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tam oan say: August 11, 2019 at 11:19 am.
A:
body {
background: url("test_logo.png") no-repeat center center fixed;
-webkit-background-size: cover;
-moz-background-size: cover;
-o-background-size: cover;
background-size: cover;
font-family: Arial, sans-serif;
}
test_logo.png is the filename of your image.
Novel mechanism of alkalosis-induced resistance to hypoxia via vascularization in zebrafish.
Oxygen sensing is a vital function of the body. In order to survive and thrive in a hyperoxia environment, fish must sense the reduced partial pressure of oxygen in order to increase blood flow to the gills and heart in a timely manner. However, the hypoxia resistance mechanisms remain unknown. In the present study, we found that alkalosis induced vascularization in zebrafish, which may be a critical resistance mechanism to hypoxia. The results showed that the livers of zebrafish exposed to alkalosis were hypoxia-resistant, and the serum MCP-1 level was significantly increased in zebrafish exposed to alkalosis. Moreover, alkalosis-induced vascularization and the production of the vasodilator NO were found in the liver. Furthermore, alkalosis promoted NO-induced apoptosis and NO production to promote vascularization in zebrafish exposed to hypoxia. We found that the renal levels of VEGF and MCP-1 and hepatic microvessel density were increased in alkalosis-induced zebrafish, which suggests that vascularization of the kidney and liver is a crucial mechanism in the adaptation of alkalosis-induced resistance to hypoxia. These findings suggest that the alkalosis resistance mechanism is associated with vascularization in the liver.Separation of Acetaminophen, N-Acetylcysteine and Deacetylated N-Acetylcysteine by Chiral Chromatography: Kinetic Separation of N-Acetylcysteine Derivatives.
The objective of this study was to determine the analytical properties and optimize be359ba680
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