Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Disseminated intravascular coagulation (DIC) was induced in rabbits by administration of antibody and antigen. The rabbits were sensitized passively by i.v. injection of antiferritin antiserum and challenged simultaneously by an i.p. inoculation of ferritin. After the challenge, circulating white blood cells, platelets and plasma fibrinogen levels showed an early fall, reaching minimum values at 3, 10 and 6 h, respectively. Fibrin thrombi appeared first at 2 h, reached a maximum at 5-7 h, and had mostly disappeared by 24 h. Formation of fibrin thrombi was frequent in the lung, liver, kidney and spleen. Early morphological changes included neutrophilic infiltration and accumulation of platelets in capillaries. Ferritin-antiferritin complexes were noted among fibrin thrombi or phagocytized by reticuloendothelial cells and neutrophils. The capacity of Kupffer cells to remove circulating immune complexes was saturated transiently; at this time fibrin thrombosis in various organs was most widespread and severe. It seems likely that formation of antigen-antibody complexes in the microcirculation initiates activation of platelets and neutrophils with subsequent release of mediators responsible for triggering DIC. Activation of complement was another possible factor inducing the reaction. In addition, blockade of the reticuloendothelial system promotes the progression of DIC. It is considered that the methods described constitute a useful model for further elucidation of immune complex-induced DIC.
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PMID:Immune complex-induced disseminated intravascular coagulation (DIC). An experimental study. 222 Mar 95

Eighteen nodules from patients with rheumatoid disease were studied histologically and immunohistochemically. A continuum of microscopic changes was observed with varying degrees of fibrinoid necrosis, mononuclear cell infiltration and healing by fibrous scarring. In two cases there was focal evidence of arteritis. Fibrin was plentiful in the necrotic areas of nodules. Small amounts of immunoglobulin were identified in plasma cells and as irregular extracellular deposits in and around areas of necrosis. In a single small vein abnormal IgG was detected. Mononuclear cells surrounding areas of necrosis stained strongly with antisera to ferritin and a cytoplasmic macrophage antigen, stained variably with muramidase (lysozyme) and negatively with alpha-1 antitrypsin antibodies. Perls' stain for ferric iron was almost entirely negative and ultrastructural x-ray microanalysis indicated that the cytoplasm of these cells were entirely free of iron. These findings confirm the chronic inflammatory nature of rheumatoid nodules but provide no support for the view that they originate in areas of vasculitis. A relative lack of cytoplasmic antiprotease along with a strong expression of ferritin appears to be a characteristic feature of macrophages in rheumatoid tissue.
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PMID:Immunohistochemical findings in rheumatoid nodules. 392 84

Arterial thrombus formation is thought to be initiated by platelet adhesion to the subendothelial matrix, but ruptured atherosclerotic plaques are characterized by substantial reduction of matrix proteins compared with stable plaques. Intraplaque erythrocytes and/or fibrin have been reported in high-risk coronary plaques. The aims of the current study were to identify factors that provide scaffolds for platelets at the sites of ruptured coronary plaques and investigate depositions of iron and bilirubin as hemoglobin catabolites in the ruptured plaques. Histological characteristics of plaque components and the thrombus interface were examined in 73 acute coronary aspirated thrombi. Necrotic debris (95%), macrophages (95%), and cholesterin clefts (81%) were observed frequently at the ruptured plaque and thrombus interface. A fibrous matrix (47%), calcification (32%), and extracellular deoxyribonucleic acid (15%) were identified as small foci. Tissue factor was localized in the necrotic core and macrophages. Fibrin and von Willebrand factor were consistently deposited within the plaques and beneath platelet aggregations. The citrullinated histone H3-immunopositive area accounted for only 0.5% of the plaque area. Bilirubin and iron depositions were detected in approximately 20% of the plaques in addition to biliverdin reductase and ferritin expression in macrophages. Fibrin and von Willebrand factor rather than matrix proteins and neutrophil extracellular traps may be major adhesive molecules at the sites of ruptured plaques. Iron and bilirubin deposits may be markers for rupture-prone plaques.
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PMID:Pathological Features of Ruptured Coronary Plaque and Thrombus Interfaces: Fibrin and von Willebrand Factor as Platelet Scaffolds on Rupture Sites. 3292 Aug 6