The global COVID-19 pandemic arising from SARS-CoV-2 has impacted many lives,gaining interest worldwide ever since it was first identified in December 2019.Till 2023,752 million cumulative cases and 6.8 million deaths...The global COVID-19 pandemic arising from SARS-CoV-2 has impacted many lives,gaining interest worldwide ever since it was first identified in December 2019.Till 2023,752 million cumulative cases and 6.8 million deaths were documented globally.COVID-19 has been rapidly evolving,affecting virus transmissibility and properties and contributing to increased disease severity.The Omicron is themost circulating variant of concern.Although success in its treatment has indicated progress in tackling the virus,limitations in delivering the current antiviral agents in battling emerging variants remain remarkable.With the latest advancements in nanotechnology for controlling infectious diseases,liposomes have the potential to counteract SARS-CoV-2 because of their ability to employ different targeting strategies,incorporating monoclonal antibodies for the active and passive targeting of infected patients.This review will present a concise summary of the possible strategies for utilizing immunoliposomes to improve current treatment against the occurrence of SARSCoV-2 and its variants.展开更多
目的系统评价糖尿病患者在接种SARS-CoV-2疫苗后的体液和细胞免疫反应。方法检索Web of Science、PubMed、中国知网、万方数据知识服务平台、维普中文科技期刊全文数据库和中国生物医学文献数据库,获取国内外于2019年12月1日至2022年5...目的系统评价糖尿病患者在接种SARS-CoV-2疫苗后的体液和细胞免疫反应。方法检索Web of Science、PubMed、中国知网、万方数据知识服务平台、维普中文科技期刊全文数据库和中国生物医学文献数据库,获取国内外于2019年12月1日至2022年5月12日公开发表的有关糖尿病患者接种SARS-CoV-2疫苗后的体液和细胞免疫反应的观察性研究,经由2名研究者独立筛选文献和提取资料后,采用美国国立卫生研究质量评价工具对纳入文献进行偏倚风险评价,使用描述性统计方法进行汇总分析。结果13篇文献共纳入66651例研究对象,其中5874例(7.9%)患有糖尿病。7篇文献报道了接种第1剂疫苗后糖尿病患者和对照组的免疫反应,其中3篇文献表明,接种1剂SARS-CoV-2疫苗后,糖尿病患者血清抗体水平和阳性率低于对照组;11篇涉及接种2剂SARS-CoV-2疫苗后的免疫反应的文献中,2篇报道了糖尿病患者可产生与对照组相似的抗体反应,9篇报道了糖尿病患者的血清抗体水平、阳性率或细胞免疫反应低于对照组。结论接种SARS-CoV-2疫苗后糖尿病患者和对照组体液和细胞免疫反应均有所增加,但糖尿病患者增加幅度普遍低于对照组。展开更多
Background:The mobilization and redistribution of severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)specific T-cells and neutralizing antibodies(nAbs)during exercise is purported to increase immune surveillan...Background:The mobilization and redistribution of severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)specific T-cells and neutralizing antibodies(nAbs)during exercise is purported to increase immune surveillance and protect against severe coronavirus disease 2019(COVID-19).We sought to determine if COVID-19 vaccination would elicit exercise-responsive SARS-CoV-2 T-cells and transiently alter nAb titers.Methods:Eighteen healthy participants completed a 20-min bout of graded cycling exercise before and/or after receiving a COVID-19 vaccine.All major leukocyte subtypes were enumerated before,during,and after exercise by flow cytometry,and immune responses to SARS-CoV-2 were determined using whole blood peptide stimulation assays,T-cell receptor(TCR)-βsequencing,and SARS-CoV-2 nAb serology.Results:COVID-19 vaccination had no effect on the mobilization or egress of major leukocyte subsets in response to intensity-controlled graded exercise.However,non-infected participants had a significantly reduced mobilization of CD4+and CD8+naive T-cells,as well as CD4+central memory T-cells,after vaccination(synthetic immunity group);this was not seen after vaccination in those with prior SARS-CoV-2 infection(hybrid immunity group).Acute exercise after vaccination robustly mobilized SARS-CoV-2 specific T-cells to blood in an intensity-dependent manner.Both groups mobilized T-cells that reacted to spike protein;however,only the hybrid immunity group mobilized T-cells that reacted to membrane and nucleocapsid antigens.nAbs increased significantly during exercise only in the hybrid immunity group.Conclusion:These data indicate that acute exercise mobilizes SARS-CoV-2 specific T-cells that recognize spike protein and increases the redistribution of nAbs in individuals with hybrid immunity.展开更多
Coronavirus disease 2019(COVID-19),caused by the highly pathogenic severe acute respiratory syndrome coronavirus 2(SARS-CoV-2),primarily impacts the respiratory tract and can lead to severe outcomes such as acute resp...Coronavirus disease 2019(COVID-19),caused by the highly pathogenic severe acute respiratory syndrome coronavirus 2(SARS-CoV-2),primarily impacts the respiratory tract and can lead to severe outcomes such as acute respiratory distress syndrome,multiple organ failure,and death.Despite extensive studies on the pathogenicity of SARS-CoV-2,its impact on the hepatobiliary system remains unclear.While liver injury is commonly indicated by reduced albumin and elevated bilirubin and transaminase levels,the exact source of this damage is not fully understood.Proposed mechanisms for injury include direct cytotoxicity,collateral damage from inflammation,drug-induced liver injury,and ischemia/hypoxia.However,evidence often relies on blood tests with liver enzyme abnormalities.In this comprehensive review,we focused solely on the different histopathological manifestations of liver injury in COVID-19 patients,drawing from liver biopsies,complete autopsies,and in vitro liver analyses.We present evidence of the direct impact of SARS-CoV-2 on the liver,substantiated by in vitro observations of viral entry mechanisms and the actual presence of viral particles in liver samples resulting in a variety of cellular changes,including mitochondrial swelling,endoplasmic reticulum dilatation,and hepatocyte apoptosis.Additional ly,we describe the diverse liver pathology observed during COVID-19 infection,encompassing necrosis,steatosis,cholestasis,and lobular inflammation.We also discuss the emergence of long-term complications,notably COVID-19-related secondary sclerosing cholangitis.Recognizing the histopathological liver changes occurring during COVID-19 infection is pivotal for improving patient recovery and guiding decision-making.展开更多
It is a challenge to coordinate carrier-kinetics performance and the redox capacity of photogenerated charges synchronously at the atomic level for boosting photocatalytic activity.Herein,the atomic Ni was introduced ...It is a challenge to coordinate carrier-kinetics performance and the redox capacity of photogenerated charges synchronously at the atomic level for boosting photocatalytic activity.Herein,the atomic Ni was introduced into the lattice of hexagonal ZnIn_(2)S_(4) nanosheets(Ni/ZnIn_(2)S_(4))via directionalsubstituting Zn atom with the facile hydrothermal method.The electronic structure calculations indicate that the introduction of Ni atom effectively extracts more electrons and acts as active site for subsequent reduction reaction.Besides the optimized light absorption range,the elevation of Efand ECBendows Ni/ZnIn_(2)S_(4) photocatalyst with the increased electron concentration and the enhanced reduction ability for surface reaction.Moreover,ultrafast transient absorption spectroscopy,as well as a series of electrochemical tests,demonstrates that Ni/ZnIn_(2)S_(4) possesses 2.15 times longer lifetime of the excited charge carriers and an order of magnitude increase for carrier mobility and separation efficiency compared with pristine ZnIn_(2)S_(4).These efficient kinetics performances of charge carriers and enhanced redox capacity synergistically boost photocatalytic activity,in which a 3-times higher conversion efficiency of nitrobenzene reduction was achieved upon Ni/ZnIn_(2)S_(4).Our study not only provides in-depth insights into the effect of atomic directional-substitution on the kinetic behavior of photogenerated charges,but also opens an avenue to the synchronous optimization of redox capacity and carrier-kinetics performance for efficient solar energy conversion.展开更多
BACKGROUND The precise role of mitochondrial carrier homolog 2(MTCH2)in promoting malignancy in gastric mucosal cells and its involvement in gastric cancer cell metastasis have not been fully elucidated.AIM To determi...BACKGROUND The precise role of mitochondrial carrier homolog 2(MTCH2)in promoting malignancy in gastric mucosal cells and its involvement in gastric cancer cell metastasis have not been fully elucidated.AIM To determine the role of MTCH2 in gastric cancer.METHODS We collected 65 samples of poorly differentiated gastric cancer tissue and adjacent tissues,constructed MTCH2-overexpressing and MTCH2-knockdown cell models,and evaluated the proliferation,migration,and invasion of human gastric epithelial cells(GES-1)and human gastric cancer cells(AGS)cells.The mito-chondrial membrane potential(MMP),mitochondrial permeability transformation pore(mPTP)and ATP fluorescence probe were used to detect mitochondrial function.Mitochondrial function and ATP synthase protein levels were detected via Western blotting.RESULTS The expression of MTCH2 and ATP2A2 in gastric cancer tissues was significantly greater than that in adjacent tissues.Overexpression of MTCH2 promoted colony formation,invasion,migration,MMP expression and ATP production in GES-1 and AGS cells while upregulating ATP2A2 expression and inhibiting cell apoptosis;knockdown of MTCH2 had the opposite effect,promoting overactivation of the mPTP and promoting apoptosis.CONCLUSION MTCH2 can increase the malignant phenotype of GES-1 cells and promote the proliferation,invasion,and migration of gastric cancer cells by regulating mitochondrial function,providing a basis for targeted therapy for gastric cancer cells.展开更多
In coronavirus disease 2019(COVID-19),severe acute respiratory syndrome coronavirus-2(SARS-CoV-2)primarily targets the respiratory system,but evidence suggests extrapulmonary organ involvement,notably in the liver.Vir...In coronavirus disease 2019(COVID-19),severe acute respiratory syndrome coronavirus-2(SARS-CoV-2)primarily targets the respiratory system,but evidence suggests extrapulmonary organ involvement,notably in the liver.Viral RNA has been detected in hepatic tissues,and in situ hybridization revealed virions in blood vessels and endothelial cells.Electron microscopy confirmed viral particles in hepatocytes,emphasizing the need for understanding hepatotropism and direct cytopathic effects in COVID-19-related liver injury.Various factors contribute to liver injury,including direct cytotoxicity,vascular changes,inflammatory responses,immune reactions from COVID-19 and vaccinations,and druginduced liver injury.Although a typical hepatitis presentation is not widely documented,elevated liver biochemical markers are common in hospitalized COVID-19 patients,primarily showing a hepatocellular pattern of elevation.Long-term studies suggest progressive cholestasis may affect 20%of patients with chronic liver disease post-SARS-CoV-2 infection.The molecular mechanisms underlying SARS-CoV-2 infection in the liver and the resulting liver damage are complex.This“Editorial”highlights the expression of the Angiotensin-converting enzyme-2 receptor in liver cells,the role of inflammatory responses,the impact of hypoxia,the involvement of the liver's vascular system,the infection of bile duct epithelial cells,the activation of hepatic stellate cells,and the contribution of monocyte-derived macrophages.It also mentions that pre-existing liver conditions can worsen the outcomes of COVID-19.Understanding the interaction of SARS-CoV-2 with the liver is still evolving,and further research is required.展开更多
基金the financial support obtained from Universiti Kebangsaan Malaysia(DIP-2021-001)ASEANIndia Science&Technology Development Fund(AISTDF)(SERB/F/3955/2022-2023).
文摘The global COVID-19 pandemic arising from SARS-CoV-2 has impacted many lives,gaining interest worldwide ever since it was first identified in December 2019.Till 2023,752 million cumulative cases and 6.8 million deaths were documented globally.COVID-19 has been rapidly evolving,affecting virus transmissibility and properties and contributing to increased disease severity.The Omicron is themost circulating variant of concern.Although success in its treatment has indicated progress in tackling the virus,limitations in delivering the current antiviral agents in battling emerging variants remain remarkable.With the latest advancements in nanotechnology for controlling infectious diseases,liposomes have the potential to counteract SARS-CoV-2 because of their ability to employ different targeting strategies,incorporating monoclonal antibodies for the active and passive targeting of infected patients.This review will present a concise summary of the possible strategies for utilizing immunoliposomes to improve current treatment against the occurrence of SARSCoV-2 and its variants.
文摘目的系统评价糖尿病患者在接种SARS-CoV-2疫苗后的体液和细胞免疫反应。方法检索Web of Science、PubMed、中国知网、万方数据知识服务平台、维普中文科技期刊全文数据库和中国生物医学文献数据库,获取国内外于2019年12月1日至2022年5月12日公开发表的有关糖尿病患者接种SARS-CoV-2疫苗后的体液和细胞免疫反应的观察性研究,经由2名研究者独立筛选文献和提取资料后,采用美国国立卫生研究质量评价工具对纳入文献进行偏倚风险评价,使用描述性统计方法进行汇总分析。结果13篇文献共纳入66651例研究对象,其中5874例(7.9%)患有糖尿病。7篇文献报道了接种第1剂疫苗后糖尿病患者和对照组的免疫反应,其中3篇文献表明,接种1剂SARS-CoV-2疫苗后,糖尿病患者血清抗体水平和阳性率低于对照组;11篇涉及接种2剂SARS-CoV-2疫苗后的免疫反应的文献中,2篇报道了糖尿病患者可产生与对照组相似的抗体反应,9篇报道了糖尿病患者的血清抗体水平、阳性率或细胞免疫反应低于对照组。结论接种SARS-CoV-2疫苗后糖尿病患者和对照组体液和细胞免疫反应均有所增加,但糖尿病患者增加幅度普遍低于对照组。
文摘Background:The mobilization and redistribution of severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)specific T-cells and neutralizing antibodies(nAbs)during exercise is purported to increase immune surveillance and protect against severe coronavirus disease 2019(COVID-19).We sought to determine if COVID-19 vaccination would elicit exercise-responsive SARS-CoV-2 T-cells and transiently alter nAb titers.Methods:Eighteen healthy participants completed a 20-min bout of graded cycling exercise before and/or after receiving a COVID-19 vaccine.All major leukocyte subtypes were enumerated before,during,and after exercise by flow cytometry,and immune responses to SARS-CoV-2 were determined using whole blood peptide stimulation assays,T-cell receptor(TCR)-βsequencing,and SARS-CoV-2 nAb serology.Results:COVID-19 vaccination had no effect on the mobilization or egress of major leukocyte subsets in response to intensity-controlled graded exercise.However,non-infected participants had a significantly reduced mobilization of CD4+and CD8+naive T-cells,as well as CD4+central memory T-cells,after vaccination(synthetic immunity group);this was not seen after vaccination in those with prior SARS-CoV-2 infection(hybrid immunity group).Acute exercise after vaccination robustly mobilized SARS-CoV-2 specific T-cells to blood in an intensity-dependent manner.Both groups mobilized T-cells that reacted to spike protein;however,only the hybrid immunity group mobilized T-cells that reacted to membrane and nucleocapsid antigens.nAbs increased significantly during exercise only in the hybrid immunity group.Conclusion:These data indicate that acute exercise mobilizes SARS-CoV-2 specific T-cells that recognize spike protein and increases the redistribution of nAbs in individuals with hybrid immunity.
文摘Coronavirus disease 2019(COVID-19),caused by the highly pathogenic severe acute respiratory syndrome coronavirus 2(SARS-CoV-2),primarily impacts the respiratory tract and can lead to severe outcomes such as acute respiratory distress syndrome,multiple organ failure,and death.Despite extensive studies on the pathogenicity of SARS-CoV-2,its impact on the hepatobiliary system remains unclear.While liver injury is commonly indicated by reduced albumin and elevated bilirubin and transaminase levels,the exact source of this damage is not fully understood.Proposed mechanisms for injury include direct cytotoxicity,collateral damage from inflammation,drug-induced liver injury,and ischemia/hypoxia.However,evidence often relies on blood tests with liver enzyme abnormalities.In this comprehensive review,we focused solely on the different histopathological manifestations of liver injury in COVID-19 patients,drawing from liver biopsies,complete autopsies,and in vitro liver analyses.We present evidence of the direct impact of SARS-CoV-2 on the liver,substantiated by in vitro observations of viral entry mechanisms and the actual presence of viral particles in liver samples resulting in a variety of cellular changes,including mitochondrial swelling,endoplasmic reticulum dilatation,and hepatocyte apoptosis.Additional ly,we describe the diverse liver pathology observed during COVID-19 infection,encompassing necrosis,steatosis,cholestasis,and lobular inflammation.We also discuss the emergence of long-term complications,notably COVID-19-related secondary sclerosing cholangitis.Recognizing the histopathological liver changes occurring during COVID-19 infection is pivotal for improving patient recovery and guiding decision-making.
基金the National Natural Science Foundation of China (22209091)the Natural Science Foundation of Shandong Province (ZR2020QB057)+1 种基金the Key Program of National Natural Science Foundation of China (22133006)the Yankuang Group 2019 Science and Technology Program (YKKJ2019AJ05JG-R60)。
文摘It is a challenge to coordinate carrier-kinetics performance and the redox capacity of photogenerated charges synchronously at the atomic level for boosting photocatalytic activity.Herein,the atomic Ni was introduced into the lattice of hexagonal ZnIn_(2)S_(4) nanosheets(Ni/ZnIn_(2)S_(4))via directionalsubstituting Zn atom with the facile hydrothermal method.The electronic structure calculations indicate that the introduction of Ni atom effectively extracts more electrons and acts as active site for subsequent reduction reaction.Besides the optimized light absorption range,the elevation of Efand ECBendows Ni/ZnIn_(2)S_(4) photocatalyst with the increased electron concentration and the enhanced reduction ability for surface reaction.Moreover,ultrafast transient absorption spectroscopy,as well as a series of electrochemical tests,demonstrates that Ni/ZnIn_(2)S_(4) possesses 2.15 times longer lifetime of the excited charge carriers and an order of magnitude increase for carrier mobility and separation efficiency compared with pristine ZnIn_(2)S_(4).These efficient kinetics performances of charge carriers and enhanced redox capacity synergistically boost photocatalytic activity,in which a 3-times higher conversion efficiency of nitrobenzene reduction was achieved upon Ni/ZnIn_(2)S_(4).Our study not only provides in-depth insights into the effect of atomic directional-substitution on the kinetic behavior of photogenerated charges,but also opens an avenue to the synchronous optimization of redox capacity and carrier-kinetics performance for efficient solar energy conversion.
基金the Medical Science Research Projects in Hebei Province,No.20221526and Natural Science Foundation,No.2022-271.
文摘BACKGROUND The precise role of mitochondrial carrier homolog 2(MTCH2)in promoting malignancy in gastric mucosal cells and its involvement in gastric cancer cell metastasis have not been fully elucidated.AIM To determine the role of MTCH2 in gastric cancer.METHODS We collected 65 samples of poorly differentiated gastric cancer tissue and adjacent tissues,constructed MTCH2-overexpressing and MTCH2-knockdown cell models,and evaluated the proliferation,migration,and invasion of human gastric epithelial cells(GES-1)and human gastric cancer cells(AGS)cells.The mito-chondrial membrane potential(MMP),mitochondrial permeability transformation pore(mPTP)and ATP fluorescence probe were used to detect mitochondrial function.Mitochondrial function and ATP synthase protein levels were detected via Western blotting.RESULTS The expression of MTCH2 and ATP2A2 in gastric cancer tissues was significantly greater than that in adjacent tissues.Overexpression of MTCH2 promoted colony formation,invasion,migration,MMP expression and ATP production in GES-1 and AGS cells while upregulating ATP2A2 expression and inhibiting cell apoptosis;knockdown of MTCH2 had the opposite effect,promoting overactivation of the mPTP and promoting apoptosis.CONCLUSION MTCH2 can increase the malignant phenotype of GES-1 cells and promote the proliferation,invasion,and migration of gastric cancer cells by regulating mitochondrial function,providing a basis for targeted therapy for gastric cancer cells.
基金Supported by Agencia Nacional de Promoción Científica y Tecnológica(PICTO-2021-COVID secuelas-00005 to JQ).
文摘In coronavirus disease 2019(COVID-19),severe acute respiratory syndrome coronavirus-2(SARS-CoV-2)primarily targets the respiratory system,but evidence suggests extrapulmonary organ involvement,notably in the liver.Viral RNA has been detected in hepatic tissues,and in situ hybridization revealed virions in blood vessels and endothelial cells.Electron microscopy confirmed viral particles in hepatocytes,emphasizing the need for understanding hepatotropism and direct cytopathic effects in COVID-19-related liver injury.Various factors contribute to liver injury,including direct cytotoxicity,vascular changes,inflammatory responses,immune reactions from COVID-19 and vaccinations,and druginduced liver injury.Although a typical hepatitis presentation is not widely documented,elevated liver biochemical markers are common in hospitalized COVID-19 patients,primarily showing a hepatocellular pattern of elevation.Long-term studies suggest progressive cholestasis may affect 20%of patients with chronic liver disease post-SARS-CoV-2 infection.The molecular mechanisms underlying SARS-CoV-2 infection in the liver and the resulting liver damage are complex.This“Editorial”highlights the expression of the Angiotensin-converting enzyme-2 receptor in liver cells,the role of inflammatory responses,the impact of hypoxia,the involvement of the liver's vascular system,the infection of bile duct epithelial cells,the activation of hepatic stellate cells,and the contribution of monocyte-derived macrophages.It also mentions that pre-existing liver conditions can worsen the outcomes of COVID-19.Understanding the interaction of SARS-CoV-2 with the liver is still evolving,and further research is required.