Hemolytic factors

S-Methylcysteine sulfoxide - precursor for 121 hemolytic factor dimethyl disulfide in cattle, but nontoxic to nonruminant animals... 

Asahi, H., Moribayashi, A., Sendo, F. and Kobayakawa, T. (1984) Hemolytic factors in Schistosoma japonicum eggs. Infection and Immunity 46, 514-518. 

Snake venoms contain direct and indirect hemolytic factors, although there is not always a very clear distinction between them. The direct hemolytic factor itself can hemolyze the red cell. Indirect lytic factor lyses the red cell very slowly however, its lytic action can be greatly accelerated by the addition of phosphatidylcholine. Indirect hemolytic factor is... 

The direct hemolytic factor is a highly basic polypeptide with a molecular weight of 7000 daltons. Usually its activity is synergistically increased with phospholipase A2. The main function of the direct hemolytic factor would appear to be to disrupt the matrix of the cell membrane organization in such a way that venom phospholipase A2 can attack membrane phosphatidylcholine more effectively. Lysophosphatidylcholine produced as a result of phospholipase A2 hydrolysis further enhances the hemolytic action. Many other snake venom components such as cardiotoxin, myotoxin, and crotamine also induce hemolysis. 

An elevation in serum bilirubin in animals of GrII and Grill, 60 min. p.i. (Table 3) was mainly due to the contained hemolytic factor (Shiomi et al, 1986) which thus induces hemolytic disorders affecting the parenchymal cells leading to hyperbilirubinemia. 

The pathogenesis of diabetic foot infection stems from three key factors neuropathy, angiopathy, and immunopathy. Aerobic gram-positive cocci, such as S. aureus and P-hemolytic streptococci, are the predominant pathogens in acutely infected diabetic foot ulcers. However, chronically infected wounds are subject to polymicrobial infection and require treatment with broad-spectrum antibiotics. 

Describe how the Rh factor may lead to hemolytic disease of the newborn... 

Complement factor H and platelet-activating factor acetylhydrolase polymorphisms and hemolytic uremic syndrome due to E. coli 0157... 

Ying L, Katz Y, Schlesinger M et al. Complement factor H gene mutation associated with autosomal recessive-atypical hemolytic uremic syndrome. Am J Hum Genet 1999 65[6] 1538—1546. 

Xu H, Iijima K, Shirakawa T et al. Platelet-activating factor acetylhydrolase gene mutation in Japanese children with Escherichia coli 0157-associated hemolytic uremic syndrome. Am J Kidney Dis 2000 36[1] 42—46. 

Louise CB, Obrig TG Shiga toxin-associated hemolytic-uremic syndrome Combined cytotoxic effects of Shiga toxin, interleukin-1 beta, and tumor necrosis factor alpha on human vascular endothelial cells in vitro. Infect Immun 1991 59 4173-4179. 

Uncertainty factors An uncertainty factor of 10 was used for interspecies variability to account for possible variability in arsine-induced hemolysis and progression to renal effects. An uncertainty factor of 3 was used for intraspecies variability assuming limited individual variability in hemolytic response (described more fully under AEGL-2 and AEGL-3). 

Intraspecies 3—An uncertainty factor of 3-fold was used, because the hemolytic response is likely to occur to a similar extent and with similar susceptibility in most individuals. This was based on the consideration that physiologic parameters (e.g., absorption, distribution, metabolism, structure of the erythrocyte and its response to arsine, and renal responses) are not likely to vary among individuals of the same species to such an extent that the response severity to arsine would be altered by an order of magnitude. Individual variability (i.e., variability in erythrocyte structure/ function or response of the kidney to hemolysis) ... 

II cytolytic Cell-associated Clonal expansion B cells IgM, IgG generated. Ig binds to cell bound antigen in the presence of complement and/or activated macrophages cell lysis occurs Rh factor incompatability, hemolytic anemeia in reaction to drugs... 

Since predators of snakes (and humans) have to deal with snake venoms as defenses, they are included here, even though they serve in predation. Snake venoms are primarily enzymes (proteins), especially of the phospholipase A2 type, which breaks down cell membrane phospholipids hydrolytically. Other snake venoms such as cobrotoxin contain peptides with 60-70 amino acid residues. Pharmacologically, they have neurotoxic, cytotoxic, anticoagulant, and other effects. The neurotoxins, in turn, can have pre- or postsynaptic effects. Snake venoms with both neurotoxic and hemolytic effects on the heart are known as cardiotoxins. Cytotoxins attach to the cells of blood vessels and cause hemorrhage. Snake venom factors may stimulate or inhibit blood clotting. Finally, platelet-active factors can contribute to hemorrhage. 

Different classifications of anemia are based in part on the pathophysiological factor inducing the decreased hemoglobin concentration. Anemias due to cell hy-poproliferation include aplastic anemia and iron deficiency anemia. Hemolytic anemia results from excessive destruction of red blood cells. Megaloblastic anemia, sideroblastic anemia, and iron deficiency anemia result from an abnormality in the maturation of red blood cells. 

Hematopoietic development of blood cells begins mainly in the spleen and liver of the fetus during early pregnancy. By the seventh month, however, the marrow of a fetus becomes the primary site of blood cell formation [1]. During childhood, the marrow of the central axial skeleton such as the pelvis, spinal cord, and ribs, and of the extremities, such as the wrist and ankle, provides the key site of hematopoiesis. Hematopoiesis at the periphery (also known as extramedullary hematopoiesis) slowly decreases with age. Chronic administration of hematopoietic growth factors can reverse this decline. Severe hemolytic anemia and hematopoietic malignancies can also reverse the process. 

The effectiveness of immunosuppressive drugs in autoimmune disorders varies widely. Nonetheless, with immunosuppressive therapy, remissions can be obtained in many instances of autoimmune hemolytic anemia, idiopathic thrombocytopenic purpura, type 1 diabetes, Hashimoto s thyroiditis, and temporal arteritis. Improvement is also often seen in patients with systemic lupus erythematosus, acute glomerulonephritis, acquired factor VIII inhibitors (antibodies), rheumatoid arthritis, inflammatory myopathy, scleroderma, and certain other autoimmune states. 

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