There are multiple sources of reactive oxygen species (ROS) in the cell. As a major site of ROS production, mitochondria have drawn considerable interest because it was recently discovered that mitochondrial ROS (mtROS) directly stimulate the production of proinflammatory cytokines and pathological conditions as diverse as malignancies, autoimmune diseases, and cardiovascular diseases all share common phenotype of increased mtROS production above basal levels. Several excellent reviews on this topic have been published, but ever-changing new discoveries mandated a more up-to-date and comprehensive review on this topic. Therefore, we update recent understanding of how mitochondria generate and regulate the production of mtROS and the function of mtROS both in physiological and pathological conditions. In addition, we describe newly developed methods to probe or scavenge mtROS and compare these methods in detail. Thorough understanding of this topic and the application of mtROS-targeting drugs in the research is significant towards development of better therapies to combat inflammatory diseases and inflammatory malignancies.

The local coordination environment of catalysts has been investigated for an extended period to obtain enhanced catalytic performance. Especially with the advancement of single-atom catalysts (SACs), research on the coordination environment has been advanced to the atomic level. The surrounding coordination atoms of central metal atoms play important roles in their catalytic activity, selectivity and stability. In recent years, remarkable improvements of the catalytic performance of SACs have been achieved by the tailoring of coordination atoms, coordination numbers and second-or higher-coordination shells, which provided new opportunities for the further development of SACs. In this review, the characterization of coordination environment, tailoring of the local coordination environment, and their related adjustable catalytic performance will be discussed. We hope this review will provide new insights on further research of SACs.

In December 2019, a new coronavirus was found in Wuhan, Hubei Province, China, and spread rapidly throughout the country, attracting global attention. On February 11, the World Health Organization (WHO) officially named the disease caused by 2019-nCoV coronavirus disease 2019 . With the increasing number of cases, health care workers (HCWs) from all over China volunteered to work in Hubei Province. Because of the strong infectivity of COVID-19, HCWs need to wear personal protective equipment (PPE), such as N95 masks, latex gloves, and protective clothing. Due to the long-term use of PPE, many adverse skin reactions may occur. Therefore, the purpose of this study is to explore the adverse skin reactions among HCWs using PPE.Questionnaires were used for the research; a quantitative study was carried out to determine the incidence of adverse skin reactions among HCWs using PPE.A total of 61 valid questionnaires were collected. The most common adverse skin reactions among HCWs wearing N95 masks were nasal bridge scarring (68.9%) and facial itching (27.9%). The most common adverse skin reactions among HCWs wearing latex gloves were dry skin (55.7%), itching (31.2%), and rash (23.0%). The most common adverse skin reactions among HCWs wearing protective clothing were dry skin (36.1%) and itching (34.4%).When most HCWs wear PPE for a long period of time, they will experience adverse skin reactions. The incidence of adverse skin reactions to the N95 mask was 95.1%, that to latex gloves was 88.5%, and that to protective clothing was 60.7%.

Objective The role of receptors for endogenous metabolic danger signals-associated molecular patterns (DAMPs) has been characterized recently as bridging innate immune sensory systems for DAMPs to initiation of inflammation in bone marrow-derived cells such as macrophages. However, it remains unknown whether endothelial cells (ECs), the cell type with the largest numbers and the first vessel cell type exposed to circulating DAMPs in the blood, can sense hyperlipidemia. This report determined whether caspase-1 plays a role in ECs in sensing hyperlipidemia and promoting EC activation. Approach and Results Using biochemical, immunological, pathological and bone marrow transplantation methods together with the generation of new apoplipoprotein E (ApoE)−/−/caspase-1−/− double knock-out mice we made the following observations: 1) early hyperlipidemia induced caspase-1 activation in ApoE−/− mouse aorta; 2) caspase-1−/−/ApoE−/− mice attenuated early atherosclerosis; 3) caspase-1−/−/ApoE−/− mice had decreased aortic expression of pro-inflammatory cytokines and attenuated aortic monocyte recruitment; and 4) caspase-1−/−/ApoE−/− mice had decreased EC activation including reduced adhesion molecule expression and cytokine secretion. Mechanistically, oxidized lipids activated caspase-1 and promoted pyroptosis in ECs by a ROS mechanism. Caspase-1 inhibition resulted in accumulation of sirtuin 1 (Sirt1) in the ApoE−/− aorta, and Sirt1 inhibited caspase-1 upregulated genes via activator protein-1 (AP-1) pathway. Conclusions Our results demonstrate for the first time that early hyperlipidemia promotes EC activation before monocyte recruitment via a caspase-1-Sirt1-AP-1 pathway, which provides an important insight into the development of novel therapeutics for blocking caspase-1 activation as early intervention of metabolic cardiovascular diseases and inflammations.