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  • 1
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    The genome sequence of taurine cattle: a window to ruminant biology and evolution (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-25
    Description: To understand the biology and evolution of ruminants, the cattle genome was sequenced to about sevenfold coverage. The cattle genome contains a minimum of 22,000 genes, with a core set of 14,345 orthologs shared among seven mammalian species of which 1217 are absent or undetected in noneutherian (marsupial or monotreme) genomes. Cattle-specific evolutionary breakpoint regions in chromosomes have a higher density of segmental duplications, enrichment of repetitive elements, and species-specific variations in genes associated with lactation and immune responsiveness. Genes involved in metabolism are generally highly conserved, although five metabolic genes are deleted or extensively diverged from their human orthologs. The cattle genome sequence thus provides a resource for understanding mammalian evolution and accelerating livestock genetic improvement for milk and meat production.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2943200/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2943200/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bovine Genome Sequencing and Analysis Consortium -- Elsik, Christine G -- Tellam, Ross L -- Worley, Kim C -- Gibbs, Richard A -- Muzny, Donna M -- Weinstock, George M -- Adelson, David L -- Eichler, Evan E -- Elnitski, Laura -- Guigo, Roderic -- Hamernik, Debora L -- Kappes, Steve M -- Lewin, Harris A -- Lynn, David J -- Nicholas, Frank W -- Reymond, Alexandre -- Rijnkels, Monique -- Skow, Loren C -- Zdobnov, Evgeny M -- Schook, Lawrence -- Womack, James -- Alioto, Tyler -- Antonarakis, Stylianos E -- Astashyn, Alex -- Chapple, Charles E -- Chen, Hsiu-Chuan -- Chrast, Jacqueline -- Camara, Francisco -- Ermolaeva, Olga -- Henrichsen, Charlotte N -- Hlavina, Wratko -- Kapustin, Yuri -- Kiryutin, Boris -- Kitts, Paul -- Kokocinski, Felix -- Landrum, Melissa -- Maglott, Donna -- Pruitt, Kim -- Sapojnikov, Victor -- Searle, Stephen M -- Solovyev, Victor -- Souvorov, Alexandre -- Ucla, Catherine -- Wyss, Carine -- Anzola, Juan M -- Gerlach, Daniel -- Elhaik, Eran -- Graur, Dan -- Reese, Justin T -- Edgar, Robert C -- McEwan, John C -- Payne, Gemma M -- Raison, Joy M -- Junier, Thomas -- Kriventseva, Evgenia V -- Eyras, Eduardo -- Plass, Mireya -- Donthu, Ravikiran -- Larkin, Denis M -- Reecy, James -- Yang, Mary Q -- Chen, Lin -- Cheng, Ze -- Chitko-McKown, Carol G -- Liu, George E -- Matukumalli, Lakshmi K -- Song, Jiuzhou -- Zhu, Bin -- Bradley, Daniel G -- Brinkman, Fiona S L -- Lau, Lilian P L -- Whiteside, Matthew D -- Walker, Angela -- Wheeler, Thomas T -- Casey, Theresa -- German, J Bruce -- Lemay, Danielle G -- Maqbool, Nauman J -- Molenaar, Adrian J -- Seo, Seongwon -- Stothard, Paul -- Baldwin, Cynthia L -- Baxter, Rebecca -- Brinkmeyer-Langford, Candice L -- Brown, Wendy C -- Childers, Christopher P -- Connelley, Timothy -- Ellis, Shirley A -- Fritz, Krista -- Glass, Elizabeth J -- Herzig, Carolyn T A -- Iivanainen, Antti -- Lahmers, Kevin K -- Bennett, Anna K -- Dickens, C Michael -- Gilbert, James G R -- Hagen, Darren E -- Salih, Hanni -- Aerts, Jan -- Caetano, Alexandre R -- Dalrymple, Brian -- Garcia, Jose Fernando -- Gill, Clare A -- Hiendleder, Stefan G -- Memili, Erdogan -- Spurlock, Diane -- Williams, John L -- Alexander, Lee -- Brownstein, Michael J -- Guan, Leluo -- Holt, Robert A -- Jones, Steven J M -- Marra, Marco A -- Moore, Richard -- Moore, Stephen S -- Roberts, Andy -- Taniguchi, Masaaki -- Waterman, Richard C -- Chacko, Joseph -- Chandrabose, Mimi M -- Cree, Andy -- Dao, Marvin Diep -- Dinh, Huyen H -- Gabisi, Ramatu Ayiesha -- Hines, Sandra -- Hume, Jennifer -- Jhangiani, Shalini N -- Joshi, Vandita -- Kovar, Christie L -- Lewis, Lora R -- Liu, Yih-Shin -- Lopez, John -- Morgan, Margaret B -- Nguyen, Ngoc Bich -- Okwuonu, Geoffrey O -- Ruiz, San Juana -- Santibanez, Jireh -- Wright, Rita A -- Buhay, Christian -- Ding, Yan -- Dugan-Rocha, Shannon -- Herdandez, Judith -- Holder, Michael -- Sabo, Aniko -- Egan, Amy -- Goodell, Jason -- Wilczek-Boney, Katarzyna -- Fowler, Gerald R -- Hitchens, Matthew Edward -- Lozado, Ryan J -- Moen, Charles -- Steffen, David -- Warren, James T -- Zhang, Jingkun -- Chiu, Readman -- Schein, Jacqueline E -- Durbin, K James -- Havlak, Paul -- Jiang, Huaiyang -- Liu, Yue -- Qin, Xiang -- Ren, Yanru -- Shen, Yufeng -- Song, Henry -- Bell, Stephanie Nicole -- Davis, Clay -- Johnson, Angela Jolivet -- Lee, Sandra -- Nazareth, Lynne V -- Patel, Bella Mayurkumar -- Pu, Ling-Ling -- Vattathil, Selina -- Williams, Rex Lee Jr -- Curry, Stacey -- Hamilton, Cerissa -- Sodergren, Erica -- Wheeler, David A -- Barris, Wes -- Bennett, Gary L -- Eggen, Andre -- Green, Ronnie D -- Harhay, Gregory P -- Hobbs, Matthew -- Jann, Oliver -- Keele, John W -- Kent, Matthew P -- Lien, Sigbjorn -- McKay, Stephanie D -- McWilliam, Sean -- Ratnakumar, Abhirami -- Schnabel, Robert D -- Smith, Timothy -- Snelling, Warren M -- Sonstegard, Tad S -- Stone, Roger T -- Sugimoto, Yoshikazu -- Takasuga, Akiko -- Taylor, Jeremy F -- Van Tassell, Curtis P -- Macneil, Michael D -- Abatepaulo, Antonio R R -- Abbey, Colette A -- Ahola, Virpi -- Almeida, Iassudara G -- Amadio, Ariel F -- Anatriello, Elen -- Bahadue, Suria M -- Biase, Fernando H -- Boldt, Clayton R -- Carroll, Jeffery A -- Carvalho, Wanessa A -- Cervelatti, Eliane P -- Chacko, Elsa -- Chapin, Jennifer E -- Cheng, Ye -- Choi, Jungwoo -- Colley, Adam J -- de Campos, Tatiana A -- De Donato, Marcos -- Santos, Isabel K F de Miranda -- de Oliveira, Carlo J F -- Deobald, Heather -- Devinoy, Eve -- Donohue, Kaitlin E -- Dovc, Peter -- Eberlein, Annett -- Fitzsimmons, Carolyn J -- Franzin, Alessandra M -- Garcia, Gustavo R -- Genini, Sem -- Gladney, Cody J -- Grant, Jason R -- Greaser, Marion L -- Green, Jonathan A -- Hadsell, Darryl L -- Hakimov, Hatam A -- Halgren, Rob -- Harrow, Jennifer L -- Hart, Elizabeth A -- Hastings, Nicola -- Hernandez, Marta -- Hu, Zhi-Liang -- Ingham, Aaron -- Iso-Touru, Terhi -- Jamis, Catherine -- Jensen, Kirsty -- Kapetis, Dimos -- Kerr, Tovah -- Khalil, Sari S -- Khatib, Hasan -- Kolbehdari, Davood -- Kumar, Charu G -- Kumar, Dinesh -- Leach, Richard -- Lee, Justin C-M -- Li, Changxi -- Logan, Krystin M -- Malinverni, Roberto -- Marques, Elisa -- Martin, William F -- Martins, Natalia F -- Maruyama, Sandra R -- Mazza, Raffaele -- McLean, Kim L -- Medrano, Juan F -- Moreno, Barbara T -- More, Daniela D -- Muntean, Carl T -- Nandakumar, Hari P -- Nogueira, Marcelo F G -- Olsaker, Ingrid -- Pant, Sameer D -- Panzitta, Francesca -- Pastor, Rosemeire C P -- Poli, Mario A -- Poslusny, Nathan -- Rachagani, Satyanarayana -- Ranganathan, Shoba -- Razpet, Andrej -- Riggs, Penny K -- Rincon, Gonzalo -- Rodriguez-Osorio, Nelida -- Rodriguez-Zas, Sandra L -- Romero, Natasha E -- Rosenwald, Anne -- Sando, Lillian -- Schmutz, Sheila M -- Shen, Libing -- Sherman, Laura -- Southey, Bruce R -- Lutzow, Ylva Strandberg -- Sweedler, Jonathan V -- Tammen, Imke -- Telugu, Bhanu Prakash V L -- Urbanski, Jennifer M -- Utsunomiya, Yuri T -- Verschoor, Chris P -- Waardenberg, Ashley J -- Wang, Zhiquan -- Ward, Robert -- Weikard, Rosemarie -- Welsh, Thomas H Jr -- White, Stephen N -- Wilming, Laurens G -- Wunderlich, Kris R -- Yang, Jianqi -- Zhao, Feng-Qi -- 062023/Wellcome Trust/United Kingdom -- 077198/Wellcome Trust/United Kingdom -- BBS/B/13438/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBS/B/13446/Biotechnology and Biological Sciences Research Council/United Kingdom -- P30 DA018310/DA/NIDA NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- U54 HG003273-04/HG/NHGRI NIH HHS/ -- U54 HG003273-04S1/HG/NHGRI NIH HHS/ -- U54 HG003273-05/HG/NHGRI NIH HHS/ -- U54 HG003273-05S1/HG/NHGRI NIH HHS/ -- U54 HG003273-05S2/HG/NHGRI NIH HHS/ -- U54 HG003273-06/HG/NHGRI NIH HHS/ -- U54 HG003273-06S1/HG/NHGRI NIH HHS/ -- U54 HG003273-06S2/HG/NHGRI NIH HHS/ -- U54 HG003273-07/HG/NHGRI NIH HHS/ -- U54 HG003273-08/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2009 Apr 24;324(5926):522-8. doi: 10.1126/science.1169588.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19390049" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Animals ; Animals, Domestic ; *Biological Evolution ; Cattle ; Evolution, Molecular ; Female ; Genetic Variation ; *Genome ; Humans ; Male ; MicroRNAs/genetics ; Molecular Sequence Data ; Proteins/genetics ; Sequence Analysis, DNA ; Species Specificity ; Synteny
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Genome remodelling in a basal-like breast cancer metastasis and xenograft (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-04-16
    Description: Massively parallel DNA sequencing technologies provide an unprecedented ability to screen entire genomes for genetic changes associated with tumour progression. Here we describe the genomic analyses of four DNA samples from an African-American patient with basal-like breast cancer: peripheral blood, the primary tumour, a brain metastasis and a xenograft derived from the primary tumour. The metastasis contained two de novo mutations and a large deletion not present in the primary tumour, and was significantly enriched for 20 shared mutations. The xenograft retained all primary tumour mutations and displayed a mutation enrichment pattern that resembled the metastasis. Two overlapping large deletions, encompassing CTNNA1, were present in all three tumour samples. The differential mutation frequencies and structural variation patterns in metastasis and xenograft compared with the primary tumour indicate that secondary tumours may arise from a minority of cells within the primary tumour.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2872544/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2872544/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ding, Li -- Ellis, Matthew J -- Li, Shunqiang -- Larson, David E -- Chen, Ken -- Wallis, John W -- Harris, Christopher C -- McLellan, Michael D -- Fulton, Robert S -- Fulton, Lucinda L -- Abbott, Rachel M -- Hoog, Jeremy -- Dooling, David J -- Koboldt, Daniel C -- Schmidt, Heather -- Kalicki, Joelle -- Zhang, Qunyuan -- Chen, Lei -- Lin, Ling -- Wendl, Michael C -- McMichael, Joshua F -- Magrini, Vincent J -- Cook, Lisa -- McGrath, Sean D -- Vickery, Tammi L -- Appelbaum, Elizabeth -- Deschryver, Katherine -- Davies, Sherri -- Guintoli, Therese -- Lin, Li -- Crowder, Robert -- Tao, Yu -- Snider, Jacqueline E -- Smith, Scott M -- Dukes, Adam F -- Sanderson, Gabriel E -- Pohl, Craig S -- Delehaunty, Kim D -- Fronick, Catrina C -- Pape, Kimberley A -- Reed, Jerry S -- Robinson, Jody S -- Hodges, Jennifer S -- Schierding, William -- Dees, Nathan D -- Shen, Dong -- Locke, Devin P -- Wiechert, Madeline E -- Eldred, James M -- Peck, Josh B -- Oberkfell, Benjamin J -- Lolofie, Justin T -- Du, Feiyu -- Hawkins, Amy E -- O'Laughlin, Michelle D -- Bernard, Kelly E -- Cunningham, Mark -- Elliott, Glendoria -- Mason, Mark D -- Thompson, Dominic M Jr -- Ivanovich, Jennifer L -- Goodfellow, Paul J -- Perou, Charles M -- Weinstock, George M -- Aft, Rebecca -- Watson, Mark -- Ley, Timothy J -- Wilson, Richard K -- Mardis, Elaine R -- 1 U01 CA114722-01/CA/NCI NIH HHS/ -- 3P50 CA68438/CA/NCI NIH HHS/ -- U01 CA114722/CA/NCI NIH HHS/ -- U10 CA076001/CA/NCI NIH HHS/ -- U54 HG003079/HG/NHGRI NIH HHS/ -- U54 HG003079-07/HG/NHGRI NIH HHS/ -- UL1 RR024992/RR/NCRR NIH HHS/ -- UL1 TR000448/TR/NCATS NIH HHS/ -- England -- Nature. 2010 Apr 15;464(7291):999-1005. doi: 10.1038/nature08989.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Genome Center at Washington University, St Louis, Missouri 63108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20393555" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Brain Neoplasms/*genetics/*secondary ; Breast Neoplasms/*genetics/pathology ; DNA Copy Number Variations/genetics ; DNA Mutational Analysis ; Disease Progression ; Female ; Gene Frequency/genetics ; Genome, Human/*genetics ; Genomics ; Humans ; Mutation/*genetics ; *Neoplasm Transplantation ; Translocation, Genetic/genetics ; Transplantation, Heterologous ; alpha Catenin/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Rapamycin-induced insulin resistance is mediated by mTORC2 loss and uncoupled from longevity (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-31
    Description: Rapamycin, an inhibitor of mechanistic target of rapamycin complex 1 (mTORC1), extends the life spans of yeast, flies, and mice. Calorie restriction, which increases life span and insulin sensitivity, is proposed to function by inhibition of mTORC1, yet paradoxically, chronic administration of rapamycin substantially impairs glucose tolerance and insulin action. We demonstrate that rapamycin disrupted a second mTOR complex, mTORC2, in vivo and that mTORC2 was required for the insulin-mediated suppression of hepatic gluconeogenesis. Further, decreased mTORC1 signaling was sufficient to extend life span independently from changes in glucose homeostasis, as female mice heterozygous for both mTOR and mLST8 exhibited decreased mTORC1 activity and extended life span but had normal glucose tolerance and insulin sensitivity. Thus, mTORC2 disruption is an important mediator of the effects of rapamycin in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3324089/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3324089/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamming, Dudley W -- Ye, Lan -- Katajisto, Pekka -- Goncalves, Marcus D -- Saitoh, Maki -- Stevens, Deanna M -- Davis, James G -- Salmon, Adam B -- Richardson, Arlan -- Ahima, Rexford S -- Guertin, David A -- Sabatini, David M -- Baur, Joseph A -- 1F32AG032833-01A1/AG/NIA NIH HHS/ -- CA129105/CA/NCI NIH HHS/ -- F32 AG032833/AG/NIA NIH HHS/ -- P30DK19525/DK/NIDDK NIH HHS/ -- R01 CA129105/CA/NCI NIH HHS/ -- R01 CA129105-05/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Mar 30;335(6076):1638-43. doi: 10.1126/science.1215135.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22461615" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue, White/metabolism ; Animals ; Carrier Proteins/genetics/metabolism ; Female ; Gluconeogenesis ; Glucose/metabolism ; Glucose Clamp Technique ; Homeostasis ; Insulin/administration & dosage/blood ; *Insulin Resistance ; Liver/metabolism ; *Longevity ; Male ; Mice ; Mice, Inbred C57BL ; Multiprotein Complexes ; Muscle, Skeletal/metabolism ; Phosphorylation ; Proteins/antagonists & inhibitors/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction ; Sirolimus/*pharmacology ; TOR Serine-Threonine Kinases/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Mutation of a gene encoding a protein with extracellular matrix motifs in Usher syndrome type IIa (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-20
    Description: Usher syndrome type IIa (OMIM 276901), an autosomal recessive disorder characterized by moderate to severe sensorineural hearing loss and progressive retinitis pigmentosa, maps to the long arm of human chromosome 1q41 between markers AFM268ZD1 and AFM144XF2. Three biologically important mutations in Usher syndrome type IIa patients were identified in a gene (USH2A) isolated from this critical region. The USH2A gene encodes a protein with a predicted size of 171.5 kilodaltons that has laminin epidermal growth factor and fibronectin type III motifs; these motifs are most commonly observed in proteins comprising components of the basal lamina and extracellular matrixes and in cell adhesion molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eudy, J D -- Weston, M D -- Yao, S -- Hoover, D M -- Rehm, H L -- Ma-Edmonds, M -- Yan, D -- Ahmad, I -- Cheng, J J -- Ayuso, C -- Cremers, C -- Davenport, S -- Moller, C -- Talmadge, C B -- Beisel, K W -- Tamayo, M -- Morton, C C -- Swaroop, A -- Kimberling, W J -- Sumegi, J -- 5PO1 DC01813-05/DC/NIDCD NIH HHS/ -- DC03402/DC/NIDCD NIH HHS/ -- EY07003/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1998 Jun 12;280(5370):1753-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9624053" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Adhesion Molecules/chemistry ; Chromosome Mapping ; Chromosomes, Human, Pair 1 ; Cochlea/chemistry ; Epidermal Growth Factor/chemistry ; Extracellular Matrix Proteins/chemistry/*genetics/physiology ; Female ; Fibronectins/chemistry ; Frameshift Mutation ; Gene Expression ; Genes, Recessive ; Glycosylation ; Hearing Loss, Sensorineural/*genetics ; Humans ; Laminin/chemistry ; Male ; Molecular Sequence Data ; Pedigree ; Retina/chemistry ; Retinitis Pigmentosa/*genetics ; Syndrome ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    Somatic mutations affect key pathways in lung adenocarcinoma (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-10-25
    Description: 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 in 188 human lung adenocarcinomas. DNA sequencing of 623 genes with known or potential relationships to cancer revealed more than 1,000 somatic mutations across the samples. Our analysis identified 26 genes that are mutated at significantly high frequencies and thus are probably involved in carcinogenesis. The frequently mutated genes include tyrosine kinases, among them the EGFR homologue ERBB4; multiple ephrin receptor genes, notably EPHA3; vascular endothelial growth factor receptor KDR; and NTRK genes. These data provide evidence of somatic mutations in primary lung adenocarcinoma for several tumour suppressor genes involved in other cancers--including NF1, APC, RB1 and ATM--and for sequence changes in PTPRD as well as the frequently deleted gene LRP1B. The observed mutational profiles correlate with clinical features, smoking status and DNA repair defects. These results are reinforced by data integration including single nucleotide polymorphism array and gene expression array. Our findings shed further light on several important signalling pathways involved in lung adenocarcinoma, and suggest new molecular targets for treatment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2694412/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2694412/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉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 -- Wilson, Richard K -- P50 CA070907/CA/NCI NIH HHS/ -- R01 CA154365/CA/NCI NIH HHS/ -- U19 CA084953/CA/NCI NIH HHS/ -- U19 CA084953-050003/CA/NCI NIH HHS/ -- U54 HG003067/HG/NHGRI NIH HHS/ -- U54 HG003067-04/HG/NHGRI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- England -- Nature. 2008 Oct 23;455(7216):1069-75. doi: 10.1038/nature07423.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Genome Center at Washington University, Department of Genetics, Washington University School of Medicine, St Louis, Missouri 63108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18948947" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma, Bronchiolo-Alveolar/*genetics ; Female ; Gene Dosage ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Humans ; Lung Neoplasms/*genetics ; Male ; Mutation/*genetics ; Proto-Oncogenes/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 6
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    Inferring nonneutral evolution from human-chimp-mouse orthologous gene trios (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-13
    Description: Even though human and chimpanzee gene sequences are nearly 99% identical, sequence comparisons can nevertheless be highly informative in identifying biologically important changes that have occurred since our ancestral lineages diverged. We analyzed alignments of 7645 chimpanzee gene sequences to their human and mouse orthologs. These three-species sequence alignments allowed us to identify genes undergoing natural selection along the human and chimp lineage by fitting models that include parameters specifying rates of synonymous and nonsynonymous nucleotide substitution. This evolutionary approach revealed an informative set of genes with significantly different patterns of substitution on the human lineage compared with the chimpanzee and mouse lineages. Partitions of genes into inferred biological classes identified accelerated evolution in several functional classes, including olfaction and nuclear transport. In addition to suggesting adaptive physiological differences between chimps and humans, human-accelerated genes are significantly more likely to underlie major known Mendelian disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clark, Andrew G -- Glanowski, Stephen -- Nielsen, Rasmus -- Thomas, Paul D -- Kejariwal, Anish -- Todd, Melissa A -- Tanenbaum, David M -- Civello, Daniel -- Lu, Fu -- Murphy, Brian -- Ferriera, Steve -- Wang, Gary -- Zheng, Xianqgun -- White, Thomas J -- Sninsky, John J -- Adams, Mark D -- Cargill, Michele -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1960-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671302" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus/genetics ; Amino Acids/metabolism ; Animals ; Biological Evolution ; Computational Biology ; *Evolution, Molecular ; Female ; Genes ; Genetic Diseases, Inborn/genetics ; *Genome ; *Genome, Human ; Humans ; Likelihood Functions ; Male ; Mice/genetics ; Models, Genetic ; Models, Statistical ; Mutation ; Pan troglodytes/*genetics ; Phylogeny ; Proteins/chemistry/genetics ; Pseudogenes ; Receptors, Odorant/genetics ; *Selection, Genetic ; Sequence Alignment ; Sequence Homology, Nucleic Acid ; Signal Transduction/genetics ; Smell/genetics ; Species Specificity
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 7
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    Concurrent activation of striatal direct and indirect pathways during action initiation (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-01-29
    Description: The basal ganglia are subcortical nuclei that control voluntary actions, and they are affected by a number of debilitating neurological disorders. The prevailing model of basal ganglia function proposes that two orthogonal projection circuits originating from distinct populations of spiny projection neurons (SPNs) in the striatum--the so-called direct and indirect pathways--have opposing effects on movement: activity of direct-pathway SPNs is thought to facilitate movement, whereas activity of indirect-pathway SPNs is presumed to inhibit movement. This model has been difficult to test owing to the lack of methods to selectively measure the activity of direct- and indirect-pathway SPNs in freely moving animals. Here we develop a novel in vivo method to specifically measure direct- and indirect-pathway SPN activity, using Cre-dependent viral expression of the genetically encoded calcium indicator (GECI) GCaMP3 in the dorsal striatum of D1-Cre (direct-pathway-specific) and A2A-Cre (indirect-pathway-specific) mice. Using fibre optics and time-correlated single-photon counting (TCSPC) in mice performing an operant task, we observed transient increases in neural activity in both direct- and indirect-pathway SPNs when animals initiated actions, but not when they were inactive. Concurrent activation of SPNs from both pathways in one hemisphere preceded the initiation of contraversive movements and predicted the occurrence of specific movements within 500 ms. These observations challenge the classical view of basal ganglia function and may have implications for understanding the origin of motor symptoms in basal ganglia disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4039389/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4039389/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cui, Guohong -- Jun, Sang Beom -- Jin, Xin -- Pham, Michael D -- Vogel, Steven S -- Lovinger, David M -- Costa, Rui M -- 243393/European Research Council/International -- ZIA AA000407-12/Intramural NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Feb 14;494(7436):238-42. doi: 10.1038/nature11846. Epub 2013 Jan 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section on In Vivo Neural Function, Laboratory for Integrative Neuroscience, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland 20892-9412, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23354054" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium Signaling ; Female ; Fiber Optic Technology/methods ; Fluorescence ; Integrases/genetics/metabolism ; Luminescent Measurements/methods ; Male ; Mice ; Models, Neurological ; Movement/*physiology ; Neostriatum/*cytology/*physiology ; Neural Pathways/*physiology ; Parkinson Disease ; Photons
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 8
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    Novel somatic and germline mutations in intracranial germ cell tumours (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-06-05
    Description: Intracranial germ cell tumours (IGCTs) are a group of rare heterogeneous brain tumours that are clinically and histologically similar to the more common gonadal GCTs. IGCTs show great variation in their geographical and gender distribution, histological composition and treatment outcomes. The incidence of IGCTs is historically five- to eightfold greater in Japan and other East Asian countries than in Western countries, with peak incidence near the time of puberty. About half of the tumours are located in the pineal region. The male-to-female incidence ratio is approximately 3-4:1 overall, but is even higher for tumours located in the pineal region. Owing to the scarcity of tumour specimens available for research, little is currently known about this rare disease. Here we report the analysis of 62 cases by next-generation sequencing, single nucleotide polymorphism array and expression array. We find the KIT/RAS signalling pathway frequently mutated in more than 50% of IGCTs, including novel recurrent somatic mutations in KIT, its downstream mediators KRAS and NRAS, and its negative regulator CBL. Novel somatic alterations in the AKT/mTOR pathway included copy number gains of the AKT1 locus at 14q32.33 in 19% of patients, with corresponding upregulation of AKT1 expression. We identified loss-of-function mutations in BCORL1, a transcriptional co-repressor and tumour suppressor. We report significant enrichment of novel and rare germline variants in JMJD1C, which codes for a histone demethylase and is a coactivator of the androgen receptor, among Japanese IGCT patients. This study establishes a molecular foundation for understanding the biology of IGCTs and suggests potentially promising therapeutic strategies focusing on the inhibition of KIT/RAS activation and the AKT1/mTOR pathway.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4532372/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4532372/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Linghua -- Yamaguchi, Shigeru -- Burstein, Matthew D -- Terashima, Keita -- Chang, Kyle -- Ng, Ho-Keung -- Nakamura, Hideo -- He, Zongxiao -- Doddapaneni, Harshavardhan -- Lewis, Lora -- Wang, Mark -- Suzuki, Tomonari -- Nishikawa, Ryo -- Natsume, Atsushi -- Terasaka, Shunsuke -- Dauser, Robert -- Whitehead, William -- Adekunle, Adesina -- Sun, Jiayi -- Qiao, Yi -- Marth, Gabor -- Muzny, Donna M -- Gibbs, Richard A -- Leal, Suzanne M -- Wheeler, David A -- Lau, Ching C -- 5T15 LM07093-18/LM/NLM NIH HHS/ -- 5T15 LM07093-19/LM/NLM NIH HHS/ -- 5U54HG003273/HG/NHGRI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- England -- Nature. 2014 Jul 10;511(7508):241-5. doi: 10.1038/nature13296. Epub 2014 Jun 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Genome Sequencing Center, Baylor College of Medicine, Houston, Texas 77030, USA. ; Texas Children's Cancer and Hematology Centers, Baylor College of Medicine, Houston, Texas 77030, USA. ; 1] Structural and Computational Biology and Molecular Biophysics Program, Baylor College of Medicine, Houston, Texas 77030, USA [2] Medical Scientist Training Program, Baylor College of Medicine, Houston, Texas 77030, USA. ; 1] Texas Children's Cancer and Hematology Centers, Baylor College of Medicine, Houston, Texas 77030, USA [2] National Center for Child Health and Development, Tokyo, 157-8535, Japan. ; Department of Anatomical and Cellular Pathology, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong. ; Department of Neurosurgery, Kumamoto University, Kumamoto, 860-0862, Japan. ; Center for Statistical Genetics, Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030, USA. ; Department of Neurosurgery, Saitama Medical University, Saitama, 350-0495, Japan. ; Department of Neurosurgery, Nagoya University, Nagoya, 466-8550, Japan. ; Department of Neurosurgery, Hokkaido University, Hokkaido Prefecture, 060-0808, Japan. ; Department of Neurosurgery, Baylor College of Medicine, Houston, Texas 77030, USA. ; Department of Pathology, Baylor College of Medicine, Houston, Texas 77030, USA. ; Medical Scientist Training Program, Baylor College of Medicine, Houston, Texas 77030, USA. ; Department of Biology, Boston College, Chestnut Hill, Maryland 02467, USA. ; 1] Texas Children's Cancer and Hematology Centers, Baylor College of Medicine, Houston, Texas 77030, USA [2] Medical Scientist Training Program, Baylor College of Medicine, Houston, Texas 77030, USA [3] Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24896186" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Brain Neoplasms/*genetics/pathology ; Child ; Female ; Germ-Line Mutation/*genetics ; Humans ; Japan ; Male ; Mutation/*genetics ; Neoplasms, Germ Cell and Embryonal/*genetics/pathology ; Oncogene Protein v-akt/genetics ; Proto-Oncogene Proteins c-kit/genetics ; Reproducibility of Results ; Signal Transduction/genetics ; TOR Serine-Threonine Kinases/genetics ; Young Adult ; ras Proteins/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 9
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    High-fat diet enhances stemness and tumorigenicity of intestinal progenitors (2016)
    Nature Publishing Group (NPG)
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    Publication Date: 2016-03-05
    Description: Little is known about how pro-obesity diets regulate tissue stem and progenitor cell function. Here we show that high-fat diet (HFD)-induced obesity augments the numbers and function of Lgr5(+) intestinal stem cells of the mammalian intestine. Mechanistically, a HFD induces a robust peroxisome proliferator-activated receptor delta (PPAR-delta) signature in intestinal stem cells and progenitor cells (non-intestinal stem cells), and pharmacological activation of PPAR-delta recapitulates the effects of a HFD on these cells. Like a HFD, ex vivo treatment of intestinal organoid cultures with fatty acid constituents of the HFD enhances the self-renewal potential of these organoid bodies in a PPAR-delta-dependent manner. Notably, HFD- and agonist-activated PPAR-delta signalling endow organoid-initiating capacity to progenitors, and enforced PPAR-delta signalling permits these progenitors to form in vivo tumours after loss of the tumour suppressor Apc. These findings highlight how diet-modulated PPAR-delta activation alters not only the function of intestinal stem and progenitor cells, but also their capacity to initiate tumours.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4846772/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4846772/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beyaz, Semir -- Mana, Miyeko D -- Roper, Jatin -- Kedrin, Dmitriy -- Saadatpour, Assieh -- Hong, Sue-Jean -- Bauer-Rowe, Khristian E -- Xifaras, Michael E -- Akkad, Adam -- Arias, Erika -- Pinello, Luca -- Katz, Yarden -- Shinagare, Shweta -- Abu-Remaileh, Monther -- Mihaylova, Maria M -- Lamming, Dudley W -- Dogum, Rizkullah -- Guo, Guoji -- Bell, George W -- Selig, Martin -- Nielsen, G Petur -- Gupta, Nitin -- Ferrone, Cristina R -- Deshpande, Vikram -- Yuan, Guo-Cheng -- Orkin, Stuart H -- Sabatini, David M -- Yilmaz, Omer H -- AI47389/AI/NIAID NIH HHS/ -- DK043351/DK/NIDDK NIH HHS/ -- K08 CA198002/CA/NCI NIH HHS/ -- K99 AG041765/AG/NIA NIH HHS/ -- K99 AG045144/AG/NIA NIH HHS/ -- P30 CA014051/CA/NCI NIH HHS/ -- P30-CA14051/CA/NCI NIH HHS/ -- R00 AG041765/AG/NIA NIH HHS/ -- R00 AG045144/AG/NIA NIH HHS/ -- R01 AI047389/AI/NIAID NIH HHS/ -- R01 CA103866/CA/NCI NIH HHS/ -- R01 CA129105/CA/NCI NIH HHS/ -- R37 AI047389/AI/NIAID NIH HHS/ -- T32DK007191/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2016 Mar 3;531(7592):53-8. doi: 10.1038/nature17173.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The David H. Koch Institute for Integrative Cancer Research at MIT, Department of Biology, MIT, Cambridge, Massachusetts 02139, USA. ; Division of Hematology/Oncology, Boston Children's Hospital and Department of Pediatric Oncology, Dana-Farber Cancer Institute, Howard Hughes Medical Institute, Harvard Stem Cell Institute, Harvard Medical School, Boston, Massachusetts 02115, USA. ; Division of Gastroenterology and Molecular Oncology Research Institute, Tufts Medical Center, Boston, Massachusetts 02111, USA. ; Departments of Pathology, Gastroenterology, and Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA. ; Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute and Harvard T. H. Chan School of Public Health, Boston, Massachusetts 02115, USA. ; Whitehead Institute for Biomedical Research, Howard Hughes Medical Institute, Department of Biology, MIT, Cambridge, Massachusetts 02142, USA. ; Broad Institute of Harvard and MIT, Cambridge, Massachusetts 02142, USA. ; Department of Medicine, University of Wisconsin-Madison, Madison, Wisconsin 53705, USA. ; Division of Digestive Diseases, University of Mississippi Medical Center, Jackson, Missisippi 39216, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26935695" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Count ; Cell Self Renewal/drug effects ; Cell Transformation, Neoplastic/*drug effects ; Colonic Neoplasms/*pathology ; Diet, High-Fat/*adverse effects ; Female ; Genes, APC ; Humans ; Intestines/*pathology ; Male ; Mice ; Obesity/chemically induced/pathology ; Organoids/drug effects/metabolism/pathology ; PPAR delta/metabolism ; Signal Transduction/drug effects ; Stem Cell Niche/drug effects ; Stem Cells/*drug effects/metabolism/*pathology ; beta Catenin/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
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    Stimulation of prostaglandin biosynthesis by urine of the human fetus may serve as a trigger for parturition (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-04-29
    Description: Urine of the human fetus stimulated prostaglandin biosynthesis in vitro by increasing the conversion of arachidonic acid into prostaglandins. The stimulatory activity in urine from fetuses delivered at term after labor of spontaneous onset was greater than that in urine from fetuses delivered by cesarean section at term before the onset of labor. Such stimulation of prostaglandin biosynthesis by the fetal membranes, by way of a substance released into the urine and thence into amniotic fluid, could serve as a signal for the initiation of parturition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strickland, D M -- Saeed, S A -- Casey, M L -- Mitchell, M D -- 5-P50-HD11149/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1983 Apr 29;220(4596):521-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6573023" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Dinoprostone ; Extraembryonic Membranes/physiology ; Female ; Fetus/*physiology ; Humans ; *Labor Onset ; *Labor, Obstetric ; Male ; Pregnancy ; Prostaglandins/*biosynthesis ; Prostaglandins E/biosynthesis ; *Urine
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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