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)

Expression of the pancreatitis-associated protein I (PAP I), an exocrine pancreatic protein, increases rapidly and strongly in acinar cells during the acute phase of pancreatitis. This is reminiscent of the response to stress of acute phase proteins. We have previously demonstrated that serum factors from rats with acute pancreatitis, but not from healthy rats, could induce endogenous PAP I gene expression in the acinar cell line AR-42J (Dusetti, N., Mallo, G., Dagorn, J.-C., Iovanna, J. L. (1994) Biochem. Biophys. Res. Commun. 204, 238-243). In the present work, we have evaluated the influence of several mediators of inflammation on rat PAP I gene transcription in these cells. Tumor necrosis factor alpha induced an increase in PAP I mRNA expression, and interferon gamma caused an even greater increase in PAP I mRNA level. These stimulations were antagonized by dexamethasone. Interleukin (IL)-1, IL-6, or dexamethasone alone were ineffective. Combinations of IL-1 with IL-6 or dexamethasone were also ineffective. IL-6 and dexamethasone together induced a marked stimulation of PAP I gene transcription, and this effect was slightly attenuated by IL-1. To analyze the cis-regulatory elements responsible for the induction of transcription, we fused a 1.2-kilobase segment of the rat PAP I promoter to the chloramphenicol acetyltransferase (CAT) gene as reporter. The resultant chimeric DNA was transfected into AR-42J cells. Addition of IL-6 or dexamethasone was ineffective, whereas their mixture increased the CAT activity 12 times. Progressive deletions of the PAP I promoter were then fused to the CAT gene, and the constructs were transfected to AR-42J cells. A 12-fold increase in CAT activity was seen upon IL-6/dexamethasone treatment with constructs containing more than 274 base pairs upstream from the cap site. In that region, two sequences are similar to the canonical IL-6 response element. Site-directed mutagenesis of these regions strongly decreased induction, showing that they were functional. PAP I should therefore be classified among acute phase proteins of class 2, whose expression is increased by IL-6 acting in combination with glucocorticoids.
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PMID:Pancreatitis-associated protein I (PAP I), an acute phase protein induced by cytokines. Identification of two functional interleukin-6 response elements in the rat PAP I promoter region. 754 77

Cholecystokinin (CCK) receptor antagonists have been reported on have an inhibitory effect on acute experimental pancreatitis, but their long-term administration is also reported to block pancreatic regeneration. We examined whether the short-term administration of KSG-504 (KSG), a synthetic CCK-A receptor antagonist, inhibited the regeneration of pancreatic acinar cells after ethionine-induced acute pancreatitis in rats. KSG (50 mg/kg), given 12 times by subcutaneous injection at 6-h intervals, prevented the reduction of protein, amylase, and trypsinogen levels, and the DNA content of the pancreas and facilitated the recovery of these values. Ornithine decarboxylase activity in pancreatic tissue and a 5-bromo-2'-deoxyuridine labeling study indicated that DNA synthesis was accelerated in rats treated with KSG. These findings suggest that the short-term administration of KSG inhibits the development of ethionine-induced acute pancreatitis and facilitates the regeneration of acinar cells.
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PMID:Effects of short-term administration of the CCK receptor antagonist, KSG-504, on regeneration of pancreatic acinar cells in acute pancreatitis in rats. 755 Aug 60

A 32-year-old man who had undergone liver transplantation for fulminant hepatitis due to HBV infection developed fatal acute necrotizing pancreatitis on the 60th post-transplant day, while showing signs of intense viral replication. Immunohistochemistry and in situ hybridization of the pancreas following autopsy showed the presence of HBsAG and HBV-DNA in the cytoplasm of acinar cells, together with the picture of necrotizing pancreatitis. Clinical and histological features seem to indicate that pancreatitis was directly caused by HBV infection.
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PMID:Fatal necrotizing pancreatitis caused by hepatitis B virus infection in a liver transplant recipient. 756 Aug 62

We investigated the cytotoxicity on Madin-Darby canine kidney (MDCK) cells of pancreatitis-associated ascitic fluid (PAAF) collected from rats with experimental necrotizing pancreatitis. PAAF reduced viability of MDCK cells in a time- and dose-dependent manner. We detected DNA fragmentation on the PAAF-treated MDCK cells, indicating that the cytocidal action of PAAF is via apoptosis. From the results obtained, we conclude that PAAF contains factor(s) inducing apoptosis on MDCK cells, and we assume that apoptotic cell death is involved in the mechanism of organ failure in acute pancreatitis.
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PMID:Induction of apoptotic cell death by pancreatitis-associated ascitic fluid in Madin-Darby canine kidney cells. 758 25

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

More than 90% of tumours of the pancreas have mutations on codon 12 of the Ki-ras oncogene. Cellular DNA from pancreatic secretions and fine-needle biopsies, obtained from 69 patients (41 men, 28 women), were amplified by the polymerase chain reaction (PCR) to demonstrate this characteristic marker. All these patients had undergone endoscopic retrograde pancreatography for suspected pancreatitis or carcinoma of the pancreas. Two different methods were developed to demonstrate the mutations. With the aid of one of these methods, enrichment PCR with analysis of the restriction fragment length (FL), mutations on codon 12 of the Ki-ras gene were demonstrated in unstimulated pancreatic secretions of 29 of 33 patients with pancreatic carcinoma. All eleven fine-needle biopsies that had been cytologically examined showed the tumour-specific mutation. After direct sequencing of enrichment PCR a codon 12 mutation was demonstrated in pancreatic secretion from 21 of 24 patients and with the single strand conformation polymorphism analysis in 17 of 33 patients. In two of these 33 patients two different Ki-ras mutations were discovered. No mutations were found in acute inflammations or stone disease, while in five patients with chronic pancreatitis mutations were demonstrated only in those two patients in whom histological examination had revealed precancerous mucinous hyperplasia. This investigation indicates that codon 12 mutations of the Ki-ras gene, found after PCR in pancreatic secretion and biopsies, constitute a sensitive and specific tumour marker whose clinical value is being assessed.
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PMID:[Ki-ras mutation as a molecular tumor marker for carcinoma of the pancreas]. 778 24

A 22-year-old Pakistani man presented with a 1-year history of recurrent attacks of pancreatitis of unknown etiology that had required hospitalization and extensive investigation in Pakistan. He was admitted with abdominal pain, fever, and weight loss. An ultrasound and computed tomographic scan of the abdomen revealed abdominal lymphadenopathy, bulky and inhomogeneous pancreas, and a large fluid collection anterior to the right lobe of the liver. The collection was aspirated but Gram-stain, Ziehl-Neelsen stain for acid-fast bacilli, and DNA analysis by a highly specific polymerase chain reaction-based assay were negative. Because of a strong clinical suspicion of tuberculosis, the patient was started on antituberculous chemotherapy; 4 weeks later the aspirate grew Mycobacterium tuberculosis (hominis). The patient improved rapidly and has remained well after 18 months follow-up. A high index of clinical suspicion and appropriate microbiological investigation is required for the diagnosis of this rare, but potentially curable cause of pancreatitis.
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PMID:Tuberculous pancreatitis: a diagnostic problem. Case report and review of literature. 779 34

Between 1979 and 1991, 48 cases of pancreatic paraffin-embedded specimens, ie 32 carcinomas and 16 islet cell tumors, confirmed by operative and pathological examination, were studied by flow cytometric nuclear DNA content measurements. 10 specimens taken from the normal pancreatic tissue nearby the tumor transection margin and another 8 specimens in pancreatitis were compared as controls. The results demonstrated that the aneuploid rate and DNA index in pancreatic carcinoma was obviously higher than that of non-pancreatic tumor (P < 0.01). In the field of pancreatic carcinoma, the S-phase fraction was much higher in aneuploid specimens (P < 0.05). Then the nuclear DNA content was a relatively independent factor to evaluate the cancerous biological behavior. The surgical resectability of pancreatic tumors with diploid DNA was significantly higher than aneuploid ones (P < 0.05), and the later carried a shorter survival time proved by Kaplan-Meier survival analysis (P < 0.05). Finally, the clinical significance of DNA content measurements in islet cell tumor was also discussed.
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PMID:[The clinical significance of nuclear DNA content measurements in pancreatic neoplasms and their Kaplan-Meier survival analysis]. 784 63

As mutations at codon 12 of the Ki-ras oncogene have been shown to occur in 90% of pancreatic adenocarcinomas, a novel strategy for the detection of these mutations in pancreatic secretions obtained at routine endoscopies was developed. Ki-ras DNA was amplified and screened for the presence of mutations at codon 12 with a combination of different rapid, non-radioactive molecular biology techniques. Examination of DNA from cell lines and paraffin-embedded tumour samples was used to establish and test the strategy employed. Pancreatic secretions from 27 patients were examined for the presence of Ki-ras mutations. Mutations at codon 12 were detected in 16/16 secretions from patients with histologically confirmed carcinoma and from one patient with carcinoma of the bile duct. In six patients a mutation identical to the one found in the pancreatic secretions was also demonstrated in paraffin-embedded fine-needle biopsy or surgical samples. Of the remaining ten patients (who had pancreatitis or cholelithiasis) mutations were not found in nine. Ki-ras codon 12 mutation was identified in one of these patients however, and mucous cell hyperplasia of pancreatic ducts was found upon histological examination. These findings establish Ki-ras polymerase chain reaction from pancreatic secretions as a valuable new diagnostic procedure for the demonstration of malignant cells, possibly at an early stage of the disease.
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PMID:Diagnosis of pancreatic adenocarcinoma by polymerase chain reaction from pancreatic secretions. 805 76

A both useful and simple classification of primary hyperlipidemias must be at the disposal of all medical doctors, namely general practitioners and cardiologists. The practical classification we have proposed and published since 1971, fulfills this aim. Three main frames of hyperlipidemias are individualized: 1) pure or essential hypercholesterolemia 2) mixed or combined hyperlipidemias 3) major hyperglyceridemia: either exogenous or endogenous. In each of these frames, some clinical specific features, as well as some very simple biologic characteristics allow sometimes an immediate orientation towards some definite varieties of primary hyperlipidemias, now perfectly identified at the level of molecular genetic (tendinosum xanthoma with or without planar xanthomas, palm creases syndrome, tuberous or tubero eruptive xanthomas, etc...). Similarly, occurrence of cardiovascular complications, chiefly coronary, in a rather early age, and with a striking repetition in other members of family, as well of attacks of acute or subacute pancreatitis in other forms, helps considerably for orientation of the diagnosis. For all these reasons, systematic reconstitution of genetic tree on, at least, three generations in absolutely necessary. Prevalence, in various populations, of the genetic origin of these various primary disorders of lipid metabolism is round one out of 500 at the heterozygote state. Even if all the genes candidates are not yet finished to be identified, much of them are now perfectly known, in their localisation on DNA and in their multiple mutations. Possibility of combination of different gene defects can be also met; and more and more are described. This extraordinary and explosive knowledge in this field is now to be described.
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PMID:[Frameworks of recognition and classification of primary hyperlipidemia]. 807 78


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