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Träfflista för sökning "WFRF:(Ohlsson Bodil) ;pers:(Axelson Jan)"

Sökning: WFRF:(Ohlsson Bodil) > Axelson Jan

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1.
  • Albrechtsson, Elin, et al. (författare)
  • The expression of retinoic Acid receptors and the effects in vitro by retinoids in human pancreatic cancer cell lines.
  • 2002
  • Ingår i: Pancreas. - 0885-3177. ; 25:1, s. 49-49
  • Tidskriftsartikel (refereegranskat)abstract
    • INTRODUCTION: Analogues of vitamin A have been shown to influence growth of malignant tissue, such as pancreatic cancer. AIMS: To study the expression of retinoic acid receptors (RAR) in pancreatic cancer cells and the effect of three different retinoids on the cell number in vitro were studied. METHODOLOGY: Cell lines were established from 13 patients who underwent surgery for pancreatic adenocarcinoma. The expression of the retinoic acid receptors (RAR) and retinoic X receptor (RXR) subtypes (alpha, beta, and gamma) was studied with western blotting and specific antibodies. The effect of incubation with all-trans-retinoic acid (atRA; tretinoin), 9-cis-retinoic acid (9-cis-RA), and 13-cis-retinoic acid (13-cis-RA; isotretinoin) on the cell number was examined with use of a Roche XTT cell proliferation kit. RESULTS: The RXRalpha receptor was expressed in all cell lines. RARalpha,beta and RXRbeta were expressed in most of them. RXRgamma was expressed in about half of the cell lines and RARgamma in only one. Incubation of the cells with retinoids showed a decreased cell number at concentrations of 104 M, except for 9-cis-RA, to which only about half of the cell lines responded. CONCLUSION: Two or more of the RAR subtypes were expressed in each pancreatic cell line. There was no uniform pattern of receptor expression; however, the cell lines responded with decreased cell number to high concentrations of atRA and 13-cis-RA but not to 9-cis-RA.
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4.
  • Axelson, Jan, et al. (författare)
  • The changes in the rat parotid glands following total parenteral nutrition and pancreatico-biliary diversion are not mediated by cholecystokinin
  • 1996
  • Ingår i: International Journal of Pancreatology. - 0169-4197. ; 20:2, s. 109-118
  • Tidskriftsartikel (refereegranskat)abstract
    • CONCLUSIONS: The results of the present study suggest that the pancreas and parotid glands both respond with hypoplasia during absence of food in the digestive tract and with hyperplasia following pancreatico-biliary diversion (PBD). Factors other than cholecystokinin (CCK) are, however, involved in the effects on the parotid glands, since infusion of CCK-8S and devazepide was without influence. BACKGROUND AND AIM: Total parenteral nutrition (TPN) causes reduced pancreatic weight, whereas PBD evokes hyperCCKemia and enlargement of the rat pancreas. The pancreas and parotid glands have in part similar morphology and function. Therefore, we studied the possible presence of alterations also in the parotid glands during TPN, after PBD and during infusion of sulfated cholecystokinin (CCK-8S) and the CCK-A receptor antagonist devazepide, respectively. MATERIALS AND RESULTS: Rats either received TPN for 7 d, or were kept under otherwise identical conditions with free access to food and water. TPN markedly reduced both pancreatic and parotid wet weight and thereby also the protein and amylase contents, and pancreatic DNA content was decreased. There was a significant correlation between the pancreas and parotid glands when comparing these parameters. The concentration of plasma CCK was unaffected by TPN. PBD caused a sevenfold increase in plasma CCK and a three fold increase in the pancreatic weight compared to control rats 28 d after the operation. The protein and DNA contents in the pancreas were found to be increased. The parotid glands increased twofold in weight, but their protein and amylase contents were not affected. There was a significant correlation between the pancreas and parotid glands when comparing weight, and protein and amylase concentrations. Infusion of CCK-8S during 28 d caused a marked increase in pancreatic wet wt and protein and DNA contents. The CCK-A receptor antagonist devazepide induced a reduction in protein and DNA contents in the pancreas. The parotid glands were not affected by either treatment. No effect on the labeling index of serous and ductal cells of the parotid gland was seen at 36 h, 3, 7, and 28 d of infusion with CCK-8S or devazepide.
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5.
  • Hjalmarsson, Claes, et al. (författare)
  • Does Epidermal Growth Factor Participate in the Regulation of Glucose, Insulin and Glucagon Levels?
  • 2006
  • Ingår i: European Surgical Research. - : S. Karger AG. - 0014-312X .- 1421-9921. ; 38:4, s. 377-384
  • Tidskriftsartikel (refereegranskat)abstract
    • <i>Background/Aims:</i> The presence of receptors for epidermal growth factor (EGF) on β cells in the rat pancreatic islets has been established, but the physiological role remains to be settled. The aim of the present study was to evaluate the effect of EGF on glucose homeostasis. <i>Methods:</i> Fasted rats were treated with intraperitoneal injections of 10, 40 or 80 µg/kg body weight, either with EGF or 1% bovine serum albumin (controls). In a second experiment, fasted rats received an intraperitoneal injection of 1 mg glucose/kg body weight, followed by an injection of EGF or bovine serum albumin. Blood was drawn before the injections and at different time points afterwards. The plasma concentrations of glucose, insulin and glucagon were measured. <i>Results:</i>A modest elevation of the concentrations of glucose and insulin in plasma during the study was found in fasted rats in experiment 1. The increase in insulin concentration was attenuated by EGF, but after glucose injection this effect was reversed. Plasma glucagon levels were dose-dependently elevated by EGF and increased instead of decreased after glucose injection. <i>Conclusion:</i> Our data suggest that EGF might play an important role in the regulation of glucagon secretion by preventing the lowering effect of glucose on plasma glucagon levels.
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6.
  • Kullenberg, Björn, et al. (författare)
  • Transforming growth factor alpha (TGF-alpha) increases cell number in a human pancreatic cancer cell line but not in normal mouse pancreas
  • 2000
  • Ingår i: International Journal of Pancreatology. - 0169-4197. ; 28:3, s. 199-205
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: The pancreas harbors growth factors such as the epidermal growth factor (EGF) family. The physiological and pathophysiological roles of growth factors in normal pancreas remain unsettled. Human pancreatic cancer overexpresses the EGF receptor, and the ligands EGF and transforming growth factor alpha (TGF-alpha). The aim of the present experiments was to study the effect of TGF-alpha in a pancreatic cancer cell line and in normal mouse pancreas. METHOD: The LN-36 cell line, established from a pancreatic duct cell adenocarcinoma, was incubated with TGF-alpha or EGF. The effect of an EGF receptor-specific, tyrosine kinase inhibitor (tyrphostin B56) with or without growth factors was also studied. The cell number was measured with the XTT-colorimetric method. TGF-alpha, the tyrphostins A25, B48, and B56, were in separate experiments infused during 1 wk to normal female mice by subcutaneous (sc) minipumps. RESULTS: The LN-36 cell line responded to TGF-alpha and EGF with increased cell number; +61% with 10(-10) M TGF-alpha and +34% with 10(-9) M EGF. Tyrphostin B56 at a concentration of 10(-5) M reduced the cell number by 76%, but when incubated together with growth factors the reduction was only 44% with TGF-alpha, and 39% with EGF. Infusion of TGF-alpha increased mouse pancreatic wet weight and protein content but was without effect on DNA synthesis, measured as incorporation of tritiated thymidine. Infusion of three different tyrphostins did not influence mice pancreas. CONCLUSION: The results support the role of TGF-alpha to maintain growth of pancreatic cancer cells by the EGF receptor. Infusion of TGF-alpha induced hypertrophy in normal mouse pancreas.
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7.
  • Ohlsson, Bodil, et al. (författare)
  • Acute taurodeoxycholate-induced pancreatitis in the rat is associated with hyperCCKemia
  • 2000
  • Ingår i: International Journal of Pancreatology. - 0169-4197. ; 27:3, s. 195-201
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Cholecystokinin (CCK) has been suggested to be involved in the development and course of acute pancreatitis. In the present study we measured plasma CCK concentrations in acute experimental pancreatitis (AEP) in the rat, and evaluated the role of circulating CCK levels on the initial pancreatic damage in pancreatitis. METHODS: Endogenous hyperCCKemia was induced by surgical biliodigestive shunt (BDS) and exogenous hyperCCKemia by infusion of CCK-8S. The CCK-A receptor antagonist devazepide was used to antagonize the effect of CCK. Pancreatitis was induced by pancreatic duct infusion of sodium taurodeoxycholate 4 wk after the BDS operation or 1 wk after the start of the infusions. Nonpancreatitic sham- and BDS-operated rats, respectively, were used as control animals as were groups of otherwise untreated rats with pancreatitis. The animals were sacrificed 6 h after induction of pancreatitis. Concentrations of CCK were determined in plasma as were protein and amylase levels in the pancreas and peritoneal exudates. The extent of pancreatic necroses was assessed microscopically. RESULTS: Pancreatitis caused an 11-20-fold increase of circulating CCK as measured after 6 h. In pancreatitic rats with induced hyperCCKemia, there was a further marked increase of plasma CCK. Pancreatic weight and edema, protein and amylase contents, and extent of necroses were the same regardless of the level of plasma CCK. Devazepide had no influence on the studied pancreatic parameters. CONCLUSION: We conclude that acute taurodeoxycholate-induced pancreatitis in the rat is associated with elevated plasma CCK concentrations. There seems, however, not to be any correlation between the degree of hyperCCKemia and the extent of initial pancreatic damage.
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8.
  • Ohlsson, Bodil, et al. (författare)
  • An evaluation of the influence of devazepide and CCK-8S on the intact and resected rat liver
  • 1998
  • Ingår i: European Surgical Research. - : S. Karger AG. - 0014-312X .- 1421-9921. ; 30:6, s. 378-384
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Recently, it has been shown that infusion of the CCK-A receptor antagonist devazepide induced proliferation of hepatocytes and bile duct epithelium in the rat liver. The aim of this study was to further evaluate the influence of devazepide and sulfated cholecystokinin-8 (CCK-8S) on the intact rat liver and rat liver after resection. METHODS: In the first experiment, either saline or devazepide was injected subcutaneously twice daily to rats for 18 and 36 h and 3 and 7 days. In the second experiment, a 70% liver resection was followed by infusion of either DMSO, devazepide, saline or CCK-8S for 2 or 7 days. Prior to sacrifice, all rats received 1 mCi/kg of tritiated thymidine intraperitoneally. The liver was excised and the contents of protein, DNA and water and incorporation of tritiated thymidine were measured. RESULTS: Intermittent injections of devazepide increased the liver protein content after 36 h, followed by a decrease after 7 days. The weight, DNA content or cell proliferation was not affected. Two days after liver resection hyperCCKemia was evoked, which was less prominent after 7 days. Devazepide lowered the plasma concentration of CCK, while the infusion of CCK-8S resulted in extremely high concentrations at both time points. The DNA synthesis measured by thymidine incorporation was increased by devazepide on day 2, whereas the weight or protein and DNA contents of the liver were not influenced. CCK-8S infusion decreased the body and liver weight throughout the study, and the protein and DNA contents after 7 days. CONCLUSIONS: Intermittent devazepide treatment did not affect the intact liver. Devazepide increased the DNA synthesis 2 days after liver resection but was without other influences on the liver regeneration. CCK-8S induced decreased body weight with ensuing negative effects on the liver regeneration. Neither devazepide nor CCK seem to be of any therapeutic use after liver resection or liver failure.
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9.
  • Ohlsson, Bodil, et al. (författare)
  • Biliodigestive shunt evokes hyperCCKemia and trophic effects in the rat pancreas, but not in the liver or gastrointestinal tract
  • 1997
  • Ingår i: Pancreas. - 0885-3177. ; 14:3, s. 255-261
  • Tidskriftsartikel (refereegranskat)abstract
    • The influence of bile on the release of cholecystokinin (CCK) and, thereby, on the regulation of exocrine pancreatic function and growth is unsettled. The aim of this study was to elucidate the effect of long-term diversion of bile from the upper small intestine on CCK release and on the pancreas, liver, and gastrointestinal tract. A surgical biliodigestive shunt was performed in rats, diverting the bile flow directly to the middle of the small intestine. The animals were killed after 4 or 12 weeks. Plasma CCK and trophic effects on the pancreas, liver, and gastrointestinal tract were determined, as were the trypsin and chymotrypsin contents in the intestine. The CCK concentration in plasma increased 10-fold at both time points studied. The pancreas doubled its weight from 4 weeks onward. Also, pancreatic protein, DNA, and amylase contents were increased throughout the study. The liver and gastrointestinal tract were unaffected. Intraluminal bile plays a role in the feedback regulation of CCK release and is involved in this way in the control of pancreatic growth but has no similar effects on the liver or gastrointestinal tract.
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10.
  • Ohlsson, Bodil, et al. (författare)
  • Devazepide-induced hyperplasia in the rat liver and bile ducts
  • 1996
  • Ingår i: European Surgical Research. - : S. Karger AG. - 0014-312X .- 1421-9921. ; 28:4, s. 299-305
  • Tidskriftsartikel (refereegranskat)abstract
    • Cholecystokinin (CCK) is a potent stimulus of pancreatic enzyme secretion and growth and is known to influence the flow of biliary secretions. It has also been suggested as a trophic stimulus of the biliary tract and liver, but confirmatory studies are lacking. The aim of the present experiment was to study the effects on the rat liver and biliary tract of long-term stimulation of CCK-8S and the CCK-A receptor antagonist devazepide, respectively. Sprague-Dawley male rats had an infusion of sulfated CCK-8, devazepide or sodium chloride by subcutaneously implanted osmotic minipumps. The animals were sacrified 36 h and 3, 7 or 28 days after the start of infusion, and all had an injection of tritiated thymidine (1 mCi/kg) intraperitoneally 1 h prior to death. The liver was dissected out, weighed and processed for its content of protein, DNA and water. After autoradiography, histologic samples were examined for labeled hepatocytes and bile duct epithelium. Devazepide caused an increase in liver protein content from 36 h on. After 3 days labeling index of hepatocytes and liver DNA concentration were increased. On day 7, induced cell proliferation was also seen in the bile duct epithelium, and the increase in liver DNA content and concentration was now more pronounced and persisted throughout the study. After 28 days devazepide also induced increased crude and relative liver weight. A transient reduction in liver weight and liver protein content and concentration was seen after 7 days of CCK-8S infusion. There were no changes of the labeling index of hepatocytes or bile duct epithelial cells or in liver DNA content in the rats receiving CCK-8S infusion. Devazepide induced hyperplastic changes in both the liver and the biliary tract, probably by interfering with the bile secretion, whereas CCK-8S did not exert any similar effects. The results do not support CCK as a hepatotrophic factor.
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