Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using a battery of 7 horseradish peroxidase marked lectins (WGA, RCA I, PHA, LCA, PNA, UEA I, LPA) or 2 unmarked lectins (Con A, VAA I) and HRP-marked antibodies, the binding to acinar cells with a postembedding technique on semithin sections of rat pancreatic tissue after olive-oil pancreatitis was studied light microscopically. The lectin binding of the normal healthy rat pancreatic tissue (Jonas et al. 1991) changed remarkably. Whereas the apical glycocalyx of acinar cells with the strong binding of WGA, RCA I, and PHA remained unchanged within the first 10 min of damage, the basolateral cell surface lost the typical specific binding of UEA I within the initial phase of pancreatitis just 2 min after injection of olive-oil. Con A and VAA I were found to be very reactive with the necrotic cells 60 min after administration of oil. The results were discussed in relation to the possible functions of the 2 main domains of the pancreatic acinar cell glycocalyx.
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PMID:Light and electron microscopic studies of lectin binding to the glycocalyx of rat pancreatic cells. II. Light microscopic changes after induction of an olive-oil pancreatitis. 128 45

Expression of intermediate filaments (IF) is regulated during development and differentiation. The authors have studied the expression of vimentin and cytokeratins (CK) 4, 7, 8, 13, 18, 19 in normal pancreas, chronic pancreatitis, and pancreas cancer using monoclonal antibodies. Immunohistochemical assays were performed on fresh frozen tissue sections and on cultured pancreas cancer cells using the streptavidin-peroxidase method. In normal pancreas, acinar cells expressed CK 8 and 18, whereas ductal cells expressed CK 7, 8, 18, and 19. CK 4 was expressed by 5-10% of pancreas duct cells in all specimens of normal pancreas. CK 13 was not detected in any epithelial cells of normal pancreas or pancreatitis. CK 7, 8, 18, and 19 were homogeneously expressed in all pancreas cancers, whereas CK 4 was expressed only in 5-50% of cells in 10/16 tumors. Foci of squamous metaplasia expressed CK 13 but showed partial loss of expression of CK 7, 8, 18, and 19. Thirteen pancreas cancer cell lines examined showed homogeneous expression of CK 7, 8, 18, and 19; 2/11 lines expressed CK 4 weakly, and 6/11 expressed vimentin. CK 13 was not detected in any of the lines. These results indicate that pancreas cancer cells consistently express cytokeratin polypeptides characteristic of ductal epithelial cells and that this phenotype is retained in pancreas cancer cell lines. In addition, squamous metaplasia is associated with a coordinate change in the expression of CK polypeptides.
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PMID:Intermediate filaments as differentiation markers of normal pancreas and pancreas cancer. 137 55

The ductular accumulation of "abnormal mucus" is the key histologic feature in cystic fibrosis. This material is periodic acid-Schiff positive and diastase resistant, suggesting that it is glycoprotein in nature. We used the avidin-biotin-peroxidase method to identify this material using antibodies to the serum glycoproteins carcinoembryonic antigen, alpha 1-antitrypsin, and alpha-fetoprotein on paraffin sections of pancreas obtained from a total of 21 patients: 9 with cystic fibrosis, 5 with chronic pancreatitis, and 7 controls. The control patients had normal pancreatic histologic findings, no alpha 1-antitrypsin or alpha-fetoprotein was demonstrated, and only the ductular epithelium reacted weakly for carcinoembryonic antigen. The pancreas in pancreatitis showed fibrosis, acinar atrophy, and ectasia of the ducts that contained only a small amount of periodic acid-Schiff-positive material. This material reacted weakly for carcinoembryonic antigen and alpha 1-antitrypsin. The appearance of the pancreas in cystic fibrosis was similar to that in chronic pancreatitis. However, the ducts contained a greater amount of periodic acid-Schiff-positive material, mostly in the form of globules that reacted strongly for carcinoembryonic antigen and alpha 1-antitrypsin and weakly for alpha-fetoprotein, as did the ductular epithelium. This study shows that the periodic acid-Schiff-positive material in cystic fibrosis contains at least the three serum glycoproteins and that the accumulation may represent a possible defect in cellular synthesis, assembly, or transport of glycoproteins in the ducts.
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PMID:Carcinoembryonic antigen, alpha 1-antitrypsin, and alpha-fetoprotein in the pancreas of patients with cystic fibrosis. 247 7

A total of 32 histologically documented cases of heterotopic pancreas was found in a review of the records of the department of pathology at the Chang Gung Memorial Hospital between 1977 and 1987. This review was done to ascertain the clinical significance of this uncommon entity. In 14 patients (44%), the aberrant pancreatic tissue was symptomatic; in the other 18 (56%), it was found incidentally. In the symptomatic group, the heterotopic pancreatic tissue was found in a duplication cyst of the ileum in one patient, in the common bile duct in one, in a Meckel's diverticulum in four, in the stomach in three, in a congenital duodenal diaphragm in one, in the duodenum in three, and in the ileum in one. The majority of heterotopic pancreatic tissue in the asymptomatic group was encountered in the jejunum (15 patients). Symptoms were related to complications, including obstruction of the common bile duct, mucosal ulcer with hemorrhage, intussusception, and intestinal obstruction, but not to pathologic conditions of the pancreas itself, such as pancreatitis or pancreatic cyst or neoplasm. In all of the clinically significant cases, the clinical symptoms disappeared completely after surgical removal of the aberrant tissue. In 28 cases (87%), diagnosis was made by frozen section during operation. Preoperative diagnosis of aberrant pancreas was not made in any of the cases. Histologically, all cases showed pancreatic excretory ducts; in 31 cases (97%), exocrine glands were present, and in 27 cases (84%), islets of Langerhans were discernible. There was no relationship between symptoms and the presence of islets, acini, or ducts. Mallory's phosphotungstic acid-hematoxylin stain was used to demonstrate zymogen granules in the acinar cells, and insulin, glucagon, and somatostatin were demonstrated with the horseradish peroxidase-antihorseradish peroxidase immunocytochemical staining technique; islets of Langerhans were also identified. Technetium Tc 99m scintigraphy was used to detect the bleeding source in a Meckel's diverticulum and an enteric duplication associated with ectopic gastric mucosa.
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PMID:Pancreatic heterotopia: a reappraisal and clinicopathologic analysis of 32 cases. 305 29

A retrospective analysis of 25 primary adenocarcinomas of the pancreas, 16 metastatic pancreatic tumors, 8 cases of chronic pancreatitis, and 3 adult normal pancreas was performed to ascertain the reactivity of monoclonal antibody (MAb) B72.3 to malignant and nonneoplastic pancreatic lesions. Formalin-fixed, paraffin-embedded sections of pancreas were evaluated by immunohistochemical techniques (avidin-biotin-peroxidase complex [ABC] method). Twenty-one of 25 malignant primary tumors were reactive, and all 16 metastatic sites expressed the B72.3 antigen. In contrast, all cases of pancreatitis and normal pancreas were either weakly reactive or nonreactive. Ten malignant and two benign pancreatic fine-needle aspirates provided results similar to those seen with fixed tissues. Because MAb B72.3 has selective reactivity for primary and metastatic pancreatic cancer, it may be of value as a diagnostic adjunct in cytologic examination or for radioimmunodetection of regional and/or distant metastases of adenocarcinoma of the pancreas.
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PMID:A tumor-associated antigen in carcinoma of the pancreas defined by monoclonal antibody B72.3. 327 79

A sandwich enzyme immunoassay was developed for human lactoferrin using polystyrene balls coated with specific IgG fraction as the first antibody and peroxidase labelled IgG fraction as the second antibody. The detection limit was 1 microgram/l. A good parallelism was observed with the curves obtained from standard lactoferrin (purified from mammary gland), plasma lactoferrin (mainly derived from granulocytes), and pancreatic lactoferrin demonstrating that the assay may be used to measure the level of the protein in different biological materials. The simplicity and the sensitivity of this assay may permit the follow-up of patients with chronic calcifying pancreatitis (in which an increase of pancreatic lactoferrin has already been demonstrated) and a study of the protein in various circumstances leading to a better understanding of its biological role.
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PMID:A non competitive enzyme immunoassay of human lactoferrin in biological fluids. 634 54

Cell necrosis in acute experimental pancreatitis is preceded by a redistribution of digestive enzymes into a lysosomal subcellular compartment. We have investigated whether endocytosis from the acinar cell lumen might contribute to this disturbance of intracellular compartmentation. In an animal model of pancreatitis involving pancreatic bile duct ligation in opossums, we have studied in vivo endocytosis of dextran 40 and [14C]dextran 70, cationized ferritin, and horseradish peroxidase from the apical surface of acinar cells before the onset of necrosis. Marker solutions were instilled into the pancreatic duct of anesthetized animals at physiological pressure. Tissue samples obtained at intervals of up to 60 min after instillation of markers were studied by electron microscopy and electron microscope autoradiography. All markers were taken up by acinar cells in control animals and in animals with obstructed pancreatic bile ducts. Markers for membrane-mediated endocytosis (cationated ferritin and horseradish peroxidase) were transported to lysosomes in both groups. In contrast, the fluid-phase tracer dextran was transported to the secretory pathway in controls but to lysosomes after duct ligation. Since dextran and luminally present secretory proteins can be expected to follow the same route after endocytosis, our findings suggest that altered intracellular targeting of endocytosed proteases might be one mechanism by which digestive zymogens reach an intracellular compartment in which premature activation can occur. This phenomenon may be a critical and early event in the pathogenesis of biliary pancreatitis.
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PMID:Luminal endocytosis and intracellular targeting by acinar cells during early biliary pancreatitis in the opossum. 753 59

Cytokeratin (CK) expression in tumors generally reflects the CK pattern of the corresponding normal epithelium. Pancreas cancers express CK of simple epithelia 7, 8, 18 and 19, as normal ductal cells. To analyze whether CK of complex or stratified epithelia are abnormally expressed in pancreas cancers, we have used polypeptide-specific mouse monoclonal antibodies (MAbs) detecting CK 5, CK 10, CK 13, CK 14 and CK 17, and an antibody detecting CK 13, CK 15 and CK 16. The streptavidin-peroxidase technique was applied on sections of fresh-frozen specimens of normal pancreas and of pancreas cancer. None of these polypeptides were expressed by normal acinar and centro-acinar cells. CK 5, CK 14 and CK 17 were expressed by less than 5% of cells in normal ducts, whereas CK 10, CK 13, CK 15 and CK 16 were not expressed at all. In tumors, CK 14, CK 15/16 and CK 17 were detected in the majority of cases studied; CK 5, CK 10 and CK 13 were present in a sub-population of pancreas cancers. CK of complex/stratified epithelia were detected in areas of glandular differentiation, but expression was more intense in areas of squamous differentiation. In pancreatitis adjacent to cancer, CK of complex/stratified epithelia were weakly detected or undetectable. These results suggest that up-regulation of these CK takes place in pancreas cancer. The CK phenotype may be of help in the differential diagnosis of this tumor.
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PMID:Intermediate filaments as differentiation markers of exocrine pancreas. II. Expression of cytokeratins of complex and stratified epithelia in normal pancreas and in pancreas cancer. 768 85

Although it is widely accepted that trypsinogen activation is an initiating event in the development of acute pancreatitis, its location inside the pancreas is not known. In our studies, acute edematous pancreatitis was induced in rats by one or two intraperitoneal injections of 50 microg cerulein/kg body weight. The pancreas was removed for examination 1 or 2 h after the first and the second cerulein injection, respectively. The cleavage product of trypsinogen activation, trypsinogen activation peptide, was specifically labeled on pancreatic tissue sections by a corresponding antibody, the signal enhanced by a biotin-avidin conjugate, and the site then visualized by coupled peroxidase activity on diaminobenzidine. The sections were examined by light microscopy. Trypsinogen activation peptide, reflecting activation of the pancreatic digestive enzyme trypsinogen, was detected inside pancreatic acinar cells in this animal model of acute pancreatitis. As early as 1 h after the first injection of cerulein, protease activation was seen within the apical pole of acinar cells. Protease activation was increased 2 h after the latter of two injections of cerulein and more evenly distributed within the cells. For the first time morphologic evidence confirms that the activation originates within the acinar cell, rather than from the interstitium or the duct lumen. The location of this activation at the apical site of the acinar cell indicates its origin from subcellular compartments involving the late steps in the secretory pathway.
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PMID:Premature trypsinogen activation during cerulein pancreatitis in rats occurs inside pancreatic acinar cells. 1082 2

Histopathological and functional changes in the pancreas were studied in 94 hamsters infected and reinfected with Trypanosoma cruzi VIC strain and in 73 non-infected normal controls. Infection in each animal was verified by microhematocrit, hemoculture, specific peroxidase anti-peroxidase, polymerase chain reaction and seroagglutination. Blood glucose and insulin were determined. The number of islets per section and the number of islet cells marked with antibodies were counted. Insulitis, neuritis, fibrosis, atrophy and inflammatory infiltrates were evaluated. Experimental chagasic infection caused pancreatitis similar to human Chagas' disease, involving acini, islets and nerves, with atrophy and fibrosis, although without correlation to the number of reinfections. Erratic blood glucose levels and a tendency to hypoinsulinemia were observed in infected animals. During the acute phase, the number of somatostatin and pancreatic polipeptide producer islet cells was lower in infected hamsters, which was eventually related to changes in blood sugar levels and hypoinsulinemia. Our findings favor the hypothesis of the existence of an endocrine form of chronic chagasic infection.
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PMID:Functional and histopathological study of the pancreas in hamsters (Mesocricetus auratus) infected and reinfected with Trypanosoma cruzi. 1532 22


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