ABSTRACT
Abstract@#Flood disasters are the common public health emergencies, mainly leading to environmental damage, water pollution, food pollution, vector breeding, infectious disease epidemic and other risk factors of sanitary and anti epidemic work. The guideline has been formulated with reference to the technical documents such as Guideline for Environmental Sanitation Disposal and Preventive Disinfection in Flooded Areas and Technical Proposal for Sanitary and Anti epidemic Measures after Flood Disasters, as well as the latest research progress at home and abroad. In order to guide the sanitary and anti epidemic measures in flooded areas, protect the health and safety of students and teachers and ensure the normal educational and teaching order, the guideline introduces the key measures that should be taken by schools, teachers and students in flood striken areas.
ABSTRACT
Sestrin-2 (SESN2) is involved in the cellular response to different stress conditions. However, the function of SESN2 in the cardiovascular system remains unknown. In the present study, we tested whether SESN2 has a beneficial effect on vascular endothelial damage induced by angiotensin II (AngII). Firstly, we found that AngII induces expression of SESN2 in human umbilical vein endothelial cells (HUVECs) in a time-dependent and dose-dependent manner. We also found that knockdown of SESN2 using small RNA interference promotes cellular toxicity of AngII, as well as a reduction in cell viability, exacerbation of oxidative stress, and stimulation of apoptosis. In addition, our results show that the c-Jun NH (2)-terminal kinase (JNK)/c-Jun pathway is activated by AngII. Inhibiting the activity of the JNK pathway abolishes the increase in SESN2 induced by AngII. Importantly, overexpression of c-Jun promotes luciferase activity of the SESN2 promoter. These findings suggest that the inductive effect of SESN2 is mediated by the JNK/c-Jun pathway. Our results indicate that the induction of SESN2 acts as a compensatory response to AngII for survival, implying that stimulating expression of SESN2 might be an effective pharmacological target for the treatment of AngII-associated cardiovascular diseases.
