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  • 1
    Electronic Resource
    Electronic Resource
    11β hydroxysteroid dehydrogenase type 2 enzyme is expressed in normotensive and hypertensive patients with renal disease (1998)
    Oxford, UK : Blackwell Publishing Ltd
    Nephrology 4 (1998), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: SUMMARY: The enzyme 11β hydroxysteroid dehydrogenase type 2 (11βHSD2) converts glucocorticoids to their 11-keto metabolites, permitting binding of aldosterone to the non-selective mineralocorticoid receptor. Recent studies have suggested that 11βHSD deficiency may be implicated in essential hypertension and renal disease. Using an antibody against a peptide deduced from the cDNA sequence, the renal expression of 11βHSD2 was examined in patients with advanced stages of renal disease and associated hypertension, patients with primary hypertension resulting in renal damage, and patients with preserved or mildly damaged renal architecture without concomitant hypertension. Despite variable degrees of tubulointerstitial damage, 11βHSD2 was expressed in distal convoluted tubules and collecting ducts in all patient groups. Collapsed tubules retained strong immunoreactivity, but decreased staining was apparent in dilated tubules. There was weak staining of the thick ascending limb of Henle. Variable glomerular expression of 11βHSD2 was observed. Our results therefore suggest that absence of renal 11βHSD2 is not a prominent feature of hypertensive nephrosclerosis, or primary renal disease associated with hypertension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1797.1998.tb00325.x
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    11β hydroxysteroid dehydrogenase type 2 enzyme is expressed in normotensive and hypertensive patients with renal disease (1998)
    Oxford, UK : Blackwell Science Ltd
    Nephrology 4 (1998), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The enzyme 11β hydroxysteroid dehydrogenase type 2 (11βHSD2) converts glucocorticoids to their 11-keto metabolites, permitting binding of aldosterone to the non-selective mineralocorticoid receptor. Recent studies have suggested that 11βHSD deficiency may be implicated in essential hypertension and renal disease. Using an antibody against a peptide deduced from the cDNA sequence, the renal expression of 11βHSD2 was examined in patients with advanced stages of renal disease and associated hypertension, patients with primary hypertension resulting in renal damage, and patients with preserved or mildly damaged renal architecture without concomitant hypertension. Despite variable degrees of tubulointerstitial damage, 11βHSD2 was expressed in distal convoluted tubules and collecting ducts in all patient groups. Collapsed tubules retained strong immunoreactivity, but decreased staining was apparent in dilated tubules. There was weak staining of the thick ascending limb of Henle. Variable glomerular expression of 11βHSD2 was observed. Our results therefore suggest that absence of renal 11βHSD2 is not a prominent feature of hypertensive nephrosclerosis, or primary renal disease associated with hypertension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1797.1998.d01-19.x
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    VASCULAR LOCALIZATION OF THE 11β-HYDROXYSTEROID DEHYDROGENASE TYPE II ENZYME (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 23 (1996), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The enzyme 11β-hydroxysteroid dehydrogenase type II (11βHSD2) confers specificity on the non-specific mineralocorticoid receptor by converting cortisol to cortisone.2. We have examined the localization of this enzyme in the human skin, myocardium and saphenous vein by immuno-histochemical techniques.3. High amounts of 11βHSD2 immunoreactivity were found in smooth muscle cells in the arterioles of the skin, heart and saphenous vein. Lower amounts of staining were also found in longitudinal and concentric smooth muscle cells lining the lumen of the saphenous vein.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1996.tb02776.x
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  • 4
    Electronic Resource
    Electronic Resource
    Development of injury in a rat model of chronic renal allograft rejection: effect of dietary protein restriction (1999)
    Springer
    Transplant international 12 (1999), S. 18-26 
    Details
    ISSN: 1432-2277
    Keywords: Key words Renal transplantation ; chronic rejection ; dietary protein restriction ; Dietary protein restriction ; chronic rejection ; renal transplantation ; Chronic rejection ; dietary protein restriction ; renal transplantation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Non-allogeneic factors such as increased nephron “workload” may contribute to chronic renal allograft rejection. Reducing dietary protein from 20 % to 8 % was tested in a model of chronic rejection: Dark Agouti kidney to Albino Surgery recipient, “tolerised” by previous donor blood transfusions. Survival, weight gain, serum creatinine concentration and creatinine clearance were similar for both groups at all times. Urinary protein was significantly (P 〈 0.05) lower in the low-protein (LP) group 1 month after transplantation. After 3 and 6 months, both groups demonstrated mild chronic rejection. After 6 months, tubular atrophy was significantly (P 〈 0.05) less in the LP group and interstitial fibrosis was marginally reduced. Glomerular hypertrophy, glomerular sclerosis, tubular dilatation, leucocyte infiltration, adhesion molecule expression and TGF-β 1 mRNA expression were similarly increased in both groups. Thus, reducing dietary protein to 8 % lowered urinary protein, but did not significantly affect the development of chronic rejection in renal allografts beyond affording a degree of protection from tubulointerstitial damage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001470050180
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  • 5
    Electronic Resource
    Electronic Resource
    Increased expression of basic fibroblast growth factor during chronic rejection in intestinal transplants is associated with macrophage infiltrates (1999)
    Springer
    Transplant international 12 (1999), S. 42-49 
    Details
    ISSN: 1432-2277
    Keywords: Key words Basic fibroblast growth factor ; chronic rejection ; small bowel transplantation ; Small bowel transplantation ; macrophage infiltration ; chronic rejection ; Chronic rejection ; small bowel transplantation ; basic fibroplast growth factor ; Macrophage infiltration ; chronic rejection ; small bowel transplantation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Long-term survival of intestinal transplants is hampered by chronic rejection (CR). Since transplants with CR demonstrate fibrotic changes, the cytokine basic fibroblast growth factor (bFGF) may be involved in the tissue remodelling of chronic intestinal rejection. The aim of this study was to investigate the bFGF gene and protein expression and distribution in chronically rejecting intestinal allografts. Orthotopic small bowel transplantation was performed in the allogeneic DA-to-AS rat combination. Cyclosporin was administered temporarily to prevent acute rejection. Controls were DA isografts and normal DA. bFGF gene expression was evaluated using reverse transcriptase polymerase chain reaction (RT-PCR) of the ileum RNA and was standardized against Glyceraldehyde-3-phosphate-dehydrogenase (GAPDH) expression. bFGF protein was determined using immunohistochemistry. To identify the bFGF-positive cell type, sequential sections were stained for cell markers. Allografts showed histological features of CR, whereas isografts preserved normal architecture. bFGF gene expression was present in normal ileum and significantly upregulated in allografts. Immunohistochemical staining showed a significant increase in bFGF protein compared to isografts. Most bFGF-positive cells were localized in the submucosa and muscularis, particularly around the neural plexus. bFGF-positive cells appeared to be ED-2-positive macrophages, strongly suggesting that the site of bFGF production is the activated macrophage. This study demonstrates increased bFGF mRNA and protein in chronically rejecting intestinal allografts that appear to be produced by macrophages.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001470050183
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  • 6
    Electronic Resource
    Electronic Resource
    EGF and TGF-β1 Gene Expression in Chronically Rejecting Small Bowel Transplants (1999)
    Springer
    Digestive diseases and sciences 44 (1999), S. 1117-1123 
    Details
    ISSN: 1573-2568
    Keywords: EPIDERMAL GROWTH FACTOR ; TRANSFORMING GROWTHFACTOR-β1 ; CHRONIC REJECTION ; SMALL BOWEL ; TRANSPLANTATION
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Long-term survival of small bowel transplants ishampered by chronic rejection. Epidermal growth factor(EGF) and transforming growth factor β (TGF-β)have opposing, regulatory roles in normal intestinal physiology and may be involved in thepathogenesis of chronic intestinal rejection. Our aimwas to investigate the expression of EGF andTGF-β1 in chronically rejecting smallbowel transplants. Orthotopic small bowel transplantation was performed inthe allogeneic DA-to-AS rat combination; Cyclosporin wasadministered temporarily to prevent acute rejection.Controls were DA isografts and normal DA rats. PreproEGF and TGF-β1 geneexpression was evaluated by northern blot analysis ofthe ileum RNA and standardized againstglyceraldehyde-3-phosphate-dehydrogenase expression.Allografts demonstrated functional impairment and histological features of chronicrejection, whereas isografts appeared normal. Allograftsdemonstrated a significant reduction of EGF mRNA whencompared to DA isografts. No significant changes were detected in TGF-β1expression in either allogeneic or syngeneic grafts. Inconclusion, this study demonstrates reduced preproEGFand preserved TGF-β1 gene expression inchronically rejecting small bowel transplants.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026659720191
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