ISSN:0885-3177    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

A previous study demonstrated that pancreatic tumor cells in culture but not other tumor cell lines, exhibit three major monocyte-related functions, i.e., endocytosis, lysosomal enzyme secretion, and luminol-enhanced chemiluminescence. All three functions could be stimulated to the same extent in pancreatic tumor cells as in monocytes by exposure to zymosan or immune complexes. In the present study, the effect of monoclonal antibodies (mabs) (BW 227/18 and BW 227119). which react with epitopes on both monocytes and pancreatic tumor cells on basal and stimulated functions, was tested. Kinetic measurement of chemiluminescence showed a quick inhibition of this activity on both cell types within 3–5 min that amounted to −50%) of the basal activity and 60–90% of the stimulated activity. The same was true for inhibition of endocytotic activity and lysosomal enzyme secretion, which were inhibited to the same extent under both basal and stimulated conditions in monocytes as well as in pancreatic tumor cells. The biochemical measurements were supported by tracer studies using cationized ferritin and electronmicroscopy, demonstrating an inhibition of the uptake of tracer into multivesicular bodies by the addition of the two mabs. The inhibitory effect of the antibodies could reflect their binding to epitopes on the plasma membrane and an interference with membrane fluidity through cross-linking.

ISSN:0885-3177    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

Glucagon is structurally related to secretin but inhibits the effects of secretin and cholecystokinin (CCK) on pancreatic secretion in vivo. Because secretin is a weak stimulant of pancreatic growth and potentiates the trophic effects of CCK, we hypothesized that glucagon might inhibit CCK-induced pancreatic growth. Four groups of 10 rats were injected with saline, glucagon (30 μg, equimolar to a known trophic dose of secretin), cerulein (0.67 μg/kg), or glucagon plus cerulein every 8 h for 5 days. The pancreas was excised, weighed, and assayed for total content of DNA, protein, amylase, chymotrypsinogen, and lipase. In control and glucagon-alone groups, the small intestine was also removed, weighed, and assayed for DNA, protein, and disaccharidase content. Glucagon alone decreased pancreatic DNA and increased lipase content. Compared with cerulein-treated animals, animals treated with glucagon and cerulein showed significant decreases in pancreatic weight and content of protein, amylase, and chymotrypsinogen. Although glucagon had significant effects on intestinal protein, maltase, and sucrase contents in certain segments, there was no clear pattern of response. The data suggest that glucagon may be an inhibitory regulator of pancreatic growth, acting to block the effects of CCK on pancreatic hypertrophy.

ISSN:0885-3177    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

Labeled somatostatin binding to pancreatic acinar membranes was examined to investigate how pancreatic secretagogues regulate somatostatin receptors in the pancreas. Pretreatment of pancreatic acini at 37°C for 120 min with not only pancreatic secretagogues, such as carbachol and bombesin, but also vasoactive intestinal peptide (VIP) and secretin reduced subsequent labeled somatostatin binding to the acinar membranes in a dose-dependent manner. The inhibitory effects of these secretagogues on labeled somatostatin binding were also time dependent. Both types of secretagogues maximally reduced subsequent somatostatin binding when acini were incubated with them for more than 120 min. However, the degree of the inhibition was greater with carbachol or bombesin than VIP or secretin: the former secretagogues reduced the binding to 40–45%, and the latter to 75–80% of a control respectively. These pancreatic secretagogues had no inhibitory effect on somatostatin binding when added directly to the binding media. Furthermore, the inhibitory effect of carbachol was attenuated by the presence of 1 mM EDTA in media for pretreatment, suggesting that intracellular pathways activated by pancreatic secretagogues may be responsible for somatostatin receptor modulation. Interestingly, when combined with VIP, pretreatment of acini with carbachol produced an additive inhibition of labeled somatostatin binding to the membranes. Results, therefore, suggest that somatostatin binding to its receptors in the pancreas may be regulated via two functionally distinct intracellular pathways.

ISSN:0885-3177    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

In order to investigate the role of renal factors in affecting trypsinogen I metabolism and excretion in chronic pancreatic disease, serum immunoreactive trypsin (IRT), urinary IRT, γ-glutamyltransferase (GGT), α-glucosidase (AGL) and RNase outputs and the molecular size distribution of serum and urine IRT were studied in 8 control subjects, 18 cases with pancreatic cancer, and 23 cases with chronic pancreatitis. Serum chromatography demonstrated that most immunoreactivity eluted as trypsinogen 1. Smaller amounts of immunoreactivity at higher molecular weights were also observed. Urine chromatography displayed both trypsinogen 1 and heavier molecular forms. An inverse linear correlation was noticed between creatinine clearance and serum trypsinogen 1 levels. Multiple regression analysis (urinary IRT output dependent and GGT, AGL, and KNase predictor variables) showed a significant linear correlation. RNase was found to be the most important parameter in explaining urinary IKI' output. Mild variations in the glomerular function seem to be able to influence serum trypsinogen 1 levels. Urinary IRT excretion is principally explained by a distrubance in the tubular reabsorption of low molecular weight proteins, such as RNase.

ISSN:0885-3177    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

The usual consumption of calories, fat, protein. and carbohydrate, and the exocrine pancreatic function estimated in duodenal juice after an intravenous injection of secretin and cholecystokinin (CCK), have been studied with the same method and by the same team in Kerala (South India) and in Marseille (France) in apparently normal children (7 Indians, 21 French), in normal adults (23 Indians, 17 French), and in patients presenting with chronic calcifying pancreatitis (8 Indian children, 28 Indian adults. 25 French adults). Although they had a low protein intake (children controls: 32.1 ± 14 g/day (SM), children pancreatitis: 51.1 ± 15, adult controls: 51.3 ± 4.9, adult pancreatitis: 55.7 ± 5.7), the exocrine secretion of Indian controls was not very much modified in comparison with Europeans. Therefore, Indians are less affected by the insufficient diet than the population of Ivory Coast previously studied by the same group. The diet of Indian patients is characterized by a moderately low protein intake and a very low h t intake (18.5 g/day + 2.3 (SM) for children 23.4 g/day ± 2.7 for adult patients). Comparison between different series of patients studied in different countries with the same method suggests that kwashiorkor or cassava consumption have no evident role in the etiology of chronic tropical pancreatitis. The possible role of a low fat diet is suggested and needs further exploration.

ISSN:0885-3177    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

Chemoprevention by a synthetic retinoid. selenium. and these agents in combination during the postinitiation stages of carcinogenesis induced in rats by azaserine was evaluated. Male Lewis rats were given three weekly injections of 30 mg/kg azaserine while being fed a purified diet. One week after completion of carcinogen treatment, groups of rats were switched to the purified diet supplemented with either a retinoid, N-(2-hydroxyethyl)retinamide, at a level of 0.5 or 1 mmol/kg diet, or with 5 ppm sodium selenite, or with a combination of retinoid and selenium. One year after the diet change, the incidence of pancreatic and other neoplasms was determined by autopsy and histologic study. The incidence of pancreatic carcinoma (including carcinoma-in-situ, CIS) among nonretinoid-treated controls was 68%. Since the dietary supplements were fed after completion of exposure to the carcinogen, the effects on both pancreatic and liver carcinogenesis were exerted during the postinitiation phase of carcinogensis. As in previous studies, the retinoid inhibited the progression of pancreatic carcinogenesis in a dose-related fashion. Selenium alone had no effect. However, the combination of retinoid plus selenium was more effective than retinoid alone, although the increase in inhibition was not large. The retinoid was also found to inhibit liver carcinogenesis induced by azaserine. Selenium, either alone or in combination with retinoid, was ineffective. Finally, testicular atrophy, noted as a toxic effect of retinoids in other studies, was not observed in this work.

ISSN:0885-3177    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

The effects of epidermal growth factor (EGF), insulin, and insulinlike growth factor I (IGF-I) were examined alone and in combination on rat pancreatic acinar cells cultured 48 h in serum free medium. IGF-I at a concentration of 2.7 nM maintained viability of cultured acinar cells comparably to EGF. In contrast, insulin was less effective in maintaining acinar viability, even at high concentrations (170nM). There were no additive or interactive effects of these growth factors on acinar viability. EGF significantly increased [3H]- phenylalanine incorporation into acinar protein and the specific activity of phenylalanine-acylated transfer RNA (tRNAphc), but did not change the apparent rate of protein synthesis when compared with insulin or IGF-I. EGF with insulin, IGF-I, or both resulted in significantly lower specific activities of tRNAphewhen compared to EGF alone, but all had comparable rates of total phe-incorporation. Acinar cells readily degraded insulin, but not EGF or IGF-I. These results demonstrate some specificity in the acinar requirement for growth factors (EGF = IGF-I >insulin) in maintaining viability in culture.

ISSN:0885-3177    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

Calcitonin gene-related peptide (CGRP)- and somatostatin (SR1F)-containing cells were identified by immunocytochemical techniques in pancreatic islet cells of the rat. CGRP-containing cells were found primarily in the peripheral portion of the pancreatic islets. In addition, CGRP-containing cells also contained somatostatin, which identifies the islet CGRP-containing cells as D cells. In the present study, we also tested the effect of CGRP on gastrin-releasing peptide (GRP; M)-stimulated release of insulin from isolated rat islets in vitro. At concentrations of 10−8– 10−8M, CGRP inhibited GRP- and CCK-8-stimulated release of insulin significantly when compared with GRP or CCK-8 alone. At the lowest concentration of CGRP (10−8M). the inhibitory effect of CGRP on CCK-8-stimulated release of insulin was statistically significant (p <0.05) and exceptionally potent (65–90% inhibition). We have also found that CGRP does not stimulate the release of SRIF from isolated islet cells. These findings suggest that CGRP may play a regulatory role in the release of insulin.

ISSN:0885-3177    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

Five patients with severe acute pancreatitis had a low contrast enhancement (CE) of the pancreas in computed tomography (CT) and underwent subtotal pancreatectomy. Microangiography and histologic studies were performed on the resected pancreases, and the findings were related to those of CE. All patients had histologically documented hemorrhagic/necrotizing pancreatitis. The more disturbed the vascular anatomy in microangiography, the more hemorrhages and necroses were found in histology. The microangiographic and histologic findings corresponded closely to the low contrast-enhanced CT of the diseased pancreas in each patient. Thus, in the early phase of severe acute pancreatitis, one can detect by noninvasive means which areas of the gland are necrotic and which edematous by a dynamic study of contrastenhanced CT of the pancreas.

ISSN:0885-3177    

出版商:OVID    

年代:1988

数据来源: OVID