@Happy Humble Hermit

Look at this shti

Shit*

Dude what in the fuck

This is my life

What are your grandparents doing about it

They are pressing for a restraining order still.

And the silver lining is that at least you live with the sane grandparents who are trying to take action

Despite being told they would hold her until court, for some reason, they just let her go

Like that, without a restraining order or anything

Women stumble onto smv and the results may surprise you

<:HMMM:513070140389326859>

Long live FOXO: unraveling the role of FOXO proteins in aging and longevity
Rute Martins, 1 Gordon J. Lithgow, 2 and Wolfgang Link

"Lifespan in C. elegans can also be modulated by its reproductive system. The removal of the worm′s germ cells extends its life by 60% (Hsin & Kenyon, 1999; Kenyon, 2010b). Germ line loss stimulates nuclear accumulation of DAF‐16/FoxO and the expression of the transcription elongation/splicing factor homolog TCER‐1 in intestinal cells. Although the precise mechanism of how the information about the reproductive status is transferred to the intestine is unclear, it has been shown that the intestinal adaptor protein KRI‐1 is required to induce DAF‐16/FoxO target gene expression and extend lifespan (Berman & Kenyon, 2006; Ganapathy et al., 2010). "

"After a person is infected with HIV, the virus seeks out the body's immune cells and attaches itself to them in the hopes of producing more virus particles. HIV's "main target" are CD4 immune cells." Nature.com

scitable/blog/viruses101/hiv_resistant_mutation?isForcedMobile=Y

"Could the Black Death protect against HIV?
People who survived the Black Death could have passed on a mutation that prevents the human immunodeficiency virus entering cells. [...] The mutation occurs on the gene for CCR-5, a receptor on the surface of macrophages. When a person becomes infected with HIV, the virus latches onto CCR5 and another protein — CD-4 — to be transported inside the macrophages.

CCR-5 is disabled in people with the full mutation, and so HIV is unable to gain access to the macrophages. If an individual inherits the mutant gene from both parents, they are essentially immune to HIV infection. People with one mutant and one normal gene can be infected, but tend to survive longer than infected people with two normal CCR-5 genes. It seems as though people without the mutation, called CCR5-Δ32, were killed by the Black Death, so that those with the mutation survived to reproduce and increase its prevalence today."

The-scientist

That’s hilarious

Freaky...

👀

Due to the selection pressures of the plague the mutation is more prevalent in European populations

Still not enough

yeah, it's a very small population

It's probably a weak link
Or these people have all in all a better immune system

As tfm said
The black death primarily killed off the poor population (with poor hygiene)

There are disadvantages with the CCR5-Δ32, but I don't remember what those were.

It might kill the protein's function

"It is likely that CCR5 plays a role in inflammatory responses to infection, though its exact role in normal immune function is unclear. Regions of this protein are also crucial for chemokine ligand binding, the functional response of the receptor, and HIV co-receptor activity." - wikipedia

"CCR5 Δ32 has an (heterozygote) allele frequency of 10% in Europe, and a homozygote frequency of 1%.

Recent research indicates that CCR5 Δ32 enhances cognition and memory. In 2016, researchers showed that removing the CCR5 gene from mice significantly improved their memory.[43] CCR5 is a powerful suppressor for neuronal plasticity, learning, and memory; CCR5 over-activation by viral proteins may contribute to HIV-associated cognitive deficits." - also wikipedia

Hmm

Ah is that that gebe the Chinese edited out from the first gene edit babies?

dunno... probably.

I can remember, that they added some hiv immunity and one article stated it also may have enhanced their cognitive abilities

lol, they're Europeanizing their babies...

But I mean, a 10% allele frequency...
It seems it has some benefits, but it's not so strong that it spreads faster

I'm sure there's some decrease in macrophage activity or something... but, if not, if it's all good, then cool.

For as much immunology work I do, I'm woefully stupid on a lot of things.

I'm a biochemist, though... that's too big for me.

I like molecules.