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18篇 您的检索式:作者名="Ulrich EM"
    题名 作者 年代 出处 被引量
1Differential toxicity and environmental fats of hexachlorocy clohexane isomers显示文摘Willett KL Ulrich EM Hires RA 1998Environmental Science & Technology1998,32,15:1
2TIMP-1,MMP-2,MMP-9,and PIILNP as serum markers for skin fibrosis in patients following severe burn trauma显示文摘Ulrich D Noah EM Von Heimburg D 0,,:1
3Epidermal growth factor--interactions with normal and malignant urothelium:in vivo and insitu studies 显示文摘Messing EM Hanson P Ulrich P 1987J Urol1987,138,5:1
4Imaging of prostate cancer metastases with SF-fluoroacetate using PET/CT 显示文摘Matthies A Ezziddin S Ulrich EM 2004Eur J Nucl Med Mol Imaging2004,31,5:1
5Differential toxicity and envi- ronmental fats of hexachlorocy clohexane isomers 显示文摘Willett KL Ulrich EM Hires RA 1998Environ- mental Science and Technology1998,32,15:1
6Decreased cyclooxygenase inhibition by aspirin in polymorphic variants of human prostaglan- din H synthase-I 显示文摘Liu W Poole EM Ulrich CM 2012Pharmacogen Gen2012,22,7:1
7TIMP-1,MMP-2,MMP-9,and PⅢNP as serum markers for skin fibrosis in patients following severe burn trauma显示文摘Ulrich D Noah EM von Heimburg D 2003Plast Reconstr Surg2003,111,4:1
8The effects of obesity and obesity-related conditions on colorectal cancer prognosis 显示文摘Siegel EM Ulrich CM Poole EM 2010Cancer Control2010,17,1:1
9Differential toxicity and environmental fates of hexachlorocyclohexane isomers显示文摘Willett KL Ulrich EM Hites RA 1998Environmental Science and Technology1998,32,15:1
10TIMP-1,MMP-2,MMP-9,and PIIINP as serum markers for skin fibrosis in patients following severe burn trauma 显示文摘Ulrich D Noah EM von Heimburg D 2003Plast Reconstr Surg2003,111,:1
11Imaging of prostate cancer metastases with 18F-fluoroacetate using PET/CT显示文摘Matthies A Ezziddin S Ulrich EM 2004Eur J Nucl Med Mol Imaging2004,31,9:1
12TIMP-1,MMP-2, MMP--9, and PIILNP as serum markers for skin fibrosis in patients following severe bum trauma 显示文摘Ulrich D Noah EM V/Heimburg D 2003Plast Reconstr Surg2003,112,5:1
13The effects of obesity and obesity-related conditions on colorectal can- cer prognosis显示文摘Siegel EM Ulrich CM Poole EM 2010Cancer Control2010,17,1:1
14Imaging of Prostate Cancer Metastases With ^18F-fluoroacetate Using PET/CT显示文摘MATTHIES A EZZIDDIN S ULRICH EM 2004Eur J Nucl Med Mol Imaging2004,31,5:1
15Oligomeric and fibrillar species of β-amyloid(A β 42) both impair mitochondrial function in P301L tau transgenic mice显示文摘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.Anne Eckert Susanne Hauptmann Isabel Scherping Jessica Meinhardt Virginie Rhein Stefan Drose Ulrich Brandt Marcus Fandrich Walter EMüller Jürgen Gotz 2015世界最新医学信息文摘2015,15,99:0
16Oligomeric and fibrillar species ofβ-amyloid(A β 42)both impair mitochondrial function in P301L tau transgenic mice显示文摘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.Anne Eckert Susanne Hauptmann Isabel Scherping Jessica Meinhardt Virginie Rhein Stefan Drose Ulrich Brandt Marcus Fandrich Walter EMüller Jürgen Gotz 2015世界最新医学信息文摘2015,15,A0:0
17Oligomeric and fibrillar species of β-amyloid(A β 42) both impair mitochondrial function in P301L tau transgenic mice显示文摘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.Anne Eckert Susanne Hauptmann Isabel Scherping Jessica Meinhardt Virginie Rhein Stefan Drose Ulrich Brandt Marcus Fandrich Walter EMüller Jürgen Gotz 2015世界最新医学信息文摘2015,15,90:0
18Oligomeric and fibrillar species of β-amyloid(A β 42) both impair mitochondrial function in P301L tau transgenic mice显示文摘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.Anne Eckert Susanne Hauptmann Isabel Scherping Jessica Meinhardt Virginie Rhein Stefan Drose Ulrich Brandt Marcus Fandrich Walter EMüller Jürgen Gotz 2016世界最新医学信息文摘2016,16,4:0
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