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| 1 | ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction-executive summary: a report of the American Heart Association Task Force on Practice Guidelines显示文摘 | Antman EM Anbe DT Ann PW | 2004 | Circulation2004，110，5： | 1 |
| 2 | Proteinaria in health and disease by measuring the urinary protein/creatin ine ratio显示文摘 | L em ann J Jr Dourm asBT | 1987 | Clin chem1987，33，21： | 1 |
| 3 | Training career adaptability to facilitate a successful school-to-work transition显示文摘 | Koen JK Ute-Christine VV Annelies EM | 2012 | J Vocat Behav2012，81，3： | 1 |
| 4 | Can paronyehiacause are- motenecrotizing soft tissue infection 显示文摘 | Julian EL Anne EM Paul L | 2011 | J Emerg Med2011，40，1： | 1 |
| 5 | Thyroid Function and Mortality in the Sudden Cardiac Death in Heart Failure Trial显示文摘 | Judith EM Anne SH AndersonJ | 2006 | Circulation2006，114，： | 1 |
| 6 | Providing Our Fellows in Training with Education on Inflammatory Bowel Disease Health Maintenance to Improve the Quality of Care in Our Health Care System显示文摘 | Ann Joo Lee Dale F. Kraemer Carmen Smotherman Emely Eid | 2016 | Inflammatory Bowel Diseases2016，，1： | 1 |
| 7 | Morphogenetic mechanisms of epithelial tubulogenesie:MDCK cell polarity is tansiently rearranged without loss of cell-cell contact during scatter factor/hepotocute growth factor-induced tubulogenesis显示文摘 | Raymond BR Keith EM | 1998 | Devel Bio1998，204，： | 1 |
| 8 | Training Career Adaptability to Facilitate A Successful School-to-work Transition显示文摘 | Jessie Koen Ute-Christine Klehe Annelies EM Van Vianen | | 0，，： | 1 |
| 9 | Managing relationship conflict and the effectiveness of organizational teams 显示文摘 | Carsten KW Dreu D Annelies EM | 2001 | Journal of Organizational Behavior2001，22，3： | 1 |
| 10 | Oligomeric 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 |
| 11 | Oligomeric 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 |
| 12 | Oligomeric 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 |
| 13 | Oligomeric 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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