Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The differentiation effects of sodium butyrate were examined in a series of human pancreatic adenocarcinoma cell lines: Panc-1, a poorly differentiated cell line; HPAF, a pleomorphic cell line isolated in this laboratory; and two clones of the parental HPAF cell line, well-differentiated CD11 and less-differentiated CD18. Incubation with 2 mM sodium butyrate induced a dramatic decrease in cell proliferation and saturation densities in culture and an increase in alkaline phosphatase activity. Of particular interest, incubation with sodium butyrate also caused a number of morphologic alterations in these cells, attributed to an induction of secretory differentiation. Following sodium butyrate treatment, CD18 cells were virtually indistinguishable from the more highly differentiated CD11 cells as evidenced by an increase in the number of profiles of rough endoplasmic reticulum and of Golgi. Intercellular and intracytoplasmic lumens, whose appearance is quite common in CD11 cells but nonexistent in untreated CD18 cells, appeared in these cells following only 5 days of sodium butyrate treatment. An increase in the cytoplasmic secretory elements was also observed in sodium butyrate-treated Panc-1 cells; however, lumen formation never occurred in these cells.
Pancreas 1991 Sep
PMID:Ultrastructural differentiation of sodium butyrate-treated human pancreatic adenocarcinoma cell lines. 194 15

Pancreatic duct fragments were isolated from rat and hamster pancreas and were cultured in an agarose matrix for up to 8 weeks (rat) or 20 weeks (hamster). The fragments consisted predominantly of duct epithelium, lesser numbers of stromal and atrophied acinar cells, and small numbers of islet cells. Hamster ducts averaged 3 micrograms protein per duct while rat ducts averaged 1 microgram, and the protein:DNA ratio of both types of ducts was less than that of whole pancreas. Estimated average duct yields of 6% (hamster) and 1% (rat) were based on the protein content of the ducts. Duct viability was shown by the incorporation of 3H-thymidine and 3H-leucine into bulk DNA and protein and by autoradiography. gamma-Glutamyl transferase and (Na + K)-ATPase specific activities were slightly elevated while amylase was depressed in the ducts when compared with whole pancreas in both species. gamma-Glutamyl transferase was localized histochemically in both duct epithelium and in surviving acinar tissue, as seen in vivo. Amylase was shown by immunohistochemistry to be present within duct lumina and in atrophied acini and their lumina. Alkaline phosphatase and Mg-ATPase specific activities were elevated in the hamster, but reduced in the rat, when compared with whole pancreas. Hamster alkaline phosphatase and Mg-ATPase were localized by histochemistry to the duct stroma, where these enzymes are not detected in vivo. Carbonic anhydrase was found in the duct epithelium of both species, as in vivo, as well as in the duct stroma, unlike in vivo. Acid glycosaminoglycans, as revealed by alcian blue staining, were found at the apical surfaces and in the lumina of both kinds of ducts. Glutathione-S-transferase and glucose-6-phosphate dehydrogenase were elevated in rat ducts, but not in hamster ducts. The polypeptide compositions of cultured ducts, freshly isolated pancreatic islets, and whole pancreas were compared by one-dimensional sodium dodecyl sulfate polyacrylamide gradient gel electrophoresis. No duct-specific polypeptides were observed; the ducts were characterized mainly by the reduction or absence of polypeptides, including some zymogens, seen in whole pancreas.
Pancreas 1987
PMID:Biochemical and histochemical characterization of cultured rat and hamster pancreatic ducts. 244 50

The influence of pancreatic secretions on growth and brush-border enzyme activity, throughout the entire small intestine, was examined in the rat. Pancreatic secretions were excluded from the gut lumen by stapling the pancreatic ducts, without interruption of bile flow. The entire small intestine was studied as four segments; the duodenum and three distal segments of equal length. Weight of intestine and mucosa, and mucosal sucrase, isomaltase, lactase, and alkaline phosphatase activity were measured 10-15 days following pancreatic duct occlusion, or sham-operation. The duodenum of pancreatic duct-occluded animals exhibited significant hypertrophy. In general, specific and total disaccharidase activities were greater in duct-occluded animals than in controls throughout the intestine. The increase was more pronounced in distal than in proximal segments. The sucrase/isomaltase ratio was significantly greater in pancreatic duct-occluded animals than in controls in the two distal segments. Alkaline phosphatase activity was not affected by pancreatic duct occlusion. The greater relative increase of disaccharidase activities and sucrase/isomaltase activity ratios in the distal segments of duct-occluded animals, indicates a more important regulatory role of pancreatic enzymes in the distal small intestine. It is concluded that regulation of intestinal brush-border enzyme activity by pancreatic secretion is selective for enzyme and site as follows: disaccharidases, but not alkaline phosphatase, are regulated; the sucrase subunit of the sucrase/isomaltase complex is most sensitive to regulation, while lactase is least sensitive; and the regulatory effect on disaccharidases is greater in distal than in proximal intestine.
Pancreas 1987
PMID:Intestinal disaccharidase activity following pancreatic duct occlusion in the rat. 311 40

Real-time ultrasonography (US), computed tomography (CT), and biochemical tests were prospectively performed to detect gallstones in 88 consecutive patients immediately after the onset of an attack of acute pancreatitis. The sensitivity of biochemical tests was 84.6% when the patients had three or more positives of five parameters [including serum bilirubin, alkaline phosphatase (AP), gamma-glutamyl transpeptidase (GGT), alanine transaminase (ALT), and alanine transaminase-aspartate transaminase (ALT-AST) ratio]. The sensitivity, specificity, and accuracy were 71.8, 98.0, and 86.4% for US, and 52.9%, 100%, and 79.5% for CT. The sensitivity, specificity, and accuracy were improved to 82.1, 100, and 93.2% by the combination of US and CT, and 94.9, 100, and 97.7% by the combination of US and biochemical tests. Adding CT to the combination of US and biochemical tests resulted in only a slight improvement in sensitivity and accuracy. In conclusion, a combination of US and biochemical tests can provide the best noninvasive method in rapidly detecting gallstones as an etiological factor in acute pancreatitis. Computed tomography is not cost-effective. A positive result of biochemical tests despite a negative finding in US calls for an intensive search for gallstones by further investigation with endoscopic retrograde cholangiography or repeated US examinations.
Pancreas 1988
PMID:Clinical significance of ultrasonography, computed tomography, and biochemical tests in the rapid diagnosis of gallstone-related pancreatitis: a prospective study. 328 69

A pancreas-specific antigen was identified by immunologic techniques and purified from saline extract of human pancreas. The purified pancreas-specific antigen was shown to be homogeneous by polyacrylamide gel electrophoresis under both denaturing and non-denaturing conditions. It had a molecular weight of 44000 as estimated by gel filtration or sodium dodecyl sulfate-gel electrophoresis, and a sedimentation coefficient of 3.4 S as analyzed by sucrose gradient centrifugation. Pancreas-specific antigen possessed an isoelectric point of 4.9 and migrated to alpha-beta region upon immunoelectrophoresis. By colorimetric assay procedures, pancreas-specific antigen exhibited no enzyme activity, such as amylase, protease, esterase, lipase, acid phosphatase, alkaline phosphatase peroxidase, deoxyribonuclease or ribonuclease. Immunoreactivity of pancreas-specific antigen was sensitive to proteolytic enzymes, perchloric acid and high temperature (70 degrees C, 10 min); but insensitive to neuraminidase or beta-glucosidase. Immunohistochemical staining revealed that pancreas-specific antigen was located in acinar cells of human pancreas. In addition, a higher concentration of pancreas-specific antigen was detected in pancreatic juice than in the saline extract of pancreas. This newly identified pancreas-specific antigen, therefore, may be a useful marker protein in physiological studies of pancreas and pancreatic secretion.
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PMID:Purification and characterization of a human pancreas-specific antigen. 678 69

In 403 patients suspected of having pancreatic cancer, we prospectively studied a combination assay of various serum tumor markers: CA19-9, DUPAN2, tissue polypeptide antigen, elastase 1, gamma-glutamyltranspeptidase, lactate dehydrogenase, lipase, amylase, and alkaline phosphatase. The diagnostic value of each marker was compared with a multivariate analysis (computer-aided multivariate and pattern analysis system for pancreatic cancer examine-1: CAMPAS-PX1). Pancreatic cancer was subsequently identified in 47 patients. CAMPAS-PX1 had higher negative in health and positive predictability than those of each marker used alone in the diagnosis of pancreatic cancer. CAMPAS-PX1 proved the most effective marker for diagnosing pancreatic cancer, but in terms of its cost/benefit ration CAMPAS-PX1 was not superior to CA19-9 used alone. In this prospective trial, we experienced poor generalizability in the statistical models (CAMPAS-PX1). We believe that selection bias was present in samples used for model building. Based on this study a new model has been designed.
Pancreas 1994 Nov
PMID:Effectiveness of multivariate analysis of tumor markers in diagnosis of pancreatic carcinoma: a prospective study in multiinstitutions. 753 33

Very late activation (VLA) receptors mediate cell adhesion to extracellular matrix, mainly by acting as adhesion receptors to fibronectin, collagen, and laminin as well as to other cells. These interactions not only regulate normal cell-extracellular matrix contact, but also are thought to be involved in metastasis and invasive tumor growth. Using immunohistochemistry [the alkaline phosphatase-anti-alkaline phosphatase (APAAP) technique] we compared the expression and distribution of VLA receptors in normal pancreatic tissue, chronic pancreatitis, and ductal pancreatic adenocarcinoma. Immunohistochemically, VLA alpha 2 and VLA alpha 6 were moderately to strongly expressed on the basal surface of ductal and acinar cells in normal pancreatic tissue, whereas centroacinar cells predominantly expressed VLA alpha 3 and VLA alpha 5. Similarly, pancreatic carcinoma showed an intensive staining for VLA alpha 2 and VLA alpha 6 with a diffuse distribution on the cell surface. Expression of VLA alpha 3 and VLA alpha 5 in pancreatic carcinoma was heterogeneous, ranging from moderate to weak and lost in about 50% of the cells. As our results suggest, cell-basement membrane interaction in ductal and acinar pancreatic cells is primarily mediated through VLA alpha 2 and VLA alpha 6, whereas VLA alpha 3 and VLA alpha 5 are the major VLA receptors on centroacinar cells. In pancreatic carcinoma a loss (VLA alpha 5) or redistribution (VLA alpha 2, VLA alpha 6) of VLAs was observed. This redistribution of VLA alpha 2 and VLA alpha 6 may reflect a loss of spatial arrangement of tumor cells and their ability to randomly interact with extracellular matrix structures during invasion and metastasis.
Pancreas 1993 Nov
PMID:Expression and distribution of VLA receptors in the pancreas: an immunohistochemical study. 825 85

One thousand twenty patients consecutively admitted because of a clinical suspicion of pancreatic cancer were investigated to evaluate the accuracy of simple clinical, laboratory, and ultrasonographic data in the diagnosis of pancreatic cancer. Age, weight loss, recent-onset diabetes mellitus, palpable abdominal mass or gallbladder, elevated serum bilirubin or alkaline phosphatase levels, and ultrasonography were significant criteria in discriminating 80 pancreatic cancers from 940 controls. The most sensitive criteria were ultrasonography (83%), weight loss (66%), and bilirubin level of > 3 mg/dl (61%); the most specific were ultrasonography (99%), recent-onset diabetes (97%), and a distended palpable gallbladder (94%). Only ultrasonography demonstrated an elevated positive predictive value (86%), while weight loss, elevated bilirubin and alkaline phosphatase, besides ultrasonography had an elevated negative predictive value (95%). These results show that advanced pancreatic cancer may be excluded with simple clinical and laboratory data; ultrasonography can confirm the diagnosis with a high degree of accuracy. We suggest that the results of any new diagnostic tests for pancreatic cancer be compared with these clinical findings.
Pancreas 1993 Mar
PMID:Clinical presentation and ultrasonography in the diagnosis of pancreatic cancer. 846 88

Dibutyltin dichloride (DBTC; 6 mg/kg body weight, i.v.) induced acute interstitial pancreatitis in rats. The course of the pancreatitis was examined within 28 days by light and electron microscopy as well as by pathobiochemistry (amylase, lipase, alkaline phosphatase, and bilirubin in serum; tin concentration in biliopancreatic juice, tissue, and concretions). The pathogenesis of the DBTC-induced pancreatitis in rats was studied by different experimental designs (in intact animals, after bile duct ligation, after surgical bypass of the bile duct). DBTC caused toxic necrosis of the biliopancreatic duct epithelium, which is then shed into the duct and forms obstructing plugs in the distal common bile duct. Interstitial pancreatitis occurred during the first 4 days, accompanied by significantly increased activities of serum alpha-amylase and lipase. After 7 days extensive infiltration of the pancreatic interstitium with mononuclear cells was observed. Twenty-eight days after administration of DBTC one-third of the rats showed periductal and interstitial fibrosis as well as an active inflammatory process in the pancreas. The findings suggest a twofold pathogenesis of the DBTC-induced pancreatitis: first, the cytotoxic effects on the biliopancreatic duct epithelium lead to epithelial necrosis with obstruction of the duct, subsequent cholestasis, and interstitial pancreatitis; and second, the hematogenic DBTC effects cause direct injury of pancreatic cells (mitochondrial damage, autophagy, cell necrosis) followed by interstitial edema and inflammation. Both processes lead to this special type of DBTC-induced acute pancreatitis with a tendency to a chronic course, when the obstruction of the duct and cholestasis persist.
Pancreas 1997 Nov
PMID:Acute interstitial pancreatitis in rats induced by dibutyltin dichloride (DBTC): pathogenesis and natural course of lesions. 936 Oct 94

We report the case of a 14 year-old male from Lima. He is a student with a history of bronchial asthma since age 4 receives conditional salbutamol, corticosteroids used for asthma attacks (a crisis in 2010, 1 month ago) Refuses surgery or transfusions. He presented with a two weeks for abdominal pain, nausea, fever, and jaundice. Epigastric pain is colicky and radiated back to righ upper quadrant, refers in addition to nausea and fever, for ten days notice jaundice of skin and sclera. On examen he was lucid, with jaundice of skin and mucous membranes. There was no palpable lymph nodes, abdomen with bowel sounds, soft, depressible, liver span of 15cm, positive Murphy, no peritonitis. The laboratory findings showed hemoglobin 13gr, MCV 90, platelets 461.000/mm3, WBC 4320/mm, lymphocytes 1700 (39%). total bilirubin: 8.8, B Direct: 7.6, ALT (alanine aminotransferase): 3016, AST (aspartate aminotransferase): 984, alkaline phosphatase: 250, albumin: 3.34gr%, globulin: 2.8, amylase: 589 (high serum amylase), TP: 17, INR: 1.6, VHA IgM positive. 89 mg glucose, urea 19 mg%, creatinine 0.5 mg Hemoglobin 13gr, MCV 90 Platelet 461000/mm3, WBC 4320/mm, Lymphocytes 1700 (39%). The nuclear magnetic resonance showed hepatomegaly associated with thickening of gallbladder wall without stones up to 11mm inside. No bile duct dilatation, bile duct 4mm, pancreas increased prevalence of body size. Mild splenomegaly and free fluid in the space of Morrison and right flank. Abdominal ultrasound revealed a gallbladder wall thickness (11mm), without stones in his light. Pancreas to increase volume with peripancreatic fluid free perivesicular with a volume of 430 cc. Findings consistent with acute acalculous cholecystitis and acute pancreatitis. CT-scan showed enlarged pancreas with predominance of body and tail with peripancreatic edema; the gallbladder was thickening. We report this case because the extrahepatic manifestations of viral hepatitis A infection are uncommon, specially the associated with acute acalculous cholecystitis and acute pancreatitis simultaneous.
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PMID:[Acute pancreatitis and acalculous cholecystitis associated with viral hepatitis A]. 2183 59


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