PubMed · 13891631
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
R FARINA, E T FALCOFF. 1962-06-11. [Complement fixation for poliomyelitis. Plaque technic].. https://pubmed.ncbi.nlm.nih.gov/13891631/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Events during ischemia/reperfusion (I/R) injury include: neutrophil-mediated endothelial cytotoxicity and activation, generation of free radicals, triggering of cytokines and chemokines, and activation of adhesion molecules and complement system. This article briefly reviews events occurring during tissue ischemia and reperfusion in relation to free tissue transfers. The consequences of tissue damage at the microcirculatory level are presented. Preventive measures of I/R injury are outlined.
Urticarial vasculitis is a clinicopathologic entity in which episodes of urticaria are accompanied by histopathologic features of cutaneous vasculitis. The histopathologic definition of vasculitis varies from report to report. In this article, vasculitis is defined as histopathologic features of blood vessel damage: There should be evidence of leukocytoclasis and vessel wall destruction, which may or may not be accompanied by fibrinoid deposits. Red blood cell extravasation and perivascular inflammatory cell infiltrate also may be present. The extent to which each of these elements must be present has been debated.
The complement system provides innate defense against microbial pathogens and is a "complement" to humoral (antibody-mediated) immunity. Consisting of plasma and membrane proteins, this proinflammatory system works in part by a cascade involving limited proteolysis whereby one component activates the next, resulting in a dramatic amplification. The overall goal is deposition of complement fragments on pathologic targets for the purposes of opsonization, lysis, and liberation of peptides that promote the inflammatory response. Deficiencies of complement components predispose to infections and autoimmune syndromes. Even though total deficiency of a complement component is rare, patients presenting with certain bacterial infections and autoimmune syndromes, especially SLE, have a much greater incidence of deficiency. This review will summarize the clinical manifestations and pathophysiology of congenital and acquired complement deficiency diseases. We will also present an algorithm for laboratory diagnosis of complement deficiency and discuss current and future therapeutic options.