Methylglyoxal, oxidative stress, and hypertension

Pathogenic mechanisms for essential hypertension are unclear despite striking efforts from numerous research teams over several decades. Increased production of reactive oxygen species (ROS) has been associated with the development of hypertension and the role of ROS in hypertension has been well documented in recent years. In this context, it is important to better understand pathways and triggering factors for increased ROS production in hypertension. This review draws a causative linkage between elevated methylglyoxal level, methylglyoxal-induced production of ROS, and advanced glycation end products in the development of hypertension. It is proposed that elevated methylglyoxal level and resulting protein glycation and ROS production may be the upstream links in the chain reaction leading to the development of hypertension.     

中国展足蛾属五新种一新纪录种(鳞翅目:织蛾科:展足蛾亚科)

报道了中国展足蛾属5新种和1新纪录种,绘制了新种的外生殖器特科。模式标本保存在南开大学生物系。     

新生儿支原体脑炎1例

本文报道了1例新生儿支原体脑炎。患儿因“皮肤黄染3天”入院,病程中有发热,入院后仍持续发热22天,热峰高达39 ℃,脑脊液检查显示白细胞计数升高、蛋白水平明显升高及葡萄糖水平显著降低,按照新生儿细菌性脑膜炎治疗后效果不佳,遂取脑脊液行宏基因组测序,第22天明确诊断为解脲支原体(Ureaplasma urealyticum, UU)感染。新生儿支原体感染以解脲支原体为主,感染主要来自母体宫内感染的垂直传播。支原体脑炎的临床表现及脑脊液改变均与新生儿细菌性脑膜炎类似,因此临床医师应重视病原学诊断,治疗宜选用大环内酯类药物。     

单细胞组学技术及其在植物保卫细胞研究中的应用

单细胞组学技术在动物研究中已经得到广泛应用,但在植物学领域尤其是保卫细胞研究中还处于起步阶段。由保卫细胞构成的气孔承担着植物生命过程中水分散发及气体交换大门的作用。将单细胞组学技术应用到保卫细胞功能解析中将有助于了解保卫细胞参与的基本生理过程。该文综述了植物单细胞组学技术的发展、保卫细胞研究现状及单细胞组学技术在植物保卫细胞研究中的初步应用,为借助该技术解决植物生物学中保卫细胞发育、代谢及对环境胁迫响应等基本问题提供研究思路和方法。     

PGC-1α Is a Key Regulator of Glucose-Induced Proliferation and Migration in Vascular Smooth Muscle Cells

Background

Atherosclerosis is a complex pathological condition caused by a number of mechanisms including the accelerated proliferation of vascular smooth muscle cells (VSMCs). Diabetes is likely to be an important risk factor for atherosclerosis, as hyperglycemia induces vascular smooth muscle cell (VSMC) proliferation and migration and may thus contribute to the formation of atherosclerotic lesions. This study was performed to investigate whether PGC-1α, a PPARγ coactivator and metabolic master regulator, plays a role in regulating VSMC proliferation and migration induced by high glucose.

Methodology/Principal Findings

PGC-1α mRNA levels are decreased in blood vessel media of STZ-treated diabetic rats. In cultured rat VSMCs, high glucose dose-dependently inhibits PGC-1α mRNA expression. Overexpression of PGC-1α either by infection with adenovirus, or by stimulation with palmitic acid, significantly reduces high glucose-induced VSMC proliferation and migration. In contrast, suppression of PGC-1α by siRNA mimics the effects of glucose on VSMCs. Finally, mechanistic studies suggest that PGC-1α-mediated inhibition of VSMC proliferation and migration is regulated through preventing ERK1/2 phosphorylation.

Conclusions/Significance

These results indicate that PGC-1α is a key regulator of high glucose-induced proliferation and migration in VSMCs, and suggest that elevation of PGC-1α in VSMC could be a useful strategy in preventing the development of diabetic atherosclerosis.