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| 1 | Effects of steroids on cerebral electrical activity显示文摘 | Watson CW Goldman PL | 1966 | Arch Neurol1966，15，： | 1 |
| 2 | Septal to posterior wall motion delay fails to predict reverser ernodeling orclinical improvement in patients undergoing cardiac resynchronization therapy显示文摘 | Marcus GM Rose E Viloria EM | 2005 | J Am Coll Cardiol2005，46，12： | 1 |
| 3 | Septal to posterior wall motion delay fails to predict reverse remodeling or clinical improvement in patients undergoing cardiac resynchronization therapy显示文摘 | Marcus GM Rose E Viloria EM | 2005 | J Am Coll Cardiol2005，46，： | 1 |
| 4 | Smoking cessation in college-aged women:a qualitative analysis of factors important to this population显示文摘 | Nademin EM Napolitano MA Xanthopoulos MS Fava JL Richardson E Marcus B | | 0，，： | 1 |
| 5 | Aspirin inhibits surface glycoprotein Ⅱb/Ⅲa,P-selection,CD63,and CD107a receptor expression on human platelets显示文摘 | Marcus EM Alex IM Christopher RB | 2003 | Blood Coagulation and Fibrinolvsis2003，14，： | 1 |
| 6 | Septal to posterior wall motion delay fails to predict reverse remodeling or clinical im- provement in patients undergoing cardiac resynchronization ther- apy显示文摘 | Marcus GM Rose E Viloria EM | 2005 | J Am Coil Cardiol2005，46，5： | 1 |
| 7 | Refusal to eat inthe elderly显示文摘 | Esther Lee Marcus Berry EM | 1998 | Nutrition Reviews1998，56，： | 1 |
| 8 | Systemic inflammatory response secondary to abdonminal compartment syndrome:stage for multiple organ failure显示文摘 | Joao B RN Ernest EM Marcus VM | 2002 | J Trauma2002，53，6： | 1 |
| 9 | 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 |
| 10 | 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 |
| 11 | 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 |
| 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 | 2016 | 世界最新医学信息文摘2016，16，4： | 0 |
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