Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.4 (trypsin)
 42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A cold-active hemagglutinin for trypsinized human type "O" erythrocytes (CAH) from blood of chickens with acute Plasmodium gallinaceum malaria was found to be associated with 19 S and 7 S globulin fractions of malarious chicken blood, but cleavage with 2-mercaptoethanol indicated that it was primarily of the IgM class of antibody. In serologic tests CAH reacted with trypsinized erythrocytes, and anti-chicken globulin. It did not react with other of the antigens or antibodies detected in the blood of malarious chickens. When the absorbed and eluted CAH was injected into normal chickens it produced an anaphylactic-like shock and caused a 25% reduction in red blood cell counts within 48 hours. Plasma samples collected during this interval showed signs of hemolysis. Reactions of blood cells from the recipient birds with fluorescein conjugated anti-chicken globulin indicated that CAH reacted with erythrocytes. The absence of fluorescent activity 3 days after injection suggested that these erythrocytes had been removed from the circulation. When normal chickens were injected with trypsinized autologous blood cells, CAH was detected within 3 days. The agglutination test again was active at temperatures below 22 degrees C and was negative when tested at 37 degrees C. In these birds the appearance of CAH was accompanied by reductions in red blood cell counts and by hemolysis. The results of these experiments suggest that CAH was not stimulated by plasmodial parasite antigen, but rather by autoantigens, which appear to be common to heterologous animal species, and which were in some manner expressed by the presence of the intracellular parasites, or by trypsin treatment. The experiments further suggest that this autohemagglutinin was partially causal of malarial anemia. The presence of other anemia factor(s) was indicated by anemia following injection of plasma that had been absorbed free of CAH.
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PMID:Pathogenesis of acute avian malaria. II. Anemia mediated by a cold-active autohemagglutinin from the blood of chickens with acute Plasmodium gallinaceum infection. 80 65

Anti-lymphocytic antibodies (ALA) have been described in a variety of autoimmune disorders. We have investigated the presence of ALA in autoimmune chronic active hepatitis (aCAH) starting in childhood. Using a modified Terasaki technique ALA were found in 17 of 18 patients with aCAH but in only one of 15 patients with alpha-1-anti-trypsin deficiency or Wilson's disease and three of 27 age-matched healthy controls (P less than 0.0005 for both). Sera from 12 patients with uncontrolled aCAH had significantly higher cytotoxicity values than sera from six children with inactive diseases (P less than 0.01). ALA were directed to T but not B lymphocytes and were not reactive with specific HLA antigens. No preferential killing was observed against CD4 or CD8 positive T lymphocytes. Characterization of ALA revealed them to be cold-reactive IgM. The possible role of ALA in aCAH is discussed.
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PMID:Anti-lymphocytic antibodies in autoimmune chronic active hepatitis starting in childhood. 278 29

Clinical and morphological features in fifteen patients with chronic cholestatic liver disease (mixed form) who had two different types of complement-fixing antimitochondrial antibodies were compared with those found in twenty-five patients with classic primary biliary cirrhosis (PBC). PBC-specific antimitochondrial antibody (M2) directed against an antigen of the inner mitochondrial membrane was always present in both groups. However, mixed-form cases had a second antimitochondrial antibody (M4) which fixed complement with a trypsin insensitive antigen probably located on the outer membrane. Histological lesions typical of chronic active hepatitis, often associated with granulomata formation and bileduct proliferation, and simultaneous increases in IgM and IgG were predominant features, indicating that these mixed-form cases may represent a separate clinical entity.
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PMID:Serological classification of chronic cholestatic liver disease by the use of two different types of antimitochondrial antibodies. 610 51

A radioimmunoassay (RIA) was developed for the detection of liver-kidney microsomal (LKM) autoantibodies. These were detected in four of 62 patients with HBsAg negative chronic active hepatitis (CAH) and in one patient with mixed connective tissue disease (MCTD). LKM antibodies were not detected in other hepatic and non-hepatic diseases. Other autoantibodies, especially anti-mitochondrial ones, do not react in this assay system. Sera positive for LKM antibodies by RIA showed a cytoplasmic staining of hepatocytes and proximal renal tubules by immunofluorescence. The LKM antigen was detected by RIA in microsomes prepared from rat liver, kidney, stomach, heart, lung, and skeletal muscle. It was destroyed after treatment with trypsin and chymotrypsin, but preserved after treatment with RNAase, DNAase and neuraminidase. Upon centrifugation of purified rat liver microsomes in CsCl gradient, LKM reactivity was detected at a density of 1.20 g/ml. In addition, the M2 antigen of the inner mitochondrial membrane specific for primary biliary cirrhosis (PBC) was localized at 1.28 g/ml in these density gradient fractions. The LKM antigen could not be solubilized. The presence of LKM antibodies characterizes a distinct subgroup of HBsAg negative CAH; they do not occur in PBC.
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PMID:Detection of liver-kidney microsomal autoantibodies by radioimmunoassay and their relation to anti-mitochondrial antibodies in inflammatory liver diseases. 646 82

Recently, attentions are being aroused as to the enzymatic network abnormalities lying behind congenital enzyme deficiency syndromes. We investigated abnormalities in activities of various hydrolytic enzymes in serum of patients with congenital adrenal hyperplasia (CAH, 21-hydroxylase deficiency). Several enzyme activities including trypsin-like enzyme, cathepsin C and esterase were significantly decreased in patients' serum. Especially the esterase activity in patients' serum was reduced to one third of controls and this may have some relations to the abnormal steroid metabolism of these patients. A multivariate analysis showed unexpectedly extensive abnormalities in enzyme interrelationships. These results suggest that wide variety of abnormal metabolism may be related to an apparent enzyme deficiency.
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PMID:Abnormalities of various serum enzyme activities in patients with congenital adrenal hyperplasia. 667 19

Antinucleolar antibody (ANoAb) was tested for in sera from 25 patients with systemic lupus erythematosus (SLE), 61 with progressive systemic sclerosis (PSS), 22 with chronic active hepatitis (CAH) and 28 healthy persons, using immunofluorescence reactivity with acetone-fixed monolayers of cultured human fibroblasts, and a procedure to reveal ANoAb when other antinuclear antibodies were concurrently present. ANoAb was found on direct testing in sera from 6 patients with SLE, 15 with PSS and 7 with CAH, but not in any of 28 sera from healthy persons; homogeneously reactive antinuclear antibody was also present in the serum of these 6 cases of SLE, in 6 of the 15 with PSS and in 3 of the 7 with CAH and, in SLE specifically, pre-treatment of fibroblast monolayers with DNase "unmasked" the presence of ANoAb in a further 7 sera which had shown only homogeneous nuclear staining in fibroblasts. ANoAb belonged to the IgG, IgM and IgA class in sera from cases of SLE and PSS, and to only the IgG and IgM class in sera from cases of CAH. ANoAb titres were highest in patients with PSS. ANoAb were sensitive to RNase in 5 cases, to RNase and DNase in 6, and were sensitive to combinations of RNase, DNase, NaC1, and trypsin in the remaining cases. We conclude that (i) fibroblast monolayers are a suitable substrate for the demonstration of ANoAb, (ii) homogeneous staining of cell nuclei may mask ANoAb, so that the incidence of ANoAb becomes higher in SLE than in PSS, (iii) low-titre ANoAb in CAH not visualized in frozen tissue sections may be detected on fibroblast monolayers, and (iv) nucleolar antigens probably include RNA, RNA bound to DNA, and RNA bound to proteins.
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PMID:Antinucleolar autoantibodies demonstrated by monolayers of human fibroblasts in sera from patients with systemic lupus erythematosus, progressive systemic sclerosis and chronic active hepatitis. 674 43

Exocrinous performance of the pancreatic gland under secretin-pancreozymin stimulation was studied in 76 patients with chronic diffuse diseases of the liver who were distinguished into 6 groups: those who suffered from chronic persistent hepatitis of viral and alcohol origin, chronic active hepatitis of viral origin, cirrhosis of the liver of viral and alcohol origin, primary biliary hepatocirrhosis. The results obtained were correlated with those from 11 normal persons (controls). Out of 76 examinees the disorders of exocrinous performance of the pancreatic gland were revealed in 75 persons. The most characteristic features were: a decrease in the basal and an increase in the stimulated volume of the pancreatic juice; a reduction of both basal and stimulated production of bicarbonates; a decrease in the trypsin and amylase fasting levels and their increment in the stimulated juice of the pancreatic gland. Disorder in the production of bicarbonates was stated as a most characteristic feature in the patients both with viral and alcohol origin of the disease but it was mostly manifest in the patients with hepatocirrhosis. Pronounced elevation of the activity of amylase and trypsin in the pancreatic juice was observed in patients with very high activity of disease development and in the patients who continuously used large amounts of alcohol. The authors suspected that alcohol abuse and the effect of hepatitis virus had an equal pathogenic impact on the liver and pancreatic gland.
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PMID:[Exocrine function of the pancreas in patients with chronic hepatitis and liver cirrhosis of various etiologies]. 814 1