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  • 1
    Keywords: Medicine ; Reproductive Medicine ; Cytology ; Medicine & Public Health ; Reproductive Medicine ; Cell Biology ; Molecular Medicine ; Springer eBooks
    Description / Table of Contents: The importance of oocyte biology for the future of fertility preservation -- The Control of Oocyte Survival by Intrinsic and Extrinsic Factors -- Oocyte Genomic Integrity -- In Vitro Activation of Dormant Follicles for Fertility Preservation -- Primate follicular development in vitro -- Vitrification of oocytes - From Basic Science to Clinical Application -- Memoir of Fertility Preservation
    Abstract: Fertility preservation has become one of the most important and fast growing fields of reproductive medicine.℗ Although there are several strategies for fertility preservation in female, most of them are still considered experimental.℗ It is important to perfect the existing technologies, but also developing new strategies should be actively sought.℗ The future development of fertility preservation strategies should be based on the sound scientific knowledge and principles.℗ One of the main objectives of fertility preservation in females is prevention of oocyte depletion. The mechanisms of oocyte loss and survival in the ovary are complex, which include genetic control both in germ cells and in somatic cells, DNA damage and repair mechanism, apoptosis and autophagy, and other poorly understood molecular mechanisms.℗ To develop clinically effective and safe strategies for fertility preservation, it is essential to know and understand the fundamentals of oocyte and ovarian biology at the molecular level.℗ Thus, the purpose of this edition is to review the current progress in research related to molecular and genetic control of oocyte development that can be applied to fertility preservation. ℗ The main topics that are discussed in this publication include molecular signaling mechanisms of oocyte activation and loss, genomic integrity of oocytes, and epigenetics. ℗
    Pages: X, 97 p. 12 illus., 9 illus. in color. : online resource.
    ISBN: 9781461482147
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  • 2
    Publication Date: 2011-03-11
    Description: In the cerebral cortex, local circuits consist of tens of thousands of neurons, each of which makes thousands of synaptic connections. Perhaps the biggest impediment to understanding these networks is that we have no wiring diagrams of their interconnections. Even if we had a partial or complete wiring diagram, however, understanding the network would also require information about each neuron's function. Here we show that the relationship between structure and function can be studied in the cortex with a combination of in vivo physiology and network anatomy. We used two-photon calcium imaging to characterize a functional property--the preferred stimulus orientation--of a group of neurons in the mouse primary visual cortex. Large-scale electron microscopy of serial thin sections was then used to trace a portion of these neurons' local network. Consistent with a prediction from recent physiological experiments, inhibitory interneurons received convergent anatomical input from nearby excitatory neurons with a broad range of preferred orientations, although weak biases could not be rejected.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3095821/" 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/PMC3095821/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bock, Davi D -- Lee, Wei-Chung Allen -- Kerlin, Aaron M -- Andermann, Mark L -- Hood, Greg -- Wetzel, Arthur W -- Yurgenson, Sergey -- Soucy, Edward R -- Kim, Hyon Suk -- Reid, R Clay -- EY10115/EY/NEI NIH HHS/ -- EY18532/EY/NEI NIH HHS/ -- EY18742/EY/NEI NIH HHS/ -- F32 EY018532/EY/NEI NIH HHS/ -- F32 EY018532-01A1/EY/NEI NIH HHS/ -- P41 RR06009/RR/NCRR NIH HHS/ -- England -- Nature. 2011 Mar 10;471(7337):177-82. doi: 10.1038/nature09802.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21390124" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium Signaling ; Interneurons/physiology ; Male ; Mice ; Microscopy, Electron, Transmission ; Microscopy, Fluorescence ; Microtomy ; Nerve Net/*anatomy & histology/*cytology/physiology/ultrastructure ; Neural Inhibition/physiology ; Neurons/*physiology/ultrastructure ; Pyramidal Cells/physiology/ultrastructure ; Synapses/physiology ; Visual Cortex/*anatomy & histology/*cytology/physiology/ultrastructure
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2012-06-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Mi-Sun -- Kondo, Takeshi -- Takada, Ichiro -- Youn, Min-Young -- Yamamoto, Yoko -- Takahashi, Sayuri -- Matsumoto, Takahiro -- Fujiyama, Sally -- Shirode, Yuko -- Yamaoka, Ikuko -- Kitagawa, Hirochika -- Takeyama, Ken-Ichi -- Shibuya, Hiroshi -- Ohtake, Fumiaki -- Kato, Shigeaki -- England -- Nature. 2012 Jun 13;486(7402):280. doi: 10.1038/nature11164.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22699624" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2012-03-31
    Description: The systematic translation of cancer genomic data into knowledge of tumour biology and therapeutic possibilities remains challenging. Such efforts should be greatly aided by robust preclinical model systems that reflect the genomic diversity of human cancers and for which detailed genetic and pharmacological annotation is available. Here we describe the Cancer Cell Line Encyclopedia (CCLE): a compilation of gene expression, chromosomal copy number and massively parallel sequencing data from 947 human cancer cell lines. When coupled with pharmacological profiles for 24 anticancer drugs across 479 of the cell lines, this collection allowed identification of genetic, lineage, and gene-expression-based predictors of drug sensitivity. In addition to known predictors, we found that plasma cell lineage correlated with sensitivity to IGF1 receptor inhibitors; AHR expression was associated with MEK inhibitor efficacy in NRAS-mutant lines; and SLFN11 expression predicted sensitivity to topoisomerase inhibitors. Together, our results indicate that large, annotated cell-line collections may help to enable preclinical stratification schemata for anticancer agents. The generation of genetic predictions of drug response in the preclinical setting and their incorporation into cancer clinical trial design could speed the emergence of 'personalized' therapeutic regimens.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3320027/" 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/PMC3320027/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barretina, Jordi -- Caponigro, Giordano -- Stransky, Nicolas -- Venkatesan, Kavitha -- Margolin, Adam A -- Kim, Sungjoon -- Wilson, Christopher J -- Lehar, Joseph -- Kryukov, Gregory V -- Sonkin, Dmitriy -- Reddy, Anupama -- Liu, Manway -- Murray, Lauren -- Berger, Michael F -- Monahan, John E -- Morais, Paula -- Meltzer, Jodi -- Korejwa, Adam -- Jane-Valbuena, Judit -- Mapa, Felipa A -- Thibault, Joseph -- Bric-Furlong, Eva -- Raman, Pichai -- Shipway, Aaron -- Engels, Ingo H -- Cheng, Jill -- Yu, Guoying K -- Yu, Jianjun -- Aspesi, Peter Jr -- de Silva, Melanie -- Jagtap, Kalpana -- Jones, Michael D -- Wang, Li -- Hatton, Charles -- Palescandolo, Emanuele -- Gupta, Supriya -- Mahan, Scott -- Sougnez, Carrie -- Onofrio, Robert C -- Liefeld, Ted -- MacConaill, Laura -- Winckler, Wendy -- Reich, Michael -- Li, Nanxin -- Mesirov, Jill P -- Gabriel, Stacey B -- Getz, Gad -- Ardlie, Kristin -- Chan, Vivien -- Myer, Vic E -- Weber, Barbara L -- Porter, Jeff -- Warmuth, Markus -- Finan, Peter -- Harris, Jennifer L -- Meyerson, Matthew -- Golub, Todd R -- Morrissey, Michael P -- Sellers, William R -- Schlegel, Robert -- Garraway, Levi A -- DP2 OD002750/OD/NIH HHS/ -- DP2 OD002750-01/OD/NIH HHS/ -- R33 CA126674/CA/NCI NIH HHS/ -- R33 CA126674-04/CA/NCI NIH HHS/ -- R33 CA155554/CA/NCI NIH HHS/ -- R33 CA155554-02/CA/NCI NIH HHS/ -- England -- Nature. 2012 Mar 28;483(7391):603-7. doi: 10.1038/nature11003.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Broad Institute of Harvard and MIT, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22460905" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Cell Lineage ; Chromosomes, Human/genetics ; Clinical Trials as Topic/methods ; *Databases, Factual ; Drug Screening Assays, Antitumor/*methods ; *Encyclopedias as Topic ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genes, ras/genetics ; Genome, Human/genetics ; Genomics ; Humans ; Mitogen-Activated Protein Kinase Kinases/antagonists & inhibitors/metabolism ; *Models, Biological ; Neoplasms/*drug therapy/genetics/metabolism/*pathology ; Pharmacogenetics ; Plasma Cells/cytology/drug effects/metabolism ; Precision Medicine/methods ; Receptor, IGF Type 1/antagonists & inhibitors/metabolism ; Receptors, Aryl Hydrocarbon/genetics/metabolism ; Sequence Analysis, DNA ; Topoisomerase Inhibitors/pharmacology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2012-03-09
    Description: Cells are organized on length scales ranging from angstrom to micrometres. However, the mechanisms by which angstrom-scale molecular properties are translated to micrometre-scale macroscopic properties are not well understood. Here we show that interactions between diverse synthetic, multivalent macromolecules (including multi-domain proteins and RNA) produce sharp liquid-liquid-demixing phase separations, generating micrometre-sized liquid droplets in aqueous solution. This macroscopic transition corresponds to a molecular transition between small complexes and large, dynamic supramolecular polymers. The concentrations needed for phase transition are directly related to the valency of the interacting species. In the case of the actin-regulatory protein called neural Wiskott-Aldrich syndrome protein (N-WASP) interacting with its established biological partners NCK and phosphorylated nephrin, the phase transition corresponds to a sharp increase in activity towards an actin nucleation factor, the Arp2/3 complex. The transition is governed by the degree of phosphorylation of nephrin, explaining how this property of the system can be controlled to regulatory effect by kinases. The widespread occurrence of multivalent systems suggests that phase transitions may be used to spatially organize and biochemically regulate information throughout biology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3343696/" 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/PMC3343696/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Pilong -- Banjade, Sudeep -- Cheng, Hui-Chun -- Kim, Soyeon -- Chen, Baoyu -- Guo, Liang -- Llaguno, Marc -- Hollingsworth, Javoris V -- King, David S -- Banani, Salman F -- Russo, Paul S -- Jiang, Qiu-Xing -- Nixon, B Tracy -- Rosen, Michael K -- P30 CA142543/CA/NCI NIH HHS/ -- P41 GM103622/GM/NIGMS NIH HHS/ -- R01 GM056322/GM/NIGMS NIH HHS/ -- R01 GM056322-13/GM/NIGMS NIH HHS/ -- R01-GM088745/GM/NIGMS NIH HHS/ -- R01-GM56322/GM/NIGMS NIH HHS/ -- RR-08630/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Mar 7;483(7389):336-40. doi: 10.1038/nature10879.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, Texas 75390-8812, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22398450" target="_blank"〉PubMed〈/a〉
    Keywords: Actin-Related Protein 2-3 Complex/metabolism ; Adaptor Proteins, Signal Transducing/chemistry/metabolism ; Binding Sites ; Biopolymers/chemistry/metabolism ; Fluorescence Recovery After Photobleaching ; HeLa Cells ; Humans ; Ligands ; Membrane Proteins/chemistry/metabolism ; Multiprotein Complexes/*chemistry/*metabolism ; Oncogene Proteins/chemistry/metabolism ; *Phase Transition ; Phosphorylation ; Proline-Rich Protein Domains ; Protein Structure, Quaternary ; Proteins/*chemistry/*metabolism ; *Signal Transduction ; Wiskott-Aldrich Syndrome Protein, Neuronal/chemistry/metabolism ; src Homology Domains
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2012-08-10
    Description: Atmospheric oxidation is a key phenomenon that connects atmospheric chemistry with globally challenging environmental issues, such as climate change, stratospheric ozone loss, acidification of soils and water, and health effects of air quality. Ozone, the hydroxyl radical and the nitrate radical are generally considered to be the dominant oxidants that initiate the removal of trace gases, including pollutants, from the atmosphere. Here we present atmospheric observations from a boreal forest region in Finland, supported by laboratory experiments and theoretical considerations, that allow us to identify another compound, probably a stabilized Criegee intermediate (a carbonyl oxide with two free-radical sites) or its derivative, which has a significant capacity to oxidize sulphur dioxide and potentially other trace gases. This compound probably enhances the reactivity of the atmosphere, particularly with regard to the production of sulphuric acid, and consequently atmospheric aerosol formation. Our findings suggest that this new atmospherically relevant oxidation route is important relative to oxidation by the hydroxyl radical, at least at moderate concentrations of that radical. We also find that the oxidation chemistry of this compound seems to be tightly linked to the presence of alkenes of biogenic origin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mauldin, R L 3rd -- Berndt, T -- Sipila, M -- Paasonen, P -- Petaja, T -- Kim, S -- Kurten, T -- Stratmann, F -- Kerminen, V-M -- Kulmala, M -- England -- Nature. 2012 Aug 9;488(7410):193-6. doi: 10.1038/nature11278.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Helsinki, Department of Physics, FI-00014 Helsinki, Finland. roy.mauldin@helsinki.fi〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22874964" target="_blank"〉PubMed〈/a〉
    Keywords: Alkenes/metabolism ; Atmosphere/*chemistry ; Finland ; Free Radicals/chemistry ; Hydroxyl Radical/chemistry ; Oxidants/*chemistry/metabolism ; Ozone/chemistry ; Sulfur Dioxide/analysis/*chemistry ; Terpenes/chemistry/metabolism ; Trees/metabolism ; Volatile Organic Compounds/analysis/chemistry/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2013-06-04
    Description: The functional importance of gene enhancers in regulated gene expression is well established. In addition to widespread transcription of long non-coding RNAs (lncRNAs) in mammalian cells, bidirectional ncRNAs are transcribed on enhancers, and are thus referred to as enhancer RNAs (eRNAs). However, it has remained unclear whether these eRNAs are functional or merely a reflection of enhancer activation. Here we report that in human breast cancer cells 17beta-oestradiol (E2)-bound oestrogen receptor alpha (ER-alpha) causes a global increase in eRNA transcription on enhancers adjacent to E2-upregulated coding genes. These induced eRNAs, as functional transcripts, seem to exert important roles for the observed ligand-dependent induction of target coding genes, increasing the strength of specific enhancer-promoter looping initiated by ER-alpha binding. Cohesin, present on many ER-alpha-regulated enhancers even before ligand treatment, apparently contributes to E2-dependent gene activation, at least in part by stabilizing E2/ER-alpha/eRNA-induced enhancer-promoter looping. Our data indicate that eRNAs are likely to have important functions in many regulated programs of gene transcription.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3718886/" 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/PMC3718886/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Wenbo -- Notani, Dimple -- Ma, Qi -- Tanasa, Bogdan -- Nunez, Esperanza -- Chen, Aaron Yun -- Merkurjev, Daria -- Zhang, Jie -- Ohgi, Kenneth -- Song, Xiaoyuan -- Oh, Soohwan -- Kim, Hong-Sook -- Glass, Christopher K -- Rosenfeld, Michael G -- CA173903/CA/NCI NIH HHS/ -- DK 039949/DK/NIDDK NIH HHS/ -- DK018477/DK/NIDDK NIH HHS/ -- HL065445/HL/NHLBI NIH HHS/ -- NS034934/NS/NINDS NIH HHS/ -- P30 CA023100/CA/NCI NIH HHS/ -- P30 CA23100/CA/NCI NIH HHS/ -- R01 CA097134/CA/NCI NIH HHS/ -- R01 CA173903/CA/NCI NIH HHS/ -- R01 DK018477/DK/NIDDK NIH HHS/ -- R01 DK039949/DK/NIDDK NIH HHS/ -- R01 HL065445/HL/NHLBI NIH HHS/ -- R01 NS034934/NS/NINDS NIH HHS/ -- R37 DK039949/DK/NIDDK NIH HHS/ -- T32 CA009523/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Jun 27;498(7455):516-20. doi: 10.1038/nature12210. Epub 2013 Jun 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, School of Medicine, University of California, San Diego, La Jolla, California 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23728302" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Cycle Proteins/metabolism ; Chromosomal Proteins, Non-Histone/metabolism ; Enhancer Elements, Genetic/*genetics ; Estradiol/pharmacology ; Estrogen Receptor alpha/metabolism ; Estrogens/*pharmacology ; Humans ; Ligands ; MCF-7 Cells ; Nucleic Acid Conformation/drug effects ; Promoter Regions, Genetic/genetics ; RNA, Untranslated/biosynthesis/*genetics/metabolism ; Transcription, Genetic/drug effects/genetics ; Transcriptional Activation/*drug effects/genetics
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2013-07-12
    Description: Manipulation of the gut microbiota holds great promise for the treatment of inflammatory and allergic diseases. Although numerous probiotic microorganisms have been identified, there remains a compelling need to discover organisms that elicit more robust therapeutic responses, are compatible with the host, and can affect a specific arm of the host immune system in a well-controlled, physiological manner. Here we use a rational approach to isolate CD4(+)FOXP3(+) regulatory T (Treg)-cell-inducing bacterial strains from the human indigenous microbiota. Starting with a healthy human faecal sample, a sequence of selection steps was applied to obtain mice colonized with human microbiota enriched in Treg-cell-inducing species. From these mice, we isolated and selected 17 strains of bacteria on the basis of their high potency in enhancing Treg cell abundance and inducing important anti-inflammatory molecules--including interleukin-10 (IL-) and inducible T-cell co-stimulator (ICOS)--in Treg cells upon inoculation into germ-free mice. Genome sequencing revealed that the 17 strains fall within clusters IV, XIVa and XVIII of Clostridia, which lack prominent toxins and virulence factors. The 17 strains act as a community to provide bacterial antigens and a TGF-beta-rich environment to help expansion and differentiation of Treg cells. Oral administration of the combination of 17 strains to adult mice attenuated disease in models of colitis and allergic diarrhoea. Use of the isolated strains may allow for tailored therapeutic manipulation of human immune disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Atarashi, Koji -- Tanoue, Takeshi -- Oshima, Kenshiro -- Suda, Wataru -- Nagano, Yuji -- Nishikawa, Hiroyoshi -- Fukuda, Shinji -- Saito, Takuro -- Narushima, Seiko -- Hase, Koji -- Kim, Sangwan -- Fritz, Joelle V -- Wilmes, Paul -- Ueha, Satoshi -- Matsushima, Kouji -- Ohno, Hiroshi -- Olle, Bernat -- Sakaguchi, Shimon -- Taniguchi, Tadatsugu -- Morita, Hidetoshi -- Hattori, Masahira -- Honda, Kenya -- England -- Nature. 2013 Aug 8;500(7461):232-6. doi: 10.1038/nature12331. Epub 2013 Jul 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉RIKEN Center for Integrative Medical Sciences (IMS-RCAI), 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23842501" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Cell Proliferation ; Clostridium/classification/genetics/*immunology ; Colitis/microbiology/pathology ; Colon/immunology/microbiology ; Disease Models, Animal ; Feces/microbiology ; Germ-Free Life ; Humans ; Inducible T-Cell Co-Stimulator Protein/metabolism ; Interleukin-10/metabolism ; Male ; Metagenome/genetics/*immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, SCID ; RNA, Ribosomal, 16S/genetics ; Rats ; Rats, Inbred F344 ; T-Lymphocytes, Regulatory/cytology/*physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2013-12-20
    Description: Plasmodium falciparum resistance to artemisinin derivatives in southeast Asia threatens malaria control and elimination activities worldwide. To monitor the spread of artemisinin resistance, a molecular marker is urgently needed. Here, using whole-genome sequencing of an artemisinin-resistant parasite line from Africa and clinical parasite isolates from Cambodia, we associate mutations in the PF3D7_1343700 kelch propeller domain ('K13-propeller') with artemisinin resistance in vitro and in vivo. Mutant K13-propeller alleles cluster in Cambodian provinces where resistance is prevalent, and the increasing frequency of a dominant mutant K13-propeller allele correlates with the recent spread of resistance in western Cambodia. Strong correlations between the presence of a mutant allele, in vitro parasite survival rates and in vivo parasite clearance rates indicate that K13-propeller mutations are important determinants of artemisinin resistance. K13-propeller polymorphism constitutes a useful molecular marker for large-scale surveillance efforts to contain artemisinin resistance in the Greater Mekong Subregion and prevent its global spread.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ariey, Frederic -- Witkowski, Benoit -- Amaratunga, Chanaki -- Beghain, Johann -- Langlois, Anne-Claire -- Khim, Nimol -- Kim, Saorin -- Duru, Valentine -- Bouchier, Christiane -- Ma, Laurence -- Lim, Pharath -- Leang, Rithea -- Duong, Socheat -- Sreng, Sokunthea -- Suon, Seila -- Chuor, Char Meng -- Bout, Denis Mey -- Menard, Sandie -- Rogers, William O -- Genton, Blaise -- Fandeur, Thierry -- Miotto, Olivo -- Ringwald, Pascal -- Le Bras, Jacques -- Berry, Antoine -- Barale, Jean-Christophe -- Fairhurst, Rick M -- Benoit-Vical, Francoise -- Mercereau-Puijalon, Odile -- Menard, Didier -- 090770/Z/09/Z/Wellcome Trust/United Kingdom -- 098051/Wellcome Trust/United Kingdom -- G0600718/Medical Research Council/United Kingdom -- Intramural NIH HHS/ -- England -- Nature. 2014 Jan 2;505(7481):50-5. doi: 10.1038/nature12876. Epub 2013 Dec 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Institut Pasteur, Parasite Molecular Immunology Unit, 75724 Paris Cedex 15, France [2] Centre National de la Recherche Scientifique, Unite de Recherche Associee 2581, 75724 Paris Cedex 15, France [3] Institut Pasteur, Genetics and Genomics of Insect Vectors Unit, 75724 Paris Cedex 15, France (F.A.); Institut Pasteur, Functional Genetics of Infectious Diseases Unit, 75724 Paris Cedex 15, France (J.B.); Centre de Physiopathologie de Toulouse-Purpan, Institut National de la Sante et de la Recherche Medicale UMR1043, Centre National de la Recherche Scientifique UMR5282, Universite Toulouse III, 31024 Toulouse Cedex 3, France Institut Pasteur, Unite de Biologie et Genetique du Paludisme, Team Malaria Targets and Drug Development, 75724 Paris Cedex 15, France (J.-C.B.). ; Institut Pasteur du Cambodge, Malaria Molecular Epidemiology Unit, Phnom Penh, Cambodia. ; Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. ; 1] Institut Pasteur, Parasite Molecular Immunology Unit, 75724 Paris Cedex 15, France [2] Centre National de la Recherche Scientifique, Unite de Recherche Associee 2581, 75724 Paris Cedex 15, France. ; Institut Pasteur, Plate-forme Genomique, Departement Genomes et Genetique, 75724 Paris Cedex 15, France. ; 1] Institut Pasteur du Cambodge, Malaria Molecular Epidemiology Unit, Phnom Penh, Cambodia [2] Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA [3] National Center for Parasitology, Entomology and Malaria Control, Phnom Penh, Cambodia. ; National Center for Parasitology, Entomology and Malaria Control, Phnom Penh, Cambodia. ; SSA WHO, Drug Monitoring in Cambodia, National Center for Parasitology, Entomology and Malaria Control, Phnom Penh, Cambodia. ; 1] Service de Parasitologie et Mycologie, Centre Hospitalier Universitaire de Toulouse, 31059 Toulouse Cedex 9, France [2] Institut Pasteur, Genetics and Genomics of Insect Vectors Unit, 75724 Paris Cedex 15, France (F.A.); Institut Pasteur, Functional Genetics of Infectious Diseases Unit, 75724 Paris Cedex 15, France (J.B.); Centre de Physiopathologie de Toulouse-Purpan, Institut National de la Sante et de la Recherche Medicale UMR1043, Centre National de la Recherche Scientifique UMR5282, Universite Toulouse III, 31024 Toulouse Cedex 3, France Institut Pasteur, Unite de Biologie et Genetique du Paludisme, Team Malaria Targets and Drug Development, 75724 Paris Cedex 15, France (J.-C.B.). ; Naval Medical Research Unit #2 Detachment, Phnom Penh, Cambodia. ; Swiss Tropical and Public Health Institute, 4051 Basel, Switzerland. ; 1] Institut Pasteur, Parasite Molecular Immunology Unit, 75724 Paris Cedex 15, France [2] Institut Pasteur du Cambodge, Malaria Molecular Epidemiology Unit, Phnom Penh, Cambodia. ; 1] MRC Centre for Genomics and Global Health, University of Oxford, Oxford OX3 7BN, UK [2] Mahidol-Oxford Tropical Medicine Research Unit, Mahidol University, Bangkok 10400, Thailand [3] Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK. ; Global Malaria Program, World Health Organization, 1211 Geneva, Switzerland. ; Centre National de Reference du Paludisme, CHU Bichat-Claude Bernard, APHP, PRES Sorbonne Paris Cite, 75018 Paris, France. ; 1] Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA [2]. ; 1] Centre National de la Recherche Scientifique, Laboratoire de Chimie de Coordination UPR8241, 31077 Toulouse Cedex 4, France [2] Universite de Toulouse, UPS, Institut National Polytechnique de Toulouse, 31077 Toulouse Cedex 4, France [3]. ; 1] Institut Pasteur, Parasite Molecular Immunology Unit, 75724 Paris Cedex 15, France [2] Centre National de la Recherche Scientifique, Unite de Recherche Associee 2581, 75724 Paris Cedex 15, France [3]. ; 1] Institut Pasteur du Cambodge, Malaria Molecular Epidemiology Unit, Phnom Penh, Cambodia [2].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24352242" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Antimalarials/*pharmacology ; Artemisinins/*pharmacology ; Blood Cells/parasitology ; Cambodia ; Drug Resistance/drug effects/*genetics ; Genetic Markers/genetics ; Half-Life ; Humans ; Malaria, Falciparum/drug therapy/*parasitology ; Mutation/genetics ; Parasitic Sensitivity Tests ; Plasmodium falciparum/*drug effects/*genetics/growth & development/isolation & ; purification ; Polymorphism, Single Nucleotide/genetics ; Protein Structure, Tertiary/genetics ; Protozoan Proteins/chemistry/*genetics ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2014-07-22
    Description: Extensive genomic characterization of human cancers presents the problem of inference from genomic abnormalities to cancer phenotypes. To address this problem, we analysed proteomes of colon and rectal tumours characterized previously by The Cancer Genome Atlas (TCGA) and perform integrated proteogenomic analyses. Somatic variants displayed reduced protein abundance compared to germline variants. Messenger RNA transcript abundance did not reliably predict protein abundance differences between tumours. Proteomics identified five proteomic subtypes in the TCGA cohort, two of which overlapped with the TCGA 'microsatellite instability/CpG island methylation phenotype' transcriptomic subtype, but had distinct mutation, methylation and protein expression patterns associated with different clinical outcomes. Although copy number alterations showed strong cis- and trans-effects on mRNA abundance, relatively few of these extend to the protein level. Thus, proteomics data enabled prioritization of candidate driver genes. The chromosome 20q amplicon was associated with the largest global changes at both mRNA and protein levels; proteomics data highlighted potential 20q candidates, including HNF4A (hepatocyte nuclear factor 4, alpha), TOMM34 (translocase of outer mitochondrial membrane 34) and SRC (SRC proto-oncogene, non-receptor tyrosine kinase). Integrated proteogenomic analysis provides functional context to interpret genomic abnormalities and affords a new paradigm for understanding cancer biology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4249766/" 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/PMC4249766/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Bing -- Wang, Jing -- Wang, Xiaojing -- Zhu, Jing -- Liu, Qi -- Shi, Zhiao -- Chambers, Matthew C -- Zimmerman, Lisa J -- Shaddox, Kent F -- Kim, Sangtae -- Davies, Sherri R -- Wang, Sean -- Wang, Pei -- Kinsinger, Christopher R -- Rivers, Robert C -- Rodriguez, Henry -- Townsend, R Reid -- Ellis, Matthew J C -- Carr, Steven A -- Tabb, David L -- Coffey, Robert J -- Slebos, Robbert J C -- Liebler, Daniel C -- NCI CPTAC -- GM088822/GM/NIGMS NIH HHS/ -- P30 CA068485/CA/NCI NIH HHS/ -- P30 DK058404/DK/NIDDK NIH HHS/ -- P30CA068485/CA/NCI NIH HHS/ -- P50 CA095103/CA/NCI NIH HHS/ -- P50CA095103/CA/NCI NIH HHS/ -- R01 GM088822/GM/NIGMS NIH HHS/ -- U24 CA159988/CA/NCI NIH HHS/ -- U24 CA160019/CA/NCI NIH HHS/ -- U24 CA160034/CA/NCI NIH HHS/ -- U24 CA160035/CA/NCI NIH HHS/ -- U24CA159988/CA/NCI NIH HHS/ -- U24CA160034/CA/NCI NIH HHS/ -- U24CA160035/CA/NCI NIH HHS/ -- U54 HG003079/HG/NHGRI NIH HHS/ -- UL1 TR000448/TR/NCATS NIH HHS/ -- England -- Nature. 2014 Sep 18;513(7518):382-7. doi: 10.1038/nature13438. Epub 2014 Jul 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Biomedical Informatics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA [2] Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA. ; Department of Biomedical Informatics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA. ; 1] Advanced Computing Center for Research and Education, Vanderbilt University, Nashville, Tennessee 37232, USA [2] Department of Electrical Engineering and Computer Science, Vanderbilt University, Tennessee 37232, USA. ; 1] Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA [2] Jim Ayers Institute for Precancer Detection and Diagnosis, Vanderbilt-Ingram Cancer Center, Nashville, Tennessee 37232, USA. ; Jim Ayers Institute for Precancer Detection and Diagnosis, Vanderbilt-Ingram Cancer Center, Nashville, Tennessee 37232, USA. ; Directorate of Fundamental and Computational Sciences, Pacific Northwest National Laboratory, Richland, Washington 99352, USA. ; Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA. ; Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, M2-B500, Seattle, Washington 98109, USA. ; Department of Genetics and Genomic Sciences, Icahn Institute of Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Box 1498, New York, New York 10029, USA. ; Office of Cancer Clinical Proteomics Research, National Cancer Institute, Bethesda, Maryland 20892, USA. ; Broad Institute of MIT and Harvard, Cambridge, Maryland 02142, USA. ; Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA. ; 1] Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA [2] Jim Ayers Institute for Precancer Detection and Diagnosis, Vanderbilt-Ingram Cancer Center, Nashville, Tennessee 37232, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25043054" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosomes, Human, Pair 20/genetics ; Colonic Neoplasms/*genetics/*metabolism ; CpG Islands/genetics ; DNA Copy Number Variations/genetics ; DNA Methylation ; *Genomics ; Hepatocyte Nuclear Factor 4/genetics ; Humans ; Microsatellite Repeats/genetics ; Mitochondrial Membrane Transport Proteins/genetics ; Mutation, Missense/genetics ; Neoplasm Proteins/analysis/genetics/metabolism ; Point Mutation/genetics ; Proteome/analysis/genetics/*metabolism ; Proteomics ; Proto-Oncogene Proteins pp60(c-src)/genetics ; RNA, Messenger/analysis/genetics/metabolism ; RNA, Neoplasm/analysis/genetics/metabolism ; Rectal Neoplasms/*genetics/*metabolism ; Transcriptome/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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