Key pathophysiologic mechanisms include: Mucosal barrier dysfunction: Impaired epithelial tight junctions allow bacterial translocation, triggering innate immune activation T-helper cell dysregulation: Predominantly Th1 and Th17 pathways drive chronic inflammation via TNF-, IL-12, IL-23 the basis for biologic therapy targets Transmural inflammation: Unlike UC (mucosal only), CD involves all layers: mucosa submucosa muscularis propria serosa Granuloma formation: Non-caseating granulomas are pathognomonic but present in only ~3050% of biopsies Fibrosis and stricture: Chronic inflammation activates myofibroblasts collagen deposition luminal narrowing obstructive symptoms Fistula formation: Transmural ulcers penetrate serosa form sinus tracts connect to adjacent bowel, bladder, vagina, or skin 7
Variable modifications included mono-methylation of arginine residues (14.01565 Da), dimethylation (28.0313 Da), and oxidation of methionine residues (15.9949 Da)
The selective mobilization of fatty acids is not based on their positional distribution in white-fat-cell triacylglycerols
Daily morning use is generally recommended for antioxidant protection and brighter-looking skin
[7] See also [edit] References [edit] Annual Review of Biochemistry