Residential Thermal Comfort in Western Agricultural and Pastoral Areas of Inner Mongolia in Shoulder Season

对内蒙古西部农牧区的81户住宅的过渡季和采暖期初的室内外环境参数进行了现场测试,并以主观问卷调查的方式对居民的着装情况和热感觉等做了统计。经过对; 调查测试的结果进行了统计分析,得出内蒙古西部农牧区的的过渡季和采暖期初的热中性温度为15.6 ℃和15.3 ℃,热期望温度为17.9; ℃和18.6 ℃, 80%居民可接受温度下限为13.1 ℃和14.3 ℃, 90%的热可接受温度范围为15.9 ~ 23.3 ℃和17.5 ~; 21.9 ℃。结果表明处于当地气候条件下和穿衣、适应措施的综合影响下,农牧区居民对偏冷环境的适应性较好。The indoor and outdoor environmental parameters of 81 houses in the; western agricultural and pastoral areas of Inner Mongolia in shoulder; season and heating periods were tested.Questionnaire about the clothing; and thermal sensation was sent to residents in the houses.By analyzing; the survey results,it was found that the acceptable neutral temperature; in shoulder season and heating periods is 15.6 ℃ and 15.5; ℃,respectively; the preferred temperature in shoulder season and heating; periods is 17.9 ℃ and 18.6 ℃,respectively; the lowest temperature that; 80% residents can accept in shoulder season and heating periods is 13.1; ℃ and 14.3 ℃, respectively; and the thermal comfort temperature at which; 90% residents feel satisfied in shoulder season and heating periods; ranges from 15.9 ℃ to 23.3 ℃ and from 17.5 ℃ to 21.9 ℃,respectively.The; results show that the residents in agricultural and pastoral areas are; better adaptable to the cold environment because of the combined; influence of local climate,dressing and adaptation measures.国家自然科学基金资助项目; 内蒙古自然科学基金资助项目; 内蒙古自然科学基金资助项目; 内蒙古研究生教育创新计划资助项

油酰乙醇胺对脂多糖诱导的THP-1细胞炎症因子表达的影响

目的探讨油酰乙醇胺(OEA)对细菌脂多糖(LPS)诱导的人急性白血病单核细胞(THP-1)中前炎症因子TNF-α、IL-1β、IL-6表达的影响,并初步探讨OEA作为过氧化物酶体增殖物激活受体-α(PPAR-α)激动剂参与对炎症调节的作用机制。方法体外培养的THP-1细胞,分别加入不同浓度的OEA(10,20,40μmol/L)或非诺贝特(100μmol/L)共同孵育1 h后,用1μg/mL LPS分别诱导6或24 h。采用RT-PCR、实时定量PCR和酶联免疫吸附检测测定细胞中TNF-α、IL-1β、IL-6 mRNA和蛋白的表达的变化,并使用实时定量PCR及Western blot方法检测PPAR-α及Toll样受体4(TLR4)的mRNA和蛋白的表达。结果相对于正常THP-1细胞,LPS诱导后细胞中炎症因子(TNF-α、IL-1β、IL-6)表达明显增加。OEA对TNF-α、IL-1β、IL-6 mRNA和蛋白的表达有抑制作用,并呈现出一定的剂量依赖性。且OEA在激活PPAR-α表达的同时能够抑制TLR4的表达。结论 OEA对LPS诱导的炎症反应有抑制作用,其机制可能与激活PPAR-α,下调TLR4的表达有关

油酰乙醇胺对血管紧张素Ⅱ诱导的血管平滑肌细胞增殖的影响

目的研究油酰乙醇胺(OEA)对血管紧张素Ⅱ(AngⅡ)刺激大鼠主动脉血管平滑肌细胞(VSMCs)增殖的抑制作用以及对p38信号通路的影响。方法分离大鼠胸主动脉,组织贴块法培养VSMCs,AngⅡ刺激VSMCs建立细胞增殖模型,不同浓度OEA(5,10,20μmol/L)作用后,用溴脱氧核苷尿嘧啶(BrdU)掺入的方法检测细胞增殖活性;流式细胞术检测细胞周期变化;Western-bolt法检测对P-p38和p38蛋白表达的影响。结果与AngⅡ组比较,随着OEA浓度升高,VSMCs的增殖受到抑制、G0/G1比例显著升高,G2/M比例显著降低,且P-p38和p38蛋白的表达量降低并呈浓度依赖关系。结论 OEA对VSMCs的增殖有抑制作用,其机制可能是抑制了p38MAPK信号通路

Numerical study on suspended sediment concentration in Jiulong Estuary-Xiamen Bay and sediment transport mechanism in tidal inlets with multi-fork

基于环境流体动力学模型(Environment Fluid Dynamic Code/EFDC)水动力和泥沙模块,该文针对九龙江口-厦门湾水域潮动力强、浅滩面积大的特点建立二维潮流泥沙数学模型并利用实测数据进行校验。模型精简适用,成功反演了该水域的水动力场和悬沙浓度场,并能正确反映浅水区域的水沙运动特征。结果表明:在潮流作用下,厦门湾水体中悬沙浓度由外向内递增,悬沙随着潮流的涨落在湾内外作中-长距离的往复运动。湾内特别是浅滩区,大潮期悬沙浓度大于小潮期且浓度随潮变化明显,小潮期悬沙场则较为稳定。采用抓斗式挖泥船(源强Q=7.5 t/h)在翔安东南侧浅滩疏浚作业对邻近保护区基本无影响,但翔安南部"五岔口"型潮汐汊道存在能远程输运近岸疏浚泥沙的"泥泵式"水动力场,促使形成环绕厦门岛东海域的带状悬沙分布,该文进一步揭示了形成该分布的水动力机制。增大疏浚强度可导致白海豚保护区被污染,悬沙带宽度增大,浓度上升。Based on hydrodynamic and sediment transport module of Environment Fluid Dynamic Code/EFDC, a 2-Dimensional mathematical model was applied to the simulation of tidal current and sediment transport in Jiulong Estuary-Xiamen Bay, which was set up with full consideration of the strong tide and large-area shoal in the study area. The model was calibrated and verified using observational data and the simulation results agreed with measured data well, which successfully re-acted the hydrodynamic field and suspended sediment transport in this area, including that of the shoal area. The research shows that, mainly controlled by tidal current, suspended sediment concentration(SSC) increases progressively from outside to inside of Xiamen Bay and suspended sediments move forth and back as tidal currents flow rectilinearly along channels. Inside the bay, especially in shoal area, SSC in spring season fluctuates tidally and is much higher than that in neap season which remains lower and more stable. Dredging in the shoal area positioned to the south east of Xiang'an using grab dredger with source strength of 7.5 t/h almost has no effect on the adjacent protection zone, however, the water area with five-forks positioned to the south of Xiang'an exists a dredge-pump-like hydrodynamic field, through which dredging-produced sediments can be transported in long distance. The special hydrodynamic field leads to the formation of ribbon-pattern distribution of suspended sediments located in the eastern waters of Xiamen island and the hydrodynamic mechanism of it is revealed. Amplifying dredging intensity can result in the pollution of White Dolphin Protection Zone, broadening of ribbon-pattern distribution and increasing of the SSC.国家自然科学基金项目(41406121)~

The effect of s-Oleylpropanolamide on the expression of cell adhesion molecules in human umbilical vein endothelial cells

目的探讨s-油酰丙醇胺对用肿瘤坏死因子α(TNF-α)诱导的人脐静脉内皮细胞黏附分子(VCAM-1,I-CAM-1,E选择素)表达的影响。方法从新鲜的脐带中分离出人脐静脉内皮细胞,培养至3~9代,用不同浓度的s-油酰丙醇胺(10,50,100μmol/L)孵育12 h后,用TNF-α(20 ng/mL)孵育8 h,采用荧光实时定量PCR和细胞酶联免疫吸附试验分别检测VCAM-1,ICAM-1,E选择素的mRNA及蛋白的表达,同时采用细胞黏附实验检测其对细胞黏附的影响。结果相对于正常的人脐静脉内皮细胞,TNF-α诱导后的人脐静脉内皮细胞黏附分子(VCAM-1,ICAM-1,E-选择素)的表达明显增加。s-油酰丙醇胺可以显著的抑制VCAM-1的表达,并呈现出一定的剂量依赖性,而且对人急性单核细胞性白血病细胞(THP-1)的黏附也有明显的抑制作用,但对ICAM-1,E-选择素的表达却没有影响。结论s-油酰丙醇胺和大多数的PPARα激动剂一样,能够抑制慢性炎症,减少单核细胞的黏附,抑制VCAM-1的表达,而对急性炎症没有作用,如对E-选择素的表达无影响。 【英文摘要】 Purpose To investigate the effect of s-Oleylpropanolamide on the expression of cell adhesion molecules such as VCAM-1,ICAM-1,E-selectin in human umbilical vein endothelial cells(HUVECs).Methods HUVECs were pretreated with different concentrations of s-Oleylpropanolamide for 12 h and then stimulated with TNF-α for 8 h.Cell Enzyme linked immunsorbendt assay.Real-time PCR and adhesion assay were performe to measure the expression of ahesion molecules in mRNA and protein levels and monocyte binding.Results s-Ol...厦门市科技计划高校创新项目(3502Z20083007);; 厦门大学“活性有机小分子的合成化学与化学生物学”创新团队项

IL-18、IL-12及相关因子在大鼠实验性自身免疫心肌炎心肌中的表达时程和特征

目的:探讨IL-18、IL-12及相关细胞因子在大鼠实验性自身免疫心肌炎(EAM)心肌中的表达时程和特征。方法:以猪心脏肌球蛋白加等体积弗氏完全佐剂,辅结核杆菌H37Ra株之乳液为抗原,于Lewis大鼠双后肢皮下注射造模(EAM);用胶原酶灌流和网筛过滤法分离纯化心肌细胞;经免疫组化技术评估心肌损伤程度;按实时荧光定量法测急性期和慢性期,IL-18、IL-12及相关因子(IL-18R,IL-18RAcPL,IL-18BP以及IL-12p40,IL-12p35,IL-12Rβ1,IL-12Rβ2)mRNA表达情况。结果:IL-18、IL-12及相关因子表达主要在急性期,免疫后2周表达增多并达峰值(P<0.01,与正常对照组比较),4周后减少,并与EAM病程正相关;IL-18、IL-12及相关因子主要在巨噬细胞表达,其受体复合物在αβT细胞表达;慢性期仅IL-18BP在心肌细胞有表达。结论:IL-18、IL-12及相关因子参与EAM病理过程,各因子主要集中于急性期巨噬细胞和αβT细胞表达

Effect of oleoylethanolamide on expression of vascular cell adhesion molecule-1 in human umbilical vein endothelial cells

目的探讨油酰乙醇胺(OEA)对肿瘤坏死因子α(TNF-α)诱导的人脐静脉内皮细胞血管细胞黏附分子-1(VCAM-1)表达的影响。方法体外培养人脐静脉内皮细胞,分别加入3种不同浓度的OEA(10,50,100μmol/L)或非诺贝特(10,50,100μmol/L)共同孵育10 h,再加入TNF-α共同孵育6 h,采用实时定量逆转录聚合酶链式反应和酶联免疫吸附剂检测测定VCAM-1以及mRNA和蛋白的表达,并采用Western blot方法检测过氧化物酶体增殖物激活受体α(PPAR-α)的蛋白表达。结果与非诺贝特相比,不同浓度的OEA更加显著地抑制人脐静脉内皮细胞VCAM-1mRNA和蛋白的表达,随着浓度的增大,抑制作用逐渐增强。Western bolt结果显示OAE能明显增强PPAR-α蛋白的表达。结论OEA对TNF-α引起的内皮细胞受损起到保护作用,其机理可能与上调过PPAR-α有关。 【英文摘要】 Purpose To investigate the effect of oleoylethanolamide(OEA) on tumor necrosis factor α(TNF-α)induced the expression of vascular cell adhesion molecule-1(VCAM-1) in human umbilical vein endothelial cells(HUVECs).Methods OEA and fenofibrate of different concentrations were incorporated in HUVECs for 10 hours respectively.Human recombinant TNF-α was then incubated with HUVECs for 6 hours.The expression of VCAM-1 in mRNA level and protein level was detected by real-time quantitative RT-PCR and enzyme linked im...厦门大学“活性有机小分子的合成化学与化学生物学”创新团队项目;; 厦门市科技局科技计划350Z20083007项

非诺贝特对小鼠急性局灶性脑缺血再灌注损伤的保护作用

目的研究非诺贝特(fenofibrate,Fen)对小鼠急性局灶性脑缺血再灌注损伤的保护作用及机制。方法线栓法制备小鼠大脑中动脉栓塞模型,缺血90 min后再灌注。非诺贝特(10,80 mg.kg-1)再灌注同时及再灌后2 h各灌胃给药1次。再灌注后24 h,测定小鼠神经功能缺失评分、脑梗死体积及脑水肿程度,实时逆转录多聚酶链反应(RT-PCR)法检测过氧化物酶体增殖物激活受体α(PPARα)mRNA的表达水平,生化法测定脑组织丙二醛(maiondialdehyde,MDA)含量及超氧化物歧化酶(superoxide dismutase,SOD)的活性,伊文思蓝(Evans blue,EB)法观察血脑屏障破坏程度;应用过氧化物酶体增殖物激活受体α拮抗剂MK886(10 mg.kg-1),观察过氧化物酶体增殖物激活受体α是否参与非诺贝特的脑保护作用。结果非诺贝特(80 mg.kg-1)可改善小鼠神经功能缺失,减小脑梗死体积,减轻脑水肿程度,减少脑缺血后脑内伊文思蓝的渗漏,上调脑损伤后脑内过氧化物酶体增殖物激活受体αmRNA的表达,减轻脑组织的脂质过氧化。MK886可拮抗非诺贝特的保护作用。结论非诺贝特可通过上调过氧化物酶体增殖物激活受体αmRNA表达、减轻脂质过氧化损伤而对小鼠急性局灶性脑缺血再灌注损伤发挥保护作用

PPARα促进自噬流抑制脑缺血后星形胶质细胞的过度激活

目的阐明过氧化物酶体增殖物激活受体α(PPARα)在脑缺血后星形胶质细胞活化中的作用及机制。方法大脑中动脉闭塞(MCAO)建立小鼠脑缺血损伤模型,缺氧缺糖再灌注(OGD/R)建立小鼠原代培养星形胶质细胞活化模型。应用PPARαnull小鼠及PPARα激动剂,观察PPARα功能缺失或者激活后对星形胶质细胞活化的影响。进一步通过观察自噬经典标记物LC3Ⅱ/LC3Ⅰ和P62表达变化,联合应用巴弗洛霉素或雷帕霉素观察自噬流的变化,应用自噬双标腺病毒(mRFP-GFP-LC3)检测自噬体和自噬溶酶体的变化,应用透射电子显微镜观察超微结构等方法,研究PPARα功能缺失或者激活后对星形胶质细胞自噬的影响。结果 PPARαnull小鼠或原代培养的PPARαnull星形胶质细胞在脑缺血损伤或OGD/R处理后,星形胶质细胞活化标记物GFAP,Neurocan等的表达较野生型对照组相比明显增加。脑缺血损伤或OGD/R处理后活化星形胶质细胞中存在自噬流障碍,自噬双标腺病毒检测及透射电子显微镜的结果均发现活化的星形胶质细胞中存在大量自噬小体的堆积,PPARαnull星形胶质细胞较野生对照组相比堆积更加明显,而PPARα激动剂可显著改善自噬流障碍,抑制星形胶质细胞的过度活化。结论 PPARα可促进脑缺血后星形胶质细胞的自噬流,抑制星形胶质细胞的过度活化。国家自然科学基金(81603093)细胞应激生物学国家重点实验室(厦门大学)开放课题基金(SKLCSB2019KF016