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1098 citation(s) found for "Au, Lewis".

P1–117: Kinetics of tau suppression in the rTg4510 inducible model of tauopathy
Lewis, Jada , Zehr, Cindy, Hutton, Mike, Knight, Joshua A. , Dickson, Dennis W. , McGowan, Eileen

Alzheimer's & Dementia | August 17, 2006 | Volume: 2 | Issue: 3S_Part_5 | Pages: No page available

10.1016/j.jalz.2006.05.493 Get It

P1–108: Gene expression changes after MAPT expression inhibition
Lewis, Jada , McKinney, Michael, Kent, Caroline, Gass, Jennifer , Heckman, Mike, Crook, Julia E. , Hutton, Michael , Golan, Maciej Przemysław

Alzheimer's & Dementia | August 17, 2006 | Volume: 2 | Issue: 3S_Part_5 | Pages: No page available

10.1016/j.jalz.2006.05.484 Get It

P1–102: Apoptosis of oligodendrocytes in an inducible model of tauopathy
Zehr, Cindy, Lin, Wenglang, Hutton, Michael , Lewis, Jada , Knight, Joshua A. , Dickson, Dennis W.

Alzheimer's & Dementia | August 17, 2006 | Volume: 2 | Issue: 3S_Part_5 | Pages: No page available

10.1016/j.jalz.2006.05.478 Get It

P1–087: Identification of toxic tau species
Berger, Zdenek , Lewis, Jada , Andorfer, Cathy, Yue, Mei, Rosenberry, T.L., Hutton, Mike

Alzheimer's & Dementia | August 17, 2006 | Volume: 2 | Issue: 3S_Part_4 | Pages: No page available

10.1016/j.jalz.2006.05.462 Get It

P3–293: Tau clearance through protein degradation pathways
Eriksen, Jason L. , Zehr, Cynthia, Berger, Zdenek , Robinson, Todd, Lewis, Jada , Hutton, Michael

Alzheimer's & Dementia | August 17, 2006 | Volume: 2 | Issue: 3S_Part_15 | Pages: No page available

10.1016/j.jalz.2006.05.1562 Get It

S2–02–06: The tauopathies: From genetics to animal models
Hutton, Mike, Melquist, Stacey , Zehr, Cynthia, Eriksen, Jason L. , Stephan, Dietrich A. , Lewis, Jada , Baker, Matthew , McGowan, Eileen , Dickson, Dennis W. , Ashe, Karen H.

Alzheimer's & Dementia | August 17, 2006 | Volume: 2 | Issue: 3S_Part_1 | Pages: No page available

10.1016/j.jalz.2006.05.086 Get It

National Center for Biomedical Ontology: Advancing Biomedicine through Structured Organization of Scientific Knowledge
Lewis, Suzanna , Mungall, Chris , Misra, Sima, Westerfield, Monte , Ashburner, Michael , Solbrig, Harold R. , Storey, Margaret‐Anne , Smith, Barry , Day-Richter, John, Noy, Natalya F., Musen, Mark A. , Rubin, Daniel L. , Sim, Ida , Chute, Christopher G. , Mungall, Christopher J

OMICS: A Journal of Integrative Biology | August 10, 2006 | Volume: 10 | Issue: 2 | Pages: 185-198

10.1089/omi.2006.10.185 | PMID 16901225 Get It

The National Center for Biomedical Ontology is a consortium that comprises leading informaticians, biologists, clinicians, and ontologists, funded by the National Institutes of Health (NIH) Roadmap, to develop innovative technology and methods that allow scientists to record, manage, and disseminate biomedical information and knowledge in machine-processable form. The goals of the Center are (1) to help unify the divergent and isolated efforts in ontology development by promoting high quality open-source, standards-based tools to create, manage, and use ontologies, (2) to create new software tools so that scientists can use ontologies to annotate and analyze biomedical data, (3) to provide a national resource for the ongoing evaluation, integration, and evolution of biomedical ontologies and associated tools and theories in the context of driving biomedical projects (DBPs), and (4) to disseminate the tools and resources of the Center and to identify, evaluate, and communicate best practices of ontology development to the biomedical community. Through the research activities within the Center, collaborations with the DBPs, and interactions with the biomedical community, our goal is to help scientists to work more effectively in the e-science paradigm, enhancing experiment design, experiment execution, data analysis, information synthesis, hypothesis generation and testing, and understand human disease. This paper is part of the special issue of OMICS on data standards.
Occult thyroid carcinoma in olmsted county, minnesota: Prevalence at autopsy compared with that in hiroshima and nagasaki. Japan
Sampson, Richard J., Woolner, Lewis B., Bahn, Robert C., Kurland, Leonard T.

Cancer | June 29, 2006 | Volume: 34 | Issue: 6 | Pages: 2072-2076

10.1002/1097-0142(197412)34:6<2072::aid-cncr2820340629>3.0.co;2-# | PMID 4474057 Get It

An inhibitor of tau hyperphosphorylation prevents severe motor impairments in tau transgenic mice
Corre, Sylvie Le, Klafki, Hans‐Wolfgang , Hübinger, Gabriele, Obermeier, Axel, Sahagún, Heidi, Monse, Barbara, Seneci, Pierfausto , Lewis, Jada , Eriksen, Jason L. , Zehr, Cynthia, Yue, Mei, Dickson, Dennis W. , Hutton, Michael , Roder, Hanno M., Plesnila, Nikolaus , McGowan, Eileen , Dickson, Dennis W

Proceedings of the National Academy of Sciences | June 12, 2006 | Volume: 103 | Issue: 25 | Pages: 9673-9678

10.1073/pnas.0602913103 | PMID 16769887 Get It

An orally bioavailable and blood–brain barrier penetrating analog of the kinase inhibitor K252a was able to prevent the typical motor deficits in the tau (P301L) transgenic mouse model (JNPL3) and markedly reduce soluble aggregated hyperphosphorylated tau. However, neurofibrillary tangle counts were not reduced in the successfully treated cohort, suggesting that the main cytotoxic effects of tau are not exerted by neurofibrillary tangles but by lower molecular mass aggregates of tau. Our findings strongly suggest that abnormal tau hyperphosphorylation plays a critical role in the development of tauopathy and suggest a previously undescribed treatment strategy for neurodegenerative diseases involving tau pathology.
Effects of Conjugated Equine Estrogen on Risk of Fractures and BMD in Postmenopausal Women With Hysterectomy: Results From the Women's Health Initiative Randomized Trial
Jackson, Rebecca D. , Wactawski‐Wende, Jean , LaCroix, Andrea Z. , Pettinger, Mary , Yood, Robert A. , Watts, Nelson B. , Robbins, John A. , Lewis, Cora E. , Beresford, Shirley A.A. , Ko, Marcia G., Naughton, Michelle J. , Satterfield, Suzanne , Bassford, Tamsen , Wactawski-Wende, Jean

Journal of Bone and Mineral Research | June 5, 2006 | Volume: 21 | Issue: 6 | Pages: 817-828

10.1359/jbmr.060312 | PMID 16753012 Get It

Abstract Further analyses from the Women's Health Initiative estrogen trial shows that CEE reduced fracture risk. The fracture reduction at the hip did not differ appreciably among risk strata. These data do not support overall benefit over risk, even in women at highest risk for fracture. Introduction: The Women's Health Initiative provided evidence that conjugated equine estrogen (CEE) can significantly reduce fracture risk in postmenopausal women. Additional analysis of the effects of CEE on BMD and fracture are presented. Materials and Methods: Postmenopausal women 50–79 years of age with hysterectomy were randomized to CEE 0.625 mg daily (n = 5310) or placebo (n = 5429) and followed for an average 7.1 years. Fracture incidence was assessed by semiannual questionnaire and verified by adjudication of radiology reports. BMD was measured in a subset of women (N = 938) at baseline and years 1, 3, and 6. A global index was used to examine whether the balance of risks and benefits differed by baseline fracture risk. Results: CEE reduced the risk of hip (hazard ratio [HR], 0.65; 95% CI, 0.45–0.94), clinical vertebral (HR, 0.64; 95% CI, 0.44–0.93), wrist/lower arm (HR, 0.58; 95% CI, 0.47–0.72), and total fracture (HR, 0.71; 95% CI, 0.64–0.80). This effect did not differ among strata according to age, oophorectomy status, past hormone use, race/ethnicity, fall frequency, physical activity, or fracture history. Total fracture reduction was less in women at the lowest predicted fracture risk in both absolute and relative terms (HR, 0.86; 95% CI, 0.68–1.08). CEE also provided modest but consistent positive effects on BMD. The HRs of the global index for CEE were relatively balanced across tertiles of summary fracture risk (lowest risk: HR, 0.81; 95% CI, 0.62–1.05; mid risk: HR, 1.09; 95% CI, 0.92–1.30; highest risk: HR, 1.04; 95% CI, 0.88–1.23; interaction, p = 0.42). Conclusions: CEE reduces the risk of fracture and increases BMD in hysterectomized postmenopausal women. Even among the women with the highest risk for fractures, when considering the effects of estrogen on other important health outcomes, a summary of the burden of monitored effects does not indicate a significant net benefit.