Biotin-deficient rats were raised on a purified ration containing raw egg white plus avidin. Urea synthesis and excretion were compared between the biotin-deficient and the pair-fed control rats. 24hrurinary urea excretion and the specific activities of carbamylphosphate synthetase, ornithine transcarbamylase, and arginase in the liver mitochondria fraction were no different between these two groups. The net urea production in the liver slice and in the isolated perfused liver of the biotin-deficient rats was similar to that of the pair-fed control. Thus the conclusion must be that biotin is not in urea in mea biosynthesis in the rat.
Animal ; Avitaminosis/metabolism ; Biotin* ; Liver/metabolism* ; Rats ; Urea/biosynthesis* ; MH - ; Substances: ; Urea ; Biotin

Vitamins are micronutrients which are essential for the maintenance of biological responses including immune system. Hence, vitamin deficiency increases a risk of infectious, allergic, and inflammatory diseases. Accumulating evidence has recently revealed the molecular and cellular mechanisms of vitamin-mediated regulation in the active and quiescent immune responses. In this review, we focus on the immunologic roles of vitamins in the regulation of homeostasis and surveillance in the gut.
Avitaminosis ; Energy Metabolism ; Homeostasis* ; Immune System ; Immunoglobulin A ; Inflammation ; Micronutrients ; Monitoring, Immunologic* ; Vitamins*

Hyperhomocysteinemia is an independent risk factor for cardiovascular, cerebrovascular and peripheral vascular diseases that are complicated by atherosclerosis and a thromboembolism. An increased level of plasma homocysteine develops from a genetic defect in the of enzyme for the homocysteine metabolism or a vitamin deficiency. Hyperhomocysteinemia has direct toxic effect on the vascular endothelium and causes damages to the antithrombotic action of vascular endothelial cells. Most cases of hyperhomocysteinemia are asymptomatic, but cardiopulmonary or cerebrovascular incidents developin rare cases. In the case of a thromboembolism with an unknown cause, hyperhomocysteinemia should be considered in a differential diagnosis. The authors report a case of pulmonary thromboembolism in a patient with hyperhomocysteinemia with a review of the relevant literature.
Atherosclerosis ; Avitaminosis ; Diagnosis, Differential ; Endothelial Cells ; Endothelium, Vascular ; Homocysteine ; Humans ; Hyperhomocysteinemia* ; Metabolism ; Peripheral Vascular Diseases ; Plasma ; Pulmonary Embolism* ; Risk Factors ; Thromboembolism