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proliferation of mesangial cells
The main aim of this study is to explore whether heparin inhibits proliferation of mesangial cells grown in high glucose concentration and to measure the effect of heparin on matrix metalloproteinases (MMPs) expression in mesangial cells.
      
The proliferation of mesangial cells on cyclosporin (CsA) test medium was studied by MTT assay and TNF-α in cultured supernatant was examined by using ELISA.
      
The results showed that cyclosporin A significantly inhibited the proliferation of mesangial cells at the concentration between 0.
      
Both forms are characterized by a differently severe proliferation of mesangial cells and by a mostly extensiv thickening of the glomerular basement membrane.
      
The proliferation of mesangial cells and thickening of the glomerular basement membrane is more severe in the lobular form of MPGN.
      
In contrast to TNF α, IL-1 β inhibited GEC proliferation; this was due to the early appearance and proliferation of mesangial cells, despite the culture being serum-free.
      
In contrast to TNF α, IL-1 β inhibited GEC proliferation; this was due to the early appearance and proliferation of mesangial cells, despite the culture being serum-free.
      
Proliferation of mesangial cells did not contribute to this development.
      
Proliferation of mesangial cells has not been observed in normal rats injected with FGF2but it has been noted in anti-Thy1.1 rats injected with FGF2.
      
Findings indicated that diet-induced hyperlipidemia can lead to proliferation of mesangial cells and accumulation of mesangial matrices, and further aggravate glomerulosclerosis in Adriamycin-induced nephrosis.
      
These findings suggest that p16INK4 and p21CIP1 function as inhibitors of the proliferation of mesangial cells, induced by growth-promoting factors, and that deregulated expression of cyclin D1 causes disturbances in the cell cycle.
      
Examination of glomerulocytes revealed early alterations in endotheliocytes, compensatory proliferation of mesangial cells, overproduction of the mesangial matrix, and metaplasia of podocytes.
      
Effects of nonenzymatic glycosylation of mesangial matrix on proliferation of mesangial cells.
      
Light microscopy of the control biopsy showed 10 glomeruli with slight proliferation of mesangial cells.
      
Kidneys ofthese young mice showed no signs of glomerulonephritis or only the slightest proliferation of mesangial cells.
      
Proliferation of mesangial cells and accumulation of extracellular matrix characterize a wide variety of progressive renal diseases.
      
Proliferation of mesangial cells without FGF-2 and scFv antibody was taken as 100%.
      
The administration of E2F decoy suppressed the proliferation of mesangial cells by 71%.
      
 

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