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glomerulonephritis/dl prolin
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Seite 1 von 22 Ergebnisse
L-arginine metabolism in immune-mediated glomerulonephritis in the rat.
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Low-protein diets slow the progression of some renal diseases. We recently found that dietary restriction of L-arginine markedly ameliorates disease in antithymocyte serum-induced glomerulonephritis in the rat, suggesting that L-arginine may play a key role in the beneficial effects of low-protein
NO mediates antifibrotic actions of L-arginine supplementation following induction of anti-thy1 glomerulonephritis.
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NO mediates antifibrotic actions of L-arginine supplementation following induction of anti-thy1 glomerulonephritis.
BACKGROUND
L-Arginine plays a complex role in renal matrix expansion, involving endogenous metabolism into nitric oxide (NO), polyamines, L-proline and agmatine. Supplementing dietary
N-acetyl-seryl-aspartyl-lysyl-proline ameliorates the progression of renal dysfunction and fibrosis in WKY rats with established anti-glomerular basement membrane nephritis.
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N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), which is hydrolyzed by angiotensin-converting enzyme, is a natural regulator of hematopoiesis. Here it is shown that Ac-SDKP inhibits TGF-beta action in mesangial cells. Because TGF-beta is thought to play a pivotal role in the development and
Tranilast ameliorates experimental mesangial proliferative glomerulonephritis.
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BACKGROUND
Immunoglobulin A nephropathy and its related animal model Thy1.1 nephritis are characterized by mesangial hypercellularity, extracellular matrix expansion and overexpression of the proproliferative and profibrotic growth factors, platelet-derived growth factor (PDGF) and transforming
Protein kinase C β inhibition ameliorates experimental mesangial proliferative glomerulonephritis.
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OBJECTIVE
Activation of protein kinase C (PKC) has been implicated in the pathogenesis of diabetic nephropathy where therapy targeting the β isoform of this enzyme has been examined. However, PKC-β is also increased in various forms of human glomerulonephritis, including IgA nephropathy.
A novel mutation in the complement regulator clusterin in recurrent hemolytic uremic syndrome.
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A novel heterozygous mutation in the clusterin gene, nucleotide position A1298C (glutamine>proline Q433P), was detected in exon 7 of a child with recurrent hemolytic uremic syndrome (HUS). The same mutation was found in the child's two siblings and mother but not in 120 controls. In addition, a
Calcium channel blockers inhibit proliferation and matrix production in rat mesangial cells: possible mechanism of suppression of AP-1 and CREB activities.
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BACKGROUND
Calcium channel blockers (CCBs) are reported to attenuate the loss of renal function in various glomerulonephritides.
METHODS
To determine the mechanism of action of these drugs, we investigated the effects of CCBs on cell proliferation and extracellular matrix (ECM) production in
[A case of pseudohypercreatininemia in a patient suffering from macroglobulinemia].
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A 56-year-old man with chronic hepatitis was admitted to the nephrology unit because of a progressive increase in serum creatinine(Cr). Blood Urea Nitrogen(BUN) and Cr, measured by the enzymatic method, were 15 and 2.0 mg/dl, respectively, in 1999, and changed to 17 and 3.8 mg/dl, respectively, on
C5b-8 and C5b-9 modulate the collagen release of human glomerular epithelial cells.
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Aside from their lytic function the late complement components C5b-9 stimulate release of prostanoids, interleukin 1 and oxygen radicals from a number of cells. Since C5b-9 has also been connected to the development of sclerosis in animal models of glomerulonephritis, we addressed the question
A new point mutation in the COL4A5 gene described in a Spanish family with X-linked Alport syndrome.
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OBJECTIVE
Alport syndrome is a hereditary glomerulonephritis, X-linked in 85% of the cases. This form is associated with mutations in the COL4A5 gene which encodes the alpha5 chain of type IV collagen. We have performed the mutational analysis of the COL4A5 gene in a Spanish family with X-linked
The effects of cyclophosphamide and azathioprine on collagen in skin and granulation tissue in rats, and the effects of cyclophosphamide on collagen in human skin.
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Granulation tissue was produced in rats by subcutaneous implantation of cellulose sponges. The effect of daily intraperitoneal injections of cyclophosphamide or azathioprine on rat skin and granulation tissue was examined after 14 and 42 days. Skin biopsies from patients with glomerulonephritis were
[The antagonistic effects of adrenomedullin on biological events governed by transforming growth factor beta in HK-2 cell line].
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OBJECTIVE
To investigate the influence of adrenomedullin (AM) on the biological events governed by transforming growth factorbeta (TGF-beta) in human tubular epithelial cell line (HK-2).
METHODS
Cell proliferation was determined by (3)H-TdR incorporation; ELISA method was used to detect the level of
Transforming growth factor-beta receptors in self-limited vs. chronic progressive nephritis in rats.
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Increases in transforming growth factor-beta (TGF-beta) expression and extracellular matrix accumulation are transient in acute self-limited mesangial proliferative glomerulonephritis induced by a single injection of anti-thymocyte serum (ATS), while these increases persist following repeated
Cytotoxicity and inhibition of normal collagen synthesis in mouse fibroblasts by lipoteichoic acid from Streptococcus pyogenes type 12.
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The toxicity of lipoteichoic acid (LTA) from Streptococcus pyogenes type 12 was investigated by using mouse fibroblasts in culture in the absence of serum. Morphologically, while low concentrations of LTA elicited a subtle effect characterized by progressive cellular degeneration with practically no
L-arginine may mediate the therapeutic effects of low protein diets.
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We have previously shown beneficial effects of dietary protein restriction on transforming growth factor beta (TGF-beta) expression and glomerular matrix accumulation in experimental glomerulonephritis. We hypothesized that these effects result from restriction of dietary L-arginine intake. Arginine
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