猪繁殖与呼吸综合征病毒(porcine reproductive and respiratory syndrome virus,PRRSV)是一种具有囊膜的单股正链RNA动脉炎病毒。PRRSV感染猪后引起猪繁殖与呼吸综合征(porcine reproductive and respiratory syndrome,PRRS),导致妊娠...猪繁殖与呼吸综合征病毒(porcine reproductive and respiratory syndrome virus,PRRSV)是一种具有囊膜的单股正链RNA动脉炎病毒。PRRSV感染猪后引起猪繁殖与呼吸综合征(porcine reproductive and respiratory syndrome,PRRS),导致妊娠母猪流产、死胎、弱胎和木乃伊胎以及各年龄段猪呼吸系统疾病,对全球养猪业造成巨大的经济损失。全面解析PRRSV感染机制有助于防控PRRS,助力生猪产业高质量发展。自噬是一种依赖于溶酶体对异常蛋白质、受损细胞器、入侵病原微生物等进行降解回收的过程,包括巨自噬、微自噬和分子伴侣介导的自噬(chaperone-mediated autophagy,CMA)3种类型。其中,巨自噬是目前研究最多的自噬类型,可进一步分为非选择性自噬和选择性自噬。自噬在维持细胞稳态、控制细胞器质量、运输胞内物质等生理过程中发挥着重要作用,还影响神经退行性疾病、自身免疫病、癌症等多种疾病的发生和发展。此外,自噬作为一种防御机制,能够清除入侵宿主细胞的病毒;然而,病毒进化出一系列策略拮抗自噬降解甚至利用自噬为自身感染服务。文章通过笔者自身的研究经历和近年来自噬在PRRSV感染过程中的研究报道,系统梳理介绍了自噬在PRRSV感染中发挥的双重作用:一方面,PRRSV非结构蛋白和结构蛋白通过多种途径诱导包括内质网自噬、线粒体自噬、聚集体自噬、脂噬等选择性自噬在内的巨自噬和CMA,随后这些诱导的巨自噬和CMA参与PRRSV复制、拮抗细胞凋亡、抑制宿主免疫反应等过程促进病毒感染;另一方面,宿主细胞通过内质网自噬等选择性巨自噬和CMA降解PRRSV非结构蛋白、激活抗病毒免疫应答等抑制病毒感染,以期从自噬角度深入揭示PRRSV感染机制。另外,文章还通过总结自噬在PRRSV感染中的作用机制,提出该研究领域仍然存在争议或尚未解答的科学问题,为今后研究提供线索;同时通过列举靶向自噬的抗病毒研究,提出自噬可作为抗PRRSV策略研发的潜在靶点,为防控PRRS提供新的思路。展开更多
Biodiversity is a critical component for sustainable human development.The recently concluded Sixteenth Conference of Parties to the Convention on Biological Diversity 2024 highlighted the need for whole of society mo...Biodiversity is a critical component for sustainable human development.The recently concluded Sixteenth Conference of Parties to the Convention on Biological Diversity 2024 highlighted the need for whole of society mobilization to address the global biodiversity crisis by translating international conservation commitments into effective local actions.A study to understand the linkages between ecological conservation measures in Aba Tibetan and Qiang Autonomous Prefecture and the United Nations Sustainable Development Goal(SDG)15 target 15.5,was undertaken,using the content analysis method that reviewed international conventions,national policies,and local government measures and practices.The study revealed that there was a strong link with between Aba’s conservation strategies and SDG 15 particularly target 15.5 in reducing natural habitat degradation,curbing biodiversity loss,and protecting endangered species.The Aba Prefecture has established 25 nature reserves,that are regulated by stringent wetland protection measures,and comprehensive legal frameworks for biodiversity conservation which is in line with SDG 15.The findings further show that that the Aba Prefecture’s efforts in ecosystem conservation,species protection,and sustainable resource utilization can be used to help meet SDG 15 target 15.5.The study also identified steps to help localize SDG aspirations and goals,by strengthening long-term data monitoring and local herder participation.These insights can be used to support other initiatives and measures in other similar biodiversity-rich regions seeking to implement global conservation goals at the local level,particularly in ecologically sensitive mountainous areas.展开更多
目的评估炎症因子与骨质疏松症(osteoporosis,OP)之间的因果关系。方法从GWAScatalog数据库中获取41个炎症因子和骨密度(bone mineral density,BMD)的GWAS数据,芬兰数据库中获取OP的GWAS数据。采用逆方差加权法(IVW)、MR-Egger回归法(M...目的评估炎症因子与骨质疏松症(osteoporosis,OP)之间的因果关系。方法从GWAScatalog数据库中获取41个炎症因子和骨密度(bone mineral density,BMD)的GWAS数据,芬兰数据库中获取OP的GWAS数据。采用逆方差加权法(IVW)、MR-Egger回归法(MER)、加权中位数法(WME)、简单中位数法和加权中值方法进行两样本孟德尔随机化分析,并以IVW法为主要分析方法。再进行敏感性分析以检验结果的可靠性,留一法评估单核苷酸多态性对结果的影响。最后进行药物预测和分子对接进一步验证炎症因子的药理价值。结果研究表明炎症因子与OP和BMD之间存在因果关系。其中肿瘤坏死因子相关的凋亡诱导配体(TRAIL)和单核细胞趋化蛋白1(MCP-1/MCAF)与OP发生风险呈正相关;肿瘤坏死因子β(TNF-β)与0~15岁人群的BMD呈负相关;白细胞介素7(IL-7)与15~30岁人群的BMD呈负相关;肝细胞生长因子(HGF)与30~45岁人群的BMD呈负相关;巨噬细胞炎性蛋白1α(MIP-1α)和巨噬细胞集落刺激因子(M-CSF)与60岁以上人群的BMD呈负相关;MIP-1α与全年龄段人群的BMD呈负相关。此外,分子对接证明了药物与蛋白质的良好结合,进一步证实了这些靶点的药理价值。结论通过孟德尔随机化方法全面评估了41种炎症因子对OP和BMD的因果效应,表明炎症因子与OP和BMD之间存在因果关联,提示OP患者可以在疾病早期通过干预炎症因子进而干预OP的发生发展过程。展开更多
文摘Biodiversity is a critical component for sustainable human development.The recently concluded Sixteenth Conference of Parties to the Convention on Biological Diversity 2024 highlighted the need for whole of society mobilization to address the global biodiversity crisis by translating international conservation commitments into effective local actions.A study to understand the linkages between ecological conservation measures in Aba Tibetan and Qiang Autonomous Prefecture and the United Nations Sustainable Development Goal(SDG)15 target 15.5,was undertaken,using the content analysis method that reviewed international conventions,national policies,and local government measures and practices.The study revealed that there was a strong link with between Aba’s conservation strategies and SDG 15 particularly target 15.5 in reducing natural habitat degradation,curbing biodiversity loss,and protecting endangered species.The Aba Prefecture has established 25 nature reserves,that are regulated by stringent wetland protection measures,and comprehensive legal frameworks for biodiversity conservation which is in line with SDG 15.The findings further show that that the Aba Prefecture’s efforts in ecosystem conservation,species protection,and sustainable resource utilization can be used to help meet SDG 15 target 15.5.The study also identified steps to help localize SDG aspirations and goals,by strengthening long-term data monitoring and local herder participation.These insights can be used to support other initiatives and measures in other similar biodiversity-rich regions seeking to implement global conservation goals at the local level,particularly in ecologically sensitive mountainous areas.
文摘目的评估炎症因子与骨质疏松症(osteoporosis,OP)之间的因果关系。方法从GWAScatalog数据库中获取41个炎症因子和骨密度(bone mineral density,BMD)的GWAS数据,芬兰数据库中获取OP的GWAS数据。采用逆方差加权法(IVW)、MR-Egger回归法(MER)、加权中位数法(WME)、简单中位数法和加权中值方法进行两样本孟德尔随机化分析,并以IVW法为主要分析方法。再进行敏感性分析以检验结果的可靠性,留一法评估单核苷酸多态性对结果的影响。最后进行药物预测和分子对接进一步验证炎症因子的药理价值。结果研究表明炎症因子与OP和BMD之间存在因果关系。其中肿瘤坏死因子相关的凋亡诱导配体(TRAIL)和单核细胞趋化蛋白1(MCP-1/MCAF)与OP发生风险呈正相关;肿瘤坏死因子β(TNF-β)与0~15岁人群的BMD呈负相关;白细胞介素7(IL-7)与15~30岁人群的BMD呈负相关;肝细胞生长因子(HGF)与30~45岁人群的BMD呈负相关;巨噬细胞炎性蛋白1α(MIP-1α)和巨噬细胞集落刺激因子(M-CSF)与60岁以上人群的BMD呈负相关;MIP-1α与全年龄段人群的BMD呈负相关。此外,分子对接证明了药物与蛋白质的良好结合,进一步证实了这些靶点的药理价值。结论通过孟德尔随机化方法全面评估了41种炎症因子对OP和BMD的因果效应,表明炎症因子与OP和BMD之间存在因果关联,提示OP患者可以在疾病早期通过干预炎症因子进而干预OP的发生发展过程。
