-Xiong, F., Xiao, D., Zhang, L. Norepinephrine causes epigenetic repression of PKC epsilon gene in rodent hearts by activating Nox1-dependent reactive oxygen species production. FASEB J. 26, 2753-2763 (2012). www.fasebj.org”
“Objectives To study the effects of Ferroptosis mutation hypaconitine used alone and combined

with liquiritin on calmodulin (CaM) expression and connexin43 (Cx43) phosphorylation on serine368 (Ser368), as well as to investigate the intervention of liquiritin on these hypaconitine-induced effects. Methods Adult Wistar rats were orally administered hypaconitine (0.23, 0.69, 2.07 mg/kg per day), liquiritin (20 mg/kg per day), or hypaconitine (2.07 mg/kg per day) plus liquiritin (20 mg/kg per day) for seven consecutive days. The mRNA expression levels of CaM and Cx43 in rat myocardial tissue were determined by real-time quantitative PCR. The protein contents of CaM and phosphorylated Cx43 (Ser368) were determined by Western blot. Key findings The results indicated that the mRNA and protein expression levels of CaM were significantly decreased by hypaconitine used alone and combined with liquiritin. Although CaM mRNA expression level

was inhibited by liquiritin, its protein expression level was upregulated. Meanwhile, although no obvious effect on Cx43 mRNA expression was observed after the drug administration, the phosphorylation level of Cx43 (Ser368) was significantly inhibited. Furthermore, the coadministration of hypaconitine and liquiritin this website significantly reduced hypaconitine-induced inhibitory action on Cx43 (Ser368) phosphorylation. Conclusions The study indicated that hypaconitine could inhibit CaM expression and Cx43 (Ser368) phosphorylation, and liquiritin could interfere with this kind of effect by synergistically inhibiting

CaM expression and by antagonizing Cx43 (Ser368) dephosphorylation induced by hypaconitine.”
“Calciphylaxis is a rare and potentially life-threatening condition. It is thought to result from arterial calcification causing complete see more vascular occlusion and subsequent cutaneous infarction. Most often, it is a complication of end-stage renal failure or hyperparathyroidism; without either of these associated conditions, it is extremely rare. We report a case of calciphylaxis in a 58-year-old white British man, who had received long-term oral prednisolone for asthma control, with prophylactic calcium supplementation. There was no history of renal failure, and the patients parathyroid function was normal. He was found to be heterozygous for the Factor V Leiden mutation. The acute presentation was seemingly precipitated by an episode of trauma and subsequent compression bandaging. The patient responded promptly to intravenous sodium thiosulfate.