238 resultados para Jeanette Winterson


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Mode of access: Internet.

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Authorship attributed to Jeanette M. Hart.

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Imperfect: v. 2 lacks plates; v. 4 lacks p. 377 to end (p. 369-[380] of the 3d vol. being inserted insted); v. 6 lacks 2d plate; v. 11 lacks "Table".

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Mode of access: Internet.

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Top Row: Suzanne P. Zeros, Leslie A. Hazle, Deborah L. Thar, Jo-Ann Uhrhammer, Susan M. Revesz, Karla M. Jackson, Laura L. Campbell, Carol T. Dekeyser, Jeanette R. Lewey, Constance B. Squibb, Kristen Eckoff, Martha J. Armantrout, Kathleen A. Duhart, Sara J. Hemming, Carrie L. Malroit, Anne Marie L. Piehl, Rita A. Dobry, Susan A. Wintermeyer

Row 2: Deborah L. Kurzeja, Elanie C. Jenkins, Mary Nehra, June Ellis, Lisa Mediodia, Mary G. Rutz, Diane L. Larson, Mark A. Kempton, Margaret M. Ulchaker, Maureen B. Schreibea, Jan E. Merrick, Holly Russell, Betsy J. hodgman, Maeve N. Boran, Theresa J. Coker, Lisa Moss, Nancy J. Deckert, Nancy R. Bailey

Row 3: Denise M. Zapinski, Michelle M. Post, Elicia baker-Rogers, Lisa A. Mast, Patricia Thomas, Karen A. Bartoluzzi, Jennifer M. Dzieciuch, Margie Von Berge, Nancy Lutz, Pamela Mrstik

Row 4: Elizabeth Doheny, Jacqueline T. Bartone, Lisa A. Pfahler, Sheryl L. Lovelace, Elizabeth A. Bazur, Janet L. Bauman, Delynn M. Dindoffer, Rebecca Waldo

Row 5: Janarl L. Harris, Jeanne M. Cancilla, Amy Garon, Alisa D. Karp, Liz Buchanan, Linda M. Ford.

Row 6: Ondreya Dillard, Linda C. Parks, Tricia Berner, Loranie A. McKaig, Susan M. Bleasdale, Heather L. Colquhoun, Valerie M. Spotts, Marcia L. Fouts

Row 7: Theresa Glick, Carrie L Giltrow, Lisa E. Chapelle, Mary H. Kiledo, Jody Kazmierczak, Patricia E. Goerke, Lisa Weingart, Laura A. Rhead, Pauletta McKivens, Nancy K. Dryer

Row 8: Mary S. Mac Taggart, Lynn M. Stephens, Ann E. Dowling, Amy L. Huntzinger, Patricia A. Schremser, Kathy Hughes, Sally Sample, Cheryl E. Easley, Rhetaugh Dumas, Janice Lindberg, Susan Boehm, Heather Hossack, Susan E. Parry, Amy D. Landau, Michele Mansour, Nancy R. Clark, Sarah Cunningham

Row 9: Rhonda B. Dean, Sandra s. Klein, Cheryl L. Goddard, Toni Rene Dawson, Sara R. Farhat, Lisa M. Kane, Kaye M. Lewandowski, Jennifer A. Blashill, Susan L. Bradley, Mary McGuiness, Ann Dameron, Karolyn L. Maron, Debra Fisher, Rebecca Vredenburg, Elaine B. Fritz, Mary A. Alphenaar, Kathy Rentenbach, Barbara J. Wolff

Row 10: Nancy L. Minegar, Mary E. Conners, Susan E. Kuzma, M. Maureen O'Conner, Elaine P. Wynter, Catherine L. Martin, Bobbi L Hall, Dawn M. Gilbert, Karen M. Kuhn, Genevieve M. Mccarthy, Anne M. Venturi, Jena Bargon, Karen Coesens, Lynne V. Duguay, Barbara A. Sterne, Jill A. Schafer, Jill A. Webster, Katharina E. Smith, Mary K. Brown

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Front Row: Marita Esteva, Kristie Aiuto, Scarlet McCarthy, Rossalyn Quaye, Jackie Pilette, Marcie Klein, Elizabeth Windram, Alison Massagli, Jeanine Seeger

Row 2: Jennifer Kinon, Jen Mayman, Lauren Maxwell, Erin Fitzgerald, Amy Ravit, Laurel LaCour, Maya Key, Amy Teunis, Nell Hurley, Erica Semeyn, Sarah Kepner

Row 3: Dawn Emick, Katie Roek, Tina Marzo, Courtney Jackson, Kendra Miller, Nora Obringer, Jaime Stilson, Danielle Starring, Anne Reader, Kate MacKenzie, Vita Scaglione

Row 4: Belinda Koo, Michelle Wolbert, Katherine Stone, Stephanie Norwell, Lisa Labadie, Jeanette Stawski, Nazema Siddiqui, Claudia Lopez, Katie Weed

Row 5: Emily Green, Tina Stutzman, Carrie Brecht, Kelly Raczak, Vanessa Giancamilli, Allison Torres, Heather Uhring, Ashley Andersen, Alyson Moskwa

Top Row: assistant coach Emily Ford, assistant coach Pam Carroll, head coach Mark Rothstein, special assistant Brady Bustany, student trainer Jennifer Nauman, student trainer Jennifer Jackson, student trainer Robin Reiter

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Reprinted in part from various periodicals.

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Ataxia-oculomotor apraxia (AOA1) is a neurological disorder with symptoms that overlap those of ataxia-telangiectasia, a syndrome characterized by abnormal responses to double-strand DNA breaks and genome instability. The gene mutated in AOA1, APTX, is predicted to code for a protein called aprataxin that contains domains of homology with proteins involved in DNA damage signalling and repair. We demonstrate that aprataxin is a nuclear protein, present in both the nucleoplasm and the nucleolus. Mutations in the APTX gene destabilize the aprataxin protein, and fusion constructs of enhanced green fluorescent protein and aprataxin, representing deletions of putative functional domains, generate highly unstable products. Cells from AOA1 patients are characterized by enhanced sensitivity to agents that cause single-strand breaks in DNA but there is no evidence for a gross defect in single-strand break repair. Sensitivity to hydrogen peroxide and the resulting genome instability are corrected by transfection with full-length aprataxin cDNA. We also demonstrate that aprataxin interacts with the repair proteins XRCC1, PARP-1 and p53 and that it co-localizes with XRCC1 along charged particle tracks on chromatin. These results demonstrate that aprataxin influences the cellular response to genotoxic stress very likely by its capacity to interact with a number of proteins involved in DNA repair.

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Cell culture and direct fluorescent antibody (DFA) assays have been traditionally used for the laboratory diagnosis of respiratory viral infections. Multiplex reverse transcriptase polymerase chain reaction (m-RT-PCR) is a sensitive, specific, and rapid method for detecting several DNIA and RNA viruses in a single specimen. We developed a m-RT-PCR assay that utilizes multiple virus-specific primer pairs in a single reaction mix combined with an enzyme-linked amplicon hybridization assay (ELAHA) using virus-specific probes targeting unique gene sequences for each virus. Using this m-RT-PCR-ELAHA, we examined the presence of seven respiratory viruses in 598 nasopharyngeal aspirate (NPA) samples from patients with suspected respiratory infection. The specificity of each assay was 100%. The sensitivity of the DFA was 79.7% and the combined DFA/culture amplified-DFA (CA-DFA) was 88.6% when compared to the m-RT-PCR-ELAHA. Of the 598 NPA specimens screened by m-RT-PCR-ELAHA, 3% were positive for adenovirus (ADM), 2% for influenza A (Flu A) virus, 0.3% for influenza B (Flu B) virus, 1% for parainfluenza type I virus (PIV1), 1% for parainfluenza type 2 virus (PIV2), 5.5% for parainfluenza type 3 virus (PIV3), and 21% for respiratory syncytial virus (RSV). The enhanced sensitivity, specificity, rapid result turnaround time and reduced expense of the m-RT-PCR-ELAHA compared to DFA and CA-DFA, suggests that this assay would be a significant improvement over traditional assays for the detection of respiratory viruses in a clinical laboratory.

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Mechanisms of speciation are not well understood, despite decades of study. Recent work has focused on how natural and sexual selection cause sexual isolation. Here, we investigate the roles of divergent natural and sexual selection in the evolution of sexual isolation between sympatric species of threespine sticklebacks. We test the importance of morphological and behavioral traits in conferring sexual isolation and examine to what extent these traits have diverged in parallel between multiple, independently evolved species pairs. We use the patterns of evolution in ecological and mating traits to infer the likely nature of selection on sexual isolation. Strong parallel evolution implicates ecologically based divergent natural and/or sexual selection, whereas arbitrary directionality implicates nonecological sexual selection or drift. In multiple pairs we find that sexual isolation arises in the same way: assortative mating on body size and asymmetric isolation due to male nuptial color. Body size and color have diverged in a strongly parallel manner, similar to ecological traits. The data implicate ecologically based divergent natural and sexual selection as engines of speciation in this group.

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The frequency and intensity of disturbance on living coral reefs have been accelerating for the past few decades, resulting in a changed seascape. What is unclear but vital for management is whether this acceleration is natural or coincident only with recent human impact. We surveyed nine uplifted early to mid-Holocene (11,000-3700 calendar [cal] yr B.P.) fringing and barrier reefs along similar to 27 km at the Huon Peninsula, Papua New Guinea. We found evidence for several episodes of coral mass mortality, but frequency was < 1 in 1500 yr. The most striking mortality event extends > 16 km along the ancient coastline, occurred ca. 9100-9400 cal yr B.P., and is associated with a volcanic ash horizon. Recolonization of the reef surface and resumption of vertical reef accretion was rapid (< 100 yr), but the post-disturbance reef communities contrasted with their pre-disturbance counterparts. Assessing the frequency, nature, and long-term ecological consequences of mass-mortality events in fossil coral reefs may provide important insights to guide management of modern reefs in this time of environmental degradation and change.

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