Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149521 (chronic pancreatitis)
 7,199 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The expression of the VLA-integrins alpha 2, alpha 3, alpha 5 and alpha 6 was studied immunohistochemically in tissue samples from ductal pancreatic cancer, chronic pancreatitis, normal pancreas and in 8 cell lines of ductal human pancreatic cancer. Furthermore, adhesion assays on purified extracellular matrix (ECM)-compounds were used to define the function of alpha 2, alpha 3, alpha 5 and alpha 6 in pancreatic cancer cells. 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, while centro-acinar cells predominantly expressed VLA alpha 3 and VLA alpha 5. Pancreatic carcinoma showed intense staining for VLA alpha 2 and VLA alpha 6 with a diffuse distribution on the cell surface. The redistribution of VLA alpha 2 and VLA alpha 6 may reflect a loss of spatial arrangement of tumor cells and their ability to interact randomly with extracellular matrix structures during invasion and metastasis. Expression of VLA alpha 3 and VLA alpha 5 in pancreatic carcinoma was heterogeneous, ranging from moderate to weak, and was lost in about 50% of the cells. Two pancreatic carcinoma cell lines (PC 3, PC 44) were further investigated in adhesion assays. Monoclonal antibodies (MAbs) against alpha 2 (GI 9, 10-G-11) were able to inhibit tumor-cell adhesion to collagen IV (59%-72%) in both cell lines. A MAb against alpha 6 (GoH3) inhibited tumor-cell adhesion to laminin (52%-86%) in both cell lines. These results suggest that alpha 2 is a collagen-binding site and alpha 6 a laminin-binding site in pancreatic cancer cells. The anti-alpha 5-MAb SAM I inhibited adhesion of PC3 to fibronectin (76%), being without effect in PC44. Adhesion of both cell lines to fibronectin was almost completely inhibited by RGDS (85%-88%). Thus, alpha 5 is a functionally important fibronectin binding site in some pancreatic carcinoma cells, suggesting further RGD-dependent fibronectin binding sites in other pancreatic carcinoma cells.
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PMID:Expression and function of VLA-alpha 2, -alpha 3, -alpha 5 and -alpha 6-integrin receptors in pancreatic carcinoma. 133 Sep 37

A colorimetric method has been used to quantify the collagen contained in 23 specimens of pancreatic tissue (11 controls and 12 chronic pancreatitis). The method takes advantage of the selective capacity of Sirius red to stain collagen protein and of rapid green to stain noncollagen protein. The results obtained by this method were compared with those of standard morphometry to determine tissue fibrosis. With the morphometric method, the values of the control group were 6.6 +/- 4.0% (fiber area/total area), and those of chronic pancreatitis 66.0 +/- 19.0% (difference 59.4, 95% confidence interval for difference: 47.2-71.6, P less than 0.001). The values obtained with the colorimetric method were 89.1 +/- 11.6 micrograms collagen/mg total protein in the control group, and 132.7 +/- 25.3 micrograms collagen/mg total protein in the chronic pancreatitis group (difference 43.6, 95% confidence interval for difference: 26.3-61.0, P less than 0.001). A highly significant correlation (r = 0.847; p less than 0.001) was observed between the amount of collagen measured colorimetrically and the degree of fibrosis determined morphometrically. These results demonstrate that the colorimetric method is a reproducible, simple, and rapid technique to quantitate fibrosis in histological preparations of pancreatic tissue.
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PMID:Quantitative measurement of fibrosis in pancreatic tissue. Evaluation of a colorimetric method. 175 28

A comparison on fibrosis in between apparently uninvolved areas in acute pancreatitis (AP) and chronic pancreatitis (CP) was both histopathologically and immunohistochemically studied. Interlobular fibrosis in the apparently uninvolved areas (AP) was found in 7 out of 9 patients and accompanied by hemosiderin deposition in 6 patients, whereas that in only 2 out of 12 patients in CP. In the 2 remaining patients of AP without fibrosis, hemorrhage with inflammation was distributed in the interlobular spaces. Hence, AP was seldomly followed by CP. Interlobular fibrosis in CP immunostained positively to both anti-collagen Types I and III, whereas that in AP in four patients only. Fibrosis in the 3 remaining patients of AP whose illness was of less than one month's duration was positive against anti-collagen Type III only. Therefore, differences in both hemosiderin deposition and immunoreactivity against anti-collagen Type I in the interlobular fibrosis, except for longer surviving patients were observed in between acute and chronic pancreatitis.
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PMID:[A comparison on between acute pancreatitis and chronic pancreatitis, special references to their fibrosis]. 179 23

Urinary excretions of hydroxyproline and fibronectin fragment (FN fragment) were serially investigated in the patients with acute pancreatitis or acute exacerbation of chronic pancreatitis. While urinary excretion of FN fragment showed the maximal level on the first day of admission, high levels of urinary hydroxyproline were observed on the second to fifth day. As to the changes in the individuals, peak level of urinary FN fragment always preceded that of hydroxyproline. And it was assumed that the elevation of FN fragment excretion on the early phase of pancreatitis reflected tissue damages of pancreas itself and complicated organs, and following elevation of hydroxyproline showed enhanced collagen metabolism induced by acute inflammation and tissue damage. According to the severity of pancreatitis, urinary excretion of FN fragment on the first day increased, and it was therefore suggested that urinary FN fragment would be one of the parameters for the assessment of the severity of acute pancreatitis.
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PMID:[Changes of the urinary excretions of hydroxyproline and fibronectin fragment in acute pancreatitis]. 194 12

It is suggested that during active phases of acute and chronic pancreatitis (aP and cP) a major breakdown of extracellular matrix occurs. Since our group previously established that serum levels of the precollagen-III-peptide (P-III-P) are good markers for changes in the extracellular matrix in liver disease (e.g. fibrosis and cirrhosis), we investigated whether this would also serve as a possible marker for pancreatitis. A total of 52 patients with pancreatitis were studied (aP = 17; cP = 35) and compared to 194 controls. Diagnosis of pancreatitis was done on the basis of established classifications. Concomitant diseases, e.g. of the liver, were excluded. Serum levels of P-III-P (three assays with polyclonal and monoclonal antibodies and Fab-Fragments), hyaluronic acid (HA) and laminin (LAM) were measured by RIA or IRMA. Patients with pancreatitis displayed elevated levels in all groups, when compared with the controls. Since the P-III-P-Fab RIA measures the Col1-fragment by 50%, which is considered to be a degradation product of P-III-P, this could mean that neogenesis of collagen is paralleled by degradation during the initial course of an acute episode of pancreatitis. The ratio (quotient) of P-III-P-Fab and P-III-PMoAb (nl = 127.3 +/- 27) is changed in patients with pancreatitis towards P-III-P-Fab (aP: 115.4 +/- 84.7*, cP: 94.9 +/- 21.8*, cP-I: 89.3 +/- 9.2*; * = p = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Parameters of connective tissue metabolism as markers in acute and chronic pancreatitis. A retrospective study with a cohort of normal subjects]. 195 31

Malnutrition is a common finding in chronic pancreatitis and its pathogenesis is multifactorial. In 14 patients with chronic pancreatitis we assessed the dietary intake, some anthropometric indices and the concentration of some serum proteins. In muscle specimens obtained by needle biopsy we examined the DNA, RNA and non-collagen alkali-soluble protein (ASP) content. In muscle we determined also the activity of cathepsin D, an enzyme involved in intracellular myofibrillar catabolism. Protein and energy intake were lower than in the normal healthy population. Plasma protein content (an index of liver protein synthesis) was generally in the normal range, whereas anthropometry and the biochemical muscle indices were generally subnormal, suggesting a depressed muscle protein content and synthesis (evaluated, respectively, by the ASP: DNA and RNA: DNA ratios). Cathepsin D activity was lower than in controls, and the percentage of 'free' activity tended to be higher but not significantly. This study suggests that muscle protein content and synthesis are reduced in patients with chronic pancreatitis, whereas liver protein synthesis is generally preserved. Possibly as a consequence of metabolic abnormalities and/or of an inadequate protein and energy intake, the nutritional status was often abnormal in our patients and a nutritional support therapy was needed.
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PMID:Muscle biopsy studies on protein-energy malnutrition in patients with chronic relapsing pancreatitis. 242 50

The proliferation of pancreatic extracellular matrix, which characterizes chronic pancreatitis, has been analysed using immunohistochemistry. The relationship of matrix components to intraductal precipitates and the presence of serum proteins in precipitates were also studied to investigate the suggestion that ductal permeability increases in chronic pancreatitis. Pancreatic tissue from organ donors was compared with that from patients with chronic calcifying or chronic obstructive pancreatitis. Frozen sections were labeled with monospecific antibodies to collagen types I, III, pro-III and IV, laminin, fibronectin, IgG, IgA, and IgM and then visualized by indirect immunofluorescence. In chronic pancreatitis, interstitial collagens and fibronectin appeared increased and disorganized in both fibrous tissue and areas that appeared histologically normal. Type IV collagen distribution was abnormal and in some sites was present with interstitial collagen. In addition, intraductal precipitates were shown to contain immunoglobulins, and defects were identified in the duct basal lamina associated with precipitates. These results demonstrate that in chronic pancreatitis interstitial collagens are extensively disorganized, the fibrosis possibly being relatively labile. The presence of serum proteins in intraductal precipitates confirms an increase in ductal permeability, and associated defects in the basal lamina appear to define a route via which serum proteins may enter the intraluminal compartment.
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PMID:Pancreatic extracellular matrix alterations in chronic pancreatitis. 357 15

We encountered a case of primary biliary cirrhosis in a nonalcoholic man who had been operated on for idiopathic retroperitoneal fibrosis 20 years previously. Chronic pancreatitis was also detected on endoscopic retrograde examination. After several episodes of digestive bleeding due to ruptured esophageal varixes, the patient died of massive hemorrhage. Postmortem examination showed stage 3 primary biliary cirrhosis and a thick retroperitoneal fibrous plaque, consisting of densely fibrotic areas of collagen with rare vessels and mononuclear cells. We suggest that idiopathic retroperitoneal fibrosis may be a new autoimmune disorder associated with primary biliary cirrhosis and that primary biliary cirrhosis is a potential cause of portal hypertension, cholestasis, or both in the course of idiopathic retroperitoneal fibrosis.
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PMID:Idiopathic retroperitoneal fibrosis and primary biliary cirrhosis. A new association? 406 68

Clinical research into patients with idiopathic chronic pancreatitis points to a possible immunopathogenetic process in a number of cases. In order to examine the behaviour between the exocrine pancreas under the influence of anti-rat-pancreas immune serum produced in rabbits, a 1.00 ml immune serum is administered once a week over a maximum 26 week period into Wistar-rats by intraperitoneal injection. By electrone-microscopy a much reduced production of enzymes apparently takes place, though to differing extent. There is also destruction of the basal membrane of acinocytes: the production of interstitial oedema, the new formation of collagen fibres and the proliferation of connective tissue cells. Under a conventional light microscope the first changes become noticeable after 8-12 weeks of study. These take the form of localised cell decay, deterioration and lysis of acinocytes; and an increasing non-specific inflammation. There is also the new formation of connective tissue. After 20-26 weeks the exocrine pancreas is characterised by reduction of parenchyma, acino-ductal metaplasia, chronic inflammatory infiltrates of differing density, fibrous and irregular calibres of the smaller and larger ducts. The findings are almost identical to the structural changes of chronic idiopathic pancreatitis in human beings. The results support the view of an immuno-pathologic aetiology for human chronic idiopathic pancreatitis.
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PMID:Serum-induced chronic pancreatitis. 722 72

The events that characterise recovery from severe biliary pancreatitis have not been defined. This study used a reversible model of necrotising pancreatitis, induced by obstructing the opossum common bile pancreatic duct (CBPD), to evaluate this phenomenon. The CBPD of opossums was obstructed with a balloon tipped catheter for five days and then decompressed by removal of the catheter. Recovery was evaluated 0-90 days after relief of obstruction. Serum bilirubin and amylase values rapidly declined, reaching control values 7-14 days after removal of the obstructing catheter. Pancreatic protein and amylase values were transiently increased shortly after relief of obstruction but returned to control values 21 days after decompression. Pancreatic ornithine decarboxylase activity and incorporation of [3H]-thymidine into DNA were transiently increased 14 days after duct decompression suggesting that regeneration occurs at approximately that time. Foci of pancreatic necrosis involved roughly 40% of the gland at time of decompression but these foci gradually disappeared and the gland resembled that of control animals 60 days after decompression. Evidence of fibrosis or collagen deposition in the pancreas was not noted at any time. These studies show that recovery after necrotising biliary pancreatitis occurs comparatively rapidly and the restitution ad integrum occurs. Recovery from necrotising acute pancreatitis in this model is not associated with the development of chronic pancreatitis.
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PMID:Biochemical and morphological changes that characterise recovery from necrotising biliary pancreatitis in the opossum. 759 Apr 43


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