137 resultados para Levinson
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Includes index.
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Mode of access: Internet.
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Mode of access: Internet.
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"Gedruckt als beilage zu den Sitzungs-berichten der Naturforscher gesellschaft vom jahre 1893."
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top row: mgr. Ritter Levinson, Harry M. Sinclair, Louis Goldstein, Theodore J. Maynard, coach Barker
William Kailes, Adelbert K. Toepper, Sidney J. Karbel, Russell Baker, Wilton A. Simpson
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back row: George Weitzel, manager Ritter Levinson, George Sibilsky, Harry MacDuff, Carlton Lindstrom, Joseph Bendey, Irving Reynolds
front row: (seated) Waldeck Levi, coach Joseph Barss, captain Daniel Petermann
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Top Row: Allison Anderson, Meghan Archer, Christopher Aten, Meredith Bajor, Sarah Belleville, Kimberly Bergere, Courtney Bernier, Diana Blanks, Julie Bluhm, Melanie Bork, Karyn Braley, Kathryn Melody Briones, Christine Brouillard, Alyson Bryson
Row 2: Amy Burk, Kelly Capellari, Carmon Carlson, Krystal Cavaliere, Jeffrey Chiambretti, Christine Cho, Renee Christopher, Holli Clewis, James Conway, Kelly Courtney, Jenna Dahn, Erin Daly, Nicole DeFauw, Stefanie DeVita, Jessica DiVirgil, Debra Dombrowski, Genevieve Donnell
Row 3: Kathleen Donnelly, Jennifer El Aile, William Faulkner, Kimberly Johnson, Danielle Alameda, Margaret Wheeler, Brian D Kaminski Jr, Bridget Fil, Rochelle Weller, Leslie Allen-Huisman, Jennifer Musbach, Kathy Feig, Lori Fellows, Shana Ferguson
Row 4: Lauren Frawley, Ashton Frederick, Molly Gacetta, Stephanie Ganger, Amanda Garcia, Megan Gdowski, Chad Godfrey, Emily Halpern
Row 5: Katherine Hammons, Natalie Hecht, Danielle Hiltz, Taylor Hosner, Jennifer Huber, Holly Huling, Nathaniel Hunt, Ana-Leonor Jay
Row 6: Rachel Jeltema, Jennifer Jones, Lindsey Jones, Sarah Kaherl, Jessica Kehbein, Kendra Leidecker, Vanessa Lelli, Meghan Lemmer, Rachel Levinson, Alexandra Lindsay
Row 7: Amanda MacDonald, Joelle Marineau, Laura Mason, Andrea Masser, Michele McKinney, Charles-Robert Moultry, Kathleen Potempa, Bonnie Hagerty, Nicole Nader, Minna Navvab, Rachael Newnam, Uche Obua, Sara Oles, Ceren Onsan-Fitzpatrick
Row 8: Emily Parobek, Dorasy Paul, Rosalynne Pinga, Sarah Pope, Laura Randall, Sarah Reits, Emma Rew, Annemarie Rozwadowski, Nicole Ruhlman, Lydia Sanok, Grace Savercool, Kimberly Schmidt, Renee Schoenborn, Lisa Schuman, Kaitlyn Seltzer, Catherine Sherwood, Elizabeth Smith
Row 9: Aimee Surma, Stephanie Swinteck, Hanna Taylor, Donnie Tietsema, Andreea Toader, Stephanie Upplegger, Meghan Visnick, Scharnice Ward, Tabytha Whitley, Kimberly Wilke, Carie Wright, Kyleen Young, Kristin Zawacki, Christina Ziegler, Carlotta Zirker
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Mode of access: Internet.
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Schizophrenia is a common disorder with high heritability and a 10-fold increase in risk to siblings of probands. Replication has been inconsistent for reports of significant genetic linkage. To assess evidence for linkage across studies, rank-based genome scan meta-analysis (GSMA) was applied to data from 20 schizophrenia genome scans. Each marker for each scan was assigned to 1 of 120 30-cM bins, with the bins ranked by linkage scores (1 = most significant) and the ranks averaged across studies (R-avg) and then weighted for sample size (rootN[affected cases]). A permutation test was used to compute the probability of observing, by chance, each bin's average rank (P-AvgRnk) or of observing it for a bin with the same place (first, second, etc.) in the order of average ranks in each permutation (P-ord). The GSMA produced significant genomewide evidence for linkage on chromosome 2q (P-AvgRnk
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We present evidence of complex balancing regulation of HTR1B transcription by common polymorphisms in its promoter. Computational analysis of the HTR1B gene predicted that a 50 segment, spanning common DNA sequence variations, T-261G, A-161T, and -182INS/DEL-181, contained a putative functional promoter. Using a secreted alkaline phosphatase (SEAP) reporter gene system, we found that the haplotype -261G_-182INS-181_A-161 enhanced transcriptional activity 2.3-fold compared with the haplotype T-261_-182INS-181_A-161. Conversely, -161T reversed this, and the net effect when -261G and -161T were in the same haplotype (-261G_-182INS-181_-161T) was equivalent to the major haplotype (T-261_-182INS-181_A-161). Electrophoretic mobility shift experiments showed that -261G and -161T modify the binding of transcription factors (TFs): -261G generates a new AP2 binding site, while alleles A-161 and -161T exhibit different binding characteristics to AP1. T-261G and A-161T were found to be in linkage disequilibrium (LD) with G861C in a European ancestry population. Interestingly, G861C has been reported to be associated with several psychiatric disorders. Our results indicate that HTR1B is the target of substantial transcriptional genetic regulation by common haplotypes, which are in LD with the HTR1B single-nucleotide polymorphism (SNP) most commonly used in association studies.
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Several linkage studies across multiple population groups provide convergent support for a susceptibility locus for schizophrenia - and, more recently, for bipolar disorder - on chromosome 6q13-q26. We genotyped 192 European-ancestry and African American (AA) pedigrees with schizophrenia from samples that previously showed linkage evidence to 6q13-q26, focusing on the MOXD1-STX7-TRARs gene cluster at 6q23.2, which contains a number of prime candidate genes for schizophrenia. Thirty-one screening single-nucleotide polymorphisms (SNPs) were selected, providing a minimum coverage of at least 1 SNP/20 kb. The association observed with rs4305745 (P = .0014) within the TRAR4 (trace amine receptor 4) gene remained significant after correction for multiple testing. Evidence for association was proportionally stronger in the smaller AA sample. We performed database searches and sequenced genomic DNA in a 30-proband subsample to obtain a high-density map of 23 SNPs spanning 21.6 kb of this gene. Single-SNP analyses and also haplotype analyses revealed that rs4305745 and/or two other polymorphisms in perfect linkage disequilibrium (LD) with rs4305745 appear to be the most likely variants underlying the association of the TRAR4 region with schizophrenia. Comparative genomic analyses further revealed that rs4305745 and/or the associated polymorphisms in complete LD with rs4305745 could potentially affect gene expression. Moreover, RT-PCR studies of various human tissues, including brain, confirm that TRAR4 is preferentially expressed in those brain regions that have been implicated in the pathophysiology of schizophrenia. These data provide strong preliminary evidence that TRAR4 is a candidate gene for schizophrenia; replication is currently being attempted in additional clinical samples.