ORCID Profile
0000-0001-9596-9188
Current Organisation
Osaka University
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Publisher: Elsevier BV
Date: 08-2019
Publisher: Wiley
Date: 16-03-2015
DOI: 10.1002/IJC.29504
Abstract: Both Yucheng and Yusho were events of accidental exposure to highly doses of polychlorinated biphenyls and dibenzofurans in Asian people. Mortality experiences caused by various diseases were reported in both cohorts with similar and dissimilar findings. We thus conducted a meta-analysis of two cohorts to reevaluate the effects of PCBs and PCDFs on major causes of mortalities. Two recently updated Yucheng and Yusho mortality studies were included. For selected diseases, standardized mortality ratios (SMR) and 95% confidence intervals (95% CI) were extracted. Meta-analyses were conducted using a random-effects model only when heterogeneity (I(2) > 50% and/or p value <0.10 by the Q test) was not found. A total of 1,803 Yucheng subjects (male, N = 830 female, N = 973) with 48,751 person-years of follow-up and 1,664 Yusho subjects (male, N = 860 female, N = 804) with 50,773 person-years are included. An increase in all-cause mortality (pooled SMR=1.2, 95% CI: 1.1-1.3, I(2) = 0.0%), all cancers (pooled SMR=1.3, 95% CI: 1.1-1.6, I(2) = 0.0%), lung cancer (pooled SMR=1.7, 95% CI: 1.2-2.3, I(2) =0.0%), heart disease (pooled SMR=1.3, 95% CI: 1.0-1.7, I(2) = 43.4%) and hepatic disease (pooled SMR=1.9, 95% CI: 1.3-2.8, I(2) = 0.0%) were found in pooled males. Significant elevation from liver cancer was found in pooled females (pooled SMR=2.0, 95% CI: 1.1-3.6, I(2) = 0.0%). This meta-analysis of Yucheng and Yusho cohorts showed similar elevation from all cancer, lung cancer, heart disease and hepatic disease mortalities in exposed men. Furthermore, a new finding of elevated liver cancer mortality in exposed women was identified.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 07-2022
DOI: 10.1161/HYPERTENSIONAHA.121.18114
Abstract: ANP (atrial natriuretic peptide), acting through NPR1 (natriuretic peptide receptor 1), provokes hypotension. Such hypotension is thought to be due to ANP inducing vasodilation via NPR1 in the vasculature however, the underlying mechanism remains unclear. Here, we investigated the mechanisms of acute and chronic blood pressure regulation by ANP. Immunohistochemical analysis of rat tissues revealed that NPR1 was abundantly expressed in endothelial cells and smooth muscle cells of small arteries and arterioles. Intravenous infusion of ANP significantly lowered systolic blood pressure in wild-type mice. ANP also significantly lowered systolic blood pressure in smooth muscle cell–specific Npr1 –knockout mice but not in endothelial cell–specific Npr1 –knockout mice. Moreover, ANP significantly lowered systolic blood pressure in Nos3 -knockout mice. In human umbilical vein endothelial cells, treatment with ANP did not influence nitric oxide production or intracellular Ca 2+ concentration, but it did hyperpolarize the cells. ANP-induced hyperpolarization of human umbilical vein endothelial cells was inhibited by several potassium channel blockers and was also abolished under knockdown of RGS2 (regulator of G-protein signaling 2), an GTPase activating protein in G-protein α-subunit. ANP increased Rgs2 mRNA expression in human umbilical vein endothelial cells but failed to lower systolic blood pressure in Rgs2 -knockout mice. Endothelial cell–specific Npr1 -overexpressing mice exhibited lower blood pressure than did wild-type mice independent of RGS2, and showed dilation of arterial vessels on synchrotron radiation microangiography. Together, these results indicate that vascular endothelial NPR1 plays a crucial role in ANP-mediated blood pressure regulation, presumably by a mechanism that is RGS2-dependent in the acute phase and RGS2-independent in the chronic phase.
Location: Philippines
Location: Japan
No related grants have been discovered for Daisuke Onozuka.