Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PANCREAS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 901 records · Page 50Linked to original sources
PubMedDate not supplied

Heterotopic pancreas of the stomach: CT findings correlated with pathologic findings in six patients.

BACKGROUND: The purpose of this study was to characterize the computed tomographic (CT) findings of heterotopic pancreas of the stomach. METHODS: CT scans of six surgically proven cases of heterotopic pancreas of the stomach were reviewed. Three were dynamic spiral CT scans, with both arterial dominant and late phase scans. In other three, both unenhanced and contrast-enhanced scans were obtained by using conventional techniques. Particular attention was given to the enhancement of the heterotopic pancreas. Pathologic and surgical findings were correlated with CT findings. RESULTS: The locations were in the gastric antrum in five cases and in the mid-body in one. Size ranged from 1 cm to 3 cm (mean = 2.1 cm). Three cases showed homogeneous, strong enhancement similar to the pancreas and consisted mainly of pancreatic acini with the same histologic features as the normal pancreas. Two cases showed poor enhancement and consisted mainly of ducts and hypertrophied muscle; pancreatic acini were a minor component. In one case appearing as a cystic lesion on CT, a pseudocyst was found with many ducts and some nests of pancreatic acini. CONCLUSIONS: Heterotopic pancreas of the stomach showed a diverse spectrum of CT findings. Good understanding of these CT findings may be helpful in making a correct diagnosis.

Adolescent↗
PubMed2006

Octreotide hardens the pancreas.

BACKGROUND AND AIMS: Leakage from pancreaticojejunostomy and development of pancreatic fistulas are the major postoperative complications in patients undergoing duodenopancreatectomy. The risk of developing these complications is higher when surgery is performed on a soft pancreas. A recent report suggests that octreotide hardens the pancreas when given intraoperatively. The present study aims at verifying this observation by measuring tissue hardness of the pancreas by a commercially available durometer in pigs with and without octreotide pretreatment. METHODS: Three groups of pigs were investigated: Group 1 (n=6) received no treatment; group 2 (n=6) was treated with 3x100 microg octreotide for 1 day; group 3 (n=6) for 5 days. Thereafter, animals were killed and the pancreas was harvested for performing measurements: Tissue hardness was assessed by a commercially available durometer, and a suture holding test was performed using a Newton dynamometer. RESULTS: There was a significant increase in tissue hardness between untreated control animals [26.3+/-2.5 S.U. (shore units)] and animals with 1 day octreotide pretreatment (29.8+/-2.6 S.U.; p=0.04) as well as between the groups treated for 1 and 5 days (34.8+/-2.8 S.U.; p=0.01). Suture holding capacity was higher in animals treated for 5 days. CONCLUSION: The present study agrees with a recent report suggesting that octreotide hardens the pancreas. Octreotide pretreatment may therefore be an advantage when performing surgery on a soft pancreas, i.e., in patients scheduled for duodenopancreatectomy for ampullary carcinomas or circumscript pancreatic tumors not associated with chronic pancreatitis.

Animals↗
PubMed2000

Pituitary adenylate cyclase-activating polypeptide in intrinsic and extrinsic nerves of the rat pancreas.

Pituitary adenylate cyclase-activating polypeptide (PACAP) is the latest member of the vasoactive intestinal polypeptide (VIP) family of neuropeptides present in nerve fibres in many peripheral organs. Using double immunohistochemistry, with VIP as a marker for intrinsic innervation and calcitonin-gene related peptide (CGRP) as a marker for mainly extrinsic innervation, the distribution and localization of PACAP were studied in the rat pancreas. PACAP was demonstrated in nerve fibres in all compartments of the pancreas and in a subpopulation of intrapancreatic VIP-containing ganglion cells. PACAP and VIP were co-stored in intra- and interlobular nerve fibres innervating acini, blood vessels, and in nerve fibres within the islets of Langerhans. No PACAP immunoreactivity was observed in the islet cells. Another population of PACAP-immunoreactive nerve fibres co-localized with CGRP innervated ducts, blood vessels and acini. PACAP/CGRP-positive nerve fibres were also demonstrated within the islets. Neonatal capsaicin reduced the PACAP-38 concentration by approximately 50%, and accordingly a marked reduction in PACAP/CGRP-immunoreactive nerve fibres in the exocrine and endocrine pancreas was observed. Bilateral subdiaphragmatic vagotomy caused a slight but significant decrease in the PACAP-38 concentration compared with controls. In conclusion, PACAP-immunoreactive nerve fibres in the rat pancreas seem to have dual origin: extrinsic, most probably sensory fibres co-storing CGRP; and intrinsic, constituting a subpopulation of VIP-containing nerve cell bodies and fibres innervating acinar cells and islet cells. Our data provide a morphological basis for the reported effects of PACAP in the pancreas and suggest that PACAP-containing nerves in the rat pancreas may have both efferent and sensory functions.

Animals↗
PubMed2006

A new technique for pancreaticogastrostomy for the soft pancreas: the transfixing suture method.

BACKGROUND/PURPOSE: Pancreatic anastomotic leakage remains a persistent problem after pancreaticoduodenectomy (PD). The presence of soft, nonfibrotic pancreatic tissue is one of the most important risk factors for pancreatic leakage. Accordingly, we devised a pancreas-transfixing suture method for pancreaticogastrostomies in patients with a soft, nonfibrotic pancreatic remnant. METHODS: The pancreas-transfixing method was applied in 103 consecutive patients after either standard PD (49 patients) or pylorus-preserving pancreaticoduodenectomy (PPPD) (54 patients) for malignant or benign disease. Of these 103 patients, 65 had a soft, nonfibrotic pancreatic remnant. For the pancreaticogastrostomy technique, an ultrasonically activated scalpel was used for transecting the pancreas. The inner layer involves a duct-to-mucosa anastomosis with an internal stent and the outer layer involves a single row of pancreas-transfixing sutures between the pancreatic remnant and the posterior gastric wall. RESULTS: Operative mortality was zero and morbidity was 22%. Only two patients (2%) developed pancreatic leaks; both resolved nonoperatively with the continuation of closed drainage. CONCLUSIONS: This technique is simple and appears to reduce the risk of pancreatic leakage, possibly by decreasing the risk of suture injury of the pancreas and by embedding the transected stump into the wall of the stomach. This novel pancreaticogastrostomy technique is an effective reconstructive procedure, especially for patients with a soft, nonfibrotic pancreas.

Adult↗
PubMed2002

The time course of gap-junctional protein connexin 32 expression in the pancreas after the induction of acute pancreatitis by caerulein in rats.

BACKGROUND: We previously demonstrated that the immunostaining of the gap-junction protein, connexin 32 (Cx 32), in the pancreas was markedly reduced in caerulein (Cn)-induced acute pancreatitis. The expression of Cx 32 in the pancreas during the course of acute pancreatitis is unclear. To address this, we examined Cx 32 mRNA and protein expression in the pancreas. METHODS: Cx 32 mRNA and protein expression in the pancreas was examined by Northern blot analysis and Western blot analysis, respectively, 1, 4, 7, and 14 days after the induction of acute pancreatitis. RESULTS: Cx 32 mRNA was identified in normal rat pancreas, and the value for the relative intensity against 18S rRNA was 0.57 +/- 0.15 (mean +/- SD). After the induction of acute pancreatitis by caerulein, the Cx 32 mRNA expression levels were increased on day 1, day 4, day 7, and day 14 compared with levels in the normal pancreas (1.63-fold, 1.61-fold, 1.49-fold, and 1.35-fold, respectively). A significant increase in Cx 32 protein expression was detected on day 1 and day 4 (1.67 +/- 0.15-fold and 1.72 +/- 0.2-fold, respectively), while Cx 32-positive spots, determined by immunohistochemical analysis, were markedly decreased on day 1 and had returned to normal by day 14. CONCLUSIONS: These results show that the expression of Cx 32 increases early on after the induction of pancreatitis by Cn, and that the normalization of Cx 32-immunostained spots in Cn-induced acute pancreatitis occurs after the increase in Cx 32 mRNA and protein expression.

Acute Disease↗
PubMed2000

Total gastrectomy with dissection of lymph nodes along the splenic artery: a pancreas-preserving method.

BACKGROUND: In Japan, the tail and body of the pancreas are generally removed for dissection of lymph nodes along the splenic artery. A new pancreas-preserving method was developed to decrease the postoperative complications due to pancreatic resection. PATIENTS AND METHODS: Between 1981 and 1989, 110 patients were registered in a randomized controlled trial, which included total gastrectomy plus dissection of lymph node along the splenic artery, either with (55 patients: Group A) or without (55: Group B) pancreas tail resection. In Group B, the splenic artery and spleen were removed and the pancreas was preserved. There were no significant differences between the two groups in terms of sex, age, location, microscopic classification, or disease stage. The postoperative complications and survival rates were compared between the two groups. RESULTS: The average number of dissected nodes along the splenic artery was 4.6 and 4.1 for Groups A and B, respectively. The amounts of blood loss during the operation were 994 ml and 904 ml for groups A and B, respectively. Anastomosis failure and/or pancreatic fistula occurred in nine patients in Group A (16%) and seven in Group B (13%). One year after the operation, a glucose tolerance test showed diabetes in 6% and impaired glucose tolerance in 33% of patients in group A, while these findings were normal in group B. The 5-year survival rates were 80% and 76.7% for groups A and B, respectively. CONCLUSIONS: The pancreas-preserving method described here was superior to the more common pancreas resecting method with regard to surgical risk and postoperative glucose tolerance.

Adult↗
PubMed2002

Pancreas and kidney transplantation.

Kidney transplantation is preferred over dialysis for management of end-stage renal disease complicating type I or type 2 diabetes, for those who are eligible. Simultaneous pancreas-kidney (SPK) or pancreas after kidney transplantation (PAK) is an important alternative to kidney transplantation alone for type I diabetes patients if the patient is able to withstand the additional risks of these procedures, because of the benefits of glucose control on other diabetic complications. Pancreas transplantation alone (PTA) is most useful for the treatment of debilitating, frequent hypoglycemia complicating type I diabetes, if renal function is adequate. One-year pancreas graft survival is best after SPK (82%) but has significantly improved after both PAK (74%) and PTA (76%). The I-year kidney graft and patient survival rates after SPK are similar to kidney transplantation alone. Pancreas transplantation normalizes glucose beyond what can be achieved with insulin therapy and has been shown to decrease progression of or improve most, if not all, diabetic end-organ complications using current immunosuppression regimens. However, the diabetologist and endocrinologist should remain involved in the care of the pancreas or kidney transplant recipient for treatment of vascular disease risk factors such as dyslipidemia, surveillance of other diabetic complications including foot ulcers, surveillance and treatment of bone loss, and management of hyperglycemia if it recurs.

Diabetic Nephropathies↗
PubMed1984

Tissue specificity of glycosphingolipids as expressed in pancreas and small intestine of blood group A and B human individuals.

A chemical investigation has been done on blood group active glycosphingolipids of both small intestine and pancreas from two individuals, one blood group A and one blood group B. Total non-acid glycolipid fractions were prepared and the major blood group fucolipids present were purified and structurally characterized by mass spectrometry, proton NMR spectroscopy, and degradation methods. The glycolipid structures identified were a blood group Leb hexaglycosylceramide, a B-hexaglycosylceramide with a type 1 (Gal beta 1 leads to 3GlcNAc) carbohydrate chain, A-hexaglycosylceramides with types 1 and 2 (Gal beta 1 leads to 4GlcNAc) carbohydrate chains, a B-heptaglycosylceramide with a type 1 carbohydrate chain, and A-heptaglycosylceramides with type 1 and 2 carbohydrate chains. In addition several minor glycolipids having more than seven sugar residues were detected by thin-layer chromatography. The small intestine and pancreas had some distinct differences in their expression of the major fucolipids. The small intestine contained only glycolipids based upon type 1 carbohydrate chain while the pancreas had both type 1 and type 2 structures. The intestines contained mainly difucosyl compounds while the pancreas tissues contained both mono- and difucosyl glycolipids. Monofucosylglycolipids based on both types 1 and 2 saccharides were present in one pancreas while the other one contained only monofucosylcomponents based on type 1 chain. The ceramides of the intestinal glycolipids were found to be more hydroxylated (trihydroxy long-chain base, hydroxy fatty acids) compared to the pancreas glycolipids (dihydroxy long-chain base, non-hydroxy fatty acids).

ABO Blood-Group System↗
PubMed1992

Cytological changes in the pancreas of transgenic mice overexpressing transforming growth factor alpha.

Transgenic mice overexpressing human transforming growth factor alpha (TGF-alpha) predictably develop an enlarged, firm pancreas. The present study investigated the changes that occur in the different components of the pancreas in these animals. The increase in size of the pancreas may be accounted for by increased connective tissue. The added collagen is mainly type I. Thin, elongate fibroblasts are frequently bordered by a basal lamina, a relationship that is normally restricted to the perineurium. Collagen is intimately associated with epithelial cells. Fingers of connective tissue extend close to acinar lumina. Redifferentiation of acinar cells produces tubular complexes. In some cases, acinar cells take on the appearance of ductular cells. In some, there is a transition to mucin-producing cells. Intermediate forms between acinar and mucin-producing cells are present. The growth factor is localized in acinar cells and decreases with redifferentiation. The pancreas of these animals routinely displays characteristics that also are observed in diseases of the exocrine pancreas in humans, including fibrosis and redifferentiation. It is likely that the changes are the result of both direct and indirect effects of TGF-alpha, some of which may parallel altered control mechanisms in human pancreatic disease. Study of this model may provide clues to understanding the initiation of fibrosis and redifferentiation in human pancreas.

Animals↗
PubMed1995

In situ hybridization shows distinct patterns of mucin gene expression in normal, benign, and malignant pancreas tissues.

BACKGROUND & AIMS: Northern blotting and immunohistochemistry have shown cell-specific patterns of mucin gene expression in the pancreas and alterations associated with neoplastic transformation. The aim of this study was to determine the presence of mucin transcripts at the single cell level in tissue samples from normal pancreas and benign and malignant pancreatic proliferative lesions. METHODS: In situ hybridization with 35S-labeled oligonucleotides was performed on sections of paraffin-embedded tissues. RESULTS: Acinar cells express only MUC1. Normal pancreatic ducts show homogeneous expression of MUC1 and MUC5B and heterogenous expression of MUC3. MUC2, MUC4, and MUC5AC are generally undetectable in all cells of normal pancreas tissue. Pancreas cancers generally express MUC1, MUC3, MUC4, MUC5B and MUC5AC. Obstructive chronic pancreatitis adjacent to pancreas cancers shows the same pattern of mucin gene expression as normal ducts. In areas of papillary hyperplasia, altered expression of MUC3, MUC5B, and MUC5AC is observed. CONCLUSIONS: In situ hybridization has confirmed that neoplastic transformation of the exocrine pancreas is accompanied by changes in mucin gene expression. Although this type of change is not restricted to cancer cells, the findings of this study suggest that analysis of mucin gene expression may be of value in the differential diagnosis of pancreatic lesions.

Adenocarcinoma↗
PubMed1993

Effects of pancreas transplantation on glomerular structure in insulin-dependent diabetic patients with their own kidneys.

Pancreas transplantation prevents or retards development of early diabetic glomerular lesions in renal allografts transplanted to patients with insulin-dependent diabetes mellitus (IDDM), but its effect on established renal lesions in native kidneys of such patients is unknown. Renal biopsy samples were taken before and 5 years after pancreas transplantation from 13 non-uraemic IDDM patients and compared with baseline and 5-year biopsy samples from 10 persistently hyperglycaemic IDDM patients who did not undergo transplantation. The two groups were similar in age, duration of diabetes, metabolic control, renal function, and blood pressure. Glomerular structures were measured by standard morphometric techniques. Haemoglobin A1 concentrations fell to within the normal range after pancreas transplantation but did not change in the comparison group. Glomerular basement membrane width did not significantly change in either group. Glomerular volume decreased and mesangial fractional volume increased in the pancreas transplant recipients but there was no significant change in total mesangial volume over 5 years. By contrast, both glomerular volume and mesangial fractional volume increased in the comparison patients, resulting in increased total mesangial volume. Diabetic glomerular lesions in patients with their own kidneys were not ameliorated by pancreas transplantation, despite 5 years of normoglycaemia. Pancreas transplantation can correct severe metabolic instability and thus improve quality of life, but it cannot yet be recommended for the treatment of established lesions of diabetic nephropathy.

Adolescent↗
PubMed1987

The organization of vagal innervation of rat pancreas using cholera toxin-horseradish peroxidase conjugate.

The present study was initiated to address the current controversy concerning the parasympathetic innervation of the pancreas, using a more sensitive tracer. The location of retrogradely labeled neurons within the dorsal motor nucleus of the vagus (DMV) was examined 48 h following injections of cholera toxin-horseradish peroxidase (CT-HRP) into designated areas of the rat pancreas. The brainstem and spinal cord were searched for any additional labeled neurons located outside of the DMV. Separate groups of animals were used for control injections into the adipose tissue of the greater omentum, the spleen, abdominal musculature, and the diaphragm. In addition, CT-HRP was dripped over the surfaces of the abdominal viscera in another group of animals. These control cases were designed to indicate whether diffusion of the neural tracer away from injection sites had occurred and had resulted in labeling of neurons which did not innervate the injected areas. Following injection of CT-HRP into the right lobe of the pancreas, labeled neurons were found primarily within the medial region of the left DMV. Injection of CT-HRP into the left lobe of the pancreas resulted in retrogradely labeled neurons predominantly within the medial region of the right DMV. Following injections into the entire pancreas, neural labeling was seen bilaterally within the DMV and was concentrated within the medial regions, with a slightly higher degree of labeling within the right DMV. No labeled neurons were seen within the nucleus ambiguus or other areas of the brainstem or spinal cord following pancreatic injections. Furthermore, no afferent labeling within the nucleus of the solitary tract (NTS) was observed, although a very small number of neurons within the nodose ganglia were labeled. The dendrites of backfilled DMV neurons could be seen extending across the midline to the contralateral DMV as well as dorsally into certain subnuclei of the NTS, and to the borders of the area postrema and the fourth ventricle. These results indicate that both the motor and sensory innervation of the rat pancreas are more restricted than has been previously suggested.

Animals↗
PubMed1994

Monitoring of kidney and simultaneous pancreas-kidney transplantation rejection by release of donor-specific, soluble HLA class I.

Using an HLA-A2-specific ELISA we monitored daily pretransplantation and posttransplantation sera from five kidney and eight simultaneous pancreas-kidney HLA-A2-negative recipients of HLA-A2-positive transplants during hospitalization. We found that, unlike liver transplants, neither kidney nor simultaneous pancreas-kidney transplants continuously secreted donor HLA proteins. However, three of four rejection episodes in kidney recipients and seven of seven rejection episodes in simultaneous pancreas-kidney recipients were accompanied by elevated serum levels of donor sHLA-A2 (> 5 ng/ml). In only one kidney patient was there a release of donor antigen without evidence of rejection, but in the simultaneous pancreas-kidney group most patients had at least one time point of detectable sHLA-A2 without strong evidence of kidney rejection. While total sHLA levels were also elevated during rejection, the rise in donor-specific sHLA was more dramatic when compared to pretransplantation background levels. We hypothesized that the release of donor sHLA class I proteins by transplanted organs might be a systemic indication of rejection in both pancreas and kidney allografts. The detection of donor sHLA in recipient sera could be an important noninvasive monitor of rejection, especially in the pancreas, which is currently difficult to monitor as a single-organ transplant.

Adult↗
PubMed1981

Studies of DNA damage in rat pancreas and liver by 6-diazo-5-oxo-L-norleucine, ethyl diazoacetate and azaserine.

One hour following intraperitoneal injection of the pancreatic and liver carcinogen azaserine, 10 mg/kg (0.06 mmol/kg), DNA damage is present in both pancreas and liver of Wistar/Lewis rats as determined with alkaline sucrose gradients. Single injections (0.06 mmol/kg) of either of 2 structural analogues of azaserine, 6-diazo-5-oxo-L-norleucine (DON) and ethyl diazoacetate (EDA), do not damage pancreatic or liver DNA. EDA administered at 0.5 mmol/kg damages liver DNA, but not pancreatic DNA. Total radioactivity in pancreas and liver of Wistar rats 1 h after intravenous injection of [14C]azaserine, (10 microCi/kg), is 2.8 and 1.3 times respectively, the level of 14C-activity in pancreas and liver following injection [14C]EDA. Three to four times as much [14C]EDA localizes in the liver of Wistar rats as in the pancreas. Azaserine (0.06 mmol/kg weekly for 6 weeks) induces atypical acinar cell nodules (AACN) in pancreas of Wistar/Lewis rats. DON (0.06 mmol/kg weekly for 6 weeks) induces an elevated incidence, but low number of AACN in pancreas. EDA (0.10 mmol/kg weekly for 6 weeks) does not induce pancreatic AACN.

Animals↗
PubMed1975

Effects of cholera toxin on cyclic adenosine 3',5'-monophosphate concentration and secretory processes in the exocrine pancreas.

1. The effect of purified cholera toxin on secretory processes of exocrine pancreas has been studied in the isolated, saline-perfused cat pancreas and in incubated pieces of rat pancreas. 2. The toxin evoked a biphasic secretory response from the perfused cat pancreas. An initial small phase, which began within minutes of toxin application, was an artefact due to the presence of NaN3 in the cholera toxin preparation as supplied; it could be entirely reproduced by NaN3 at the concentration expected during toxin stimulation. A second, sustained phase of secretion, due to the action of the toxin proper, began within 30-60 min, increasing in magnitude for many hours and persisting in the absence of toxin. It was accompanied by a parellel rise in tissue cyclic AMP concentration, and could be potentiated by theophylline. 3. The composition of the secretion stimulated by cholera toxin resembled that evoked by secretin; e.g. it contained a high concentration of bicarbonate and only basal amounts of digestive enzymes. 4. Similarly, cholera toxin did not stimulate enzyme secretion by incubated rat pancreas, despite large rises in tissue cyclic AMP concentration. 5. Because cholera toxin has thus far been shown to have no other effect than that of stimulating adenylate cyclase, these observations support the conclusion that cyclic AMP does mediate the electrolyte secretory response of the pancreas to secretin, but offers no evidence that cyclic AMP plays a similar role in the regulation of pancreatic enzyme secretion stimulated by cholecystokinin-pancreozymin or acetylcholine.

Animals↗
PubMed1976

Hypertrophy and hyperplasia of the neonatal rat exocrine pancreas induced by orally administered soybean trypsin inhibitor.

Measurement of RNA, DNA, protein and phospholipid synthesis in the neonatal rat pancreas following the oral administration of partially purified soybean trypsin inhibitor demonstrates an enhanced synthesis of all these constituents. Evidence of true hyperplasia in addition to this cellular hypertrophy is provided by an increased mitotic activity in the exocrine pancreas following a wave of enhanced [3H] thymidine incorporation into DNA. Complete inhibition of the stimulated RNA synthesis by low doses of actinomycin D indicates the importance of transcription as a regulatory step in the response of the exocrine pancreas to trophic stimulation by this means. Collateral observations of [3H] thymidine and [14C] orotic acid incorporation into liver DNA and RNA, respectively, fail to demonstrate comparable changes confirming the probable specificity of the trypsin inhibitor induced effect on the exocrine pancreas. It is suggested that the pronounced trophic effect of orally administered soybean trypsin inhibitor in the neonatal rat pancreas may serve as a useful model for the study of regulatory mechanisms of nucleic acid and protein synthesis in the mammalian pancreas.

Administration, Oral↗
PubMed1986

Isolation and characterization of two oncofetal glycoproteins from hamster pancreas using concanavalin A and preparative electrophoresis.

Pancreatic fetal acinar antigens in the Syrian golden hamster, which are associated with development of the pancreas, have been previously described. In this study, two major antigens were isolated from fetal pancreas using affinity chromatography on Con A-Sepharose and preparative electrophoresis. Homogenates from fetal and adult pancreas were analyzed for their ability to bind to concanavalin A. This lectin allowed obtention of eluted fractions accounting for 2 and 0.7%, respectively, of the protein content in crude extracts. Concanavalin A-positive fraction from fetal pancreas contained two major carbohydrate-reactive glycoproteins of relative molecular weight (Mr) 80 000 and 58 000 in SDS-polyacrylamide gel electrophoresis. Both behaved as fetal antigens in nitrocellulose blot immunoassay. Similar experiments with chemically induced tumors of the pancreas led to a concanavalin A fraction containing the 80 and 58 kDa fetal glycoproteins; but in this case, the fraction was quite heterogeneous. Our data provide new support for the existence of differentiation antigens in the acinar cells of the pancreas, and indicate that two major ones are glycoproteins. Moreover, both are expressed in pancreatic tumors.

Animals↗
PubMed2004

Ethanol consumption potentiates viral pancreatitis and may inhibit pancreas regeneration: preliminary findings.

Alcohol abuse is often associated with acute pancreatitis. The pathogenesis of alcoholic pancreatitis remains poorly understood, in part because of the lack of a suitable animal model to study the mechanism or mechanisms of this disease. It has been proposed that ethanol predisposes or sensitizes the pancreas to the effects of co-factors, and the combination of the effects of ethanol on the pancreas and the actions of these co-factors results in alcoholic pancreatitis. A number of viruses are known to infect the pancreas, and we have suggested that one co-factor that could be involved in the development of alcoholic pancreatitis is a viral infection. One of the most-studied groups of viruses that infect the pancreas and cause pancreatitis in human beings is the coxsackieviruses. We have shown that short-term (5-14 days) and subchronic (>28 days) administration of ethanol to mice increases the severity of coxsackie B3-induced pancreas damage. We hypothesize that consumption of ethanol would result in an impairment of pancreas regeneration after injury, similar to the effect of ethanol on liver regeneration. With the use of the murine model of coxsackie B3-mediated alcoholic pancreatitis we have obtained preliminary data to support the hypothesis. Specifically, consumption of ethanol by mice is associated with changes in the replication of acinar cells and their organization into acini after viral-mediated injury. We believe that this model will be a valuable tool to study the biochemical and molecular mechanisms involved in alcoholic pancreatitis.

Alcoholism↗