关键词： 新冠肺炎   焦虑量表   信度   效度   临界值  

摘要： 目的研究旨在对原版新冠肺炎焦虑情绪量表(C-19ASS)进行本土化调试,验证其稳定性与可靠性,确定其临界值,以判断量表是否能作为测量我国公众的新冠肺炎所致焦虑情绪的可靠工具。方法对C-19ASS进行翻译,形成中文版新冠肺炎焦虑情绪量表(C-19ASS-C)。基于按年龄和地区分层抽样的方法,采用C-19ASS-C和中文版新冠肺炎恐惧量表(FCV-19S-C)对1354名西安市城区居民开展调查。结果在探索性因子分析和验证性因子分析中依据共同度和因子载荷剔除不符合要求的条目5和9后得到了C-19ASS-C-7。探索性因子分析共提取两个公因子,分别对应“回避”和“坚持”维度。验证性因子分析显示适配指标良好。总量表的Cronbachα为0.833,OMEGA系数为0.835。两个维度的组合信度分别为0.7433和0.8291,收敛效度分别为0.4913和0.5488,区分效度分别为0.7009和0.7408。C-19ASS-C-7得分与FCV-19S-C得分存在显著正相关关系(r=0.496,P<0.01)。通过ROC曲线得到C-19ASS-C-7的最佳临界值为14分。根据临界值得出本研究的1354名受访者中约有64%的受访者存在由新冠肺炎所导致的焦虑情绪。结论C-19ASS-C-7具有良好的信度和效度,可以作为测量我国公众的新冠肺炎所致焦虑情绪的工具。政策决策者应及时对采取措施以减少公众的不良情绪,提升当前疫情防控的整体效能。

关键词： 公立医院   脆弱性分析   应急体系   疫情防控  

摘要： 医院应急体系既是卫生应急体系的重要组成部分,也是卫生应急体系有效发挥作用的关键环节。在应对新型冠状病毒感染疫情过程中,医院应急体系发挥了积极作用,但也暴露出应急体系不完善、能力不足、机制不健全等诸多问题与短板。本研究通过对宁夏56家二级以上公立医院应急体系建设情况调研,分析目前医院应急体系存在的主要问题,从而对建立和完善应急体系及机制,提升医院应急能力等方面提出对策建议。

关键词： 新型冠状病毒感染   淋巴细胞计数   奥密克戎变异株  

摘要： 目的探讨新型冠状病毒奥密克戎变异株感染患者淋巴细胞计数与预后关系。方法收集首都医科大学附属北京安贞医院2022年12月8日至2023年1月31日在院且于2023年2月1日前出院的新型冠状病毒奥密克戎变异株感染1313例患者的病历资料;根据淋巴细胞计数三分位数将患者分为3组,T1组(淋巴细胞计数≤0.59×10^(9)/L)433例;T2组[淋巴细胞计数(>0.59~1.07)×10^(9)/L]437例;T3组(淋巴细胞计数>1.07×10^(9)/L)443例。比较3组患者一般资料,采用Kaplan-Meier生存曲线分析各组患者生存情况。根据临床预后,将患者分为存活组与死亡组,使用限制性立方样条图分析患者淋巴细胞计数与预后关系,使用Cox回归模型分析不同模型中各指标与患者预后关系。结果1313例新型冠状病毒奥密克戎变异株感染患者,存活1038例(79.1%),死亡275例(20.9%)。T1组死亡比例、男性比例、年龄大于T2、T3组,体重指数小于T2、T3组(均P<0.05)。死亡组患者全程淋巴细胞计数均低于存活组,差异均有统计学意义(均P<0.001)。Kaplan-Meier生存曲线结果显示,T1组累积死亡率显著高于T2、T3组(P<0.001)。Cox回归分析结果显示,模型1(调整性别、年龄、体重指数)、模型2(模型1+既往病史)、模型3(模型2+血常规指标)校正后入院淋巴细胞计数均与患者预后显著相关(风险比分别为0.32、0.27、0.46,均P<0.01)。模型3校正后,限制性立方样条图显示,入院淋巴细胞计数与患者预后呈非线性关系(P=0.003);当入院淋巴细胞计数<0.844×10^(9)/L时,淋巴细胞计数降低与死亡风险升高相关(风险比=0.122,95%置信区间:0.054~0.275,P<0.001)。结论新型冠状病毒奥密克戎变异株感染患者入院淋巴细胞计数与预后呈非线性关系,淋巴细胞计数<0.844×10^(9)/L时,淋巴细胞计数越低,患者死亡风险越大。

关键词： 化湿宣肺合剂   新型冠状病毒   网络药理学   分子对接  

摘要： 目的:通过网络药理学和分子对接探寻化湿宣肺合剂用于防治新型冠状病毒(SARS-CoV-2)的活性化合物、作用靶点及通路,探索其可能的作用机制。方法:借助TCMSP、ETCM等数据库检索化湿宣肺合剂中药物的化学成分和作用靶点,使用Cytoscape软件构建其“中药-活性成分-相关靶点”网络图,通过GO富集和KEGG通路注释分析预测潜在的作用机制,并将化湿宣肺合剂中的核心成分与SARS-CoV-2、血管紧张素转化酶Ⅱ(ACE2)进行分子对接验证。结果:经筛选获得化湿宣肺合剂共280个活性化合物与4713个作用靶点,关键靶点涉及病毒感染、AKT1、TNF、MAPK及VEGF等。GO富集分析得到细胞组成(CC)功能条目599个,KEGG通路获得113条(P<0.05),主要涉及甲型流感(Influenza A)信号通路、TLR(Toll-like receptor)信号通路、PI3K-Akt信号通路、HIF-1信号通路等。分子对接结果显示化湿宣肺合剂中连翘苷、绿原酸、阿魏酸、木犀草素等核心成分与核心蛋白的亲和力较强。结论:化湿宣肺合剂中的连翘苷、绿原酸、木犀草素等核心成分可能通过与ACE2、3CL等的结合来抑制病毒的侵袭和复制,并可能通过调节IL6、MAPK3、MAPK1、IL1β、CCL2、EGFR和NOS3等关键靶点而在新冠肺炎的治疗中发挥作用,或为治疗新型冠状病毒肺炎的活性化合物。

关键词： COVID-19   Vaccine trial   Homologous booster   Heterologous booster   ChAdOx1 nCov-19   COVISHIELD   BBV152   Covaxin   Immunogenicity   Safety  

摘要： Background Primary SARS-CoV-2 vaccination has been shown to wane with time and provide lower protection from disease with new viral variants, prompting the WHO to recommend the administration of booster doses. We determined the safety and immunogenicity of homologous or heterologous boosters with ChAdOx1 nCoV-19 (COVISHIELDTM) or BBV152 (COVAXIN (R)), the two vaccines used widely for primary immunization in India, in participants who had already received two primary doses of these vaccines. Methods Participants primed with two doses each of COVISHIELDTM or COVAXIN (R) 12-36 weeks previously, were randomised to receive either COVISHIELDTM or COVAXIN (R) booster in a 1:1 ratio. The primary outcome was day 28 post-booster anti-spike IgG seropositivity and secondary outcomes were anti-spike IgG levels and assessment of safety and reactogenicity. The results of 90 days intention-to-treat analysis are presented. This trial is registered with ISRCTN (CTRI/2021/08/035648). Findings In the COVISHIELDTM primed group with 200 participants, the seropositivity 28 days post booster in the heterologous COVAXIN (R) arm was 99% and non-inferior to the homologous COVISHIELDTM arm, which was also 99% (difference 0%;95% CI: -2.8% to 2.7%). The geometric mean concentration (GMC) of anti-spike antibodies following heterologous COVAXIN (R) boost on day 28 was 36,190.78 AU/mL (95% CI: 30,526.64-42,905.88) while the GMC following homologous COVISHIELDTM boost was 97,445.09 AU/mL (82,626.97-114,920.7). In the COVAXIN (R) primed group with 204 participants, the seropositivity 28 days post booster in the heterologous COVISHIELDTM arm was 100% and non inferior to the homologous COVAXIN (R) arm which was 96% (difference 4%, 95% CI: 0.2%-7.8%). The GMC following heterologous COVISHIELDTM boost was 241,681.6 AU/mL (95% CI: 201,380.2-290,048.3) compared to homologous COVAXIN (R) boost, which was 48,473.94 AU/mL (95% CI: 38,529.56-60,984.95). The day 28 geometric mean ratio (GMR) of the anti-spike I

摘要： The authors regret that there has been an error published within Fig. 5 of this article. The authors inadvertently pasted the anti-spike plots for the "≥70 years" group instead of the pseudo-neutralising antibody plots (pages 808–809) to Fig. 5A a...

摘要： Coronavirus disease 2019 (COVID-19) has caused formidable global health crisis, and multiple vaccination programs have been rolled out to curb the spread of the pandemic. Genetic disorders like primary immunodeficiency diseases severely compromise...

关键词： SARS-CoV-2   Vaccine   Microangiopathic hemolytic anemia   Thrombotic microangiopathy   AstraZeneca   AZD1222  

摘要： Vaccine-associated thrombotic thrombocytopenic purpura (TTP) is a rare type of acquired TTP recently reported after COVID-19 vaccination. Merely four cases are ascribed to the ChAdOx1 nCoV-19 vaccine in the medical literature till the preparation of this study. In this case report, we describe a 43-year-old man who developed symptoms of TTP four days after receiving the second dose of the ChAdOx1 nCoV-19 vaccine. Peripheral blood smear demonstrated multiple schistocytes. Given a high plasmic score, he received plasma exchange, corticosteroids, and rituximab, and later, low ADAMTS 13 activity and high-titer ADAMTS inhibition antibody confirmed the diagnosis of COVID-19 vaccine-associated TTP. COVID-19 vaccine-associated TTP is an infrequent consequence of SARS-CoV-2 vaccination but with a substantial mortality rate which must be considered as one of the crucial differential diagnoses of post-COVID-19 vaccine thrombocytopenia besides vaccine-induced immune thrombotic thrombocytopenia and Immune thrombocytopenic purpura.

关键词： SARS-CoV-2   COVID-19   CoronaVac   nCoV-19   antibodies  

摘要： Background: The pandemic unleashed by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has infected more than 500 million people worldwide and caused more than 6 million deaths. Cellular and humoral immunity induced by infection or immunization are key factors in controlling the viral burden and avoiding the recurrence of coronavirus disease. The duration and effectiveness of immunity after infection is relevant to pandemic policy interventions, including the timing of vaccine boosters. Objectives: We sought to evaluate longitudinal binding and functional antibodies against SARS-CoV-2 receptor-binding domain in police officers and health care workers with a history of coronavirus disease 2019 and compare with SARS-CoV-2-naive individuals after vaccination with adenovirus-based ChAdOx1 nCoV-19 (AstraZeneca-Fiocruz) or the inactivated CoronaVac vaccine (Sinovac-Butantan Institute). Methods: A total of 208 participants were vaccinated. Of these, 126 (60.57%) received the ChAdOx1 nCoV-19 vaccine and 82 (39.42%) received the CoronaVac vaccine. Prevaccination and postvaccination blood was collected, and the amount of anti-SARS-CoV-2 IgG and the neutralizing ability of the antibodies to block the interaction between angiotensin-converting enzyme 2 and receptor-binding domain were determined. Results: Subjects with preexisting SARS-CoV-2 immunity and who received a single dose of ChAdOx1 nCoV-19 or CoronaVac have similar or superior antibody levels when compared with levels in seronegative individuals even after 2 doses of the vaccine. Neutralizing antibody titers of seropositive individuals were higher with a single dose of either ChAdOx1 nCoV-19 or CoronaVac compared with those of seronegative individuals. After 2 doses, both groups reached a plateau response. Conclusions: Our data reinforce the importance of vaccine boosters to increase specific binding and neutralizing SARSCoV-2 antibodies. (J Allergy Clin Immunol Global

关键词： ACE2 receptor   Binding affinity  

摘要： ContextSince the outbreak of COVID-19 in 2019, the 2019-nCovcoronavirus has appeared diverse mutational characteristics due to its ownflexible conformation. One multiple-mutant strain (Omicron) with surprisinglyinfective activity outburst, and affected the biological activities of currentdrugs and vaccines, making the epidemic significantly difficult to prevent andcontrol, and seriously threaten health around the world. Importunatelyexploration of mutant characteristics for novel coronavirus Omicron can supplystrong theoretical guidance for learning binding mechanism of mutant ***'s more, full acknowledgement of key mutated-residues on Omicron strain canprovide new methodology of the novel pathogenic mechanism to human ACE2receptor, as well as the subsequent vaccine *** this research, 3D structures of 32 single-point mutationsof 2019-nCov were firstly constructed, and 32-sites multiple-mutant Omicronwere finally obtained based one the wild-type virus by homology modeling *** total number of 33 2019-nCov/ACE2 complex systems were acquired byprotein-protein docking, and optimized by using preliminary molecular dynamicsimulations. Binding free energies between each 2019-nCov mutation system andhuman ACE2 receptor were calculated, and corresponding binding patternsespecially the regions adjacent to mutation site were analyzed. The resultsindicated that one total number of 6 mutated sites on the Omicron strain playedcrucial role in improving binding capacities from 2019-nCov to ACE2 ***, we performed long-term molecular dynamic simulations andprotein-protein binding energy analysis for the selected 6 mutations. 3infected individuals, the mutants T478K, Q493R and G496S with lower bindingenergies -66.36, -67.98 and -67.09 kcal/mol also presents the high *** findings indicated that the 3 mutations T478K, Q493R and G496S play thecrucial roles in enhancing binding affinity of Omicron to human ACE2 *** th