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https://www.selleckchem.com/products/sulfosuccinimidyl-oleate-sodium.html Developmental toxicity profiles were partly different in male and female offspring, males being more sensitive to increased liver weight, PROD induction and decreased thyroxine concentrations. MoE assessment indicated that the 95th percentile of current maternal PCB 180 concentrations do not exceed the estimated tolerable human lipid-based PCB 180 concentration. Although PCB 180 is much less potent than dioxin-like compounds, it shares several toxicological targets suggesting a potential for interactions. The electrophysiological (EP) effects and safety of renal artery denervation (RDN) in chronic kidney disease (CKD) are unclear. The purpose of this study was to investigate the arrhythmogenicity of RDN in a rabbit model of CKD. Eighteen New Zealand white rabbits were randomized to control (n = 6), CKD (n = 6), and CKD-RDN (n = 6) groups. A 5/6 nephrectomy was selected for the CKD model. RDN was applied in the CKD-RDN group. All rabbits underwent cardiac EP studies for evaluation. Immunohistochemistry, myocardial fibrosis, and renal catecholamine levels were evaluated. The CKD group (34.8% ± 9.2%) had a significantly higher ventricular arrhythmia (VA) inducibility than the control (8.6% ± 3.8%; P <.01) and CKD-RDN (19.5% ± 6.3%; P = .01) groups. In the CKD-RDN group, ventricular fibrosis was significantly decreased compared to the CKD group (7.4% ± 2.0 % vs 10.4% ± 3.7%; P=.02). Sympathetic innervation in the CKD group was significantly increased compared to the control and CKD-RDN groups [left ventricle 4.1 ± 1.8 vs 0.8 ± 0.5 (10 μm /mm ), P <.01; 4.1 ± 1.8 vs 0.9± 0.6 (10 μm /mm ), P <.01; right ventricle 3.6 ± 1.0 vs 1.0 ± 0.4 (10 μm /mm ), P <.01; 3.6 ± 1.0 vs 1.0± 0.5 (10 μm /mm ), P <.01]. Neuromodulation by RDN demonstrated protective effects with less structural and electrical remodeling, leading to attenuated VAs. In a rabbit model of CKD, RDN plays a therapeutic role by lowering the

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