With the reduction of sequencing costs,optimization of algorithms,and improvement of multi-omics integration capabilities,transcriptomics,as a core technology for analyzing gene expression dynamics and discovering key...With the reduction of sequencing costs,optimization of algorithms,and improvement of multi-omics integration capabilities,transcriptomics,as a core technology for analyzing gene expression dynamics and discovering key functional molecules,has shown great potential in the field of disease prevention and control[1,2].The multi-continental transcriptomics study of tick-borne poxvirus not only provides a new perspective for understanding the evolution and transmission of vector-mediated viruses,but also reflects the trend of transcriptomics research and highlights its key role in disease prevention and control[3].展开更多
Objective Patients with severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)infection frequently develop central nervous system damage,yet the mechanisms driving this pathology remain unclear.This study investi...Objective Patients with severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)infection frequently develop central nervous system damage,yet the mechanisms driving this pathology remain unclear.This study investigated the primary pathways and key factors underlying brain tissue damage induced by the SARS-CoV-2 beta variant(lineage B.1.351).Methods K18-hACE2 and C57BL/6 mice were intranasally infected with the SARS-CoV-2 beta variant.Viral replication,pathological phenotypes,and brain transcriptomes were analyzed.Gene Ontology(GO)analysis was performed to identify altered pathways.Expression changes of host genes were verified using reverse transcription-quantitative polymerase chain reaction and Western blot.Results Pathological alterations were observed in the lungs of both mouse strains.However,only K18-hACE2 mice exhibited elevated viral RNA loads and infectious titers in the brain at 3 days post-infection,accompanied by neuropathological injury and weight loss.GO analysis of infected K18-hACE2 brain tissue revealed significant dysregulation of genes associated with innate immunity and antiviral defense responses,including type I interferons,pro-inflammatory cytokines,Toll-like receptor signaling components,and interferon-stimulated genes.Neuroinflammation was evident,alongside activation of apoptotic and pyroptotic pathways.Furthermore,altered neural cell marker expression suggested viral-induced neuroglial activation,resulting in caspase 4 and lipocalin 2 release and disruption of neuronal molecular networks.Conclusion These findings elucidate mechanisms of neuropathogenicity associated with the SARS-CoV-2 beta variant and highlight therapeutic targets to mitigate COVID-19-related neurological dysfunction.展开更多
Objective This study aimed to evaluate the relationships of white blood cell(WBC)count,platelet(PLT)count,and PLT-to-WBC ratio(PWR)with muscle mass in Chinese older adults.Methods This cross-sectional analysis involve...Objective This study aimed to evaluate the relationships of white blood cell(WBC)count,platelet(PLT)count,and PLT-to-WBC ratio(PWR)with muscle mass in Chinese older adults.Methods This cross-sectional analysis involved 4,033 Chinese older adults aged≥65 years from the Healthy Ageing and Biomarkers Cohort Study.Muscle mass and total skeletal muscle mass index(TSMI)were measured by bioelectric impedance analysis.WBC,PLT,and PWR were measured using standard methods.Multivariate linear regression was used to examine the associations of WBC count,PLT count,and PWR with TSMI.Results High WBC count,PLT count,and PWR were associated with low TSMI,with coefficients of-0.0091(95%confidence interval[CI]:-0.0142 to-0.0041),-0.0119(95%CI:-0.0170 to-0.0068),and-0.0051(95%CI:-0.0102 to-0.0001).The associations between the three inflammatory indices and TSMI were linear.Stratified analyses indicated that the relationship between inflammatory markers and TSMI was more evident in male participants and in individuals aged<80 years than in their counterparts.Conclusion Elevated WBC count,PLT count,and PWR correlated with muscle mass loss.This study highlights the importance of regular monitoring of inflammatory markers as a potential strategy for the screening and management of sarcopenia in older adults.展开更多
文摘With the reduction of sequencing costs,optimization of algorithms,and improvement of multi-omics integration capabilities,transcriptomics,as a core technology for analyzing gene expression dynamics and discovering key functional molecules,has shown great potential in the field of disease prevention and control[1,2].The multi-continental transcriptomics study of tick-borne poxvirus not only provides a new perspective for understanding the evolution and transmission of vector-mediated viruses,but also reflects the trend of transcriptomics research and highlights its key role in disease prevention and control[3].
基金supported by the National Key Research and Development Program of China(2023YFC3041500).
文摘Objective Patients with severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)infection frequently develop central nervous system damage,yet the mechanisms driving this pathology remain unclear.This study investigated the primary pathways and key factors underlying brain tissue damage induced by the SARS-CoV-2 beta variant(lineage B.1.351).Methods K18-hACE2 and C57BL/6 mice were intranasally infected with the SARS-CoV-2 beta variant.Viral replication,pathological phenotypes,and brain transcriptomes were analyzed.Gene Ontology(GO)analysis was performed to identify altered pathways.Expression changes of host genes were verified using reverse transcription-quantitative polymerase chain reaction and Western blot.Results Pathological alterations were observed in the lungs of both mouse strains.However,only K18-hACE2 mice exhibited elevated viral RNA loads and infectious titers in the brain at 3 days post-infection,accompanied by neuropathological injury and weight loss.GO analysis of infected K18-hACE2 brain tissue revealed significant dysregulation of genes associated with innate immunity and antiviral defense responses,including type I interferons,pro-inflammatory cytokines,Toll-like receptor signaling components,and interferon-stimulated genes.Neuroinflammation was evident,alongside activation of apoptotic and pyroptotic pathways.Furthermore,altered neural cell marker expression suggested viral-induced neuroglial activation,resulting in caspase 4 and lipocalin 2 release and disruption of neuronal molecular networks.Conclusion These findings elucidate mechanisms of neuropathogenicity associated with the SARS-CoV-2 beta variant and highlight therapeutic targets to mitigate COVID-19-related neurological dysfunction.
基金supported by the National Natural Science Foundation of China(grant nos.82025030,82222063,and 82388102)the National Key Research and Development Program of China(grant no.2023YFC3603400)。
文摘Objective This study aimed to evaluate the relationships of white blood cell(WBC)count,platelet(PLT)count,and PLT-to-WBC ratio(PWR)with muscle mass in Chinese older adults.Methods This cross-sectional analysis involved 4,033 Chinese older adults aged≥65 years from the Healthy Ageing and Biomarkers Cohort Study.Muscle mass and total skeletal muscle mass index(TSMI)were measured by bioelectric impedance analysis.WBC,PLT,and PWR were measured using standard methods.Multivariate linear regression was used to examine the associations of WBC count,PLT count,and PWR with TSMI.Results High WBC count,PLT count,and PWR were associated with low TSMI,with coefficients of-0.0091(95%confidence interval[CI]:-0.0142 to-0.0041),-0.0119(95%CI:-0.0170 to-0.0068),and-0.0051(95%CI:-0.0102 to-0.0001).The associations between the three inflammatory indices and TSMI were linear.Stratified analyses indicated that the relationship between inflammatory markers and TSMI was more evident in male participants and in individuals aged<80 years than in their counterparts.Conclusion Elevated WBC count,PLT count,and PWR correlated with muscle mass loss.This study highlights the importance of regular monitoring of inflammatory markers as a potential strategy for the screening and management of sarcopenia in older adults.
