不同术前皮肤准备方案与手术切口感染的关系研究

目的:研究不同术前皮肤准备方案与手术切口感染(SSI)的关系,为降低临床SSI发生率提供参考。方法:选择自2015年1月～2019年12月在医院行手术治疗的患者1810例为本次研究对象。根据析因设计表,将因素A:是否剃毛(1不剃毛;2剃毛),B:清洁方式(1清水清洁;2肥皂水清洁),C:术前备皮时间(1术前1 d;2术前2 h)配对分为8个组:A1B1C1组226例,A1B2C1组229例,A1B1C2组216例,A1B2C2组232例,A2B1C1组221例,A2B2C1组241例,A2B1C2组221例,A2B2C2组224例,比较各组手术部位及切口类型分布、术后SSI发生率,并采用析因分析法分析术前皮肤准备后各组菌落计数的相关性及交互作用。结果:各组患者的手术部位及切口类型之间的差异不存在统计学意义(P0.05)。A1B1C1组及A2B1C1组的SSI发生率较高,分别为12.83%和14.48%。A1水平的SSI发生率是8.75%,与A2水平的8.27%相比,差异不存在统计学意义(P0.05)。B1、C1水平的SSI发生率分别是11.31%、10.03%,明显高于B2、C2水平的5.83%、6.94%,差异均存在统计学意义(P0.05)。各组术前皮肤准备后的菌落计数差异存在统计学意义(P0.05),析因分析结果显示,B、C单因素分析差异存在统计学意义(P0.05),且A与C,B与C间具有交互作用,而A、B、C间具有二级交互作用(P0.05)。结论:术前皮肤准备对降低SSI发生具有重要作用,实际操作时,建议在较短的时间内利用肥皂水或其他消毒水进行皮肤清洗并完成备皮。     

Long-Term Existence of SARS-CoV-2 in COVID-19 Patients: Host Immunity,Viral Virulence,and Transmissibility

Virologica Sinica - COVID-19 patients can recover with a median SARS-CoV-2 clearance of 20 days post initial symptoms (PIS). However, we observed some COVID-19 patients with existing...     

Plant adaptation to climate change—Where are we?

Climate change poses critical challenges for population persistence in natural communities, for agriculture and environmental sustainability, and for food security. In this review, we discuss recent progress in climatic adaptation in plants. We evaluate whether climate change exerts novel selection and disrupts local adaptation, whether gene flow can facilitate adaptive responses to climate change, and whether adaptive phenotypic plasticity could sustain populations in the short term. Furthermore, we discuss how climate change influences species interactions. Through a more in‐depth understanding of these eco‐evolutionary dynamics, we will increase our capacity to predict the adaptive potential of plants under climate change. In addition, we review studies that dissect the genetic basis of plant adaptation to climate change. Finally, we highlight key research gaps, ranging from validating gene function to elucidating molecular mechanisms, expanding research systems from model species to other natural species, testing the fitness consequences of alleles in natural environments, and designing multifactorial studies that more closely reflect the complex and interactive effects of multiple climate change factors. By leveraging interdisciplinary tools (e.g., cutting‐edge omics toolkits, novel ecological strategies, newly developed genome editing technology), researchers can more accurately predict the probability that species can persist through this rapid and intense period of environmental change, as well as cultivate crops to withstand climate change, and conserve biodiversity in natural systems.     

In memory of Professor Tang Yan‐Cheng: New perspectives in systematic and evolutionary biology

In China, three institutes for botanical research were established in the 1920s. They were the Department of Botany, Biological Laboratory of the Science Society of China (1922, Nanjing), the Fan Memorial Institute of Biology (1928, Beiping), and the Institute of Botany, Beiping Academy of Sciences (1929, Beiping).     

Antibody response and therapy in COVID-19 patients: what can be learned for vaccine development?

Science China Life Sciences - The newly emerged severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has infected millions of people and caused tremendous morbidity and mortality worldwide....     

Three proline rotamases involved in calcium homeostasis play differential roles in stress tolerance,virulence and calcineurin regulation of Beauveria bassiana

FK506‐sensitive proline rotamases (FPRs), also known as FK506‐binding proteins (FKBPs), can mediate immunosuppressive drug resistance in budding yeast but their physiological roles in filamentous fungi remain opaque. Here, we report that three FPRs (cytosolic/nuclear 12.15‐kD Fpr1, membrane‐associated 14.78‐kD Fpr2 and nuclear 50.43‐kD Fpr3) are all equally essential for cellular Ca²⁺ homeostasis and contribute significantly to calcineurin activity at different levels in the insect‐pathogenic fungus Beauveria bassiana although the deletion of fpr1 alone conferred resistance to FK506. Radial growth, conidiation, conidial viability and virulence were less compromised in the absence of fpr1 or fpr2 than in the absence of fpr3, which abolished almost all growth on scant media and reduced growth moderately on rich media. The Δfpr3 mutant was more sensitive to Na⁺, K⁺, Mn²⁺, Ca²⁺, Cu²⁺, metal chelate, heat shock and UVB irradiation than was Δfpr2 while both mutants were equally sensitive to Zn²⁺, Mg²⁺, Fe²⁺, H₂O₂ and cell wall‐perturbing agents. In contrast, the Δfpr1 mutant was less sensitive to fewer stress cues. Most of 32 examined genes involved in DNA damage repair, Na⁺/K⁺ detoxification or osmotolerance and Ca²⁺ homeostasis were downregulated sharply in Δfpr2 and Δfpr3 but rarely so affected in Δfpr1, coinciding well with their phenotypic changes. These findings uncover important, but differential, roles of three FPRs in the fungal adaptation to insect host and environment and provide novel insight into their essential roles in calcium signalling pathway.     

Cleavage and degradation of EDEM1 promotes coxsackievirus B3 replication via ATF6a‐mediated unfolded protein response signalling

Our previous study of coxsackievirus B3 (CVB3)‐induced unfolded protein responses (UPR) found that overexpression of ATF6a enhances CVB3 VP1 capsid protein production and increases viral particle formation. These findings implicate that ATF6a signalling benefits CVB3 replication. However, the mechanism by which ATF6a signalling is transduced to promote virus replication is unclear. In this study, using a Tet‐On inducible ATF6a HeLa cell line, we found that ATF6a signalling downregulated the protein expression of the endoplasmic reticulum (ER) degradation‐enhancing α‐mannosidase‐like protein 1 (EDEM1), resulting in accumulation of CVB3 VP1 protein; in contrast, expression of a dominant negative ATF6a had the opposite effect. Furthermore, we found that EDEM1 was cleaved by both CVB3 protease 3C and virus‐activated caspase and subsequently degraded via the ubiquitin‐proteasome pathway. However, overexpression of EDEM1 caused VP1 degradation, likely via a glycosylation‐independent and ubiquitin‐lysosome pathway. Finally, we demonstrated that CRISPR/Cas9‐mediated knockout of EDEM1 increased VP1 accumulation and thus CVB3 replication. This is the first study to report the ER protein quality control of non‐enveloped RNA virus and reveals a novel mechanism by which CVB3 evades host ER quality control pathways through cleavage and degradation of the UPR target gene EDEM1, to ultimately benefit its own replication.