| 1. |
- Albrechtsson, Elin, et al.
(författare)
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The expression of retinoic Acid receptors and the effects in vitro by retinoids in human pancreatic cancer cell lines.
- 2002
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Ingår i: Pancreas. - 0885-3177. ; 25:1, s. 49-49
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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. |
- Dahlström, Ulf, 1946-, et al.
(författare)
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Hjärtsvikt hos äldre
- 2001
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Ingår i: Nordisk geriatrik. - 1403-2082. ; 1, s. 30-36
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 5. |
- Kullenberg, Björn, et al.
(författare)
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Transforming growth factor alpha (TGF-alpha) increases cell number in a human pancreatic cancer cell line but not in normal mouse pancreas
- 2000
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Ingår i: International Journal of Pancreatology. - 0169-4197. ; 28:3, s. 199-205
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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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| 6. |
- Lindström, Eva, et al.
(författare)
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Pin within a bile duct stone.
- 2002
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Ingår i: Gastrointestinal Endoscopy. - : Elsevier BV. - 1097-6779 .- 0016-5107. ; 55:7, s. 912-912
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Tidskriftsartikel (refereegranskat)
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| 7. |
- Monstein, Hans-Jurg, et al.
(författare)
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Differential expression of gastrin, cholecystokinin-A and cholecystokinin-B receptor mRNA in human pancreatic cancer cell lines
- 2001
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Ingår i: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 1502-7708 .- 0036-5521. ; 36:7, s. 738-743
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: It has been assumed that gastrin stimulates the growth of pancreatic cancer in an autocrine way through co-expression of gastrin and the cholecystokinin-B receptor (CCK-BR). However, pancreatic cancer cell lines established directly from patients have revealed a great heterogeneity in cell proliferation when exposed to CCK, gastrin and their receptor antagonists. The aim of this study was therefore to examine co-expression of CCK-A and CCK-B receptor (CCK-AR and CCK-BR), and gastrin mRNA as well as the secretion of CCK and gastrin peptides in these cell lines. METHODS: Fourteen cell lines were established from primary pancreatic cancers or their metastases. Total RNA was isolated from the cell lines and reverse-transcribed into single-stranded cDNA. A PCR technique based on Taq polymerase-antibody interaction and CCK-AR, CCK-BR and gastrin-specific primers, followed by Southern blot analysis, were the methods used. The incubation mediums were analysed for the presence of secreted CCK/proCCK and gastrin/progastrin peptides by specific radioimmunoassays (RIA). RESULTS: By means of nested Reverse-Transcribed Polymerase Chain Reaction (nested RT-PCR), combined with Southem blot analysis of the PCR amplified products, CCK-AR and gastrin mRNA co-expression was detected in cell lines LPC-6p and LPC-10m, whereas CCK-BR and gastrin mRNA could be detected in cell lines LPC-8p and LPC-12m. A low level of secreted CCK peptides was detected in cell line LPC-6p, which also expressed CCK-AR mRNA. In no other cases were CCK or gastrin peptides detected in the cell culture mediums. CONCLUSION: The lack of CCK-BR and gastrin mRNA co-expression, and not detectable levels of secreted CCK and gastrin in culture media, does not lend support to the hypothesis that concomitant gene-expression of CCK receptors and gastrin or CCK are essential to maintaining pancreatic cancer cell proliferation.
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| 8. |
- Monstein, Hans-Jurg, et al.
(författare)
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Oxytocin and oxytocin-receptor mRNA expression in the human gastrointestinal tract : A polymerase chain reaction study
- 2004
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Ingår i: Regulatory Peptides. - : Elsevier BV. - 0167-0115 .- 1873-1686. ; 119:1-2, s. 39-44
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Tidskriftsartikel (refereegranskat)abstract
- Background/aim: Oxytocin (OT) has a wide range of effects throughout the body. However, the role of OT on the gastrointestinal (GI) tract has to be settled. So far, the few studies performed reveal no conclusive results. The aim of this study was to examine the expression of OT and OT-receptor mRNA in the human GI tract. Material and methods: Full-thickness biopsies from all segments of the GI tract and the gallbladder were collected during operations at the Department of Surgery, Malmö University Hospital. Biopsies were taken and put immediately into fluid nitrogen and stored at -70°C until total RNA was extracted after mechanical tissue homogenization. Subsequently, poly A + mRNA was isolated from the total RNA extract using an automated nucleic acid extractor and converted into single-stranded cDNA. PCR amplifications were carried out using gene-specific OT and OT-receptor primers. The specificity of the PCR amplicons was further confirmed by Southern blot analyses using gene specific OT and OT-receptor hybridization probes. Results: Expression of OT and OT-receptor mRNA was detected in nearly all segments of the GI tract analyzed. In most of the biopsy specimens analyzed, co-expression of both OT and OT-receptor mRNA appeared to take place. Conclusion: The present study demonstrates that OT and OT-receptor mRNAs are expressed throughout the GI tract. A possible physiological and/or pathophysiological role of OT and OT-receptor expression in the human GI tract and the cellular location of its expression remain to be shown. © 2004 Elsevier B.V. All rights reserved.
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| 9. |
- Ohlsson, Bodil, et al.
(författare)
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Achalasia: A vagal disease
- 2004
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Ingår i: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 1502-7708 .- 0036-5521. ; 39:6, s. 527-530
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Tidskriftsartikel (refereegranskat)abstract
- Background: Achalasia is considered to be a primary motor disorder of the oesophagus. However, there is increasing evidence to suggest extra- oesophageal involvement in this disease. Vagal disturbances at different levels and extra- oesophageal dysmotility have been reported in several studies. The aim of this study was to examine cardiovascular reflexes in patients with achalasia further to evaluate the involvement of the autonomic nervous system outside the oesophagus in this entity. Methods: Five patients ( age range 38 - 58 years, median 45 years) diagnosed with achalasia were assessed for the autonomic nerve function by the heart rate reaction to deep breathing ( E/ I ratio) and to tilt ( acceleration and brake index). The blood pressure reaction to tilt was also assessed. The results were compared with a control group comprising 56 healthy individuals ( age range 16 - 59 years, median 40 years). Results: Patients with achalasia had a significantly decreased E/ I ratio compared with controls ( absolute values 1.13 ( 0.23) ( median value ( interquartile range)) versus 1.38 ( 0.14): P = 0.0309, age corrected values - 1.39 ( 1.49) versus - 0.25 ( 1.20): P = 0.0457). This reflects impairment of the vagus nerve. In contrast, sympathetic nerves were not affected, as the acceleration index and brake index and postural blood pressure reaction were not disturbed in patients. Conclusion: Patients with achalasia have autonomic nerve dysfunction in the vagal nerve outside the oesophagus.
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| 10. |
- Ohlsson, Bodil, et al.
(författare)
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Acute taurodeoxycholate-induced pancreatitis in the rat is associated with hyperCCKemia
- 2000
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Ingår i: International Journal of Pancreatology. - 0169-4197. ; 27:3, s. 195-201
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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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