Surveillance of emerging infectious diseases for biosecurity

Emerging infectious diseases, such as COVID-19, continue to pose significant threats to human beings and their surroundings. In addition, biological warfare, bioterrorism, biological accidents, and harmful consequences arising from dual-use biotechnology also pose a challenge for global biosecurity. Improving the early surveillance capabilities is necessary for building a common biosecurity shield for the global community of health for all. Furthermore, surveillance could provide early warning and situational awareness of biosecurity risks. However, current surveillance systems face enormous challenges, including technical shortages, fragmented management, and limited international cooperation. Detecting emerging biological risks caused by unknown or novel pathogens is of particular concern. Surveillance systems must be enhanced to effectively mitigate biosecurity risks. Thus, a global strategy of meaningful cooperation based on efficient integration of surveillance at all levels, including interdisciplinary integration of techniques and interdepartmental integration for effective management, is urgently needed. In this paper, we review the biosecurity risks by analyzing potential factors at all levels globally. In addition to describing biosecurity risks and their impact on global security, we also focus on analyzing the challenges to traditional surveillance and propose suggestions on how to integrate current technologies and resources to conduct effective global surveillance.

Effects of Simvastatin on Endoplasmic Reticulum Stress-Mediated Apoptosis in Atherosclerotic Calcification

Objective:The effectiveness of statins in reducing atherosclerotic calcification remains controversial.The aim of this study was to confirm that simvastatin reduces atherosclerotic calcification and stabilizes plaque by restricting endoplasmic reticulum stress(ERS)-mediated apoptosis.Methods:Twenty-four 8-week-old male apolipoprotein E(ApoE)-/-mice(C57BL/6J genetic background)were selected and randomly divided into model(n=12)and simvastatin(n=12)groups.Twelve male C57BL/6J mice were selected as control group(n=12).The mice were adaptively fed for 2 weeks and were put on a high-fat diet thereafter.After 9 weeks,they were treated with simvastatin(20 mg/kg)or phosphate-buffered saline daily for 8 weeks.Aortic sinus samples were obtained from ApoE-/-and C57BL/6J mice for hematoxylin and eosin,von Kossa,alizarin Red S,terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling,and immunohistochemical staining after in vivo treatment with simvastatin.In addition,mouse vascular smooth muscle cells were analyzed after exposure to simvastatin in vitro.Results:Administration of simvastatin in vivo drastically attenuated the atherosclerosis,calcification,and apoptosis,and decreased the serum levels of triglycerides,total cholesterol,low-density lipoprotein cholesterol,and high-density lipoprotein cholesterol.The expression levels of glucose-regulated protein,78 kDa(GRP78),C/EBP homologous protein(CHOP),and caspase 12(CASP12)in the aortic sinus decreased in the simvastatin group compared with the model group.In vitro,simvastatin or simvastatin plus ERS inhibitor(taurine)attenuated calcification and apoptosis,and reduced the expression of ERS-related proteins GRP78,CHOP,and CASP12.Conclusion:Treatment with simvastatin suppressed atherosclerotic calcification.This effect may be mediated through the inhibition of ERS-related apoptosis.