570 research outputs found
Design and Development of Fast Response, Wide Dynamic Range Neutron Flux Monitor for the Large Helical Device
Bifurcation Phenomena of a Magnetic Island at a Rational Surface in a Magnetic-Shear Control Experiment
Three states of a magnetic island are observed when the magnetic shear at the rational surface is modified using inductive current associated with the neutral beam current drive in the Large Helical Device. One state is the healed magnetic island with a zero island width. The second state is the saturated magnetic island with partial flattening of the T_e profile. The third state is characterized by the global flattening of the T_e profile in the core region. As the plasma assumes each of the three states consecutively through a bifurcation process a clear hysteresis in the relation between the size of the magnetic island and the magnetic shear is observed
Protective effect of 17β-estradiol on ischemic acute renal failure through the PI3K/Akt/eNOS pathway
Estrogens attenuate renal injury induced by ischemia/reperfusion (I/R), an effect that is related to nitric oxide production in the post-ischemic kidney. The compound 17β-estradiol (E2-β) acting via estrogen receptors (ERs) is known to activate endothelial nitric oxide synthase (eNOS) through the phosphatidylinositol-3 kinase (PI3K)/Akt pathway. We determined if this pathway contributes to the renoprotective effect of E2-β in the uninephrectomized ischemia reperfusion rat model of acute renal injury. Treatment with E2-β suppressed the I/R-induced increases in blood urea nitrogen, plasma creatinine, urine flow, and fractional excretion of sodium while augmenting creatinine clearance, renal blood flow, and urine osmolality, indicating attenuation of renal injury. Phosphorylation of Akt and eNOS protein was significantly increased 30–60 min after reperfusion in estradiol-treated compared to vehicle-treated rats. The protective effects of E2-β and protein phosphorylation were reversed by the PI3K inhibitor wortmannin or the ER antagonist tamoxifen. Furthermore, the E2-β-induced renoprotective effects were not seen in eNOS knockout mice with renal injury. We conclude that the E2-β-induced renoprotective effect is due to activation of the PI3K/Akt pathway followed by increased eNOS phosphorylation in the post-ischemic kidney
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