Sentence examples for models of glomerulonephritis from inspiring English sources

In two different rat models of glomerulonephritis we detected changes in the expression pattern of meprinβ, both in the glomeruli as well as in the proximal tubules.

Antibodies against MIF can decrease inflammation in experimental models of glomerulonephritis, arthritis and allograft rejection [ 26, 27, 28].

Depletion of platelets reduces influx of hemopoietic cells into the glomeruli, decreases resident cell proliferation and improves renal function in animal models of glomerulonephritis.

In experimental models of glomerulonephritis, mice that are deficient in TNFα receptor [ 10], and rats administered inhibitory TNFα antibodies [ 11] had reduced glomerular injury.

Fibrin deposition in human glomerulonephritis and arthritis is associated with more severe disease [ 13, 14]; in animal models of glomerulonephritis, arthritis and nerve injury fibrin exacerbates inflammation and tissue damage [ 3, 15- 17].

This notion is supported by the observation that CCR2 knockout mice had exacerbated disease in a model of glomerulonephritis [ 33].

Its use as an anti-fibrotic molecule has been shown in a rat model of glomerulonephritis [ 93].

Activation of NF- κB is observed in both animal (rat model of glomerulonephritis) and human (diabetic nephropathy) renal diseases [ 105, 106].

In a rodent model of glomerulonephritis, urinary leukotriene concentrations were elevated at initial stages of disease, followed by a decline at more advanced phases [ 35].

In the model of glomerulonephritis with mesangial proliferation induced by the injection of anti-thymocyte antibodies, an increase is observed in the glomerular expression of ET-1 and ETB receptors [ 141].

In a rat model of glomerulonephritis, Tie2 is over-expressed by ECs, and Ang-1 and Ang-2 are over-expressed by podocytes in a time-dependent manner during the repair phase [ 20].