Silent Spring, by Rachel Carson (https://en.wikipedia.org/wiki/Silent_Spring), https://archive.org/details/fp_Silent_Spring-Rachel_Carson-1962

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A Hug without u is just toxic!

Pretty sure it wasn’t formal.

No, I rather not hear from him ever again.

Agreed! And yeah, still down, I just checked.

This is exactly why I’m not a gambler. ;-) I really prefer it when people say things like, “wow, thanks, here have a fiver.”

Dude’s a superhero, and needn’t be a ‘lone ranger’. Agreed. As the Fediverse expands, it will be the work of many; it just has to be that way.

MBIN FTW. KBIN has been “We are working on resolving the issues” for some days now. I hope Ernest is ok.

I have a login for lemmy.ml, as I have several from when I was switching over from Reddit. I’m thinking from what I’m reading here, that it’s not an instance I want to associate with.

A little chortle now and then. Keeps things from getting to ‘heavy’.

From the abstract: "By investigating an intergenic haplotype on chr21q22—which has been independently linked to inflammatory bowel disease, ankylosing spondylitis, primary sclerosing cholangitis and Takayasu’s arteritis3,4,5,6—we identify that the causal gene, ETS2, is a central regulator of human inflammatory macrophages and delineate the shared disease mechanism that amplifies ETS2 expression. "

I guess you owe me five bucks.

It was her all along!

A disease-associated gene desert directs macrophage inflammation through ETS2 https://www.nature.com/articles/s41586-024-07501-1

Abstract

Increasing rates of autoimmune and inflammatory disease present a burgeoning threat to human health1. This is compounded by the limited efficacy of available treatments1 and high failure rates during drug development2, highlighting an urgent need to better understand disease mechanisms. Here we show how functional genomics could address this challenge. By investigating an intergenic haplotype on chr21q22—which has been independently linked to inflammatory bowel disease, ankylosing spondylitis, primary sclerosing cholangitis and Takayasu’s arteritis3,4,5,6—we identify that the causal gene, ETS2, is a central regulator of human inflammatory macrophages and delineate the shared disease mechanism that amplifies ETS2 expression. Genes regulated by ETS2 were prominently expressed in diseased tissues and more enriched for inflammatory bowel disease GWAS hits than most previously described pathways. Overexpressing ETS2 in resting macrophages reproduced the inflammatory state observed in chr21q22-associated diseases, with upregulation of multiple drug targets, including TNF and IL-23. Using a database of cellular signatures7, we identified drugs that might modulate this pathway and validated the potent anti-inflammatory activity of one class of small molecules in vitro and ex vivo. Together, this illustrates the power of functional genomics, applied directly in primary human cells, to identify immune-mediated disease mechanisms and potential therapeutic opportunities.

People are always talking ‘miles per gallon’. I had a nerdy friend who kept the data and tracked ‘dollars per mile’.

https://foodstruct.com/food/cheesecake 5.5g per 100g serving, and it’s a pretty balanced protein. The fat combined with carbs makes it relatively low glycemic index at 50. Also at about 5:1 carbs to protein it’s pretty close to the 4:1 ratio recommended for endurance athletes by Edmund R. Burke, PhD. One of my professors would say, “There are no junk foods only junk diets.”

With air conditioning. Hey buddy, can you buy me a $10 cup ‘o coffee? Tho’ I could def. see this being a sort of funky, off beat vacation destination.

Hair cut, shoe shine, 15$ Beers, 20$ burgers. It’s intriguing. Non-denominational meditation space.

Second question: How does one afford to live in an airport?

You mispelled 42 minutes of doomscrolling. ;-)

Thank you, that’s most helpful. And no I won’t take your words blindly. Trust, and verify. :-) I’ll need to make sure my bank/ credit union is on with GNU Taler, tho’ it sounds unlikely, at this time.

FedNow looks very interesting.