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In ME/CFS patients, dysfunction of the TRPM3 calcium channel, which is critical for calcium permeability and NK cell function, results in diminished NK cell activity and disrupted calcium signaling [146]

Many published studies are constrained by small sample sizes, non-standardised dosing protocols, or an overreliance on extrapolated data from human or rodent models

present in ~40% of PV patients Plethora (facial redness/ruddy complexion) due to increased RBC mass and skin hyperemia Headache, dizziness, and visual disturbances from hyperviscosity and reduced cerebral blood flow Splenomegaly palpable in 7090% of PV patients from extramedullary hematopoiesis Thrombotic events (DVT, stroke, MI, Budd-Chiari syndrome) major complications from hyperviscosity Erythromelalgia burning pain/redness of hands and feet due to platelet-mediated microvascular occlusion Gout from elevated uric acid due to increased cell turnover Hypertension common comorbidity in PV Bleeding tendency paradoxically, despite elevated platelets, qualitative platelet dysfunction can cause GI bleeding Signs and symptoms that are routinely associated with a confirmed diagnosis of anemia or polycythemia (e.g., tachycardia, fatigue, pallor with anemia

Methylation doesnt directly produce glutathione, but it does play a part in the process that synthesizes glutathione

Thalidomide (THD) alleviates radiation induced lung fibrosis (RILF) via down-regulation of TGF-beta/Smad3 signaling pathway in an Nrf2-dependent manner

GPX4 reduces phospholipid hydroperoxides (PL-OOH) to their corresponding non-toxic phospholipid alcohol (PL-OH) using GSH as an electron donor, thereby preserving membrane integrity 95