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Träfflista för sökning "hsv:(MEDICIN OCH HÄLSOVETENSKAP) hsv:(Klinisk medicin) hsv:(Gastroenterologi) srt2:(1990-1999)"

Sökning: hsv:(MEDICIN OCH HÄLSOVETENSKAP) hsv:(Klinisk medicin) hsv:(Gastroenterologi) > (1990-1999)

  • Resultat 41-50 av 58
  • Föregående 1234[5]6Nästa
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41.
  • Ohlsson, Bodil, et al. (författare)
  • The effect of bombesin, cholecystokinin, gastrin, and their antagonists on proliferation of pancreatic cancer cell lines
  • 1999
  • Ingår i: Scandinavian Journal of Gastroenterology. - : Taylor & Francis. - 1502-7708 .- 0036-5521. ; 34:12, s. 1224-1229
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: The role of cholecystokinin (CCK) and gastrin in the development and growth of pancreatic cancer cells is controversial. The aim of this study was to evaluate the role of CCK-8S, gastrin-17, bombesin, and their antagonists on cell lines from patients with pancreatic cancer. METHODS: Cell lines were established from pancreatic cancers operated on at our department. The cells were grown in 10% fetal calf serum (FCS). The effects of CCK-8S, gastrin-17, bombesin, and their antagonists in different concentrations and for different time intervals were studied. The cell number was evaluated with the XTT method. RESULTS: The cell line LN 36 responded with increased cell number to stimulation by gastrin-17 and decreased cell number to inhibition by the CCK-B receptor antagonist L-365,260. In contrast, LPC 1 responded with increased cell number to CCK-8S and decreased cell number to the CCK-A receptor antagonist devazepide. LPC 2, 6, and 7 were stimulated by CCK-8S, gastrin-17, and their antagonists. LPC 3 showed decreased cell number after inhibition by the antagonists, and LPC 5 and 10 showed increased cell number after stimulation by CCK-8S and gastrin-17. LPC 4 was stimulated by CCK-8S, and LPC 8 was stimulated by all substances except gastrin-17. Intermittent administration of the substances to LN 36 led to a greater effect on the cell number than administration every day, which was not the case with LPC 1 and LPC 3. Bombesin led to an increased growth in LPC 5 but not in LPC 3. CONCLUSION: CCK-8S and gastrin-17 led to an increased cell number in some cell lines. A blockade of the CCK-A and CCK-B receptors by their antagonists led to an increased, an unaffected, or a decreased cell number of the cell lines. The effect of bombesin on different cell lines also varied. This shows a great heterogenicity among pancreatic cancer cells from different patients.
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42.
  • Olsson, Rolf, et al. (författare)
  • Estrogen-progestogen therapy for low bone mineral density in primary biliary cirrhosis
  • 1999
  • Ingår i: Liver. - : Wiley-Blackwell. - 0106-9543. ; 19:3, s. 188-192
  • Tidskriftsartikel (refereegranskat)abstract
    • AIMS/BACKGROUND: Patients with primary biliary cirrhosis (PBC) often have osteoporosis of the high-turnover type, suggesting that estrogen could have a beneficial effect. However, the cholestatic potential of estrogen could imply a risk of increased cholestasis in a disease characterized by cholestasis. The aim of the present study was to test whether hormone replacement therapy (HRT) could be used to increase bone mineral density (BMD) in PBC patients with osteoporosis, without causing deterioration of the liver function. METHODS: Nine female PBC patients with osteoporosis and one with osteopenia were offered HRT for two years. The change in BMD was compared to the change in ten age-matched female PBC patients who had less severe or no osteopenia and who did not receive HRT. Liver function tests were checked at six-month intervals. RESULTS: HRT patients showed a statistically significant increase in lumbar spine BMD and total body BMD whereas control patients showed a significant decrease in lumbar and total body BMD. In contrast to the controls, HRT patients also showed a decrease in truncal fat (-3.8%). Neither of the groups showed any statistically significant changes in the liver function tests. CONCLUSIONS: HRT is safe and effective in female PBC patients with osteoporosis.
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43.
  • Pettersson, Anna, et al. (författare)
  • HLA genotypes in coeliac disease and healthy individuals carrying gliadin antibodies
  • 1993
  • Ingår i: European Journal of Gastroenterology and Hepatology. - : Lippincott Williams & Wilkins. - 0954-691X. ; 5:6, s. 445-450
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: Coeliac disease is closely associated with the presence of gliadin antibodies and certain HLA class II alleles. The aim of this study was to compare the HLA genotype in gliadin antibody-positive individuals without coeliac disease with that in patients with clinically verified coeliac disease.Design: HLA genotyping was carried out in 65 patients with coeliac disease and the results were compared with those from 19 gliadin antibody-positive and 96 antibody-negative healthy blood donors.Methods: Immunoglobulin G and A gliadin antibodies were measured with a micro-enzyme-linked immunosorbent assay technique. Restriction fragment length polymorphism typing for determination of HLA was carried out by means of Southern blot analysis of restriction digests.Results: Coeliac disease was significantly correlated with the presence of HLA-DR3 and DQ2, whereas DQ1, DQ7, DR1, DR4 and DR5 were all under-represented in coeliac disease patients. Of the extended haplotypes, only DR3-DQ2 was associated with the disease, while DR1-DQ1, DR4-DQ7 and DR5-DQ7 were under-represented. The correlation between DR3-DQ2 and coeliac disease depended on homozygosity; 29% of the patients and 4% of the controls were homozygous for DQ2 compared with 18 and 1%, respectively, for DR3. Only five out of 19 of the gliadin antibody-positive healthy blood donors had HLA genotypes characteristic of coeliac disease, while 15 were DQ1-positive which would be expected to confer protection.Conclusion: These findings suggest that the presence or development of gliadin antibodies is independent of the HLA genotype.
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44.
  • Raab, Y, et al. (författare)
  • A technique for segmental rectal and colonic perfusion in humans.
  • 1992
  • Ingår i: American Journal of Gastroenterology. - 0002-9270 .- 1572-0241. ; 87:10, s. 1453-9
  • Tidskriftsartikel (refereegranskat)abstract
    • To enable a better characterization of pathophysiologic processes in colon and rectum, we have developed a perfusion technique for collection of soluble substances and cells from standardized intestinal segments. A tube with balloons attached to its outer wall was endoscopically introduced into the rectum and sigmoid colon, and its position ascertained fluoroscopically. The balloons delimited two segments, one in the sigmoid colon and one in the rectum. The segments were simultaneously perfused by a buffer at 37 degrees C. After a 30-min rinsing period, perfusate and cells were collected at 20-min intervals. Of 51 attempted perfusions, 45 were successfully completed. Recovered volumes equaled those infused. Leakage from the proximal intestine to the segments was negligible. In 18 healthy volunteers, the mean perfusate concentration from the rectal segment was 57.5 (27.5-120.2) mg/L for albumin, 1.3 (1.0-1.7) micrograms/L for eosinophil cationic protein, 5.1 (2.8-9.5) ng/L for prostaglandin E2, and 61.7 (41.7-89.1) micrograms/L for hyaluronan, and all values were lower in the sigmoid segment. Steady state conditions were achieved from the second perfusion period. The perfusate contained 4-80 x 10(4) cells, more than 95% of which were epithelial cells. The technique is safe, has a good subject compliance, and seems to be a valuable tool in investigations on quantitative release of soluble substances and cells in, e.g., colorectal inflammation.
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45.
  • Raab, Y, et al. (författare)
  • Enhanced intestinal synthesis of interleukin-6 is related to the disease severity and activity in ulcerative colitis.
  • 1994
  • Ingår i: Digestion. - 0012-2823 .- 1421-9867. ; 55:1, s. 44-9
  • Tidskriftsartikel (refereegranskat)abstract
    • The concentration of interleukin-6 (IL-6) was measured in the perfusion fluid from investigated rectal and sigmoid segments in patients with ulcerative colitis (UC). The colorectal release of this substance from segments with active inflammation was greatly increased compared with that found in healthy controls and correlated to the mucosal damage defined by plasma protein leakage and endoscopic findings. The perfusate/serum ratio of IL-6 was significantly higher than the corresponding ratio of albumin, indicating that the increased amount of IL-6 detected in the perfusion fluid was synthesized in the inflamed colorectal mucosa. A strong correlation between the concentrations of IL-6 and of tumor necrosis factor-alpha in perfusion fluid suggests that macrophages/monocytes are cells of importance in the stimulated local synthesis of IL-6. The calculated total colorectal release of IL-6 was significantly correlated to the serum concentrations of C-reactive protein and alpha 1-antitrypsin, demonstrating that the acute phase response in patients with UC reflects the amount of locally produced IL-6.
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46.
  • Raab, Y, et al. (författare)
  • Eosinophil activation in ulcerative colitis : studies on mucosal release and localization of eosinophil granule constituents.
  • 1998
  • Ingår i: Digestive Diseases and Sciences. - 0163-2116 .- 1573-2568. ; 43:5, s. 1061-70
  • Tidskriftsartikel (refereegranskat)abstract
    • Activation of eosinophil granulocytes (eosinophils) seems to contribute to the pathophysiology of several inflammatory conditions. This process was evaluated in 18 patients with ulcerative colitis and in 18 healthy controls using intraluminal segmental perfusion of the sigmoid colon and rectum and immunoanalysis for eosinophil cationic protein (ECP) in the perfusate. Immunohistochemistry for eosinophils and neutrophils was made in simultaneously taken biopsies and in biopsies from surgical specimens taken from additional 10 patients. The mucosal release of ECP was increased severalfold in patients with UC. The bowel biopsies demonstrated a lamina propria infiltrated with eosinophils. The degree of eosinophil activation/degranulation was related to the intensity of the inflammatory reaction. Activated eosinophils and extracellular deposits of ECP were, in particular, seen in crypt abscesses and in areas with damaged surface epithelium. Since ECP is highly cytotoxic, its release at the site of inflammatory bowel lesions might reflect a potential pathophysiological mechanism.
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47.
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48.
  • Raab, Y, et al. (författare)
  • Neutrophil mucosal involvement is accompanied by enhanced local production of interleukin-8 in ulcerative colitis.
  • 1993
  • Ingår i: Gut. - 0017-5749 .- 1468-3288. ; 34:9, s. 1203-6
  • Tidskriftsartikel (refereegranskat)abstract
    • The concentration of myeloperoxidase, a neutrophil granule constituent, was measured in the perfusion fluid from sigmoid and rectal segments in patients with ulcerative colitis. The concentrations of myeloperoxidase were increased severalfold in the patients with ulcerative colitis compared with healthy controls pointing to an enhanced neutrophil activity. The release of myeloperoxidase correlated to an enhanced local release of the neutrophil activating peptide interleukin-8 (IL-8). Increased values of tumour necrosis factor (TNF-alpha) were also found during intestinal perfusion of the patients and correlated with those of IL-8. The results obtained are compatible with the hypothesis that local mucosal recruitment/activation of neutrophils in ulcerative colitis is mediated by an enhanced IL-8 synthesis. TNF-alpha may be one relevant factor as a stimulus to IL-8 synthesis.
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49.
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50.
  • Shev, S, et al. (författare)
  • The importance of cofactors in the histologic progression of minimal and mild chronic hepatitis C
  • 1997
  • Ingår i: Liver. - : Wiley-Blackwell. - 0106-9543. ; 17:5, s. 215-223
  • Tidskriftsartikel (refereegranskat)abstract
    • A follow-up liver biopsy was done 9-16 years (mean 12 years) after initial biopsy in 20 untreated Swedish patients infected with hepatitis C (8 men, 12 women; mean age 30 years at initial biopsy) in whom first biopsy had been classified as chronic persistent hepatitis. A significant progression of liver damage was found when using Histology Activity Index (HAI) scoring according to Knodell (p=0.006 for total HAI score; p=0.03 for grading, i.e., sum of HAI components 1, 2, and 3; p=0.01 for staging, i.e., HAI component 4, fibrosis). Fourteen of 20 (70%) patients had increased while 6 had decreased or unchanged HAI scores on follow-up biopsy. Occasional heavy alcohol drinkers (n=6) had an increased follow-up HAI score as compared with nondrinkers (p<0.05). Eight of 14 who deteriorated on follow-up versus 0 of 6 with improved or unchanged liver histology were anti-HBc positive (p=0.04). There was no significant correlation between HCV genotype and prognosis; however, the only two patients with liver cirrhosis on follow-up had genotype 1b. In conclusion, most patients with minimal or mild chronic hepatitis C in the present study had histologic progression on the latest biopsy. Cofactors such as alcohol abuse and exposure to hepatitis B may have a greater influence than HCV alone in determining the rate of deterioration of liver disease.
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