FFS

Dear scientists,

Please, for the love of God, please, make your papers more understandable.

Fuck you

Sincerely,

A college student on the verge of tears

vitamin sea, if you will

Journey to the Microcosmos- Flatworms: Simple Wiggly Tubes

Images Originally Captured by Jam’s Germs

Quote Voiced by Jam’s Germs

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“

To students taking exams right now:

You are smarter than you know

It is almost over, just keep holding on

You are not your grades, and your grades don’t define your intelligence

Trust and believe in yourself

Stop comparing yourself to others

Remember to drink water (not just coffee)

Study discovers that mitochondria transmit signals in the immune and nervous systems

The new study has revealed that mitochondria play a crucial role in the regulation of the NF-κB signaling pathway.

Mitochondria are primarily known as the powerhouse of the cell. However, these cellular organelles are required not only for providing energy: Professor Konstanze Winklhofer and her group at the Faculty of Medicine at Ruhr University Bochum, Germany, recently discovered that mitochondria play an important role in signal transduction in innate immune pathways.

They regulate a signaling pathway that helps to eliminate pathogens, but can cause damage through inflammation upon overactivation. The research team published their findings in the EMBO Journal.

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