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Oligomeric and fibrillar species of β-amyloid(Aβ42) both impair mitochondrial function in P301l tau transgenic mice

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世界最新医学信息文摘 2016年第4期 8-8页

作者： Anne Eckert Susanne Hauptmann Isabel Scherping Jessica Meinhardt Virginie Rhein Stefan Drse Ulrich Brandt marcus Fndrich Walter E.Müller Jiirgen Gtz

We recently provided evidence for a mitochondrial dysfunction in P301l tau transgenic mice,a strain modeling the tau pathology of Alzheimer's disease(AD)and frontotemporal dementia(FTD).In addition to tau aggregates,the AD brain is further characterized by Aβpeptide-containing *** we addressed the role of Aβ,this indicated a synergistic action of tau and Aβpathology on the *** the present study,we compared the toxicity of different Aβ42 conformations in light of recent studies suggesting that oligomeric rather than fibrillar Aβmight be the actual toxic ***,both oligomeric and fibrillar,but not disaggregated(mainly monomeric)Aβ42 caused a decreased mitochondrial membrane potential in cortical brain cells obtained from FTD P301l tau transgenic *** was not observed with cerebellar preparations indicating selective vulnerability of cortical ***,we found reductions in state 3 respiration,the respiratory control ratio,and uncoupled respiration when incubating P301l tau mitochondria either with oligomeric or fibrillar preparations of Aβ***,we found that aging specifically increased the sensitivity of mitochondria to oligomeric Aβ42 damage indicating that oligomeric and fibrillar Aβ42 are both toxic,but exert different degrees of toxicity.

关键词： Alzheimer’s disease Amyloid aggregates Amyloid β-peptide Amyloid toxicity Fibrils Frontotemporal dementia Globulomer Mitochondria Oligomer Protein aggregation Respiration Tau Transgenic mice

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长效局麻药减轻FMlP诱导的大鼠急性肺损伤的作用

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麻醉与镇痛 2012年第3期8卷 52-57页

作者： marcus T. Schley, MD Matthias Casutt, MD Christoph Haberthar, PhD Martin Dusch, MD Roman Rukwied, PhD Martin Schmelz, MD, PhD Joachim Schmeck, MD,PhD Guido K. Schupfer, MD, PhD , Christoph J, Konrad, MD, PhD 徐妍君(译) 李士通(校) Department of Anaesthesiology and Operative Intensive Care Medicine Kantonsspital Lucerne Switzerland Department of Anaesthesiology and Intensive Care Medicine University of Heidelberg Heidelberg Germany Department of Anaesthesiology University of Mainz Mainz Germany 不详

背景内皮素-1（endothelin-1，ET-1）可介导肺部疾病，是一个强有力的血管收缩药。与血栓素A2一起参与了肺水肿的形成。利多卡因和甲哌卡因可以缓解肺动脉压的升高以及肺水肿的进展。我们利用增加肺动脉压、促使ET—1释放的实验模型验... 详细信息

背景内皮素-1（endothelin-1，ET-1）可介导肺部疾病，是一个强有力的血管收缩药。与血栓素A2一起参与了肺水肿的形成。利多卡因和甲哌卡因可以缓解肺动脉压的升高以及肺水肿的进展。我们利用增加肺动脉压、促使ET—1释放的实验模型验证普鲁卡因、布比卡因、罗哌卡因的作用。方法用Krebs-Henseleit羟乙基淀粉缓冲液灌注大鼠离体肺脏，测量肺动脉压及肺脏质量，加入10^-1-10^7mg／kg浓度的布比卡因、罗哌卡因、普鲁卡因，用免疫酶标技术检测ET-1水平，放射免疫法检验血栓素A2水平，用N-甲酰-甲硫氨酰．亮氨酰苯丙氨酸（FMlP）来激活人多形核中性粒细胞。结果与对照组（P〈0．05）相比，治疗组布比卡因、罗哌卡因、普鲁卡因明显减轻了肺动脉压的升高（P〈0．05），导致肺脏质量的减轻。除了普鲁卡因，在剂量为10^-3-10^-6mg／kg的范围中，长效局麻药布比卡因、罗哌卡因（P〈0．05）降低了ET-1的水平，降低炎症发生率，且不影响肺结构。结论布比卡因、罗哌卡因能缓解FMlP诱导的肺动脉压升高，减轻肺水肿，减少ET-1释放。利多卡因和甲哌卡因能更有效地缓解肺动脉压升高以及肺水肿形成，但是长效局麻药能通过抑制ET-1的释放增强抗炎能力。

关键词：急性肺损伤长效局麻药 FMlP 减轻大鼠 ET-1水平多形核中性粒细胞布比卡因

Oligomeric and fibrillar species of β-amyloid(Aβ42) both impair mitochondrial function in P301l tau transgenic mice

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世界最新医学信息文摘 2015年第A期 8-8页

作者： Anne Eckert Susanne Hauptmann Isabel Scherping Jessica Meinhardt Virginie Rhein Stefan Dr?se Ulrich Brandt marcus F?ndrich Walter E.Müller Jürgen G?tz

We recently provided evidence for a mitochondrial dysfunction in P301 l tau transgenic mice, a strain modeling the tau pathology of alzheimer's disease(ad) and frontotemporal dementia(ftd). in addition to tau aggregates, the ad brain is further characterized by Aβ peptide-containing plaques. When we addressed the role of Aβ, this indicated a synergistic action of tau and Aβ pathology on the mitochondria. In the present study, we compared the toxicity of different Aβ42 conformations in light of recent studies suggesting that oligomeric rather than fibrillar Aβ might be the actual toxic species. Interestingly, both oligomeric and fibrillar, but not disaggregated(mainly monomeric) Aβ42 caused a decreased mitochondrial membrane potential in cortical brain cells obtained from FTD P301 l tau transgenic mice. This was not observed with cerebellar preparations indicating selective vulnerability of cortical neurons. Furthermore, we found reductions in state 3 respiration, the respiratory control ratio, and uncoupled respiration when incubating P301 l tau mitochondria either with oligomeric or fibrillar preparations of Aβ42. Finally, we found that aging specifically increased the sensitivity of mitochondria to oligomeric Aβ42 damage indicating that oligomeric and fibrillar Aβ42 are both toxic, but exert different degrees of toxicity.

关键词： Alzheimer’s disease Amyloid aggregates Amyloid β-peptide Amyloid toxicity Fibrils Frontotemporal dementia Globulomer Mitochondria oligomer Protein aggregation respiration tau transgenic mice

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Oligomeric and fibrillar species of β-amyloid(A β 42) both impair mitochondrial function in P301l tau transgenic mice

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世界最新医学信息文摘 2015年第99期 1-1页

作者： Anne Eckert Susanne Hauptmann Isabel Scherping Jessica Meinhardt Virginie Rhein Stefan Dr?se Ulrich Brandt marcus F?ndrich Walter E.Müller Jürgen G?tz

We recently provided evidence for a mitochondrial dysfunction in P301l tau transgenic mice, a strain modeling the tau pathology of alzheimer's disease(ad) and frontotemporal dementia(ftd). in addition to tau aggregates, the ad brain is further characterized by Aβ peptide-containing plaques. When we addressed the role of Aβ, this indicated a synergistic action of tau and Aβ pathology on the mitochondria. In the present study, we compared the toxicity of different Aβ42 conformations in light of recent studies suggesting that oligomeric rather than fibrillar Aβ might be the actual toxic species. Interestingly, both oligomeric and fibrillar, but not disaggregated(mainly monomeric) Aβ42 caused a decreased mitochondrial membrane potential in cortical brain cells obtained from FTD P301l tau transgenic mice. This was not observed with cerebellar preparations indicating selective vulnerability of cortical neurons. Furthermore, we found reductions in state 3 respiration, the respiratory control ratio, and uncoupled respiration when incubating P301l tau mitochondria either with oligomeric or fibrillar preparations of Aβ42. Finally, we found that aging specifically increased the sensitivity of mitochondria to oligomeric Aβ42 damage indicating that oligomeric and fibrillar Aβ42 are both toxic, but exert different degrees of toxicity.

认知干预对慢性乙型肝炎患者心理状态和治疗依从性的影响

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中国临床康复 2005年第12期9卷 44-45页

作者：张姝娜安平曹艳雪戴文颖卞丽吕丹王佳贺沈阳市传染病医院肝病研究所辽宁省沈阳市110006 中国医科大学附属第一医院感染科辽宁省沈阳市110001

目的:研究认知干预对慢性乙型肝炎患者心理状态及抗病毒治疗依从性的影响,为慢性乙型肝炎的康复干预介入提供依据。方法:选择2003-06/2003-12沈阳市传染病医院肝病研究所收治的慢性乙型肝炎患者76例为研究对象。按病例来诊先后顺序分为... 详细信息

目的:研究认知干预对慢性乙型肝炎患者心理状态及抗病毒治疗依从性的影响,为慢性乙型肝炎的康复干预介入提供依据。方法:选择2003-06/2003-12沈阳市传染病医院肝病研究所收治的慢性乙型肝炎患者76例为研究对象。按病例来诊先后顺序分为干预组38例与对照组38例。全部患者能够按计划随访并完成测查。对照组实施抗病毒药物治疗,干预组在相同抗病毒药物治疗下实行针对性的认知干预。抗病毒治疗前后让患者填写症状自评量表,评价两组心理状态差异、抗病毒依从性及抗病毒疗效。结果:干预组在接受认知干预后症状自评量表中抑郁、焦虑、敌对及恐怖方面评分明显较干预前改善(t=6.383,3.498,3.216,4.953,P<0.01)。干预组抗病毒依从率明显优于对照组(97%,84%,χ2=6.832,P<0.05);干预组抗病毒治疗应答率明显优于对照组(95%,76%,χ2=6.801,P<0.05)。结论:对慢性乙型肝炎患者进行认知干预,有助于建立良好的医患关系,提高患者对慢性乙肝的认知行为,从而有效提高其对抗病毒治疗的依从性,提高疗效。

关键词：认知肝炎,乙型,慢性/心理学病人依从

维普期刊数据库

Thermal decomposition of normal decane:reaction mechanisms,product distributions and rate constants

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Thermal decomposition of normal decane:reaction mechanisms,p...

中国化学会第28届学术年会

作者： Guona li1,Tianlei Zhang1,Chunying li2,Yongmei Du2,Jian lü2,Wenliang Wang1,1 Key laboratory for Macromolecular Science of Shaanxi Province,School of Chemistry and Chemical Engineering,Shaanxi Normal University,Xi''an,710062 2 Xi''an Modern Chemistry Research Institute,Xi''an,710065

＜正＞The thermal decomposition of n-decane has been investigated theoretically by employing CBS-QB3/6-311G（d,p）// B3lYP/6-311G（d,p）method,variational transition state theory and Rice-Ramsperger-Kassel-marcus *** calculated results show that the pyrolysis mechanism of n-decane follows a free radical chain mechanism,which

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宝马世界

城市环境设计 2020年第4期126卷 134-149页

作者：沃尔夫·狄·普瑞克斯 Paul Kath Tom Wiscombe Waltraut Hoheneder Mona Marbach Hans Aescht Beatrix Basting Guy Bebiè Chris Beccone Johannes Behrens Marcelo Bernardi Pawel Bodzak Verena Boyer Antja Bulthaup Claudia Buhmann Timo Carl Jan Chaldil Ing Tse Chen Tadeusz Chimiak Andrea Christmann Patrick Erhardt Stephan Exsternbrink Wolfgang Fiel Benedikt Frass Helmut Fr?tscher Volker Gessendorfer Andrea Graser lukas Haller Markus Henning Armin Hess Jens Hoff Tamas Horvath Robert Huebser Astrid Jagersberger Marin Jurycz Gregor Kassl Areta Keller Markus Klausecker Tobias Klein Martin Konrad Quirin Krumbholz Caroline Kufferath Marion lattenmayer Stefan laub Wolfgang leitgeb Andreas Mieling Karin Miesenberger Dennis Milam Elke Müller Henrike Münker Claudia Nehammer Martin Oberascher Alexander Ott Stefan Pfefferle Florian Pfeifer Markus Pillhofer Ekkehard Rehfeld Goswin Rothenthal Wolfgang Ruthensteiner Jasmin Sauerbier Florian Schafschetzy Kristina Schinegger Karolin Schmidbaur Patrick Schneider Katharina Schneider Hubert Schoba Angus Schoenberger Andrea Sch?ning Anja Sorger Gernot Stangl Mark Steinmetz Sigrid Steinwender Martina Tippelskirch Dionicio Valdez Pascal Vauclair Akvile Rimantaite Andreas Weissenbach Heribert Wolfmayer Irina Zahler 2007 Ari Marcopoulos Gerald Zugmann Hélène Binet Duccio Malagamba marcus Buck Christian Richters Richard Walch

项目大事记/CHRONOlOGY竞赛（一等奖）/Competition（1st Prize）:2001规划设计起始时间/Start of Planning:11/2001施工起始时间/Start of Construction:08/2003投入使用/Opening:20/10/2007-21/10/2007项目参数/PROJECT DATA用地面积/Site Area:约25 000m2/Approx. 25 000m2建筑毛面积/Gross Floor Area:约73 000m2（除坡道）=100%/Approx.73 000m2（excluding ramps）=100%地上建筑毛面积/Gross Floor Area above ground:约28 500m2=40%/Approx.28 500m2=40%地下建筑毛面积/Gross Floor Area underground:约44 500m2=60%/Approx.44 500m2=60%

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