How complement pathways generate C3b, anaphylatoxins and C5b–9; why endothelial injury is tissue-specific and what positive, negative and retracted clinical findings show.
How standardized pine bark extract becomes metabolites, what is known about eNOS, COX and 5-LOX, and where clinical trials show positive or negative results.
HS, HA, syndecan and glypican architecture; shear signaling, eNOS, SOD3, and antithrombin. Revised Starling forces, rheology, renal and brain barriers, indirect PBR and biomarkers, and positive and negative repair trials.
ADMA release from methylated proteins, DDAH1 and DDAH2 catalytic evidence, AGXT2, arginine transport, and NOS inhibition. Clinical associations, measurement methods, and why a reference interval is not a treatment threshold.
Reading CV, TIR, and AGP; sensor chemistry, mitochondria, PARP/GAPDH, Brownlee's four branches, eNOS, and glycocalyx. Clinical findings, meal strategies, and limits of transferring targets between populations.
Detailed analysis of EGb 761 composition, PAF antagonism, erythrocyte rheology, endothelial NO and mitochondrial mechanisms. Clinical data on dementia, tinnitus, Raynaud's and glaucoma are compared with model limitations, interactions and specialist practice.