Alzheimer s disease,among the most common neurodegenerative disorders,is chara cterized by progressive cognitive impairment.At present,the Alzheimer’s disease main risk remains genetic ris ks,but major environmental ...Alzheimer s disease,among the most common neurodegenerative disorders,is chara cterized by progressive cognitive impairment.At present,the Alzheimer’s disease main risk remains genetic ris ks,but major environmental fa ctors are increasingly shown to impact Alzheimer’s disease development and progression.Microglia,the most important brain immune cells,play a central role in Alzheimer’s disease pathogenesis and are considered environmental and lifestyle"sensors."Factors like environmental pollution and modern lifestyles(e.g.,chronic stress,poor dietary habits,sleep,and circadian rhythm disorde rs)can cause neuroinflammato ry responses that lead to cognitive impairment via microglial functioning and phenotypic regulation.However,the specific mechanisms underlying interactions among these facto rs and microglia in Alzheimer’s disease are unclear.Herein,we:discuss the biological effects of air pollution,chronic stress,gut micro biota,sleep patterns,physical exercise,cigarette smoking,and caffeine consumption on microglia;consider how unhealthy lifestyle factors influence individual susceptibility to Alzheimer’s disease;and present the neuroprotective effects of a healthy lifestyle.Toward intervening and controlling these environmental risk fa ctors at an early Alzheimer’s disease stage,understanding the role of microglia in Alzheimer’s disease development,and to rgeting strategies to to rget microglia,co uld be essential to future Alzheimer’s disease treatments.展开更多
目的研究不同剂量直径≤2.5μm的细颗粒物(PM2.5)诱导卵清蛋白(OVA)致哮喘小鼠肺损伤的程度。方法雄性BALB/c小鼠被随机分为正常对照组、OVA哮喘组、(1、5、15)mg/m L PM2.5处理的OVA哮喘组。收集支气管肺泡灌洗液(BALF)进行Gimsa染色...目的研究不同剂量直径≤2.5μm的细颗粒物(PM2.5)诱导卵清蛋白(OVA)致哮喘小鼠肺损伤的程度。方法雄性BALB/c小鼠被随机分为正常对照组、OVA哮喘组、(1、5、15)mg/m L PM2.5处理的OVA哮喘组。收集支气管肺泡灌洗液(BALF)进行Gimsa染色观察白细胞数量,ELISA检测小鼠血清γ干扰素(IFN-γ)、白细胞介素17(IL-17)和IL-10的含量;实时定量PCR进行外周血单个核细胞(PBMC)Toll样受体4(TLR4)、核因子κB(NF-κB)的mRNA水平;Western blot法检测T细胞表达的T盒(T-bet)、维甲酸相关孤核受体γt(RORγt)和叉头盒P3(FOXP3)蛋白水平;HE染色观察小鼠肺组织病变情况。结果与对照组相比,OVA哮喘组小鼠的肺泡间隔增厚,肺泡腔增大,且出现较明显的炎性细胞浸润,BALF中与炎症反应相关的白细胞数目增多;与OVA哮喘组相比,15 mg/m L PM2.5诱导的哮喘小鼠上述变化极其明显。与对照组相比,OVA哮喘组小鼠血清中IFN-γ、IL-10显著降低,而IL-17显著增加;与OVA哮喘组相比,15 mg/m L PM2.5处理的OVA哮喘组IFN-γ、IL-10含量显著减少,而IL-17含量显著增加。与对照组相比,OVA哮喘组小鼠PBMC中TLR4、NF-κB表达量明显增加,与OVA哮喘组相比,15 mg/m L PM2.5处理OVA哮喘组TLR4、NF-κB表达量显著增加。与对照组相比,OVA哮喘组小鼠T-bet和FOXP3蛋白水平明显降低,RORγt蛋白水平明显升高;与OVA哮喘组相比,15 mg/m L PM2.5处理OVA哮喘组小鼠T-bet和FOXP3蛋白水平极显著降低,而RORγt蛋白水平显著增加。结论 15 mg/m L PM2.5通过激活TLR4/NF-κB信号通路促进OVA诱发的哮喘和肺损伤。展开更多
We report our numerical simulation on dispersive waves （DWs） generated in the Kr-filled Kagome hollow-core photonic crystal fiber, by deploying the unidirectional pulse propagation equation. Relatively strong disper...We report our numerical simulation on dispersive waves （DWs） generated in the Kr-filled Kagome hollow-core photonic crystal fiber, by deploying the unidirectional pulse propagation equation. Relatively strong dispersive waves are simultaneously generated at 2.5μm and 4.6μm. It is deciphered that the interplay between plasma currents due to Kr ionization and nonlinear effects plays a key role in DW generation. Remarkably, this kind of DW generation is corroborated by the plasma-corrected phase-matching condition.展开更多
The present study was designed to alert the public opinion and policy makers on the supposed enhancing effects of exposure to ambient air particulate matter with aerodynamic diameters < 2.5 mm (PM 2.5 ) on non-alco...The present study was designed to alert the public opinion and policy makers on the supposed enhancing effects of exposure to ambient air particulate matter with aerodynamic diameters < 2.5 mm (PM 2.5 ) on non-alcoholic fatty liver disease (NAFLD), the most common chronic liver disease in Western countries. For far too long literature data have been fixated on pulmonary diseases and/or cardiovascular disease, as consequence of particulate exposure, ignoring the link between the explosion of obesity with related syndromes such as NAFLD and air pollution, the worst characteristics of nowadays civilization. In order to delineate a clear picture of this major health problem, further studies should investigate whether and at what extent cigarette smoking and exposure to ambient air PM 2.5 impact the natural history of patients with obesity-related NAFLD,i.e. , development of non alcoholic steatohepatitis, disease characterized by a worse prognosis due its progression towards fibrosis and hepatocarcinoma.展开更多
基金supported by the National Natural Science Foundation of China,Nos.82071190 and 82371438(to LC)Innovative Strong School Project of Guangdong Medical University,No.4SG21230G(to LC)Scientific Research Foundation of Guangdong Medical University,No.GDMUM2020017(to CL)。
文摘Alzheimer s disease,among the most common neurodegenerative disorders,is chara cterized by progressive cognitive impairment.At present,the Alzheimer’s disease main risk remains genetic ris ks,but major environmental fa ctors are increasingly shown to impact Alzheimer’s disease development and progression.Microglia,the most important brain immune cells,play a central role in Alzheimer’s disease pathogenesis and are considered environmental and lifestyle"sensors."Factors like environmental pollution and modern lifestyles(e.g.,chronic stress,poor dietary habits,sleep,and circadian rhythm disorde rs)can cause neuroinflammato ry responses that lead to cognitive impairment via microglial functioning and phenotypic regulation.However,the specific mechanisms underlying interactions among these facto rs and microglia in Alzheimer’s disease are unclear.Herein,we:discuss the biological effects of air pollution,chronic stress,gut micro biota,sleep patterns,physical exercise,cigarette smoking,and caffeine consumption on microglia;consider how unhealthy lifestyle factors influence individual susceptibility to Alzheimer’s disease;and present the neuroprotective effects of a healthy lifestyle.Toward intervening and controlling these environmental risk fa ctors at an early Alzheimer’s disease stage,understanding the role of microglia in Alzheimer’s disease development,and to rgeting strategies to to rget microglia,co uld be essential to future Alzheimer’s disease treatments.
文摘目的研究不同剂量直径≤2.5μm的细颗粒物(PM2.5)诱导卵清蛋白(OVA)致哮喘小鼠肺损伤的程度。方法雄性BALB/c小鼠被随机分为正常对照组、OVA哮喘组、(1、5、15)mg/m L PM2.5处理的OVA哮喘组。收集支气管肺泡灌洗液(BALF)进行Gimsa染色观察白细胞数量,ELISA检测小鼠血清γ干扰素(IFN-γ)、白细胞介素17(IL-17)和IL-10的含量;实时定量PCR进行外周血单个核细胞(PBMC)Toll样受体4(TLR4)、核因子κB(NF-κB)的mRNA水平;Western blot法检测T细胞表达的T盒(T-bet)、维甲酸相关孤核受体γt(RORγt)和叉头盒P3(FOXP3)蛋白水平;HE染色观察小鼠肺组织病变情况。结果与对照组相比,OVA哮喘组小鼠的肺泡间隔增厚,肺泡腔增大,且出现较明显的炎性细胞浸润,BALF中与炎症反应相关的白细胞数目增多;与OVA哮喘组相比,15 mg/m L PM2.5诱导的哮喘小鼠上述变化极其明显。与对照组相比,OVA哮喘组小鼠血清中IFN-γ、IL-10显著降低,而IL-17显著增加;与OVA哮喘组相比,15 mg/m L PM2.5处理的OVA哮喘组IFN-γ、IL-10含量显著减少,而IL-17含量显著增加。与对照组相比,OVA哮喘组小鼠PBMC中TLR4、NF-κB表达量明显增加,与OVA哮喘组相比,15 mg/m L PM2.5处理OVA哮喘组TLR4、NF-κB表达量显著增加。与对照组相比,OVA哮喘组小鼠T-bet和FOXP3蛋白水平明显降低,RORγt蛋白水平明显升高;与OVA哮喘组相比,15 mg/m L PM2.5处理OVA哮喘组小鼠T-bet和FOXP3蛋白水平极显著降低,而RORγt蛋白水平显著增加。结论 15 mg/m L PM2.5通过激活TLR4/NF-κB信号通路促进OVA诱发的哮喘和肺损伤。
基金Supported by the National Natural Science Foundation of China under Grant Nos 11674243 and 11674242
文摘We report our numerical simulation on dispersive waves （DWs） generated in the Kr-filled Kagome hollow-core photonic crystal fiber, by deploying the unidirectional pulse propagation equation. Relatively strong dispersive waves are simultaneously generated at 2.5μm and 4.6μm. It is deciphered that the interplay between plasma currents due to Kr ionization and nonlinear effects plays a key role in DW generation. Remarkably, this kind of DW generation is corroborated by the plasma-corrected phase-matching condition.
文摘The present study was designed to alert the public opinion and policy makers on the supposed enhancing effects of exposure to ambient air particulate matter with aerodynamic diameters < 2.5 mm (PM 2.5 ) on non-alcoholic fatty liver disease (NAFLD), the most common chronic liver disease in Western countries. For far too long literature data have been fixated on pulmonary diseases and/or cardiovascular disease, as consequence of particulate exposure, ignoring the link between the explosion of obesity with related syndromes such as NAFLD and air pollution, the worst characteristics of nowadays civilization. In order to delineate a clear picture of this major health problem, further studies should investigate whether and at what extent cigarette smoking and exposure to ambient air PM 2.5 impact the natural history of patients with obesity-related NAFLD,i.e. , development of non alcoholic steatohepatitis, disease characterized by a worse prognosis due its progression towards fibrosis and hepatocarcinoma.
