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Hypoxia induces PAI-1 expression via remarkable nuclear accumulation of HIF-1alpha and partially via NF-kappaB activation in HPTECs. TNF-alpha can synergistically enhance this hypoxia-induced PAI-1 expression.

In order to evaluate the quantitative cavitation-erosion resistance of materials, a pressure-detector-installed specimen was developed, which can measure both the impact load produced by cavitation bubble collapse and the volume loss simultaneously. Test specimens (pressure-detection rod) used were nine kinds of metals and were exposed to vibratory cavitation. A linear relation was obtained for all materials between the accumulated impact energy ∑Fi2 calculated from the distribution of impact loads and the volume loss, independent of test conditions. Impact energy accumulated during the incubation period and the energy for a unit material removal in steady-state period were obtained from the relation. These values are very Important concerning quantitative erosion resistance evaluation. That is, when the distribution of impact loads is acquired for different cavitation conditions, the volume loss can be estimated. This idea was applied to the venturi cavitation erosion. The experimental results for venturi test corresponds well with the prediction using these impact energy values. It was concluded that the quantitative impact energy values of materials can be determined independent of the apparatus and the test condition by using the newly developed pressure-detector-installed specimen.

To examine the effect of chronic administration of recombinant human erythropoietin (rHuEPO) on endogenous nitric oxide (NO) activity, we treated Sprague-Dawley rats with rHuEPO (100 IU kg-1 or 300 IU kg-1) or a corresponding vehicle for 2 weeks, administered subcutaneously on alternate days. Treatment elicited increases in haematocrit and systolic blood pressure in a dose-dependent fashion. Simultaneous administration of NG-nitro-L-arginine methyl ester (L-NAME, 20 mg dl-1 of drinking water), but not aminoguanidine (400 mg dl-1), induced a further significant rise in blood pressure. The effect of L-NAME was inhibited by a large dose of L-arginine (2.0 g dl-1). Polycythaemia and hypertension induced by chronic rHuEPO therapy were associated with increased urinary NO2- and NO3- (NOx-) excretion, while co-administration of L-NAME, but not aminoguanidine, reduced NOx- excretion. Our results indicate that chronic rHuEPO treatment has a significant pressor effect, but induces a compensatory increase in the steady-state release of NO by constitutive NO synthase in normal rats. Such enhanced NO synthesis may act as a protective mechanism against the hypertensive effect of rHuEPO.

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