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Background and Summary of Retrospective Studies Homocystinuria caused by congenital CBS and MTHFR defects or by genetic alteration of cobalamin metabolism is characterized by clinical problems including frequent arterial and venous thromboembolism and premature atherosclerosis (McCully, 1983

BCL-2 family inhibitors Senescent cells enter a near-permanent cell cycle arrest and activate an anti-apoptotic program to persist in the tissue where they contribute to inflammation