67 results on '"Fulton, Robert A."'
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2. Study: Prenatal supplements fail to meet nutrient needs
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Fulton, Robert
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Dietary supplements -- Reports -- Research ,College teachers -- Reports -- Research ,Pregnant women -- Research -- Reports ,Health - Abstract
Although drugstore shelves might suggest otherwise, affordable dietary supplements that provide critical nutrients in appropriate doses for pregnant women are virtually nonexistent, researchers have found. In a new study published [...]
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- 2023
3. Continuous glucose monitors for pregnant patients?
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Fulton, Robert
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Dextrose ,Glucose ,Patient monitoring equipment ,Pregnant women ,Health - Abstract
Patients with pregestational diabetes may benefit from use of a continuous subcutaneous insulin infusion pump paired with a continuous glucose monitor. Use of the tools has been associated with a [...]
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- 2023
4. All in stride: Few age limitations for joint replacement
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Fulton, Robert
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Company business planning ,Health ,Health care industry - Abstract
Kathy Blackwell is not going to allow a couple of aching joints stop her from living her best life. The 73-year-old resident of Simi Valley, Calif, a bedroom community about [...]
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- 2023
5. All in stride: Few age limitations for joint replacement
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Fulton, Robert
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Joint replacement ,Health - Abstract
Joint replacements are getting more common, with about 790,000 total knee replacements and more than 450,000 hip replacements performed annually in the United States, according to the American College of [...]
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- 2023
6. USPSTF maintains 'insufficient' evidence for lipid disorder screenings in kids and teens
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Fulton, Robert
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Cholesterol -- Reports -- Analysis ,Medical societies -- Analysis -- Reports ,Teenagers -- Analysis -- Reports ,Youth -- Analysis -- Reports ,Medical screening -- Analysis -- Reports ,Health - Abstract
THE U.S. PREVENTIVE SERVICES Task Force has again determined that current evidence is insufficient to recommend screening for lipid disorders among asymptomatic children and patients aged 20 years or younger. [...]
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- 2023
7. Can you spot hypermobility spectrum disorder?
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Fulton, Robert
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Fibromyalgia -- Diagnosis -- Care and treatment -- Comparative analysis ,Therapeutics, Physiological -- Patient outcomes ,Physical therapy -- Patient outcomes ,Diagnostic errors -- Prevention ,Joints -- Hypermobility ,Health - Abstract
Joint hypermobility syndrome, popularly known as being double-jointed, may be a common but underrecognized disorder in adults that is difficult to diagnose and often mistaken for fibromyalgia or other conditions. [...]
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- 2023
8. Study: Most prenatal supplements fail to meet nutrient needs
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Fulton, Robert
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Prenatal care -- Research ,Dietary supplements -- Composition -- Health aspects -- Standards ,Product quality -- Research ,Pregnant women -- Care and treatment -- Food and nutrition ,Pharmaceutical research ,Software quality ,Product defect/failure ,Health - Abstract
ALTHOUGH DRUGSTORE SHELVES might suggest otherwise, affordable dietary supplements that provide critical nutrients in appropriate doses for pregnant women are virtually nonexistent, researchers have found. In a new study published [...]
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- 2023
9. Haploinsufficiency for DNA methyltransferase 3A predisposes hematopoietic cells to myeloid malignancies
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Cole, Christopher B., Russler-Germain, David A., Ketkar, Shamika, Verdoni, Angela M., Smith, Amanda M., Bangert, Celia V., Helton, Nichole M., Guo, Mindy, Klco, Jeffery M., O'Laughlin, Shelly, Fronick, Catrina, Fulton, Robert, Chang, Gue Su, Petti, Allegra A., Miller, Christopher A., and Ley, Timothy J.
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Methyltransferases -- Research ,Gene mutation -- Research ,Hematopoietic growth factors -- Research ,Myeloid leukemia -- Diagnosis -- Care and treatment ,T cells -- Research ,Health care industry - Abstract
The gene that encodes de novo DNA methyltransferase 3A (DNMT3A) is frequently mutated in acute myeloid leukemia genomes. Point mutations at position R882 have been shown to cause a dominant negative loss of DNMT3A methylation activity, but 15% of DNMT3A mutations are predicted to produce truncated proteins that could either have dominant negative activities or cause loss of function and haploinsufficiency. Here, we demonstrate that 3 of these mutants produce truncated, inactive proteins that do not dimerize with WT DNMT3A, strongly supporting the haploinsufficiency hypothesis. We therefore evaluated hematopoiesis in mice heterozygous for a constitutive null Dnmt3a mutation. With no other manipulations, [Dnmt3a.sup.+/-] mice developed myeloid skewing over time, and their hematopoietic stem/progenitor cells exhibited a long-term competitive transplantation advantage. [Dnmt3a.sup.+/-] mice also spontaneously developed transplantable myeloid malignancies after a long latent period, and 3 of 12 tumors tested had cooperating mutations in the Ras/MAPK pathway. The residual Dnmt3a allele was neither mutated nor downregulated in these tumors. The bone marrow cells of [Dnmt3a.sup.+/-] mice had a subtle but statistically significant DNA hypomethylation phenotype that was not associated with gene dysregulation. These data demonstrate that haploinsufficiency for Dnmt3a alters hematopoiesis and predisposes mice (and probably humans) to myeloid malignancies by a mechanism that is not yet clear., Introduction The DNA methyltransferase 3A (DNMT3A) gene is mutated in approximately 37% of acute myeloid leukemia (AML) patients with a normal karyotype (and ~25% of all AML cases) (1) and [...]
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- 2017
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10. Integrated genomic and molecular characterization of cervical cancer
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Burk, Robert D., Chen, Zigui, Saller, Charles, Tarvin, Katherine, Carvalho, Andre L., Scapulatempo-Neto, Cristovam, Silveira, Henrique C., Fregnani, Jos H., Creighton, Chad J., Anderson, Matthew L., Castro, Patricia, Wang, Sophia S., Yau, Christina, Benz, Christopher, Robertson, A. Gordon, Mungall, Karen, Lim, Lynette, Bowlby, Reanne, Sadeghi, Sara, Brooks, Denise, Sipahimalani, Payal, Mar, Richard, Ally, Adrian, Clarke, Amanda, Mungall, Andrew J., Tam, Angela, Lee, Darlene, Chuah, Eric, Schein, Jacqueline E., Tse, Kane, Kasaian, Katayoon, Ma, Yussanne, Marra, Marco A., Mayo, Michael, Balasundaram, Miruna, Thiessen, Nina, Dhalla, Noreen, Carlsen, Rebecca, Moore, Richard A., Holt, Robert A., Jones, Steven J. M., Wong, Tina, Pantazi, Angeliki, Parfenov, Michael, Kucherlapati, Raju, Hadjipanayis, Angela, Seidman, Jonathan, Kucherlapati, Melanie, Ren, Xiaojia, Xu, Andrew W., Yang, Lixing, Park, Peter J., Lee, Semin, Rabeno, Brenda, Huelsenbeck-Dill, Lori, Borowsky, Mark, Cadungog, Mark, Iacocca, Mary, Petrelli, Nicholas, Swanson, Patricia, Ojesina, Akinyemi I., Le, Xuan, Sandusky, George, Adebamowo, Sally N., Akeredolu, Teniola, Adebamowo, Clement, Reynolds, Sheila M., Shmulevich, Ilya, Shelton, Candace, Crain, Daniel, Mallery, David, Curley, Erin, Gardner, Johanna, Penny, Robert, Morris, Scott, Shelton, Troy, Liu, Jia, Lolla, Laxmi, Chudamani, Sudha, Wu, Ye, Birrer, Michael, McLellan, Michael D., Bailey, Matthew H., Miller, Christopher A., Wyczalkowski, Matthew A., Fulton, Robert S., Fronick, Catrina C., Lu, Charles, Mardis, Elaine R., Appelbaum, Elizabeth L., Schmidt, Heather K., Fulton, Lucinda A., Cordes, Matthew G., Li, Tiandao, Ding, Li, Wilson, Richard K., Rader, Janet S., Behmaram, Behnaz, Uyar, Denise, Bradley, William, Wrangle, John, Pastore, Alessandro, Levine, Douglas A., Dao, Fanny, Gao, Jianjiong, Schultz, Nikolaus, Sander, Chris, Ladanyi, Marc, Einstein, Mark, Teeter, Randall, Benz, Stephen, Wentzensen, Nicolas, Felau, Ina, Zenklusen, Jean C., Bodelon, Clara, Demchok, John A., Yang, Liming, Sheth, Margi, Ferguson, Martin L., Tarnuzzer, Roy, Yang, Hannah, Schiffman, Mark, Zhang, Jiashan, Wang, Zhining, Davidsen, Tanja, Olaniyan, Olayinka, Hutter, Carolyn M., Sofia, Heidi J., Gordenin, Dmitry A., Chan, Kin, Roberts, Steven A., Klimczak, Leszek J., Van Waes, Carter, Chen, Zhong, Saleh, Anthony D., Cheng, Hui, Parfitt, Jeremy, Bartlett, John, Albert, Monique, Arnaout, Angel, Sekhon, Harman, Gilbert, Sebastien, Peto, Myron, Myers, Jerome, Harr, Jodi, Eckman, John, Bergsten, Julie, Tucker, Kelinda, Zach, Leigh Anne, Karlan, Beth Y., Lester, Jenny, Orsulic, Sandra, Sun, Qiang, Naresh, Rashi, Pihl, Todd, Wan, Yunhu, Zaren, Howard, Sapp, Jennifer, Miller, Judy, Drwiega, Paul, Murray, Bradley A., Zhang, Hailei, Cherniack, Andrew D., Sougnez, Carrie, Pedamallu, Chandra Sekhar, Lichtenstein, Lee, Meyerson, Matthew, Noble, Michael S., Heiman, David I., Voet, Doug, Getz, Gad, Saksena, Gordon, Kim, Jaegil, Shih, Juliann, Cho, Juok, Lawrence, Michael S., Gehlenborg, Nils, Lin, Pei, Beroukhim, Rameen, Frazer, Scott, Gabriel, Stacey B., Schumacher, Steven E., Leraas, Kristen M., Lichtenberg, Tara M., Zmuda, Erik, Bowen, Jay, Frick, Jessica, Gastier-Foster, Julie M., Wise, Lisa, Gerken, Mark, Ramirez, Nilsa C., Danilova, Ludmila, Cope, Leslie, Baylin, Stephen B., Salvesen, Helga B., Vellano, Christopher P., Ju, Zhenlin, Diao, Lixia, Zhao, Hao, Chong, Zechen, Ryan, Michael C., Martinez-Ledesma, Emmanuel, Verhaak, Roeland G., Averett Byers, Lauren, Yuan, Yuan, Chen, Ken, Ling, Shiyun, Mills, Gordon B., Lu, Yiling, Akbani, Rehan, Seth, Sahil, Liang, Han, Wang, Jing, Han, Leng, Weinstein, John N., Bristow, Christopher A., Zhang, Wei, Mahadeshwar, Harshad S., Sun, Huandong, Tang, Jiabin, Zhang, Jianhua, Song, Xingzhi, Protopopov, Alexei, Shaw, Kenna R. Mills, Chin, Lynda, Olabode, Oluwole, DiSaia, Philip, Radenbaugh, Amie, Haussler, David, Zhu, Jingchun, Stuart, Josh, Chalise, Prabhakar, Koestler, Devin, Fridley, Brooke L., Godwin, Andrew K., Madan, Rashna, Ciriello, Giovanni, Martinez, Cathleen, Higgins, Kelly, Bocklage, Therese, Auman, J. Todd, Perou, Charles M., Tan, Donghui, Parker, Joel S., Hoadley, Katherine A., Wilkerson, Matthew D., Mieczkowski, Piotr A., Skelly, Tara, Veluvolu, Umadevi, Hayes, D. Neil, Rathmell, W. Kimryn, Hoyle, Alan P., Simons, Janae V., Wu, Junyuan, Mose, Lisle E., Soloway, Matthew G., Balu, Saianand, Meng, Shaowu, Jefferys, Stuart R., Bodenheimer, Tom, Shi, Yan, Roach, Jeffrey, Thorne, Leigh B., Boice, Lori, Huang, Mei, Jones, Corbin D., Zuna, Rosemary, Walker, Joan, Gunderson, Camille, Snowbarger, Carie, Brown, David, Moxley, Katherine, Moore, Kathleen, Andrade, Kelsi, Landrum, Lisa, Mannel, Robert, McMeekin, Scott, Johnson, Starla, Nelson, Tina, Elishaev, Esther, Dhir, Rajiv, Edwards, Robert, Bhargava, Rohit, Tiezzi, Daniel G., Andrade, Jurandyr M., Noushmehr, Houtan, Gilberto Carlotti, Carlos, Jr, Tirapelli, Daniela Pretti da Cunha, Weisenberger, Daniel J., Van Den Berg, David J., Maglinte, Dennis T., Bootwalla, Moiz S., Lai, Phillip H., Triche, Timothy, Jr, Swisher, Elizabeth M., Agnew, Kathy J., Shelley, Carl Simon, Laird, Peter W., Schwarz, Julie, Grigsby, Perry, and Mutch, David
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Cervical cancer -- Genetic aspects -- Care and treatment -- Causes of ,Gene mutation -- Health aspects ,Environmental issues ,Science and technology ,Zoology and wildlife conservation - Abstract
Cervical cancer remains one of the leading causes of cancer-related deaths worldwide. Here we report the extensive molecular characterization of 228 primary cervical cancers, one of the largest comprehensive genomic studies of cervical cancer to date. We observed notable APOBEC mutagenesis patterns and identified SHKBP1, ERBB3, CASP8, HLA-A and TGFBR2 as novel significantly mutated genes in cervical cancer. We also discovered amplifications in immune targets CD274 (also known as PD-L1) and PDCD1LG2 (also known as PD-L2), and the BCAR4 long non-coding RNA, which has been associated with response to lapatinib. Integration of human papilloma virus (HPV) was observed in all HPV18-related samples and 76% of HPV16-related samples, and was associated with structural aberrations and increased target-gene expression. We identified a unique set of endometrial-like cervical cancers, comprised predominantly of HPV-negative tumours with relatively high frequencies of KRAS, ARID1A and PTEN mutations. Integrative clustering of 178 samples identified keratin-low squamous, keratin-high squamous and adenocarcinoma-rich subgroups. These molecular analyses reveal new potential therapeutic targets for cervical cancers., Author(s): The Cancer Genome Atlas Research Network; Albert Einstein College of Medicine; Robert D. Burk [1]; Zigui Chen [1]; Analytical Biological Services; Charles Saller [2]; Katherine Tarvin [2]; Barretos Cancer [...]
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- 2017
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11. Quaternary stratigraphy and evidence for multiple glacial episodes in the north Okanagan Valley, British Columbia
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Nichol, Craig, Monahan, Patrick, Fulton, Robert, Ping, Jianhua, Wei, Xioahua, and Thomson, Skye
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Okanagan Valley -- Natural history ,Geology, Stratigraphic -- Research ,Interglacial periods -- Research ,Geological research ,Sediments (Geology) -- Natural history ,Earth sciences - Abstract
This study investigates the Quaternary stratigraphy of the north Okanagan Valley to inform hydrogeological studies. The north Okanagan Valley extends from the north end of Okanagan Lake to Enderby in the southern interior of British Columbia, Canada. Prior surficial geology mapping, provincial and private borehole data, historical seismic profiling, and a new 5 km high-resolution seismic reflection profile were examined to characterize up to 580 m thickness of unconsolidated sediments. A mixture of glacial and interglacial sediments of uncertain Pleistocene age infills bedrock lows that extend below sea level. These are unconformably overlain by a sand and gravel unit of at least Early Wisconsin age (>65 000 years BP). It is in turn unconformably onlapped by nonglacial, organic-rich, lacustrine and alluvial deposits of Middle Wisconsin age (65 000-23 000 years BP). This unit was eroded and overlain by a fine sand to silty sand unit deposited immediately prior to, or during, the Fraser Glaciation advance (>23 000 years BP). Diamict and glacial deposits including valley-side kame overlie these sands at some of the valley margins. Glaciolacustrine sediments of the end of the Fraser Glaciation have no appreciable organic matter and overlie the fine sands in the main Okanagan Valley; these form the majority of the surface outcrop. Recessional glaciodeltaic sediments overlie, and in some places may interfinger with, these glaciolacustrine sediments, which indicates an open proglacial lake environment during late glacial stages. These materials and fan-shaped periglacial debris flow deposits are incised by late Holocene fluvial downcutting. The north Okanagan Valley stratigraphy preserves the record of several glacial and interglacial periods, which suggests that overdeepening of the bedrock surface of the Okanagan Valley may be older than previously suggested. La presente etude analyse la stratigraphie du Quaternaire du nord de la vallee de l'Okanagan dans le but d'obtenir des donnees pour des etudes hydrogeologiques. Le nord de la vallee de l'Okanagan s'etend de l'extremite nord du lac kanagan jusqu';! Enderby dans le sud interieur de la Colombie-Britannique, Canada. Une cartographie anterieure de la geologie de surface, des donnees provinciales et privees de de forages, des profils sismiques historiques et un nouveau profil sismique reflexion a haute resolution, d'une longueur de 5 km, ont ete examines dans le but de caracteriser des sediments non consolides atteignant une epaisseur de 580 m. Un melange de sediments glaciaires et interglaciaires, d'age Pleistocene incertain, remplit des creux du socle qui s'etendent sous le niveau de la mer. Une unite de sable et de gravier, d'age au moins Wisconsin precoce (>65 000 annees avant le present), repose de facon discordante sur ces sediments. Des depots lacustres et alluviaux, riches en matiere organique, datant du Wisconsin moyen (65 000-23 000 annees avant le present), recouvrent a leur tour et de maniere discordante transgressive l'unite de sable. Cette derniere unite a ete erodee et recouverte d'une unite de sable fin a silteux deposee immediatement avant, ou durant, l'avancee glaciaire Fraser (>23 000 annees avant le present). Des depots glaciaires et de diamictons, incluant des kames, recouvrent ces sables a certains endroits sur le bord de la vallee. Les sediments glacio-lacustres de la fin de la glaciation Fraser ne contiennent pas de matiere organique en quantite appreciable et ils recouvrent les sables fins de la vallee principale de l'Okanagan; ces sediments forment la plus grande partie des affleurements en surface. Des sediments glacio-deltaiques de recession recouvrent et parfois se melent a ces sediments glacio-lacustres, indiquant un environnement de lac proglaciaire ouvert durant les derniers stades glaciaires. Ces materiaux et les debris d'ecoulement periglaciaire en forme d'eventail ont ete recoupes par une erosion fluviale verticale a l'Holocene tardif.La stratigraphie du nord de la vallee de l'Okanagan preserve le profil de plusieurs periodes glaciaires et interglaciaires, ce qui suggere que l'incision de la surface du socle de la vallee de l'Okanagan pourrait etre plus ancienne que suggere anterieurement. [Traduit par la Redaction], Introduction The Okanagan Basin is an 8000 [km.sup.2] watershed located in the interior of southern British Columbia, Canada (Fig. 1). Its dominant feature is the 1-4 km wide, north-south trending, [...]
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- 2015
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12. Role of TP53 mutations in the origin and evolution of therapy--related acute myeloid leukaemia
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Wong, Terrence N., Ramsingh, Giridharan, Young, Andrew L., Miller, Christopher A., Touma, Waseem, Welch, John S., Lamprecht, Tamara L., Shen, Dong, Hundal, Jasreet, Fulton, Robert S., Heath, Sharon, Baty, Jack D., Klco, Jeffery M., Ding, Li, Mardis, Elaine R., Westervelt, Peter, DiPersio, John F., Walter, Matthew J., Graubert, Timothy A., Ley, Timothy J., Druley, Todd E., Link, Daniel C., and Wilson, Richard K.
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Gene mutations -- Health aspects ,Environmental issues ,Science and technology ,Zoology and wildlife conservation - Abstract
Therapy-related acute myeloid leukaemia (t-AML) and therapy-related myelodysplastic syndrome (t-MDS) are well-recognized complications of cytotoxic chemotherapy and/or radiotherapy (1). There are several features that distinguish t-AML from denovo AML, including a higher incidence of TP53 mutations (2,3), abnormalities of chromosomes 5 or 7, complex cytogenetics and a reduced response to chemotherapy (4). However, it is not clear how prior exposure to cytotoxic therapy influences leukaemogenesis. In particular, the mechanism by which TP53 mutations are selectively enriched in t-AML/t-MDS is unknown. Here, by sequencing the genomes of 22 patients with t-AML, we show that the total number of somatic single-nucleotide variants and the percentage of chemotherapy-related transversions are similar in t-AML and denovo AML, indicating that previous chemotherapy does not induce genome-wide DNA damage. W e identified four cases of t-AML/ t-MDS in which the exact TP53 mutation found at diagnosis was also present at low frequencies (0.003-0.7%) in mobilized blood leukocytes or bone marrow 3-6 years before the development of t-AML/tMDS, including two cases in which the relevant TP53 mutation was detected before any chemotherapy. Moreover, functional TP53 mutations were identified in small populations of peripheral blood cells of healthy chemotherapy-naive elderly individuals. Finally, in mouse bone marrow chimaeras containing both wild-type and [Tp53.sup.+/-] haematopoietic stem/progenitor cells (HSPCs), the [Tp53.sup.+/-] HSPCs preferentially expanded after exposure to chemotherapy. These data suggest that cytotoxic therapy does not directly induce TP53 mutations. Rather, they support a model in which rare HSPCs carrying age-related TP53 mutations are resistant to chemotherapy and expand preferentially after treatment. The early acquisition of TP53 mutations in the founding HSPC clone probably contributes to the frequent cytogenetic abnormalities and poor responses to chemotherapy that are typical of patients with t-AML/t-MDS., t-AML and t-MDS are clonal haematopoietic disorders that typically develop 1-5 years after exposure to chemotherapy or radiotherapy (1). To understand better how prior cytotoxic therapy contributes to the high [...]
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- 2015
13. Mammalian Y chromosomes retain widely expressed dosage-sensitive regulators
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Bellott, Daniel W., Hughes, Jennifer F., Skaletsky, Helen, Brown, Laura G., Pyntikova, Tatyana, Cho, Ting-Jan, Koutseva, Natalia, Zaghlul, Sara, Graves, Tina, Rock, Susie, Kremitzki, Colin, Fulton, Robert S., Dugan, Shannon, Ding, Yan, Morton, Donna, Khan, Ziad, Lewis, Lora, Buhay, Christian, Wang, Qiaoyan, Watt, Jennifer, Holder, Michael, Lee, Sandy, Nazareth, Lynne, Rozen, Steve, Muzny, Donna M., Warren, Wesley C., Gibbs, Richard A., Wilson, Richard K., and Page, David C.
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Spermatogenesis -- Research ,Evolutionary biology -- Research ,X chromosome -- Physiological aspects -- Research ,Y chromosome -- Physiological aspects -- Research ,Environmental issues ,Science and technology ,Zoology and wildlife conservation - Abstract
The human X and Y chromosomes evolved from an ordinary pair of autosomes, but millions of years ago genetic decay ravaged the Y chromosome, and only three per cent of its ancestral genes survived. We reconstructed the evolution of the Y chromosome across eight mammals to identify biases in gene content and the selective pressures that preserved the surviving ancestral genes. Our findings indicate that survival was nonrandom, and in two cases, convergent across placental and marsupial mammals. We conclude that the gene content of the Y chromosome became specialized through selection to maintain the ancestral dosage of homologous X-Ygene pairs that function as broadly expressed regulators of transcription, translation and protein stability. We propose that beyond its roles in testis determination and spermatogenesis, the Y chromosome is essential for male viability, and has unappreciated roles in Turner's syndrome and in phenotypic differences between the sexes in health and disease., The human X and Y chromosomes evolved from autosomes over the past 300 million years (1). Only 3% of ancestral genes survive on the human Y chromosome (2,3), compared to [...]
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- 2014
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14. Whole-genome analysis informs breast cancer response to aromatase inhibition
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Ellis, Matthew J., Ding, Li, Shen, Dong, Luo, Jingqin, Suman, Vera J., Wallis, John W., Van Tine, Brian A., Hoog, Jeremy, Goiffon, Reece J., Goldstein, Theodore C., Ng, Sam, Lin, Li, Crowder, Robert, Snider, Jacqueline, Ballman, Karla, Weber, Jason, Chen, Ken, Koboldt, Daniel C., Kandoth, Cyriac, Schierding, William S., McMichael, Joshua F., Miller, Christopher A., Lu, Charles, Harris, Christopher C., McLellan, Michael D., Wendl, Michael C., DeSchryver, Katherine, Allred, D. Craig, Esserman, Laura, Unzeitig, Gary, Margenthaler, Julie, Babiera, G. V., Marcom, P. Kelly, Guenther, J. M., Leitch, Marilyn, Hunt, Kelly, Olson, John, Tao, Yu, Maher, Christopher A., Fulton, Lucinda L., Fulton, Robert S., Harrison, Michelle, Oberkfell, Ben, Du, Feiyu, Demeter, Ryan, Vickery, Tammi L., Elhammali, Adnan, Piwnica-Worms, Helen, McDonald, Sandra, Watson, Mark, Dooling, David J., Ota, David, Chang, Li-Wei, Bose, Ron, Ley, Timothy J., Piwnica-Worms, David, Stuart, Joshua M., Wilson, Richard K., and Mardis, Elaine R.
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Gene mutations -- Health aspects ,Breast cancer -- Drug therapy -- Genetic aspects ,Environmental issues ,Science and technology ,Zoology and wildlife conservation - Abstract
To correlate the variable clinical features of oestrogen-receptor-positive breast cancer with somatic alterations, we studied pretreatment tumour biopsies accrued from patients in two studies of neoadjuvant aromatase inhibitor therapy by massively parallel sequencing and analysis. Eighteen significantly mutated genes were identified, including five genes (RUNX1, CBFB, MYH9, MLL3 and SF3B1) previously linked to haematopoietic disorders. Mutant MAP3K1 was associated with luminal A status, low-grade histology and low proliferation rates, whereas mutant TP53 was associated with the opposite pattern. Moreover, mutant GATA3 correlated with suppression of proliferation upon aromatase inhibitor treatment. Pathway analysis demonstrated that mutations in MAP2K4, a MAP3K1 substrate, produced similar perturbations as MAP3K1 loss. Distinct phenotypes in oestrogen-receptor-positive breast cancer are associated with specific patterns of somatic mutations that map into cellular pathways linked to tumour biology, but most recurrent mutations are relatively infrequent. Prospective clinical trials based on these findings will require comprehensive genome sequencing., Author(s): Matthew J. Ellis [1, 2, 3, 25]; Li Ding [4, 5, 25]; Dong Shen [4, 5, 25]; Jingqin Luo [3, 6]; Vera J. Suman [7]; John W. Wallis [4, [...]
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- 2012
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15. Strict evolutionary conservation followed rapid gene loss on human and rhesus Y chromosomes
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Hughes, Jennifer F., Skaletsky, Helen, Brown, Laura G., Pyntikova, Tatyana, Graves, Tina, Fulton, Robert S., Dugan, Shannon, Ding, Yan, Buhay, Christian J., Kremitzki, Colin, Wang, Qiaoyan, Shen, Hua, Holder, Michael, Villasana, Donna, Nazareth, Lynne V., Cree, Andrew, Courtney, Laura, Veizer, Joelle, Kotkiewicz, Holland, Cho, Ting-Jan, Koutseva, Natalia, Rozen, Steve, Muzny, Donna M., Warren, Wesley C., Gibbs, Richard A., Wilson, Richard K., and Page, David C.
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Rhesus monkey -- Genetic aspects ,Chimpanzees -- Genetic aspects ,Human genetics -- Research ,Human chromosomes -- Properties ,Y chromosome -- Properties ,Evolutionary genetics -- Research ,Chromosome mapping -- Methods ,Environmental issues ,Science and technology ,Zoology and wildlife conservation - Abstract
The human X and Y chromosomes evolved from an ordinary pair of autosomes during the past 200-300 million years (1-3). The human MSY (male-specific region of Y chromosome) retains only three percent of the ancestral autosomes' genes owing to genetic decay (4,5). This evolutionary decay was driven by a series of five 'stratification' events. Each event suppressed X-Y crossing over within a chromosome segment or 'stratum', incorporated that segment into the MSY and subjected its genes to the erosive forces that attend the absence of crossing over (2,6). The last of these events occurred 30 million years ago, 5 million years before the human and Old World monkey lineages diverged. Although speculation abounds regarding ongoing decay and looming extinction of the human Y chromosome (7-10), remarkably little is known about how many MSY genes were lost in the human lineage in the 25 million years that have followed its separation from the Old World monkey lineage. To investigate this question, we sequenced the MSY of the rhesus macaque, an Old World monkey, and compared it to the human MSY. We discovered that during the last 25 million years MSY gene loss in the human lineage was limited to the youngest stratum (stratum 5), which comprises three percent of the human MSY. In the older strata, which collectively comprise the bulk of the human MSY, gene loss evidently ceased more than 25 million years ago. Likewise, the rhesus MSY has not lost any older genes (from strata 1-4) during the past 25 million years, despite its major structural differences to the human MSY. The rhesus MSY is simpler, with few amplified gene families or palindromes that might enable intrachromosomal recombination and repair. We present an empirical reconstruction of human MSY evolution in which each stratum transitioned from rapid, exponential loss of ancestral genes to strict conservation through purifying selection., The human Y chromosome no longer engages in crossing over with its once-identical partner, the X chromosome, except in its pseudoautosomal regions. During evolution, X-Y crossing over was suppressed in [...]
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- 2012
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16. Clonal evolution in relapsed acute myeloid leukaemia revealed by whole-genome sequencing
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Ding, Li, Ley, Timothy J., Larson, David E., Miller, Christopher A., Koboldt, Daniel C., Welch, John S., Ritchey, Julie K., Young, Margaret A., Lamprecht, Tamara, McLellan, Michael D., McMichael, Joshua F., Wallis, John W., Lu, Charles, Shen, Dong, Harris, Christopher C., Dooling, David J., Fulton, Robert S., Fulton, Lucinda L., Chen, Ken, Schmidt, Heather, Kalicki-Veizer, Joelle, Magrini, Vincent J., Cook, Lisa, McGrath, Sean D., Vickery, Tammi L., Wendl, Michael C., Heath, Sharon, Watson, Mark A., Link, Daniel C., Tomasson, Michael H., Shannon, William D., Payton, Jacqueline E., Kulkarni, Shashikant, Westervelt, Peter, Walter, Matthew J., Graubert, Timothy A., Mardis, Elaine R., Wilson, Richard K., and DiPersio, John F.
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Nucleotide sequencing -- Health aspects ,DNA sequencing -- Health aspects ,Clonal selection theory -- Abnormalities ,Environmental issues ,Science and technology ,Zoology and wildlife conservation - Abstract
Most patients with acute myeloid leukaemia (AML) die from progressive disease after relapse, which is associated with clonal evolution at the cytogenetic level (1,2). To determine the mutational spectrum associated with relapse, we sequenced the primary tumour and relapse genomes from eight AML patients, and validated hundreds of somatic mutations using deep sequencing; this allowed us to define clonality and clonal evolution patterns precisely at relapse. In addition to discovering novel, recurrently mutated genes (for example, WAC, SMC3, DIS3, DDX41 and DAXX) in AML, we also found two major clonal evolution patterns during AML relapse: (1) the founding clone in the primary tumour gained mutations and evolved into the relapse clone, or (2) a subclone of the founding clone survived initial therapy, gained additional mutations and expanded at relapse. In all cases, chemotherapy failed to eradicate the founding clone. The comparison of relapse-specific versus primary tumour mutations in all eight cases revealed an increase in transversions, probably due to DNA damage caused by cytotoxic chemotherapy. These data demonstrate that AML relapse is associated with the addition of new mutations and clonal evolution, which is shaped, in part, by the chemotherapy that the patients receive to establish and maintain remissions., To investigate the genetic changes associated with AML relapse, and to determine whether clonal evolution contributes to relapse, we performed whole-genome sequencing of primary tumour-relapse pairs and matched skin samples [...]
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- 2012
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17. A novel retinoblastoma therapy from genomic and epigenetic analyses
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Zhang, Jinghui, Benavente, Claudia A., McEvoy, Justina, Flores-Otero, Jacqueline, Ding, Li, Chen, Xiang, Ulyanov, Anatoly, Wu, Gang, Wilson, Matthew, Wang, Jianmin, Brennan, Rachel, Rusch, Michael, Manning, Amity L., Ma, Jing, Easton, John, Shurtleff, Sheila, Mullighan, Charles, Pounds, Stanley, Mukatira, Suraj, Gupta, Pankaj, Neale, Geoff, Zhao, David, Lu, Charles, Fulton, Robert S., Fulton, Lucinda L., Hong, Xin, Dooling, David J., Ochoa, Kerri, Naeve, Clayton, Dyson, Nicholas J., Mardis, Elaine R., Bahrami, Armita, Ellison, David, Wilson, Richard K., Downing, James R., and Dyer, Michael A.
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Gene mutations -- Research ,Retinoblastoma -- Genetic aspects -- Development and progression -- Diagnosis -- Research -- Risk factors ,Gene therapy -- Health aspects -- Research ,Environmental issues ,Science and technology ,Zoology and wildlife conservation - Abstract
Retinoblastoma is an aggressive childhood cancer of the developing retina that is initiated by the biallelic loss of RB1. Tumours progress very quickly following RB1 inactivation but the underlying mechanism is not known. Here we show that the retinoblastoma genome is stable, but that multiple cancer pathways can be epigenetically deregulated. To identify the mutations that cooperate with RB1 loss, we performed whole-genome sequencing of retinoblastomas. The overall mutational rate was very low; RB1 was the only known cancer gene mutated. We then evaluated the role of RB1 in genome stability and considered non-genetic mechanisms of cancer pathway deregulation. For example, the proto-oncogene SYK is upregulated in retinoblastoma and is required for tumour cell survival. Targeting SYK with a small-molecule inhibitor induced retinoblastoma tumour cell death in vitro and in vivo. Thus, retinoblastomas may develop quickly as a result of the epigenetic deregulation of key cancer pathways as a direct or indirect result of RB1 loss., Retinoblastoma is a rare childhood cancer of the retina that can develop in a sporadic or a heritable form and is fatal if untreated. When the RB1 gene was first [...]
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- 2012
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18. Sequencing a mouse acute promyelocytic leukemia genome reveals genetic events relevant for disease progression
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Wartman, Lukas D., Larson, David E., Xiang, Zhifu, Ding, Li, Chen, Ken, Lin, Ling, Cahan, Patrick, Klco, Jeffery M., Welch, John S., Li, Cheng, Payton, Jacqueline E., Uy, Geoffrey L., Varghese, Nobish, Ries, Rhonda E., Hoock, Mieke, Koboldt, Daniel C., McLellan, Michael D., Schmidt, Heather, Fulton, Robert S., Abbott, Rachel M., Cook, Lisa, McGrath, Sean D., Fan, Xian, Dukes, Adam F., Vickery, Tammi, Kalicki, Joelle, Lamprecht, Tamara L., Graubert, Timothy A., Tomasson, Michael H., Mardis, Elaine R., Wilson, Richard K., and Ley, Timothy J.
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Nucleotide sequencing -- Research -- Genetic aspects ,DNA sequencing -- Research -- Genetic aspects ,Cancer -- Genetic aspects ,Health care industry - Abstract
Acute promyelocytic leukemia (APL) is a subtype of acute myeloid leukemia (AML). It is characterized by the t(15;17)(q22;q11.2) chromosomal translocation that creates the promyelocytic leukemia-retinoic acid receptor a (PML-RARA) fusion oncogene. Although this fusion oncogene is known to initiate APL in mice, other cooperating mutations, as yet ill defined, are important for disease pathogenesis. To identify these, we used a mouse model of APL, whereby PML-RARA expressed in myeloid cells leads to a myeloproliferative disease that ultimately evolves into APL. Sequencing of a mouse APL genome revealed 3 somatic, nonsynonymous mutations relevant to APL pathogenesis, of which 1 (Jakl V657F) was found to be recurrent in other affected mice. This mutation was identical to the JAK1 V658F mutation previously found in human APL and acute lym-phoblastic leukemia samples. Further analysis showed that JAK1 V658F cooperated in vivo with PML-RARA, causing a rapidly fatal leukemia in mice. We also discovered a somatic 150-kb deletion involving the lysine (K)-specific demethylase 6A (Kdm6a, also known as Utx) gene, in the mouse APL genome. Similar deletions were observed in 3 out of 14 additional mouse APL samples and 1 out of 150 human AML samples. In conclusion, whole genome sequencing of mouse cancer genomes can provide an unbiased and comprehensive approach for discovering functionally relevant mutations that are also present in human leukemias., Introduction Recent studies have shown that whole genome sequencing is a valid, unbiased approach that can identify novel mutations and structural variants that may be important drivers of acute myeloid [...]
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- 2011
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19. Evidence-based practice in group care: the effects of policy, research, and organizational practices
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Stuart, Carol, Sanders, Larry, Gurevich, Maria, and Fulton, Robert
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Social group work -- Methods ,Case management (Social services) -- Methods ,Family and marriage ,Sociology and social work - Abstract
This article describes the effect of a province-wide vision of evidence-based and outcome-based services for children and youth and the challenges of implementing evidence-based practice (EBP) and evidence-based treatment (EBT) [...]
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- 2011
20. DNMT3A mutations in acute myeloid leukemia
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Ley, Timothy J., Li Ding, Walter, Matthew J., McLellan, Michael D., Lamprecht, Tamara, Larson, David E., Kandoth, Cyriac, Payton, Jacqueline E., Baty, Jack, Welch, John, Harris, Christopher C., Lichti, Cheryl F., Townsend, R. Reid, Fulton, Robert S., Dooling, David J., Koboldt, Daniel C., Schmidt, Heather, Qunyuan Zhang, Osborne, John R., Ling Lin, O'aughlin, Michelle, McMichael, Joshua F., Delehaunty, Kim D., McGrath, Sean D., Fulton, Lucinda A., Magrini, Vincent J., Vickery, Tammi L., Hundal, Jasreet, Cook, Lisa L., Conyers, Joshua J., Swift, Gary W., Reed, Jerry P., Alldredge, Patricia A., Wylie, Todd, Walker, Jason, Kalicki, Joelle, Watson, Mark A., Heath, Sharon, Shannon, William D., Varghese, Nobish, Nagarajan, Rakesh, Westervelt, Peter, Tomasson, Michael H., Link, Daniel C., Graubert, Timothy A., DiPersio, John F., Mardis, Elaine R., and Wilson, Richard K.
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Amino acids -- Chemical properties ,Amino acids -- Health aspects ,Nucleotide sequencing -- Usage - Abstract
A study was conducted to evaluate whether DNMT3A is recurrently mutated in acute myeloid leukemia samples and whether DNMT3A mutations are associated with poor survival rates. Results indicated that sNMT3A mutations are highly recurrent in such patients and are independently associated with poor outcomes.
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- 2010
21. Chimpanzee and human Y chromosomes are remarkably divergent in structure and gene content
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Hughes, Jennifer F., Skaletsky, Helen, Pyntikova, Tatyana, Graves, Tina A., van Daalen, Saskia K.M., Minx, Patrick J., Fulton, Robert S., McGrath, Sean D., Locke, Devin P., Friedman, Cynthia, Trask, Barbara J., Mardis, Elaine R., Warren, Wesley C., Repping, Sjoerd, Rozen, Steve, Wilson, Richard K., and Page, David C.
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Man -- Genetic aspects -- Research ,Chimpanzees -- Research -- Genetic aspects ,Human beings -- Genetic aspects -- Research ,Environmental issues ,Science and technology ,Zoology and wildlife conservation - Abstract
The human Y chromosome began to evolve from an autosome hundreds of millions of years ago, acquiring a sex-determining function and undergoing a series of inversions that suppressed crossing over with the X chromosome (1,2). Little is known about the recent evolution of the Y chromosome because only the human Y chromosome has been fully sequenced. Prevailing theories hold that Y chromosomes evolve by gene loss, the pace of which slows over time, eventually leading to a paucity of genes, and stasis (3,4). These theories have been buttressed by partial sequence data from newly emergent plant and animal Y chromosomes (5-8), but they have not been tested in older, highly evolved Y chromosomes such as that of humans. Here we finished sequencing of the male-specific region of the Y chromosome (MSY) in our closest living relative, the chimpanzee, achieving levels of accuracy and completion previously reached for the human MSY. By comparing the MSYs of the two species we show that they differ radically in sequence structure and gene content, indicating rapid evolution during the past 6 million years. The chimpanzee MSY contains twice as many massive palindromes as the human MSY, yet it has lost large fractions of the MSY protein-coding genes and gene families present in the last common ancestor. We suggest that the extraordinary divergence of the chimpanzee and human MSYs was driven by four synergistic factors: the prominent role of the MSY in sperm production, 'genetic hitchhiking' effects in the absence of meiotic crossing over, frequent ectopic recombination within the MSY, and species differences in mating behaviour. Although genetic decay may be the principal dynamic in the evolution of newly emergent Y chromosomes, wholesale renovation is the paramount theme in the continuing evolution of chimpanzee, human and perhaps other older MSYs., This study required that we first complete the sequencing of the chimpanzee MSY (9-11) using large-insert bacterial artificial chromosome (BAC) clones and the iterative mapping and sequencing strategy used to [...]
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- 2010
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22. Recurring mutations found by sequencing an acute myeloid leukemia genome
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Mardis, Elaine R., Ding, Li, Dooling, David J., Larson, David E., McLellan, Michael D., Chen, Ken, Koboldt, Daniel C., Fulton, Robert S., Delehaunty, Kim D., McGrath, Sean D., Fulton, Lucinda A., Locke, Devin P., Magrini, Vincent J., Abbott, Rachel M., Vickery, Tammi L., Reed, Jerry S., Robinson, Jody S., Wylie, Todd, Smith, Scott M., Carmichael, Lynn, Eldred, James M., Harris, Christopher C., Walker, Jason, Peck, Joshua P., Du, Feiyu, Dukes, Adam F., Sanderson, Gabriel E., Brummett, Anthony M., Clark, Eric, McMichael, Joshua F., Meyer, Rick J., Schindler, Jonathan K., Pohl, Craig S., Wallis, John W., Xiaoqi Shi, Ling Lin, Schmidt, Heather, Tang, Tuzhu, Haipek,Carrie, and Wiechert, Madeline E.
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Gene mutations -- Research ,Nucleotide sequencing -- Research - Abstract
The study aims to investigate and understand the DNA mutations that are responsible for sequencing of an acute myeloid leukemia (AML) genome. The results indicate that recurrent mutations that may be relevant for pathogenesis by comparing the sequences of tumor and skin genomes of a patient with AML-M1 have been identified.
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- 2009
23. Acquired copy number alterations in adult acute myeloid leukemia genomes
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Walter, Matthew J., Payton, Jacqueline E., Ries, Rhonda E., Shannon, William D., Deshmukh, Hrishikesh, Zhao, Yu, Baty, Jack, Heath, Sharon, Westervelt, Peter, Watson, Mark A., Tomasson, Michael H., Nagarajan, Rakesh, O'Gara, Brian P., Bloomfield, Clara D., Mrozek, Krzysztof, Seizer, Rebecca R., Richmond, Todd A., Kitzman, Jacob, Geoghegan, Joel, Eis, Peggy S., Maupin, Rachel, Fulton, Robert S., McLellan, Michael, Wilson, Richard K., Mardis, Elaine R., Link, Daniel C., Graubert, Timothy A., DiPersio, John F., and Ley, Timothy J.
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Genomes -- Identification and classification ,Genomes -- Health aspects ,Cancer -- Genetic aspects ,Cancer -- Research ,Science and technology - Abstract
Cytogenetic analysis of acute myeloid leukemia (AML) cells has accelerated the identification of genes important for AML pathogenesis. To complement cytogenetic studies and to identify genes altered in AML genomes, we performed genome-wide copy number analysis with paired normal and tumor DNA obtained from 86 adult patients with de novo AML using 1.85 million feature SNP arrays. Acquired copy number alterations (CNAs) were confirmed using an ultra-dense array comparative genomic hybridization platform. A total of 201 somatic CNAs were found in the 86 AML genomes (mean, 2.34 CNAs per genome), with French-American-British system M6 and M7 genomes containing the most changes (10-29 CNAs per genome). Twenty-four percent of AML patients with normal cytogenetics had CNA, whereas 40% of patients with an abnormal karyotype had additional CNA detected by SNP array, and several CNA regions were recurrent. The mRNA expression levels of 57 genes were significantly altered in 27 of 50 recurrent CNA regions AML | array CGH | genomics | SNP array
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- 2009
24. Characterizing a model human gut microbiota composed of members of its two dominant bacterial phyla
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Mahowald, Michael A., Rey, Federico E., Seedorf, Henning, Turnbaugh, Peter J., Fulton, Robert S., Wollam, Aye, Shah, Neha, Wang, Chunyan, Magrini, Vincent, Wilson, Richard K., Cantarel, Brandi L., Coutinho, Pedro M., Henrissat, Bernard, Crock, Lara W., Russell, Alison, Verberkmoes, Nathan C., Hettich, Robert L., and Gordon, Jeffrey I.
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Microbiota (Symbiotic organisms) -- Research ,Science and technology - Abstract
The adult human distal gut microbial community is typically dominated by 2 bacterial phyla (divisions), the Firmicutes and the Bacteroidetes. Little is known about the factors that govern the interactions between their members. Here, we examine the niches of representatives of both phyla in vivo. Finished genome sequences were generated from Eubacterium rectale and E. eligens, which belong to Clostridium Cluster XIVa, one of the most common gut Firmicute clades. Comparison of these and 25 other gut Firmicutes and Bacteroidetes indicated that the Firmicutes possess smaller genomes and a disproportionately smaller number of glycan-degrading enzymes. Germ-free mice were then colonized with E. rectale and/or a prominent human gut Bacteroidetes, Bacteroides thetaiotaomicron, followed by whole-genome transcriptional profiling, high-resolution proteomic analysis, and biochemical assays of microbial--microbial and microbial--host interactions. B. thetaiotaomicron adapts to E. rectale by up-regulating expression of a variety of polysaccharide utilization loci encoding numerous glycoside hydrolases, and by signaling the host to produce mucosal glycans that it, but not E. rectale, can access. E. rectale adapts to B. thetaiotaomicron by decreasing production of its glycan-degrading enzymes, increasing expression of selected amino acid and sugar transporters, and facilitating glycolysis by reducing levels of NADH, in part via generation of butyrate from acetate, which in turn is used by the gut epithelium. This simplified model of the human gut microbiota illustrates niche specialization and functional redundancy within members of its major bacterial phyla, and the importance of host glycans as a nutrient foundation that ensures ecosystem stability. human gut Firmicutes and Bacteroidetes | carbohydrate metabolism gnotobiotic mice | gut microbiome | nutrient sharing
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- 2009
25. Somatic mutations affect key pathways in lung adenocarcinoma
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Ding, Li, Getz, Gad, Wheeler, David A., Mardis, Elaine R., McLellan, Michael D., Cibulskis, Kristian, Sougnez, Carrie, Greulich, Heidi, Muzny, Donna M., Morgan, Margaret B., Fulton, Lucinda, Fulton, Robert S., Zhang, Qunyuan, Wendl, Michael C., Lawrence, Michael S., Larson, David E., Chen, Ken, Dooling, David J., Sabo, Aniko, Hawes, Alicia C., Shen, Hua, Jhangiani, Shalini N., Lewis, Lora R., Hall, Otis, Zhu, Yiming, Mathew, Tittu, Ren, Yanru, Yao, Jiqiang, Scherer, Steven E., Clerc, Kerstin, Metcalf, Ginger A., Ng, Brian, Milosavljevic, Aleksandar, Gonzalez-Garay, Manuel L., Osborne, John R., Meyer, Rick, Shi, Xiaoqi, Tang, Yuzhu, Koboldt, Daniel C., Lin, Ling, Abbott, Rachel, Miner, Tracie L., Pohl, Craig, Fewell, Ginger, Haipek, Carrie, Schmidt, Heather, Dunford-Shore, Brian H., Kraja, Aldi, Crosby, Seth D., Sawyer, Christopher S., Vickery, Tammi, Sander, Sacha, Robinson, Jody, Winckler, Wendy, Baldwin, Jennifer, Chirieac, Lucian R., Dutt, Amit, Fennell, Tim, Hanna, Megan, Johnson, Bruce E., Onofrio, Robert C., Thomas, Roman K., Tonon, Giovanni, Weir, Barbara A., Zhao, Xiaojun, Ziaugra, Liuda, Zody, Michael C., Giordano, Thomas, Orringer, Mark B., Roth, Jack A., Spitz, Margaret R., Wistuba, Ignacio I., Ozenberger, Bradley, Good, Peter J., Chang, Andrew C., Beer, David G., Watson, Mark A., Ladanyi, Marc, Broderick, Stephen, Yoshizawa, Akihiko, Travis, William D., Pao, William, Province, Michael A., Weinstock, George M., Varmus, Harold E., Gabriel, Stacey B., Lander, Eric S., Gibbs, Richard A., Meyerson, Matthew, and Wilson, Richard K.
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Gene mutations -- Research -- Physiological aspects -- Genetic aspects ,Nucleotide sequencing -- Research -- Physiological aspects -- Genetic aspects ,Adenocarcinoma -- Genetic aspects -- Research -- Care and treatment -- Prognosis -- Diagnosis ,DNA sequencing -- Research -- Physiological aspects -- Genetic aspects ,Lung cancer -- Genetic aspects -- Research -- Care and treatment -- Diagnosis -- Prognosis ,Environmental issues ,Science and technology ,Zoology and wildlife conservation ,Diagnosis ,Care and treatment ,Physiological aspects ,Genetic aspects ,Research ,Prognosis - Abstract
Determining the genetic basis of cancer requires comprehensive analyses of large collections of histopathologically well-classified primary tumours. Here we report the results of a collaborative study to discover somatic mutations [...]
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- 2008
26. The genome of Cyanothece 51142, a unicellular diazotrophic cyanobacterium important in the marine nitrogen cycle
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Welsh, Eric A., Liberton, Michelle, Stockel, Jana, Loh, Thomas, Elvitigala, Thanura, Wang, Chunyan, Wollam, Aye, Fulton, Robert S., Clifton, Sandra W., Jacobs, Jon M., Aurora, Rajeev, Ghosh, Bijoy K., Sherman, Louis A., Smith, Richard D., Wilson, Richard K., and Pakrasi, Himadri B.
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Cyanobacteria -- Genetic aspects ,Nitrogen-fixing microorganisms -- Genetic aspects ,Science and technology - Abstract
Unicellular cyanobacteria have recently been recognized for their contributions to nitrogen fixation in marine environments, a function previously thought to be filled mainly by filamentous cyanobacteria such as Trichodesmium. To begin a systems level analysis of the physiology of the unicellular N2-fixing microbes, we have sequenced to completion the genome of Cyanothece sp. ATCC 51142, the first such organism. Cyanothece 51142 performs oxygenic photosynthesis and nitrogen fixation, separating these two incompatible processes temporally within the same cell, while concomitantly accumulating metabolic products in inclusion bodies that are later mobilized as part of a robust diurnal cycle. The 5,460,377-bp Cyanothece 51142 genome has a unique arrangement of one large circular chromosome, four small plasmids, and one linear chromosome, the first report of a linear element in the genome of a photosynthetic bacterium. On the 429,701-bp linear chromosome is a cluster of genes for enzymes involved in pyruvate metabolism, suggesting an important role for the linear chromosome in fermentative processes. The annotation of the genome was significantly aided by simultaneous global proteomic studies of this organism. Compared with other nitrogen-fixing cyanobacteria, Cyanothece 51142 contains the largest intact contiguous cluster of nitrogen fixation-related genes. We discuss the implications of such an organization on the regulation of nitrogen fixation. The genome sequence provides important information regarding the ability of Cyanothece 51142 to accomplish metabolic compartmentalization and energy storage, as well as how a unicellular bacterium balances multiple, often incompatible, processes in a single cell. diurnal rhythm | linear chromosome | nitrogen fixation | optical mapping | proteomics
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- 2008
27. Integrated genomic characterization of oesophageal carcinoma
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Kim, Jihun, Bowlby, Reanne, Mungall, Andrew J., Robertson, A. Gordon, Odze, Robert D., Cherniack, Andrew D., Shih, Juliann, Pedamallu, Chandra Sekhar, Cibulskis, Carrie, Dunford, Andrew, Meier, Samuel R., Kim, Jaegil, Raphael, Benjamin J., Wu, Hsin-Ta, Wong, Alexandra M., Willis, Joseph E., Bass, Adam J., Derks, Sarah, Garman, Katherine, McCall, Shannon J., Wiznerowicz, Maciej, Pantazi, Angeliki, Parfenov, Michael, Thorsson, Vsteinn, Shmulevich, Ilya, Dhankani, Varsha, Miller, Michael, Sakai, Ryo, Wang, Kenneth, Schultz, Nikolaus, Shen, Ronglai, Arora, Arshi, Weinhold, Nils, Snchez-Vega, Francisco, Kelsen, David P., Zhang, Julia, Felau, Ina, Demchok, John, Rabkin, Charles S., Camargo, M. Constanza, Zenklusen, Jean Claude, Bowen, Jay, Leraas, Kristen, Lichtenberg, Tara M., Curtis, Christina, Seoane, Jose A., Ojesina, Akinyemi I., Beer, David G., Gulley, Margaret L., Pennathur, Arjun, Luketich, James D., Zhou, Zhongren, Weisenberger, Daniel J., Akbani, Rehan, Lee, Ju-Seog, Liu, Wenbin, Mills, Gordon B., Zhang, Wei, Reid, Brian J, Hinoue, Toshinori, Laird, Peter W., Shen, Hui, Piazuelo, M. Blanca, Schneider, Barbara G., McLellan, Michael, Taylor-Weiner, Amaro, Lawrence, Michael, Cibulskis, Kristian, Stewart, Chip, Getz, Gad, Lander, Eric, Gabriel, Stacey B., Ding, Li, McLellan, Michael D., Miller, Christopher A., Appelbaum, Elizabeth L., Cordes, Matthew G., Fronick, Catrina C., Fulton, Lucinda A., Mardis, Elaine R., Wilson, Richard K., Schmidt, Heather K., Fulton, Robert S., Ally, Adrian, Balasundaram, Miruna, Carlsen, Rebecca, Chuah, Eric, Dhalla, Noreen, Holt, Robert A., Jones, Steven J. M., Kasaian, Katayoon, Brooks, Denise, Li, Haiyan I., Ma, Yussanne, Marra, Marco A., Mayo, Michael, Moore, Richard A., Mungall, Karen L., Schein, Jacqueline E., Sipahimalani, Payal, Tam, Angela, Thiessen, Nina, Wong, Tina, Beroukhim, Rameen, Bullman, Susan, Murray, Bradley A., Saksena, Gordon, Schumacher, Steven E., Gabriel, Stacey, Meyerson, Matthew, Hadjipanayis, Angela, Kucherlapati, Raju, Ren, Xiaojia, Park, Peter J., Lee, Semin, Kucherlapati, Melanie, Yang, Lixing, Baylin, Stephen B., Hoadley, Katherine A., Bootwalla, Moiz S., Lai, Phillip H., Van Den Berg, David J., Berrios, Mario, Holbrook, Andrea, Hwang, Jun-Eul, Jang, Hee-Jin, Weinstein, John N., Lu, Yiling, Sohn, Bo Hwa, Mills, Gordon, Seth, Sahil, Protopopov, Alexei, Bristow, Christopher A., Mahadeshwar, Harshad S., Tang, Jiabin, Song, Xingzhi, Zhang, Jianhua, Cho, Juok, Defrietas, Timothy, Frazer, Scott, Gehlenborg, Nils, Heiman, David I., Lawrence, Michael S., Lin, Pei, Noble, Michael S., Voet, Doug, Zhang, Hailei, Polak, Paz, Chin, Lynda, Bernard, Brady, Iype, Lisa, Reynolds, Sheila M., Abeshouse, Adam, Armenia, Joshua, Kundra, Ritika, Ladanyi, Marc, Lehmann, Kjong-Van, Gao, Jianjiong, Sander, Chris, Chakravarty, Debyani, Zhang, Hongxin, Radenbaugh, Amie, Hegde, Apruva, Penny, Robert, Crain, Daniel, Gardner, Johanna, Curley, Erin, Mallery, David, Morris, Scott, Paulauskis, Joseph, Shelton, Troy, Shelton, Candace, Frick, Jessica, Gastier-Foster, Julie M., Gerken, Mark, Leraas, Kristen M., Ramirez, Nilsa C., Wise, Lisa, Zmuda, Erik, Tarvin, Katherine, Saller, Charles, Park, Young Soo, Button, Michael, Carvalho, Andre L., Reis, Rui Manuel, Matsushita, Marcus Medeiros, Lucchesi, Fabiano, de Oliveira, Antonio Talvane, Le, Xuan, Paklina, Oxana, Setdikova, Galiya, Lee, Jae-Hyuck, Bennett, Joseph, Iacocca, Mary, Huelsenbeck-Dill, Lori, Potapova, Olga, Voronina, Olga, Liu, Ouida, Fulidou, Victoria, Cates, Crystal, Sharp, Alexis, Behera, Madhusmitara, Force, Seth, Khuri, Fadio, Owonikoko, Taofeek, Pickens, Allan, Ramalingam, Suresh, Sica, Gabriel, Dinjens, Winand, van Nistelrooij, Anna, Wijnhoven, Bas, Sandusky, George, Stepa, Serghei, Juhl, Hartmut, Zornig, Carsten, Kwon, Sun Young, Kelsen, David, Kim, Hark Kyun, Bartlett, John, Parfitt, Jeremy, Chetty, Runjan, Darling, Gail, Knox, Jennifer, Wong, Rebecca, El-Zimaity, Haila, Liu, Geoffrey, Boussioutas, Alex, Park, Do Young, Kemp, Rafael, Carlotti, Carlos Gilberto, da Cunha Tirapelli, Daniela Pretti, Saggioro, Fabiano Pinto, Sankarankutty, Ajith Kumar, Noushmehr, Houtan, dos Santos, Jose Sebastio, Trevisan, Felipe Amstalden, Eschbacher, Jennifer, Dubina, Michael, Mozgovoy, Eugene, Carey, Frank, Chalmers, Sally, Forgie, Ian, Godwin, Andrew, Reilly, Colleen, Madan, Rashna, Naima, Zaid, Ferrer-Torres, Daysha, Vinco, Michele, Rathmell, W. Kimryn, Dhir, Rajiv, Luketich, James, Ajani, Jaffer A., Janjigian, Yelena, Tang, Laura, Cheong, Jae-Ho, Chudamani, Sudha, Liu, Jai, Lolla, Laxmi, Naresh, Rashi, Pihl, Todd, Sun, Qiang, Wan, Yunhu, Wu, Ye, Demchok, John A., Ferguson, Martin L., Shaw, Kenna R. Mills, Sheth, Margi, Tarnuzzer, Roy, Wang, Zhining, Yang, Liming, Hutter, Carolyn M., Sofia, Heidi J., and Zhang, Jiashan
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DNA sequencing -- Methods ,Esophageal cancer -- Genetic aspects ,Environmental issues ,Science and technology ,Zoology and wildlife conservation - Abstract
Oesophageal cancers are prominent worldwide; however, there are few targeted therapies and survival rates for these cancers remain dismal. Here we performed a comprehensive molecular analysis of 164 carcinomas of the oesophagus derived from Western and Eastern populations. Beyond known histopathological and epidemiologic distinctions, molecular features differentiated oesophageal squamous cell carcinomas from oesophageal adenocarcinomas. Oesophageal squamous cell carcinomas resembled squamous carcinomas of other organs more than they did oesophageal adenocarcinomas. Our analyses identified three molecular subclasses of oesophageal squamous cell carcinomas, but none showed evidence for an aetiological role of human papillomavirus. Squamous cell carcinomas showed frequent genomic amplifications of CCND1 and SOX2 and/or TP63, whereas ERBB2, VEGFA and GATA4 and GATA6 were more commonly amplified in adenocarcinomas. Oesophageal adenocarcinomas strongly resembled the chromosomally unstable variant of gastric adenocarcinoma, suggesting that these cancers could be considered a single disease entity. However, some molecular features, including DNA hypermethylation, occurred disproportionally in oesophageal adenocarcinomas. These data provide a framework to facilitate more rational categorization of these tumours and a foundation for new therapies., Author(s): The Cancer Genome Atlas Research Network; Analysis Working Group: Asan University; Jihun Kim [1]; BC Cancer Agency; Reanne Bowlby [2]; Andrew J. Mungall [2]; A. Gordon Robertson [2]; Brigham [...]
- Published
- 2017
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- View/download PDF
28. Evolution of genes and genomes on the Drosophila phylogeny
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Clark, Andrew G., Eisen, Michael B., Smith, Douglas R., Bergman, Casey M., Oliver, Brian, Markow, Therese A., Kaufman, Thomas C., Kellis, Manolis, Gelbart, William, Iyer, Venky N., Pollard, Daniel A., Sackton, Timothy B., Larracuente, Amanda M., Singh, Nadia D., Abad, Jose P., Abt, Dawn N., Adryan, Boris, Aguade, Montserrat, Akashi, Hiroshi, Anderson, Wyatt W., Aquadro, Charles F., Ardell, David H., Arguello, Roman, Artieri, Carlo G., Barbash, Daniel A., Barker, Daniel, Barsanti, Paolo, Batterham, Phil, Batzoglou, Serafim, Begun, Dave, Bhutkar, Arjun, Blanco, Enrico, Bosak, Stephanie A., Bradley, Robert K., Brand, Adrianne D., Brent, Michael R., Brooks, Angela N., Brown, Randall H., Butlin, Roger K., Caggese, Corrado, Calvi, Brian R., Bernardo de Carvalho, A., Caspi, Anat, Castrezana, Sergio, Celniker, Susan E., Chang, Jean L., Chapple, Charles, Chatterji, Sourav, Chinwalla, Asif, Civetta, Alberto, Clifton, Sandra W., Comeron, Josep M., Costello, James C., Coyne, Jerry A., Daub, Jennifer, David, Robert G., Delcher, Arthur L., Delehaunty, Kim, Do, Chuong B., Ebling, Heather, Edwards, Kevin, Eickbush, Thomas, Evans, Jay D., Filipski, Alan, Findeiß, Sven, Freyhult, Eva, Fulton, Lucinda, Fulton, Robert, Garcia, Ana C. L., Gardiner, Anastasia, Garfield, David A., Garvin, Barry E., Gibson, Greg, Gilbert, Don, Gnerre, Sante, Godfrey, Jennifer, Good, Robert, Gotea, Valer, Gravely, Brenton, Greenberg, Anthony J., Griffiths-Jones, Sam, Gross, Samuel, Guigo, Roderic, Gustafson, Erik A., Haerty, Wilfried, Hahn, Matthew W., Halligan, Daniel L., Halpern, Aaron L., Halter, Gillian M., Han, Mira V., Heger, Andreas, Hillier, LaDeana, Hinrichs, Angie S., Holmes, Ian, Hoskins, Roger A., Hubisz, Melissa J., Hultmark, Dan, Huntley, Melanie A., Jaffe, David B., Jagadeeshan, Santosh, Jeck, William R., Johnson, Justin, Jones, Corbin D., Jordan, William C., Karpen, Gary H., Kataoka, Eiko, Keightley, Peter D., Kheradpour, Pouya, Kirkness, Ewen F., Koerich, Leonardo B., Kristiansen, Karsten, Kudrna, Dave, Kulathinal, Rob J., Kumar, Sudhir, Kwok, Roberta, Lander, Eric, Langley, Charles H., Lapoint, Richard, Lazzaro, Brian P., Lee, So-Jeong, Levesque, Lisa, Li, Ruiqiang, Lin, Chiao-Feng, Lin, Michael F., Lindblad-Toh, Kerstin, Llopart, Ana, Long, Manyuan, Low, Lloyd, Lozovsky, Elena, Lu, Jian, Luo, Meizhong, Machado, Carlos A., Makalowski, Wojciech, Marzo, Mar, Matsuda, Muneo, Matzkin, Luciano, McAllister, Bryant, McBride, Carolyn S., McKernan, Brendan, McKernan, Kevin, Mendez-Lago, Maria, Minx, Patrick, Mollenhauer, Michael U., Montooth, Kristi, Mount, Stephen M., Mu, Xu, Myers, Eugene, Negre, Barbara, Newfeld, Stuart, Nielsen, Rasmus, Noor, Mohamed A. F., O'Grady, Patrick, Pachter, Lior, Papaceit, Montserrat, Parisi, Matthew J., Parisi, Michael, Parts, Leopold, Pedersen, Jakob S., Pesole, Graziano, Phillippy, Adam M., Ponting, Chris P., Pop, Mihai, Porcelli, Damiano, Powell, Jeffrey R., Prohaska, Sonja, Pruitt, Kim, Puig, Marta, Quesneville, Hadi, Ravi Ram, Kristipati, Rand, David, Rasmussen, Matthew D., Reed, Laura K., Reenan, Robert, Reily, Amy, Remington, Karin A., Rieger, Tania T., Ritchie, Michael G., Robin, Charles, Rogers, Yu-Hui, Rohde, Claudia, Rozas, Julio, Rubenfield, Marc J., Ruiz, Alfredo, Russo, Susan, Salzberg, Steven L., Sanchez-Gracia, Alejandro, Saranga, David J., Sato, Hajime, Schaeffer, Stephen W., Schatz, Michael C., Schlenke, Todd, Schwartz, Russell, Segarra, Carmen, Singh, Rama S., Sirot, Laura, Sirota, Marina, Sisneros, Nicholas B., Smith, Chris D., Smith, Temple F., Spieth, John, Stage, Deborah E., Stark, Alexander, Stephan, Wolfgang, Strausberg, Robert L., Strempel, Sebastian, Sturgill, David, Sutton, Granger, Sutton, Granger G., Tao, Wei, Teichmann, Sarah, Tobari, Yoshiko N., Tomimura, Yoshihiko, Tsolas, Jason M., Valente, Vera L. S., Venter, Eli, Craig Venter, J., Vicario, Saverio, Vieira, Filipe G., Vilella, Albert J., Villasante, Alfredo, Walenz, Brian, Wang, Jun, Wasserman, Marvin, Watts, Thomas, Wilson, Derek, Wilson, Richard K., Wing, Rod A., Wolfner, Mariana F., Wong, Alex, Ka-Shu Wong, Gane, Wu, Chung-I, Wu, Gabriel, Yamamoto, Daisuke, Yang, Hsiao-Pei, Yang, Shiaw-Pyng, Yorke, James A., Yoshida, Kiyohito, Zdobnov, Evgeny, Zhang, Peili, Zhang, Yu, Zimin, Aleksey V., Baldwin, Jennifer, Abdouelleil, Amr, Abdulkadir, Jamal, Abebe, Adal, Abera, Brikti, Abreu, Justin, Christophe Acer, St, Aftuck, Lynne, Alexander, Allen, An, Peter, Anderson, Erica, Anderson, Scott, Arachi, Harindra, Azer, Marc, Bachantsang, Pasang, Barry, Andrew, Bayul, Tashi, Berlin, Aaron, Bessette, Daniel, Bloom, Toby, Blye, Jason, Boguslavskiy, Leonid, Bonnet, Claude, Boukhgalter, Boris, Bourzgui, Imane, Brown, Adam, Cahill, Patrick, Channer, Sheridon, Cheshatsang, Yama, Chuda, Lisa, Citroen, Mieke, Collymore, Alville, Cooke, Patrick, Costello, Maura, D'Aco, Katie, Daza, Riza, De Haan, Georgius, DeGray, Stuart, DeMaso, Christina, Dhargay, Norbu, Dooley, Kimberly, Dooley, Erin, Doricent, Missole, Dorje, Passang, Dorjee, Kunsang, Dupes, Alan, Elong, Richard, Falk, Jill, Farina, Abderrahim, Faro, Susan, Ferguson, Diallo, Fisher, Sheila, Foley, Chelsea D., Franke, Alicia, Friedrich, Dennis, Gadbois, Loryn, Gearin, Gary, Gearin, Christina R., Giannoukos, Georgia, Goode, Tina, Graham, Joseph, Grandbois, Edward, Grewal, Sharleen, Gyaltsen, Kunsang, Hafez, Nabil, Hagos, Birhane, Hall, Jennifer, Henson, Charlotte, Hollinger, Andrew, Honan, Tracey, Huard, Monika D., Hughes, Leanne, Hurhula, Brian, Erii Husby, M, Kamat, Asha, Kanga, Ben, Kashin, Seva, Khazanovich, Dmitry, Kisner, Peter, Lance, Krista, Lara, Marcia, Lee, William, Lennon, Niall, Letendre, Frances, LeVine, Rosie, Lipovsky, Alex, Liu, Xiaohong, Liu, Jinlei, Liu, Shangtao, Lokyitsang, Tashi, Lokyitsang, Yeshi, Lubonja, Rakela, Lui, Annie, MacDonald, Pen, Magnisalis, Vasilia, Maru, Kebede, Matthews, Charles, McCusker, William, McDonough, Susan, Mehta, Teena, Meldrim, James, Meneus, Louis, Mihai, Oana, Mihalev, Atanas, Mihova, Tanya, Mittelman, Rachel, Mlenga, Valentine, Montmayeur, Anna, Mulrain, Leonidas, Navidi, Adam, Naylor, Jerome, Negash, Tamrat, Nguyen, Thu, Nguyen, Nga, Nicol, Robert, Norbu, Choe, Norbu, Nyima, Novod, Nathaniel, O'Neill, Barry, Osman, Sahal, Markiewicz, Eva, Oyono, Otero L., Patti, Christopher, Phunkhang, Pema, Pierre, Fritz, Priest, Margaret, Raghuraman, Sujaa, Rege, Filip, Reyes, Rebecca, Rise, Cecil, Rogov, Peter, Ross, Keenan, Ryan, Elizabeth, Settipalli, Sampath, Shea, Terry, Sherpa, Ngawang, Shi, Lu, Shih, Diana, Sparrow, Todd, Spaulding, Jessica, Stalker, John, Stange-Thomann, Nicole, Stavropoulos, Sharon, Stone, Catherine, Strader, Christopher, Tesfaye, Senait, Thomson, Talene, Thoulutsang, Yama, Thoulutsang, Dawa, Topham, Kerri, Topping, Ira, Tsamla, Tsamla, Vassiliev, Helen, Vo, Andy, Wangchuk, Tsering, Wangdi, Tsering, Weiand, Michael, Wilkinson, Jane, Wilson, Adam, Yadav, Shailendra, Young, Geneva, Yu, Qing, Zembek, Lisa, Zhong, Danni, Zimmer, Andrew, Zwirko, Zac, Alvarez, Pablo, Brockman, Will, Butler, Jonathan, Chin, CheeWhye, Grabherr, Manfred, Kleber, Michael, Mauceli, Evan, and MacCallum, Iain
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Environmental issues ,Science and technology ,Zoology and wildlife conservation - Abstract
Author(s): Drosophila 12 Genomes Consortium; Project Leaders; Andrew G. Clark (corresponding author) [1]; Michael B. Eisen (corresponding author) [2, 3]; Douglas R. Smith (corresponding author) [4]; Casey M. Bergman (corresponding [...]
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- 2007
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29. Genomic and metabolic adaptations of methanobrevibacter smithii to the human gut
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Samuel, Buck S., Hansen, Elizabeth E., Manchester, Jill K., Coutinho, Pedro M., Henrissat, Bernard, Fulton, Robert, Latreille, Philippe, Kim, Kung, Wilson, Richard K., and Gordon, Jeffrey I.
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Genomics -- Research ,Gnosticism -- Research ,Metabolomics -- Research ,Methanobacteriaceae -- Research ,Mutualism (Biology) -- Research ,Science and technology - Abstract
The human gut is home to trillions of microbes, thousands of bacterial phylotypes, as well as hydrogen-consuming methanogenic archaea. Studies in gnotobiotic mice indicate that Methanobrevibacter smithii, the dominant archaeon in the human gut ecosystem, affects the specificity and efficiency of bacterial digestion of dietary polysaccharides, thereby influencing host calorie harvest and adiposity. Metagenomic studies of the gut microbial communities of genetically obese mice and their lean littermates have shown that the former contain an enhanced representation of genes involved in polysaccharide degradation, possess more archaea, and exhibit a greater capacity to promote adiposity when transplanted into germ-free recipients. These findings have led to the hypothesis that M. smithii may be a therapeutic target for reducing energy harvest in obese humans. To explore this possibility, we have sequenced its 1,853,160-bp genome and compared it to other human gut-associated M. smithii strains and other Archaea. We have also examined M. smithii's transcriptome and metabolome in gnotobiotic mice that do or do not harbor Bacteroides thetaiotaomicron, a prominent saccharolytic bacterial member of our gut microbiota. Our results indicate that M. smithii is well equipped to persist in the distal intestine through (i) production of surface glycans resembling those found in the gut mucosa, (ii) regulated expression of adhesin-like proteins, (iii) consumption of a variety of fermentation products produced by saccharolytic bacteria, and (iv) effective competition for nitrogenous nutrient pools. These findings provide a framework for designing strategies to change the representation and/or properties of M. smithii in the human gut microbiota. archaeal-bacterial mutualism | comparative microbial genomics | functional genomics and metabolomics | gnotobiotic mice | human gut microbiota
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- 2007
30. Identification and analysis of functional elements in 1% of the human genome by the ENCODE pilot project
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Birney, Ewan, Stamatoyannopoulos, John A., Dutta, Anindya, Guigo, Roderic, Gingeras, Thomas R., Margulies, Elliott H., Weng, Zhiping, Snyder, Michael, Dermitzakis, Emmanouil T., Thurman, Robert E., Kuehn, Michael S., Taylor, Christopher M., Neph, Shane, Koch, Christoph M., Asthana, Saurabh, Malhotra, Ankit, Adzhubei, Ivan, Greenbaum, Jason A., Andrews, Robert M., Flicek, Paul, Boyle, Patrick J., Cao, Hua, Carter, Nigel P., Clelland, Gayle K., Davis, Sean, Day, Nathan, Dhami, Pawandeep, Dillon, Shane C., Dorschner, Michael O., Fiegler, Heike, Giresi, Paul G., Goldy, Jeff, Hawrylycz, Michael, Haydock, Andrew, Humbert, Richard, James, Keith D., Johnson, Brett E., Johnson, Ericka M., Frum, Tristan T., Rosenzweig, Elizabeth R., Karnani, Neerja, Lee, Kirsten, Lefebvre, Gregory C., Navas, Patrick A., Neri, Fidencio, Parker, Stephen C. J., Sabo, Peter J., Sandstrom, Richard, Shafer, Anthony, Vetrie, David, Weaver, Molly, Wilcox, Sarah, Yu1, Man, Collins, Francis S., Dekker, Job, Lieb, Jason D., Tullius, Thomas D., Crawford, Gregory E., Sunyaev, Shamil, Noble, William S., Dunham, Ian, Denoeud, France, Reymond, Alexandre, Kapranov, Philipp, Rozowsky, Joel, Zheng, Deyou, Castelo, Robert, Frankish, Adam, Harrow, Jennifer, Ghosh, Srinka, Sandelin, Albin, Hofacker, Ivo L., Baertsch, Robert, Keefe, Damian, Dike, Sujit, Cheng, Jill, Hirsch, Heather A., Sekinger, Edward A., Lagarde, Julien, Abril, Josep F., Shahab, Atif, Flamm, Christoph, Fried, Claudia, Hackermuller, Jorg, Hertel, Jana, Lindemeyer, Manja, Missal, Kristin, Tanzer, Andrea, Washietl, Stefan, Korbel, Jan, Emanuelsson, Olof, Pedersen, Jakob S., Holroyd, Nancy, Taylor, Ruth, Swarbreck, David, Matthews, Nicholas, Dickson, Mark C., Thomas, Daryl J., Weirauch, Matthew T., Gilbert, James, Drenkow, Jorg, Bell, Ian, Zhao, XiaoDong, Srinivasan, K.G., Sung, Wing-Kin, Ooi, Hong Sain, Chiu, Kuo Ping, Foissac, Sylvain, Alioto, Tyler, Brent, Michael, Pachter, Lior, Tress, Michael L., Valencia, Alfonso, Choo, Siew Woh, Choo, Chiou Yu, Ucla, Catherine, Manzano, Caroline, Wyss, Carine, Cheung, Evelyn, Clark, Taane G., Brown, James B., Ganesh, Madhavan, Patel, Sandeep, Tammana, Hari, Chrast, Jacqueline, Henrichsen, Charlotte N., Kai, Chikatoshi, Kawai, Jun, Nagalakshmi, Ugrappa, Wu, Jiaqian, Lian, Zheng, Lian, Jin, Newburger, Peter, Zhang, Xueqing, Bickel, Peter, Mattick, John S., Carninci, Piero, Hayashizaki, Yoshihide, Weissman, Sherman, Hubbard, Tim, Myers, Richard M., Rogers, Jane, Stadler, Peter F., Lowe, Todd M., Wei, Chia-Lin, Ruan, Yijun, Struhl, Kevin, Gerstein, Mark, Antonarakis, Stylianos E., Fu, Yutao, Green, Eric D., Karaoz, Ulaş, Siepel, Adam, Taylor, James, Liefer, Laura A., Wetterstrand, Kris A., Good, Peter J., Feingold, Elise A., Guyer, Mark S., Cooper, Gregory M., Asimenos, George, Dewey, Colin N., Hou, Minmei, Nikolaev, Sergey, Montoya-Burgos, Juan I., Loytynoja, Ari, Whelan, Simon, Pardi, Fabio, Massingham, Tim, Huang, Haiyan, Zhang, Nancy R., Holmes, Ian, Mullikin, James C., Ureta-Vidal, Abel, Paten, Benedict, Seringhaus, Michael, Church, Deanna, Rosenbloom, Kate, Kent, W. James, Stone, Eric A., Batzoglou, Serafim, Goldman, Nick, Hardison, Ross C., Haussler, David, Miller, Webb, Sidow, Arend, Trinklein, Nathan D., Zhang, Zhengdong D., Barrera, Leah, Stuart, Rhona, King, David C., Ameur, Adam, Enroth, Stefan, Bieda, Mark C., Kim, Jonghwan, Bhinge, Akshay A., Jiang, Nan, Liu, Jun, Yao, Fei, Vega, Vinsensius B., Lee, Charlie W.H., Ng, Patrick, Yang, Annie, Moqtaderi, Zarmik, Zhu, Zhou, Xu, Xiaoqin, Squazzo, Sharon, Oberley, Matthew J., Inman, David, Singer, Michael A., Richmond, Todd A., Munn, Kyle J., Rada-Iglesias, Alvaro, Wallerman, Ola, Komorowski, Jan, Fowler, Joanna C., Couttet, Phillippe, Bruce, Alexander W., Dovey, Oliver M., Ellis, Peter D., Langford, Cordelia F., Nix, David A., Euskirchen, Ghia, Hartman, Stephen, Urban, Alexander E., Kraus, Peter, Van Calcar, Sara, Heintzman, Nate, Hoon Kim, Tae, Wang, Kun, Qu, Chunxu, Hon, Gary, Luna, Rosa, Glass, Christopher K., Rosenfeld, M. Geoff, Aldred, Shelley Force, Cooper, Sara J., Halees, Anason, Lin, Jane M., Shulha, Hennady P., Zhang, Xiaoling, Xu, Mousheng, Haidar, Jaafar N. S., Yu, Yong, Birney*, Ewan, Iyer, Vishwanath R., Green, Roland D., Wadelius, Claes, Farnham, Peggy J., Ren, Bing, Harte, Rachel A., Hinrichs, Angie S., Trumbower, Heather, Clawson, Hiram, Hillman-Jackson, Jennifer, Zweig, Ann S., Smith, Kayla, Thakkapallayil, Archana, Barber, Galt, Kuhn, Robert M., Karolchik, Donna, Armengol, Lluis, Bird, Christine P., de Bakker, Paul I. W., Kern, Andrew D., Lopez-Bigas, Nuria, Martin, Joel D., Stranger, Barbara E., Woodroffe, Abigail, Davydov, Eugene, Dimas, Antigone, Eyras, Eduardo, Hallgrimsdottir, Ingileif B., Huppert, Julian, Zody, Michael C., Abecasis, Goncalo R., Estivill, Xavier, Bouffard, Gerard G., Guan, Xiaobin, Hansen, Nancy F., Idol, Jacquelyn R., Maduro, Valerie V.B., Maskeri, Baishali, McDowell, Jennifer C., Park, Morgan, Thomas, Pamela J., Young, Alice C., Blakesley, Robert W., Baylor College of Medicine, Human Genome Sequencing Center, Muzny, Donna M., Sodergren, Erica, Wheeler, David A., Worley, Kim C., Jiang, Huaiyang, Weinstock, George M., Gibbs, Richard A., Graves, Tina, Fulton, Robert, Mardis, Elaine R., Wilson, Richard K., Clamp, Michele, Cuff, James, Gnerre, Sante, Jaffe, David B., Chang, Jean L., Lindblad-Toh, Kerstin, Lander, Eric S., Koriabine, Maxim, Nefedov, Mikhail, Osoegawa, Kazutoyo, Yoshinaga, Yuko, Zhu, Baoli, and de Jong, Pieter J.
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Environmental issues ,Science and technology ,Zoology and wildlife conservation - Abstract
Author(s): The ENCODE Project Consortium; Analysis Coordination; Ewan Birney (corresponding author) [1]; John A. Stamatoyannopoulos (corresponding author) [2]; Anindya Dutta (corresponding author) [3]; Roderic Guigó (corresponding author) [4, 5]; Thomas [...]
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- 2007
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31. Tumor Evolution in Two Patients with Basal-like Breast Cancer: A Retrospective Genomics Study of Multiple Metastases
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Hoadley, Katherine A., Siegel, Marni B., Kanchi, Krishna L., Miller, Christopher A., Ding, Li, Zhao, Wei, He, Xiaping, Parker, Joel S., Wendl, Michael C., Fulton, Robert S., Demeter, Ryan T., Wilson, Richard K., Carey, Lisa A., Perou, Charles M., and Mardis, Elaine R.
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Breast cancer -- Genetic aspects -- Development and progression -- Care and treatment ,Gene expression -- Health aspects ,Cancer metastasis -- Genetic aspects -- Development and progression -- Care and treatment ,Biological sciences - Abstract
Background Metastasis is the main cause of cancer patient deaths and remains a poorly characterized process. It is still unclear when in tumor progression the ability to metastasize arises and whether this ability is inherent to the primary tumor or is acquired well after primary tumor formation. Next-generation sequencing and analytical methods to define clonal heterogeneity provide a means for identifying genetic events and the temporal relationships between these events in the primary and metastatic tumors within an individual. Methods and Findings We performed DNA whole genome and mRNA sequencing on two primary tumors, each with either four or five distinct tissue site-specific metastases, from two individuals with triple-negative/basal-like breast cancers. As evidenced by their case histories, each patient had an aggressive disease course with abbreviated survival. In each patient, the overall gene expression signatures, DNA copy number patterns, and somatic mutation patterns were highly similar across each primary tumor and its associated metastases. Almost every mutation found in the primary was found in a metastasis (for the two patients, 52/54 and 75/75). Many of these mutations were found in every tumor (11/54 and 65/75, respectively). In addition, each metastasis had fewer metastatic-specific events and shared at least 50% of its somatic mutation repertoire with the primary tumor, and all samples from each patient grouped together by gene expression clustering analysis. TP53 was the only mutated gene in common between both patients and was present in every tumor in this study. Strikingly, each metastasis resulted from multiclonal seeding instead of from a single cell of origin, and few of the new mutations, present only in the metastases, were expressed in mRNAs. Because of the clinical differences between these two patients and the small sample size of our study, the generalizability of these findings will need to be further examined in larger cohorts of patients. Conclusions Our findings suggest that multiclonal seeding may be common amongst basal-like breast cancers. In these two patients, mutations and DNA copy number changes in the primary tumors appear to have had a biologic impact on metastatic potential, whereas mutations arising in the metastases were much more likely to be passengers., Author(s): Katherine A. Hoadley 1,2, Marni B. Siegel 1,2, Krishna L. Kanchi 3, Christopher A. Miller 3, Li Ding 3, Wei Zhao 1,2, Xiaping He 2, Joel S. Parker 1,2, [...]
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- 2016
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32. Comparison of the localization of an electron as determined by the two-particle distribution function and by the single-particle sharing index
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&Fulton, Robert L.
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Dynamics of a particle -- Research ,Wave functions -- Research ,Chemicals, plastics and rubber industries - Abstract
A simple set of wave functions which span states ranging from single determinant ground and double excited states through states mimicking correlated states were used to compare the measure of the delocalization of a particle based on the two-particle distribution function and that based on the single-particle density matrix. It is learnt that the values of the integrated atom-atom measures agree for a range of wave functions involving combinations of the two single determinant wave functions but disagree for a different range of these wave functions and for the singly excited wave functions.
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- 2006
33. The complete genome sequence of a chronic atrophic gastritis Helicobacter pylori strain: evolution during disease progression
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Oh, Jung D., Kling-Backhed, Helene, Giannakis, Marios, Xu, Jian, Fulton, Robert S., Fulton, Lucinda A., Cordum, Holland S., Wang, Chunyan, Elliott, Glendoria, Edwards, Jennifer, Mardis, Elaine R., Engstrand, Lars G., and Gordon, Jeffrey I.
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Stomach cancer -- Research ,Helicobacter pylori -- Research ,Science and technology - Abstract
Helicobacter pylori produces acute superficial gastritis in nearly all of its human hosts. However, a subset of individuals develops chronic atrophic gastritis (ChAG), a condition characterized in part by diminished numbers of acid-producing parietal cells and increased risk for development of gastric adenocarcinoma. Previously, we used a gnotobiotic transgenic mouse model with an engineered ablation of parietal cells to show that loss of parietal cells provides an opportunity for a H. pylori isolate from a patient with ChAG (HPAG1) to bind to, enter, and persist within gastric stem cells. This finding raises the question of how ChAG influences H. pylori genome evolution, physiology, and tumorigenesis. Here we describe the 1,596,366-bp HPAG1 genome. Custom HPAG1 Affymetrix GeneChips, representing 99.6% of its predicted ORFs, were used for whole-genome genotyping of additional H. pylori ChAG isolates obtained from Swedish patients enrolled in a case-control study of gastric cancer, as well as ChAG- and cancer-associated isolates from an individual who progressed from ChAG to gastric adenocarcinoma. The results reveal a shared gene signature among ChAG strains, as well as genes that may have been lost or gained during progression to adenocarcinoma. Whole-genome transcriptional profiling of HPAG1's response to acid during in vitro growth indicates that genes encoding components of metal uptake and utilization pathways, outer membrane proteins, and virulence factors are among those associated with H. pylori's adaptation to ChAG. acid regulation | comparative microbial genomics | ecogenomics | functional genomics | gastric cancer
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- 2006
34. Identification of genes subject to positive selection in uropathogenic strains of Escherichia coil: a comparative genomics approach
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Chen, Swaine L., Hung, Chia-Seui, Xu, Jian, Reigstad, Christopher S., Magrini, Vincent, Sabo, Aniko, Blasiar, Darin, Bieri, Tamberlyn, Meyer, Rekha R., Ozersky, Philip, Armstrong, Jon R., Fulton, Robert S., Latreille, J. Phillip, Spieth, John, Hooton, Thomas M., Mardis, Elaine R., Hultgren, Scott J., and Gordon, Jeffrey I.
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Escherichia coli -- Physiological aspects ,Science and technology - Abstract
Escherichia coil is a model laboratory bacterium, a species that is widely distributed in the environment, as well as a mutualist and pathogen in its human hosts. As such, E. coli represents an attractive organism to study how environment impacts microbial genome structure and function. Uropathogenic E. coli (UPEC) must adapt to life in several microbial communities in the human body, and has a complex life cycle in the bladder when it causes acute or recurrent urinary tract infection (UTI). Several studies designed to identify virulence factors have focused on genes that are uniquely represented in UPEC strains, whereas the role of genes that are common to all E. coli has received much less attention. Here we describe the complete 5,065,741-bp genome sequence of a UPEC strain recovered from a patient with an acute bladder infection and compare it with six other finished E. coli genome sequences. We searched 3,470 ortholog sets for genes that are under positive selection only in UPEC strains. Our maximum likelihood-based analysis yielded 29 genes involved in various aspects of cell surface structure, DNA metabolism, nutrient acquisition, and UTI. These results were validated by resequencing a subset of the 29 genes in a panel of 50 urinary, periurethral, and rectal E. coli isolates from patients with UTI. These studies outline a computational approach that may be broadly applicable for studying strain-specific adaptation and pathogenesis in other bacteria. uropathogenic Escherichia coil | ecogenomics
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- 2006
35. After the duplication: gene loss and adaptation in Saccharomyces genomes
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Cliften, Paul F., Fulton, Robert S., Wilson, Richard K., and Johnston, Mark
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Saccharomyces -- Genetic aspects ,DNA replication -- Research ,Biological sciences - Abstract
The ancient duplication of the Saccharomyces cerevisiae genome and subsequent massive loss of duplicated genes is apparent when it is compared to the genomes of related species that diverged before the duplication event. To learn more about the evolutionary effects of the duplication event, we compared the S. cerevisiae genome to other Saccharomyces genomes. We demonstrate that the whole genome duplication occurred before S. castellii diverged from S. cerevisiae. In addition to more accurately dating the duplication event, this finding allowed us to study the effects of the duplication on two separate lineages. Analyses of the duplication regions of the genomes indicate that most of the duplicated genes (~85%) were lost before the speciation. Only a small amount of paralogous gene loss (4-6%) occurred after speciation. On the other hand, S. castellii appears to have lost several hundred genes that were not retained as duplicated paralogs. These losses could be related to genomic rearrangements that reduced the number of chromosomes from 16 to 9. In addition to S. castellii, other Saccharomyces sensu lato species likely diverged from S. cerevisiae after the duplication. A thorough analysis of these species will likely reveal other important outcomes of the whole genome duplication.
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- 2006
36. Generation and annotation of the DNA sequences of human chromosomes 2 and 4
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Hillier, LaDeana W., Graves, Tina A., Fulton, Robert S., Fulton, Lucinda A., Pepin, Kymberlie H., Minx, Patrick, Wagner-McPherson, Caryn, Layman, Dan, Wylie, Kristine, Sekhon, Mandeep, Becker, Michael C., Fewell, Ginger A., Delehaunty, Kimberly D., Miner, Tracie L., Nash, William E., Kremitzki, Colin, Oddy, Lachlan, Du, Hui, Sun, Hui, Bradshaw-Cordum, Holland, Ali, Johar, Carter, Jason, Cordes, Matt, Harris, Anthony, Isak, Amber, van Brunt, Andrew, Nguyen, Christine, Du, Feiyu, Courtney, Laura, Kalicki, Joelle, Ozersky, Philip, Abbott, Scott, Armstrong, Jon, Belter, Edward A., Caruso, Lauren, Cedroni, Maria, Cotton, Marc, Davidson, Teresa, Desai, Anu, Elliott, Glendoria, Erb, Thomas, Fronick, Catrina, Gaige, Tony, Haakenson, William, Haglund, Krista, Holmes, Andrea, Harkins, Richard, Kim, Kyung, Kruchowski, Scott S., Strong, Cynthia Madsen, Grewal, Neenu, Goyea, Ernest, Hou, Shunfang, Levy, Andrew, Martinka, Scott, Mead, Kelly, McLellan, Michael D., Meyer, Rick, Randall-Maher, Jennifer, Tomlinson, Chad, Dauphin-Kohlberg, Sara, Kozlowicz-Reilly, Amy, Shah, Neha, Swearengen-Shahid, Sharhonda, Snider, Jacqueline, Strong, Joseph T., Thompson, Johanna, Yoakum, Martin, Leonard, Shawn, Pearman, Charlene, Trani, Lee, Radionenko, Maxim, Waligorski, Jason E., Wang, Chunyan, Rock, Susan M., Tin-Wollam, Aye-Mon, Maupin, Rachel, Latreille, Phil, Wendl, Michael C., Yang, Shiaw-Pyng, Pohl, Craig, Wallis, John W., Spieth, John, Bieri, Tamberlyn A., Berkowicz, Nicolas, Nelson, Joanne O., Osborne, John, Ding, Li, Meyer, Rekha, Sabo, Aniko, Shotland, Yoram, Sinha, Prashant, Wohldmann, Patricia E., Cook, Lisa L., Hickenbotham, Matthew T., Eldred, James, Williams, Donald, Jones, Thomas A., She, Xinwei, Ciccarelli, Francesca D., Izaurralde, Elisa, Taylor, James, Schmutz, Jeremy, Myers, Richard M., Cox, David R., Huang, Xiaoqiu, McPherson, John D., Mardis, Elaine R., Clifton, Sandra W., Warren, Wesley C., Chinwalla, Asif T., Eddy, Sean R., Marra, Marco A., Ovcharenko, Ivan, Furey, Terrence S., Miller, Webb, Eichler, Evan E., Bork, Peer, Suyama, Mikita, Torrents, David, Waterston, Robert H., and Wilson, Richard K.
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Environmental issues ,Science and technology ,Zoology and wildlife conservation - Abstract
Author(s): LaDeana W. Hillier [1]; Tina A. Graves [1]; Robert S. Fulton [1]; Lucinda A. Fulton [1]; Kymberlie H. Pepin [1]; Patrick Minx [1]; Caryn Wagner-McPherson [1]; Dan Layman [1]; [...]
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- 2005
- Full Text
- View/download PDF
37. The DNA sequence of the human X chromosome
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Ross, Mark T., Grafham, Darren V., Coffey, Alison J., Scherer, Steven, McLay, Kirsten, Muzny, Donna, Platzer, Matthias, Howell, Gareth R., Burrows, Christine, Bird, Christine P., Frankish, Adam, Lovell, Frances L., Howe, Kevin L., Ashurst, Jennifer L., Fulton, Robert S., Sudbrak, Ralf, Wen, Gaiping, Jones, Matthew C., Hurles, Matthew E., Andrews, T. Daniel, Scott, Carol E., Searle, Stephen, Ramser, Juliane, Whittaker, Adam, Deadman, Rebecca, Carter, Nigel P., Hunt, Sarah E., Chen, Rui, Cree, Andrew, Gunaratne, Preethi, Havlak, Paul, Hodgson, Anne, Metzker, Michael L., Richards, Stephen, Scott, Graham, Steffen, David, Sodergren, Erica, Wheeler, David A., Worley, Kim C., Ainscough, Rachael, Ambrose, Kerrie D., Ansari-Lari, M. Ali, Aradhya, Swaroop, Ashwell, Robert I. S., Babbage, Anne K., Bagguley, Claire L., Ballabio, Andrea, Banerjee, Ruby, Barker, Gary E., Barlow, Karen F., Barrett, Ian P., Bates, Karen N., Beare, David M., Beasley, Helen, Beasley, Oliver, Beck, Alfred, Bethel, Graeme, Blechschmidt, Karin, Brady, Nicola, Bray-Allen, Sarah, Bridgeman, Anne M., Brown, Andrew J., Brown, Mary J., Bonnin, David, Bruford, Elspeth A., Buhay, Christian, Burch, Paula, Burford, Deborah, Burgess, Joanne, Burrill, Wayne, Burton, John, Bye, Jackie M., Carder, Carol, Carrel, Laura, Chako, Joseph, Chapman, Joanne C., Chavez, Dean, Chen, Ellson, Chen, Guan, Chen, Yuan, Chen, Zhijian, Chinault, Craig, Ciccodicola, Alfredo, Clark, Sue Y., Clarke, Graham, Clee, Chris M., Clegg, Sheila, Clerc-Blankenburg, Kerstin, Clifford, Karen, Cobley, Vicky, Cole, Charlotte G., Conquer, Jen S., Corby, Nicole, Connor, Richard E., David, Robert, Davies, Joy, Davis, Clay, Davis, John, Delgado, Oliver, DeShazo, Denise, Dhami, Pawandeep, Ding, Yan, Dinh, Huyen, Dodsworth, Steve, Draper, Heather, Dugan-Rocha, Shannon, Dunham, Andrew, Dunn, Matthew, Durbin, K. James, Dutta, Ireena, Eades, Tamsin, Ellwood, Matthew, Emery-Cohen, Alexandra, Errington, Helen, Evans, Kathryn L., Faulkner, Louisa, Francis, Fiona, Frankland, John, Fraser, Audrey E., Galgoczy, Petra, Gilbert, James, Gill, Rachel, Glockner, Gernot, Gregory, Simon G., Gribble, Susan, Griffiths, Coline, Grocock, Russell, Gu, Yanghong, Gwilliam, Rhian, Hamilton, Cerissa, Hart, Elizabeth A., Hawes, Alicia, Heath, Paul D., Heitmann, Katja, Hennig, Steffen, Hernandez, Judith, Hinzmann, Bernd, Ho, Sarah, Hoffs, Michael, Howden, Phillip J., Huckle, Elizabeth J., Hume, Jennifer, Hunt, Paul J., Hunt, Adrienne R., Isherwood, Judith, Jacob, Leni, Johnson, David, Jones, Sally, de Jong, Pieter J., Joseph, Shirin S., Keenan, Stephen, Kelly, Susan, Kershaw, Joanne K., Khan, Ziad, Kioschis, Petra, Klages, Sven, Knights, Andrew J., Kosiura, Anna, Kovar-Smith, Christie, Laird, Gavin K., Langford, Cordelia, Lawlor, Stephanie, Leversha, Margaret, Lewis, Lora, Liu, Wen, Lloyd, Christine, Lloyd, David M., Loulseged, Hermela, Loveland, Jane E., Lovell, Jamieson D., Lozado, Ryan, Lu, Jing, Lyne, Rachael, Ma, Jie, Maheshwari, Manjula, Matthews, Lucy H., McDowall, Jennifer, McLaren, Stuart, McMurray, Amanda, Meidl, Patrick, Meitinger, Thomas, Milne, Sarah, Miner, George, Mistry, Shailesh L., Morgan, Margaret, Morris, Sidney, Muller, Ines, Mullikin, James C., Nguyen, Ngoc, Nordsiek, Gabriele, Nyakatura, Gerald, O'Dell, Christopher N., Okwuonu, Geoffery, Palmer, Sophie, Pandian, Richard, Parker, David, Parrish, Julia, Pasternak, Shiran, Patel, Dina, Pearce, Alex V., Pearson, Danita M., Pelan, Sarah E., Perez, Lesette, Porter, Keith M., Ramsey, Yvonne, Reichwald, Kathrin, Rhodes, Susan, Ridler, Kerry A., Schlessinger, David, Schueler, Mary G., Sehra, Harminder K., Shaw-Smith, Charles, Shen, Hua, Sheridan, Elizabeth M., Shownkeen, Ratna, Skuce, Carl D., Smith, Michelle L., Sotheran, Elizabeth C., Steingruber, Helen E., Steward, Charles A., Storey, Roy, Swann, R. Mark, Swarbreck, David, Tabor, Paul E., Taudien, Stefan, Taylor, Tineace, Teague, Brian, Thomas, Karen, Thorpe, Andrea, Timms, Kirsten, Tracey, Alan, Trevanion, Steve, Tromans, Anthony C., d'Urso, Michele, Verduzco, Daniel, Villasana, Donna, Waldron, Lenee, Wall, Melanie, Wang, Qiaoyan, Warren, James, Warry, Georgina L., Wei, Xuehong, West, Anthony, Whitehead, Siobhan L., Whiteley, Mathew N., Wilkinson, Jane E., Willey, David L., Williams, Gabrielle, Williams, Leanne, Williamson, Angela, Williamson, Helen, Wilming, Laurens, Woodmansey, Rebecca L., Wray, Paul W., Yen, Jennifer, Zhang, Jingkun, Zhou, Jianling, Zoghbi, Huda, Zorilla, Sara, Buck, David, Reinhardt, Richard, Poustka, Annemarie, Rosenthal, Andre, Lehrach, Hans, Meindl, Alfons, Minx, Patrick J., Hillier, LaDeana W., Willard, Huntington F., Wilson, Richard K., Waterston, Robert H., Rice, Catherine M., Vaudin, Mark, Coulson, Alan, Nelson, David L., Weinstock, George, Sulston, John E., Durbin, Richard, Hubbard, Tim, Gibbs, Richard A., Beck, Stephan, Rogers, Jane, and Bentley, David R.
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Environmental issues ,Science and technology ,Zoology and wildlife conservation - Abstract
Author(s): Mark T. Ross (corresponding author) [1]; Darren V. Grafham [1]; Alison J. Coffey [1]; Steven Scherer [2]; Kirsten McLay [1]; Donna Muzny [2]; Matthias Platzer [3]; Gareth R. Howell [...]
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- 2005
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38. The DNA sequence of human chromosome 7
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Hillier, LaDeana W., Fulton, Robert S., Fulton, Lucinda A., Graves, Tina A., Pepin, Kymberlie H., Wagner-McPherson, Caryn, Layman, Dan, Maas, Jason, Jaeger, Sara, Walker, Rebecca, Wylie, Kristine, Sekhon, Mandeep, Becker, Michael C., O'Laughlin, Michelle D., Schaller, Mark E., Fewell, Ginger A., Delehaunty, Kimberly D., Miner, Tracie L., Nash, William E., Cordes, Matt, Du, Hui, Sun, Hui, Edwards, Jennifer, Bradshaw-Cordum, Holland, Ali, Johar, Andrews, Stephanie, Isak, Amber, VanBrunt, Andrew, Nguyen, Christine, Du, Feiyu, Lamar, Betty, Courtney, Laura, Kalicki, Joelle, Ozersky, Philip, Bielicki, Lauren, Scott, Kelsi, Holmes, Andrea, Harkins, Richard, Harris, Anthony, Strong, Cynthia Madsen, Hou, Shunfang, Tomlinson, Chad, Dauphin-Kohlberg, Sara, Kozlowicz-Reilly, Amy, Leonard, Shawn, Rohlfing, Theresa, Rock, Susan M., Tin-Wollam, Aye-Mon, Abbott, Amanda, Minx, Patrick, Maupin, Rachel, Strowmatt, Catrina, Latreille, Phil, Miller, Nancy, Johnson, Doug, Murray, Jennifer, Woessner, Jeffrey P., Wendl, Michael C., Yang, Shiaw-Pyng, Schultz, Brian R., Wallis, John W., Spieth, John, Bieri, Tamberlyn A., Nelson, Joanne O., Berkowicz, Nicolas, Wohldmann, Patricia E., Cook, Lisa L., Hickenbotham, Matthew T., Eldred, James, Williams, Donald, Bedell, Joseph A., Mardis, Elaine R., Clifton, Sandra W., Chissoe, Stephanie L., Marra, Marco A., Raymond, Christopher, Haugen, Eric, Gillett, Will, Zhou, Yang, James, Rose, Phelps, Karen, Iadanoto, Shawn, Bubb, Kerry, Simms, Elizabeth, Levy, Ruth, Clendenning, James, Kaul, Rajinder, Kent, W. James, Furey, Terrence S., Baertsch, Robert A., Brent, Michael R., Keibler, Evan, Flicek, Paul, Bork, Peer, Suyama, Mikita, Bailey, Jeffrey A., Portnoy, Matthew E., Torrents, David, Chinwalla, Asif T., Gish, Warren R., Eddy, Sean R., McPherson, John D., Olson, Maynard V., Eichler, Evan E., Green, Eric D., Waterston, Robert H., and Wilson, Richard K.
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Environmental issues ,Science and technology ,Zoology and wildlife conservation - Abstract
Author(s): LaDeana W. Hillier [1]; Robert S. Fulton [1]; Lucinda A. Fulton [1]; Tina A. Graves [1]; Kymberlie H. Pepin [1]; Caryn Wagner-McPherson [1]; Dan Layman [1]; Jason Maas [1]; [...]
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- 2003
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39. The male-specific region of the human Y chromosome is a mosaic of discrete sequence classes
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Skaletsky, Helen, Kuroda-Kawaguchi, Tomoko, Minx, Patrick J., Cordum, Holland S., Hillier, LaDeana, Brown, Laura G., Repping, Sjoerd, Pyntikova, Tatyana, Ali, Johar, Bieri, Tamberlyn, Chinwalla, Asif, Delehaunty, Andrew, Delehaunty, Kim, Du, Hui, Fewell, Ginger, Fulton, Lucinda, Fulton, Robert, Graves, Tina, Hou, Shun-Fang, Latrielle, Philip, Leonard, Shawn, Mardis, Elaine, Maupin, Rachel, McPherson, John, Miner, Tracie, Nash, William, Nguyen, Christine, Ozersky, Philip, Pepin, Kymberlie, Rock, Susan, Rohlfing, Tracy, Scott, Kelsi, Schultz, Brian, Strong, Cindy, Tin-Wollam, Aye, Yang, Shiaw-Pyng, Waterston, Robert H., Wilson, Richard K., Rozen, Steve, and Page, David C.
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Environmental issues ,Science and technology ,Zoology and wildlife conservation - Abstract
Author(s): Helen Skaletsky [1]; Tomoko Kuroda-Kawaguchi [1]; Patrick J. Minx [2]; Holland S. Cordum [2]; LaDeana Hillier [2]; Laura G. Brown [1]; Sjoerd Repping [3]; Tatyana Pyntikova [1]; Johar Ali [...]
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- 2003
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40. Initial sequencing and comparative analysis of the mouse genome
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Chinwalla, Asif T., Cook, Lisa L., Delehaunty, Kimberly D., Fewell, Ginger A., Fulton, Lucinda A., Fulton, Robert S., Graves, Tina A., Hillier, LaDeana W., Mardis, Elaine R., McPherson, John D., Miner, Tracie L., Nash, William E., Nelson, Joanne O., Nhan, Michael N., Pepin, Kymberlie H., Pohl, Craig S., Ponce, Tracy C., Schultz, Brian, Thompson, Johanna, Trevaskis, Evanne, Waterston, Robert H., Wendl, Michael C., Wilson, Richard K., Yang, Shiaw-Pyng, An, Peter, Berry, Eric, Birren, Bruce, Bloom, Toby, Brown, Daniel G., Butler, Jonathan, Daly, Mark, David, Robert, Deri, Justin, Dodge, Sheila, Foley, Karen, Gage, Diane, Gnerre, Sante, Holzer, Timothy, Jaffe, David B., Kamal, Michael, Karlsson, Elinor K., Kells, Cristyn, Kirby, Andrew, Kulbokas, III, Edward J., Lander, Eric S., Landers, Tom, Leger, J. P., Levine, Rosie, Lindblad-Toh, Kerstin, Mauceli, Evan, Mayer, John H., McCarthy, Megan, Meldrim, Jim, Mesirov, Jill P., Nicol, Robert, Nusbaum, Chad, Seaman, Steven, Sharpe, Ted, Sheridan, Andrew, Singer, Jonathan B., Santos, Ralph, Spencer, Brian, Stange-Thomann, Nicole, Vinson, Jade P., Wade, Claire M., Wierzbowski, Jamey, Wyman, Dudley, Zody, Michael C., Birney, Ewan, Goldman, Nick, Kasprzyk, Arkadiusz, Mongin, Emmanuel, Rust, Alistair G., Slater, Guy, Stabenau, Arne, Ureta-Vidal, Abel, Whelan, Simon, Ainscough, Rachel, Attwood, John, Bailey, Jonathon, Barlow, Karen, Beck, Stephan, Burton, John, Clamp, Michele, Clee, Christopher, Coulson, Alan, Cuff, James, Curwen, Val, Cutts, Tim, Davies, Joy, Eyras, Eduardo, Grafham, Darren, Gregory, Simon, Hubbard, Tim, Hunt, Adrienne, Jones, Matthew, Joy, Ann, Leonard, Steven, Lloyd, Christine, Matthews, Lucy, McLaren, Stuart, McLay, Kirsten, Meredith, Beverley, Mullikin, James C., Ning, Zemin, Oliver, Karen, Overton-Larty, Emma, Plumb, Robert, Potter, Simon, Quail, Michael, Rogers, Jane, Scott, Carol, Searle, Steve, Shownkeen, Ratna, Sims, Sarah, Wall, Melanie, West, Anthony P., Willey, David, Williams, Sophie, Abril, Josep F., Guigo, Roderic, Parra, Genis, Agarwal, Pankaj, Agarwala, Richa, Church, Deanna M., Hlavina, Wratko, Maglott, Donna R., Sapojnikov, Victor, Alexandersson, Marina, Pachter, Lior, Antonarakis, Stylianos E., Dermitzakis, Emmanouil T., Reymond, Alexandre, Ucla, Catherine, Baertsch, Robert, Diekhans, Mark, Furey, Terrence S., Hinrichs, Angela, Hsu, Fan, Karolchik, Donna, Kent, W. James, Roskin, Krishna M., Schwartz, Matthias S., Sugnet, Charles, Weber, Ryan J., Bork, Peer, Letunic, Ivica, Suyama, Mikita, Torrents, David, Zdobnov, Evgeny M., Botcherby, Marc, Brown, Stephen D., Campbell, Robert D., Jackson, Ian, Bray, Nicolas, Couronne, Olivier, Dubchak, Inna, Poliakov, Alex, Rubin, Edward M., Brent, Michael R., Flicek, Paul, Keibler, Evan, Korf, Ian, Batalov, S., Bult, Carol, Frankel, Wayne N., Carninci, Piero, Hayashizaki, Yoshihide, Kawai, Jun, Okazaki, Yasushi, Cawley, Simon, Kulp, David, Wheeler, Raymond, Chiaromonte, Francesca, Collins, Francis S., Felsenfeld, Adam, Guyer, Mark, Peterson, Jane, Wetterstrand, Kris, Copley, Richard R., Mott, Richard, Dewey, Colin, Dickens, Nicholas J., Emes, Richard D., Goodstadt, Leo, Ponting, Chris P., Winter, Eitan, Dunn, Diane M., von Niederhausern, Andrew C., Weiss, Robert B., Eddy, Sean R., Johnson, L. Steven, Jones, Thomas A., Elnitski, Laura, Kolbe, Diana L., Eswara, Pallavi, Miller, Webb, O'Connor, Michael J., Schwartz, Scott, Muzny, Donna M., Glusman, Gustavo, Smit, Arian, Green, Eric D., Hardison, Ross C., Yang, Shan, Haussler, David, Hua, Axin, Roe, Bruce A., Kucherlapati, Raju S., Montgomery, Kate T., Li, Jia, Li, Ming, Lucas, Susan, Ma, Bin, McCombie, W. Richard, Morgan, Michael, Pevzner, Pavel, Tesler, Glenn, Schultz, Jorg, Smith, Douglas R., Tromp, John, and Worley, Kim C.
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Environmental issues ,Science and technology ,Zoology and wildlife conservation - Abstract
Author(s): Mouse Genome Sequencing Consortium ; Genome Sequencing Center: ; Asif T. Chinwalla [1, 47]; Lisa L. Cook [1]; Kimberly D. Delehaunty [1]; Ginger A. Fewell [1]; Lucinda A. Fulton [...]
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- 2002
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41. Nonlinear dynamics analysis of a laminated printed wiring board
- Author
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He, Xiaoling and Fulton, Robert E.
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Electronic packaging -- Research ,Printed circuits -- Design and construction ,Nonlinear theories -- Usage ,Vibration research -- Reports ,Laminated materials -- Research ,Electronics - Abstract
Nonlinear laminate theory is applied for the printed wiring board (PWB) dynamic response analysis. Equations of motion for the nonlinear elastic deformation of the isotropic laminates are derived for the dynamic response of a simply supported PWB. Numerical results are generated for the nonlinear response characterization of the PWB deformation. Comparisons are made between the response of linear and nonlinear systems. Results show that PWB is in large deflection under high acceleration or certain pressure load. Nonlinear theory gives more accurate results for the large deflection than the linear theory does. Besides, lamina stresses are analyzed and illustrated from finite difference computation. The analytical derivation in modal approach and the stress analysis provide the basis for PWB reliability studies, especially the defect and failure induced by the dynamic stress field. [DOI: 10.1115/1.1457454] Keywords: Nonlinear Dynamics, Vibration, Printed Wiring Board, Laminated Plate
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- 2002
42. A physical map of the human genome
- Author
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McPherson, John D., Marra, Marco, Hillier, LaDeana, Waterston, Robert H., Chinwalla, Asif, Wallis, John, Sekhon, Mandeep, Wylie, Kristine, Mardis, Elaine R., Wilson, Richard K., Fulton, Robert, Kucaba, Tamara A., Wagner-McPherson, Caryn, and Barbazuk, William B.
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Nucleotide sequencing -- Methods ,DNA sequencing -- Methods ,Human genome -- Structure -- Methods ,Cloning -- Methods ,Chromosome mapping -- Methods ,Environmental issues ,Science and technology ,Zoology and wildlife conservation ,International Human Genome Sequencing Consortium - Abstract
The human genome is by far the largest genome to be sequenced, and its size and complexity present many challenges for sequence assembly. The International Human Genome Sequencing Consortium constructed a map of the whole genome to enable the selection of clones for sequencing and for the accurate assembly of the genome sequence. Here we report the construction of the whole-genome bacterial artificial chromosome (BAC) map and its integration with previous landmark maps and information from mapping efforts focused on specific chromosomal regions. We also describe the integration of sequence data with the map., Author(s): John D. McPherson [sup.1] , Marco Marra [sup.1] [sup.29] , LaDeana Hillier [sup.1] , Robert H. Waterston [sup.1] , Asif Chinwalla [sup.1] , John Wallis [sup.1] , Mandeep Sekhon [...]
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- 2001
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43. Initial sequencing and analysis of the human genome
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Lander, Eric S., Linton, Lauren M., Birren, Bruce, Nusbaum, Chad, Zody, Michael C., Baldwin, Jennifer, Devon, Keri, Dewar, Ken, Doyle, Michael, FitzHugh, William, Funke, Roel, Gage, Diane, Harris, Katrina, Heaford, Andrew, Howland, John, Kann, Lisa, Lehoczky, Jessica, LeVine, Rosie, McEwan, Paul, McKernan, Kevin, Meldrim, James, Mesirov, Jill P., Miranda, Cher, Morris, William, Naylor, Jerome, Raymond, Christina, Rosetti, Mark, Santos, Ralph, Sheridan, Andrew, Sougnez, Carrie, Stange-Thomann, Nicole, Stojanovic, Nikola, Subramanian, Aravind, Wyman, Dudley, Rogers, Jane, Sulston, John, Ainscough, Rachael, Beck, Stephan, Bentley, David, Burton, John, Clee, Christopher, Carter, Nigel, Coulson, Alan, Deadman, Rebecca, Deloukas, Panos, Dunham, Andrew, Dunham, Ian, Durbin, Richard, French, Lisa, Grafham, Darren, Gregory, Simon, Hubbard, Tim, Humphray, Sean, Hunt, Adrienne, Jones, Matthew, Lloyd, Christine, McMurray, Amanda, Matthews, Lucy, Mercer, Simon, Milne, Sarah, Mullikin, James C., Mungall, Andrew, Plumb, Robert, Ross, Mark, Shownkeen, Ratna, Sims, Sarah, Waterston, Robert H., Wilson, Richard K., Hillier, LaDeana W., McPherson, John D., Marra, Marco A., Mardis, Elaine R., Fulton, Lucinda A., Chinwalla, Asif T., Pepin, Kymberlie H., Gish, Warren R., Chissoe, Stephanie L., Wendl, Michael C., Delehaunty, Kim D., Miner, Tracie L., Delehaunty, Andrew, Kramer, Jason B., Cook, Lisa L., Fulton, Robert S., Johnson, Douglas L., Minx, Patrick J., Clifton, Sandra W., Hawkins, Trevor, Branscomb, Elbert, Predki, Paul, Richardson, Paul, Wenning, Sarah, Slezak, Tom, Doggett, Norman, Cheng, Jan-Fang, Olsen, Anne, Lucas, Susan, Elkin, Christopher, Uberbacher, Edward, Frazier, Marvin, Gibbs, Richard A., Muzny, Donna M., Scherer, Steven E., Bouck, John B., Sodergren, Erica J., Worley, Kim C., Rives, Catherine M., Gorrell, James H., Metzker, Michael L., Naylor, Susan L., Kucherlapati, Raju S., Nelson, David L., Weinstock, George M., Sakaki, Yoshiyuki, Fujiyama, Asao, Hattori, Masahira, Yada, Tetsushi, Toyoda, Atsushi, Itoh, Takehiko, Kawagoe, Chiharu, Watanabe, Hidemi, Totoki, Yasushi, Taylor, Todd, Weissenbach, Jean, Heilig, Roland, Saurin, William, Artiguenave, Francois, Brottier, Philippe, Bruls, Thomas, Pelletier, Eric, Robert, Catherine, Wincker, Patrick, Rosenthal, Andre, Platzer, Matthias, Nyakatura, Gerald, Taudien, Stefan, Rump, Andreas, Smith, Douglas R., Doucette-Stamm, Lynn, Rubenfield, Marc, Weinstock, Keith, Lee, Hong Mei, Dubois, JoAnn, Yang, Huanming, Yu, Jun, Wang, Jian, Huang, Guyang, Gu, Jun, Hood, Leroy, Rowen, Lee, Madan, Anup, Qin, Shizen, Davis, Ronald W., Federspiel, Nancy A., Abola, A. Pia, Proctor, Michael J., Roe, Bruce A., Chen, Feng, Pan, Huaqin, Ramser, Juliane, Lehrach, Hans, Reinhardt, Richard, McCombie, W. Richard, de la Bastide, Melissa, Dedhia, Neilay, Blocker, Helmut, Hornischer, Klaus, Nordsiek, Gabriele, Agarwala, Richa, Aravind, L., Bailey, Jeffrey A., Bateman, Alex, Batzoglou, Serafim, Birney, Ewan, Bork, Peer, Brown, Daniel G., Burge, Christopher B., Cerutti, Lorenzo, Chen, Hsiu-Chuan, Church, Deanna, Clamp, Michele, Copley, Richard R., Doerks, Tobias, Eddy, Sean R., Eichler, Evan E., Furey, Terrence S., Galagan, James, Gilbert, James G. R., Harmon, Cyrus, Hayashizaki, Yoshihide, Haussler, David, Hermjakob, Henning, Hokamp, Karsten, Jang, Wonhee, Johnson, L. Steven, Jones, Thomas A., Kasif, Simon, Kaspryzk, Arek, Kennedy, Scot, Kent, W. James, Kitts, Paul, Koonin, Eugene V., Korf, Ian, Kulp, David, Lancet, Doron, Lowe, Todd M., McLysaght, Aoife, Mikkelsen, Tarjei, Moran, John V., Mulder, Nicola, Pollara, Victor J., Ponting, Chris P., Schuler, Greg, Schultz, Jorg, Slater, Guy, Smit, Arian F. A., Stupka, Elia, Szustakowki, Joseph, Thierry-Mieg, Danielle, Thierry-Mieg, Jean, Wagner, Lukas, Wallis, John, Wheeler, Raymond, Williams, Alan, Wolf, Yuri I., Wolfe, Kenneth H., Yang, Shiaw-Pyng, Yeh, Ru-Fang, Collins, Francis, Guyer, Mark S., Peterson, Jane, Felsenfeld, Adam, Wetterstrand, Kris A., Myers, Richard M., Schmutz, Jeremy, Dickson, Mark, Grimwood, Jane, Cox, David R., Olson, Maynard V., Kaul, Rajinder, Raymond, Christopher, Shimizu, Nobuyoshi, Kawasaki, Kazuhiko, Minoshima, Shinsei, Evans, Glen A., Athanasiou, Maria, Schultz, Roger, Patrinos, Aristides, and Morgan, Michael J.
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Environmental issues ,Science and technology ,Zoology and wildlife conservation - Abstract
Author(s): International Human Genome Sequencing Consortium; Whitehead Institute for Biomedical Research, Center for Genome Research:; Eric S. Lander [1]; Lauren M. Linton [1]; Bruce Birren [1]; Chad Nusbaum [1]; Michael [...]
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- 2001
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- View/download PDF
44. A physical map of the human genome
- Author
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McPherson, John D., Marra, Marco, Hillier, LaDeana, Waterston, Robert H., Chinwalla, Asif, Wallis, John, Sekhon, Mandeep, Wylie, Kristine, Mardis, Elaine R., Wilson, Richard K., Fulton, Robert, Kucaba, Tamara A., Wagner-McPherson, Caryn, Barbazuk, William B., Gregory, Simon G., Humphray, Sean J., French, Lisa, Evans, Richard S., Bethel, Graeme, Whittaker, Adam, Holden, Jane L., McCann, Owen T., Dunham, Andrew, Soderlund, Carol, Scott, Carol E., Bentley, David R., Schuler, Gregory, Chen, Hsiu-Chuan, Jang, Wonhee, Green, Eric D., Idol, Jacquelyn R., Maduro, Valerie V. Braden, Montgomery, Kate T., Lee, Eunice, Miller, Ashley, Emerling, Suzanne, Kucherlapati, Raju, Gibbs, Richard, Scherer, Steve, Gorrell, J. Harley, Sodergren, Erica, Clerc-Blankenburg, Kerstin, Tabor, Paul, Naylor, Susan, Garcia, Dawn, de Jong, Pieter J., Catanese, Joseph J., Nowak, Norma, Osoegawa, Kazutoyo, Qin, Shizhen, Rowen, Lee, Madan, Anuradha, Dors, Monica, Hood, Leroy, Trask, Barbara, Friedman, Cynthia, Massa, Hillary, Cheung, Vivian G., Kirsch, Ilan R., Reid, Thomas, Yonescu, Raluca, Weissenbach, Jean, Bruls, Thomas, Heilig, Roland, Branscomb, Elbert, Olsen, Anne, Doggett, Norman, Cheng, Jan-Fang, Hawkins, Trevor, Myers, Richard M., Shang, Jin, Ramirez, Lucia, Schmutz, Jeremy, Velasquez, Olivia, Dixon, Kami, Stone, Nancy E., Cox, David R., Haussler, David, Kent, W. James, Furey, Terrence, Rogic, Sanja, Kennedy, Scot, Jones, Steven, Rosenthal, Andre, Wen, Gaiping, Schilhabel, Markus, Gloeckner, Gernot, Nyakatura, Gerald, Siebert, Reiner, Schlegelberger, Brigitte, Korenberg, Julie, Chen, Xiao-Ning, Fujiyama, Asao, Hattori, Masahira, Toyoda, Atsushi, Yada, Tetsushi, Park, Hong-Seok, Sakaki, Yoshiyuki, Shimizu, Nobuyoshi, Asakawa, Shuichi, Kawasaki, Kazuhiko, Sasaki, Takashi, Shintani, Ai, Shimizu, Atsushi, Shibuya, Kazunori, Kudoh, Jun, Minoshima, Shinsei, Ramser, Juliane, Seranski, Peter, Hoff, Celine, Poustka, Annemarie, Reinhardt, Richard, and Lehrach, Hans
- Subjects
Environmental issues ,Science and technology ,Zoology and wildlife conservation - Abstract
Author(s): The International Human Genome Mapping Consortium ; Washington University School of Medicine, Genome Sequencing Center: ; John D. McPherson (corresponding author) [1]; Marco Marra [1]; LaDeana Hillier [1]; Robert [...]
- Published
- 2001
- Full Text
- View/download PDF
45. Perspectives in conflict: the response to transfusion-associated AIDS
- Author
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Corless, Inge B., Stowell, Christopher P., Fulton, Robert, and Weeks, O. Duane
- Subjects
AIDS (Disease) -- Care and treatment ,Blood transfusion -- Health aspects ,Blood banks -- Management ,Health ,Health care industry ,Law - Abstract
The epidemiological model of AIDS did not prevail when discussions were held in the early 1980s about the safety of the US blood supply. Public health and medical rationales supported action, yet scientific and commercial concerns demanded certainty, thus introducing a crucial delay.
- Published
- 1999
46. Identification of the motor vehicle accident victim who abuses alcohol: an opportunity to reduce trauma
- Author
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Mancino, Michael, Cunningham, Michael R., Davidson, Pattie, and Fulton, Robert L.
- Subjects
Drinking and traffic accidents -- Research ,Alcoholism -- Research ,Wounds and injuries -- Care and treatment ,Health ,Psychology and mental health - Abstract
There seems to be a strong association between people repeatedly injured in motor vehicle accidents (MVAs) and alcohol abuse. One hundred fifty patients admitted to the emergency room following an MVA were interviewed regarding past MVA injuries, drug and alcohol abuse, and drunk-driving arrests. They were also tested for blood alcohol levels. Thirty-seven percent of the participants were drunk, 42% were alcohol abusers, 68% had been involved in other MVAs, and 43% had been injured in other MVAs. Participants involved in other MVAs were more likely to abuse drugs and have been previously arrested for drunk driving.
- Published
- 1996
47. Production techniques for the Superconducting Super Collider low energy booster quadrupole magnet
- Author
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Morrison, Michael E., Behrsing, Gerd U., and Fulton, Robert L.
- Subjects
Superconducting magnets -- Energy use ,Business ,Electronics ,Electronics and electrical industries ,Superconducting Super Collider -- Research - Abstract
The manufacturing techniques used for a prototype quadrupole magnet, developed at Lawrence Berkeley Laboratory (LBL) for the Superconducting Super Collider (SSC) Low Energy Booster (LEB), are described. The SSC LEB Ring employs 96 dipoles and 90 quadrupoles connected in series to form the magnetic lattice, requiring the use of a 21.9 mm x 23.0 mm hollow conductor for the quadrupoles. Due to the large conductor size and small bend radii required, development of special fixtures was necessary. A unique coil-forming method with close attention paid to tooling design and special assembly procedures was required to manufacture this prototype to stringent specifications.
- Published
- 1994
48. Correlation of analytical and experimental approaches to determine thermally induced PWB warpage
- Author
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Yeh, Chao-Pin, Ume, Charles, Fulton, Robert E., Wyatt, Karl W., and Stafford, John W.
- Subjects
Printed circuits -- Research ,Surfaces, Deformation of -- Analysis ,Finite element method -- Usage ,Business ,Engineering and manufacturing industries ,Science and technology - Abstract
Studies on thermally induced printed wiring board technology warpage and finite element analysis reveal that these methods are in accord with the data obtained using the shadow Moire method. Accurate mechanical property data will further enhance the process efficiency. The finite element method can be extended to warpage measurement at temperatures up to 250 degrees Celsius.
- Published
- 1993
49. The Amerindian 'man-woman' gender, liminality, and cultural continuity
- Author
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Fulton, Robert and Anderson, Steven W.
- Subjects
Native Americans -- Culture ,Shamans -- Analysis ,Ethnology -- Research - Published
- 1992
50. What's up with billet?
- Author
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Fulton, Robert, III
- Subjects
Company business management ,Disabled persons -- Equipment and supplies ,Rugby football players -- Management ,Wheelchairs -- Usage - Abstract
An avid quad-rugby player and successful businessman, Lance Seadbrook wanted more style for his everyday wheelchair. He began searching for a customizer. He found Glen Kegler, a master machinist and [...]
- Published
- 2005
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