@greg_price11 You need to understand that Pepsi, General Mills.. etc. help write the SNAP policy. Every government agency has connections to corporate America, and they fund democrats to distract you.
@InterestingSTEM I know its more humane that other methods. But this slaughter process takes far too long. I can see the worry in its eyes. I have avoided pig since i first saw this 6 years ago, and im fine without eating it.
@RealAlexJones Im pretty sure a deal was made, and it was with the same people behind his attempted assassination. This is the real power that controls US international policies.
This is and has been normal policy for universities. They love diversity at least since the 90s when I went to collage. I remember being denied being an RA because I never said the word diversity in my essay. I asked the administration about it and they admitted they do a word count on “diversity”. Highest count wins. And they have quotas for admittance from shithole countries with scholarships.
@KaySpillne3394@TRobinsonNewEra Germans need to take back their country and remove the puppet regime at any cost. Your culture and heritage depends on it.
I tested the current leading AI models joke abilities.
“There is a new book coming out of the romanic beginnings of Prince Harry and Megans relationship, titled: When Harry met Silly”
Ok here are the results
1. 🧠 GPT-4o caught the joke on first prompt, but was unsure, he suspected it was a play on harry met sally
2. 🤖 ChatGPT-5 second prompt when i said it was a joke completly got the movie reference
3. 🧞 Grok(Expert) got the joke on second prompt but did not mention movie reference
4. 🌌 Gemini still processing the joke
Key Publications / Evidence
1.“Acetaminophen‐Induced Oxidant Stress and Cell Injury in Cultured Mouse Hepatocytes: Protection by N‑Acetyl Cysteine”
— Bajt et al. (2004), Toxicological Sciences
This in vitro hepatocyte study showed that exposure to acetaminophen caused rapid depletion of glutathione (GSH), followed by increased oxidative stress (measured by ROS indicators) and then cell injury.
2.“Role of glutathione depletion in the cytotoxicity of acetaminophen in a primary culture system of rat hepatocytes”
— Older classic toxicology work
This study backs up the mechanistic idea that depletion of glutathione is central to acetaminophen’s cytotoxicity in liver cells (i.e. in overdose).
3.“Acetaminophen decreases intracellular glutathione levels and modulates cytokine production in human alveolar macrophages and type II pneumocytes in vitro”
— PubMed / in vitro human lung cells
This one is interesting because it’s outside the liver. They reported that even “clinically relevant concentrations” of acetaminophen (0.05‑1 mM) reduced intracellular reduced-glutathione in human pulmonary macrophages (up to ~53% drop) and in type II pneumocytes (up to ~34%) over 1–4 h exposures.
4.“Effect of acetaminophen on glutathione levels in several regions of rat brain”
— study of regional brain GSH
This animal study found that acetaminophen reduced reduced-glutathione (GSH) in brain regions: e.g. hypothalamus (~ −20%), medulla oblongata (~ −14%), cerebral cortex, etc.
5.Biochemical / modeling review: “The biochemistry of acetaminophen hepatotoxicity and rescue”
— This review (and modeling work) shows how one of the major detoxification pathways for the reactive metabolite of acetaminophen (NAPQI) is conjugation with glutathione, and that overproduction of NAPQI (as in overdose) can “use up” glutathione stores, causing depletion.
6.“Glutathione Reductase Is Inhibited by Acetaminophen‑glutathione Conjugate”
— Roušar et al. (2009)
This is a more mechanistic twist: they synthesized the acetaminophen–glutathione conjugate and showed that it inhibits glutathione reductase (the enzyme that helps regenerate reduced GSH from GSSG) in both yeast and rat hepatocyte lysates. So not only consumption, but interference with regeneration.
7.“Paracetamol‑Induced Glutathione Consumption: Is There a Link …” and related commentary
— Sestili & Fimognari, plus commentaries
These more recent papers discuss the hypothesis that even therapeutic (non‑overdose) doses may modestly consume glutathione, especially in susceptible individuals or under oxidative stress.