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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, U.K. and Cambridge, USA : Blackwell Science Ltd
    Histopathology 33 (1998), S. 0 
    ISSN: 1365-2559
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: There have been several cell kinetic studies of thymoma, but the effectiveness of using Ki67 antibody as a tool to measure proliferative activity in this tumour was rarely evaluated. We carried out an immunohistochemical study using this antibody to assess the clinicopathological correlation and the prognostic significance of this technique.〈section xml:id="abs1-2"〉〈title type="main"〉Methods and resultsNinety-one cases of thymoma were collected. Double immunostaining with Ki67 and cytokeratin KL-1 antibodies was performed on paraffin sections. Ki67 labelling index (LI) was expressed as a percentage of Ki67 immunopositive nuclei by counting at least 1000 epithelial cells. The LIs were correlated with stages, histological subtypes based on both Lattes–Bernatz and Müller–Hermelink–Kirchner classifications, and length of survival. There were statistically significant differences of LIs between stage I and stage III and between stage I and stage IV tumours. Histologically, statistically significant differences were identified between predominantly epithelial thymoma and every other subtype of the Lattes–Bernatz classification and between well-differentiated thymic carcinoma and medullary or mixed thymomas of the Müller–Hermelink–Kirchner classification. Regarding the prognostic implication of Ki67 LI, although there appeared a trend that patients with tumours of higher LIs had slightly worse survival, the difference was not statistically significant in both univariate and multivariate survival analyses.〈section xml:id="abs1-3"〉〈title type="main"〉ConclusionsWe have demonstrated the proliferative potential in thymoma is associated with stage and histology. However, its clinical usefulness is limited on account of the overlap of LIs and lack of prognostic significance.
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  • 2
    ISSN: 0003-2670
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    Publication Date: 2012-03-20
    Description: The conversion of chemical energy into mechanical force by AAA+ (ATPases associated with diverse cellular activities) ATPases is integral to cellular processes, including DNA replication, protein unfolding, cargo transport and membrane fusion. The AAA+ ATPase motor cytoplasmic dynein regulates ciliary trafficking, mitotic spindle formation and organelle transport, and dissecting its precise functions has been challenging because of its rapid timescale of action and the lack of cell-permeable, chemical modulators. Here we describe the discovery of ciliobrevins, the first specific small-molecule antagonists of cytoplasmic dynein. Ciliobrevins perturb protein trafficking within the primary cilium, leading to their malformation and Hedgehog signalling blockade. Ciliobrevins also prevent spindle pole focusing, kinetochore-microtubule attachment, melanosome aggregation and peroxisome motility in cultured cells. We further demonstrate the ability of ciliobrevins to block dynein-dependent microtubule gliding and ATPase activity in vitro. Ciliobrevins therefore will be useful reagents for studying cellular processes that require this microtubule motor and may guide the development of additional AAA+ ATPase superfamily inhibitors.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321072/" 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/PMC3321072/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Firestone, Ari J -- Weinger, Joshua S -- Maldonado, Maria -- Barlan, Kari -- Langston, Lance D -- O'Donnell, Michael -- Gelfand, Vladimir I -- Kapoor, Tarun M -- Chen, James K -- R01 CA136574/CA/NCI NIH HHS/ -- R01 GM038839/GM/NIGMS NIH HHS/ -- R01 GM052111/GM/NIGMS NIH HHS/ -- R01 GM052111-14/GM/NIGMS NIH HHS/ -- R01 GM065933/GM/NIGMS NIH HHS/ -- R01 GM52111/GM/NIGMS NIH HHS/ -- R01 GM65933/GM/NIGMS NIH HHS/ -- R01 GM71772/GM/NIGMS NIH HHS/ -- England -- Nature. 2012 Mar 18;484(7392):125-9. doi: 10.1038/nature10936.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22425997" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Cilia/drug effects/metabolism/pathology ; Cytoplasm/*enzymology ; Cytoplasmic Dyneins/*antagonists & inhibitors/metabolism ; Enzyme Inhibitors/*chemistry/*pharmacology ; Hedgehog Proteins/metabolism ; Kinetochores/drug effects/metabolism ; Kruppel-Like Transcription Factors/metabolism ; Melanosomes/drug effects/metabolism ; Mice ; Microtubules/drug effects/metabolism ; Molecular Weight ; Movement/drug effects ; NIH 3T3 Cells ; Peroxisomes/drug effects/physiology ; Protein Transport/drug effects ; Quinazolinones/*chemistry/*pharmacology ; Signal Transduction/drug effects ; Spindle Apparatus/drug effects/metabolism/pathology
    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: 2012-06-23
    Description: Sirtuin proteins regulate diverse cellular pathways that influence genomic stability, metabolism and ageing. SIRT7 is a mammalian sirtuin whose biochemical activity, molecular targets and physiological functions have been unclear. Here we show that SIRT7 is an NAD(+)-dependent H3K18Ac (acetylated lysine 18 of histone H3) deacetylase that stabilizes the transformed state of cancer cells. Genome-wide binding studies reveal that SIRT7 binds to promoters of a specific set of gene targets, where it deacetylates H3K18Ac and promotes transcriptional repression. The spectrum of SIRT7 target genes is defined in part by its interaction with the cancer-associated E26 transformed specific (ETS) transcription factor ELK4, and comprises numerous genes with links to tumour suppression. Notably, selective hypoacetylation of H3K18Ac has been linked to oncogenic transformation, and in patients is associated with aggressive tumour phenotypes and poor prognosis. We find that deacetylation of H3K18Ac by SIRT7 is necessary for maintaining essential features of human cancer cells, including anchorage-independent growth and escape from contact inhibition. Moreover, SIRT7 is necessary for a global hypoacetylation of H3K18Ac associated with cellular transformation by the viral oncoprotein E1A. Finally, SIRT7 depletion markedly reduces the tumorigenicity of human cancer cell xenografts in mice. Together, our work establishes SIRT7 as a highly selective H3K18Ac deacetylase and demonstrates a pivotal role for SIRT7 in chromatin regulation, cellular transformation programs and tumour formation in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3412143/" 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/PMC3412143/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barber, Matthew F -- Michishita-Kioi, Eriko -- Xi, Yuanxin -- Tasselli, Luisa -- Kioi, Mitomu -- Moqtaderi, Zarmik -- Tennen, Ruth I -- Paredes, Silvana -- Young, Nicolas L -- Chen, Kaifu -- Struhl, Kevin -- Garcia, Benjamin A -- Gozani, Or -- Li, Wei -- Chua, Katrin F -- 1018438-142/PHS HHS/ -- 3T32DK007217-36S1/DK/NIDDK NIH HHS/ -- DP2OD007447/OD/NIH HHS/ -- GM 30186/GM/NIGMS NIH HHS/ -- HG 4558/HG/NHGRI NIH HHS/ -- K08 AG028961/AG/NIA NIH HHS/ -- R01 AG028867/AG/NIA NIH HHS/ -- R01 GM030186/GM/NIGMS NIH HHS/ -- R01 GM079641/GM/NIGMS NIH HHS/ -- T32 CA009302/CA/NCI NIH HHS/ -- U01 DA025956/DA/NIDA NIH HHS/ -- U01 DA025956-01/DA/NIDA NIH HHS/ -- U01DA025956/DA/NIDA NIH HHS/ -- England -- Nature. 2012 Jul 5;487(7405):114-8. doi: 10.1038/nature11043.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Stanford University, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22722849" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Adenovirus E1A Proteins/genetics/metabolism ; Animals ; Base Sequence ; Binding Sites ; Cell Line, Tumor ; Cell Proliferation ; Cell Transformation, Neoplastic/genetics/*metabolism/pathology ; Chromatin/metabolism ; Contact Inhibition ; Disease Progression ; Histone Deacetylases/*metabolism ; Histones/*metabolism ; Humans ; Lysine/*metabolism ; Mice ; Neoplasm Transplantation ; Nucleotide Motifs ; Phenotype ; Promoter Regions, Genetic ; Repressor Proteins/metabolism ; Sirtuins/deficiency/genetics/*metabolism ; Transcription, Genetic ; Transplantation, Heterologous ; ets-Domain Protein Elk-4/metabolism
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2013-03-30
    Description: Compared with atoms, molecules have a rich internal structure that offers many opportunities for technological and scientific advancement. The study of this structure could yield critical insights into quantum chemistry, new methods for manipulating quantum information, and improved tests of discrete symmetry violation and fundamental constant variation. Harnessing this potential typically requires the preparation of cold molecules in their quantum rovibrational ground state. However, the molecular internal structure severely complicates efforts to produce such samples. Removal of energy stored in long-lived vibrational levels is particularly problematic because optical transitions between vibrational levels are not governed by strict selection rules, which makes laser cooling difficult. Additionally, traditional collisional, or sympathetic, cooling methods are inefficient at quenching molecular vibrational motion. Here we experimentally demonstrate that the vibrational motion of trapped BaCl(+) molecules is quenched by collisions with ultracold calcium atoms at a rate comparable to the classical scattering, or Langevin, rate. This is over four orders of magnitude more efficient than traditional sympathetic cooling schemes. The high cooling rate, a consequence of a strong interaction potential (due to the high polarizability of calcium), along with the low collision energies involved, leads to molecular samples with a vibrational ground-state occupancy of at least 90 per cent. Our demonstration uses a novel thermometry technique that relies on relative photodissociation yields. Although the decrease in vibrational temperature is modest, with straightforward improvements it should be possible to produce molecular samples with a vibrational ground-state occupancy greater than 99 per cent in less than 100 milliseconds. Because sympathetic cooling of molecular rotational motion is much more efficient than vibrational cooling in traditional systems, we expect that the method also allows efficient cooling of the rotational motion of the molecules. Moreover, the technique should work for many different combinations of ultracold atoms and molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rellergert, Wade G -- Sullivan, Scott T -- Schowalter, Steven J -- Kotochigova, Svetlana -- Chen, Kuang -- Hudson, Eric R -- England -- Nature. 2013 Mar 28;495(7442):490-4. doi: 10.1038/nature11937.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physics and Astronomy, University of California, Los Angeles, California 90095, USA. wgr6@ucla.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23538830" 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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  • 6
    Publication Date: 2015-10-04
    Description: Structural variants are implicated in numerous diseases and make up the majority of varying nucleotides among human genomes. Here we describe an integrated set of eight structural variant classes comprising both balanced and unbalanced variants, which we constructed using short-read DNA sequencing data and statistically phased onto haplotype blocks in 26 human populations. Analysing this set, we identify numerous gene-intersecting structural variants exhibiting population stratification and describe naturally occurring homozygous gene knockouts that suggest the dispensability of a variety of human genes. We demonstrate that structural variants are enriched on haplotypes identified by genome-wide association studies and exhibit enrichment for expression quantitative trait loci. Additionally, we uncover appreciable levels of structural variant complexity at different scales, including genic loci subject to clusters of repeated rearrangement and complex structural variants with multiple breakpoints likely to have formed through individual mutational events. Our catalogue will enhance future studies into structural variant demography, functional impact and disease association.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4617611/" 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/PMC4617611/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sudmant, Peter H -- Rausch, Tobias -- Gardner, Eugene J -- Handsaker, Robert E -- Abyzov, Alexej -- Huddleston, John -- Zhang, Yan -- Ye, Kai -- Jun, Goo -- Hsi-Yang Fritz, Markus -- Konkel, Miriam K -- Malhotra, Ankit -- Stutz, Adrian M -- Shi, Xinghua -- Paolo Casale, Francesco -- Chen, Jieming -- Hormozdiari, Fereydoun -- Dayama, Gargi -- Chen, Ken -- Malig, Maika -- Chaisson, Mark J P -- Walter, Klaudia -- Meiers, Sascha -- Kashin, Seva -- Garrison, Erik -- Auton, Adam -- Lam, Hugo Y K -- Jasmine Mu, Xinmeng -- Alkan, Can -- Antaki, Danny -- Bae, Taejeong -- Cerveira, Eliza -- Chines, Peter -- Chong, Zechen -- Clarke, Laura -- Dal, Elif -- Ding, Li -- Emery, Sarah -- Fan, Xian -- Gujral, Madhusudan -- Kahveci, Fatma -- Kidd, Jeffrey M -- Kong, Yu -- Lameijer, Eric-Wubbo -- McCarthy, Shane -- Flicek, Paul -- Gibbs, Richard A -- Marth, Gabor -- Mason, Christopher E -- Menelaou, Androniki -- Muzny, Donna M -- Nelson, Bradley J -- Noor, Amina -- Parrish, Nicholas F -- Pendleton, Matthew -- Quitadamo, Andrew -- Raeder, Benjamin -- Schadt, Eric E -- Romanovitch, Mallory -- Schlattl, Andreas -- Sebra, Robert -- Shabalin, Andrey A -- Untergasser, Andreas -- Walker, Jerilyn A -- Wang, Min -- Yu, Fuli -- Zhang, Chengsheng -- Zhang, Jing -- Zheng-Bradley, Xiangqun -- Zhou, Wanding -- Zichner, Thomas -- Sebat, Jonathan -- Batzer, Mark A -- McCarroll, Steven A -- 1000 Genomes Project Consortium -- Mills, Ryan E -- Gerstein, Mark B -- Bashir, Ali -- Stegle, Oliver -- Devine, Scott E -- Lee, Charles -- Eichler, Evan E -- Korbel, Jan O -- P01HG007497/HG/NHGRI NIH HHS/ -- R01 CA166661/CA/NCI NIH HHS/ -- R01 HG002385/HG/NHGRI NIH HHS/ -- R01 HG002898/HG/NHGRI NIH HHS/ -- R01CA166661/CA/NCI NIH HHS/ -- R01GM59290/GM/NIGMS NIH HHS/ -- R01HG002898/HG/NHGRI NIH HHS/ -- R01HG007068/HG/NHGRI NIH HHS/ -- RR029676-01/RR/NCRR NIH HHS/ -- RR19895/RR/NCRR NIH HHS/ -- T32 GM008666/GM/NIGMS NIH HHS/ -- U41 HG007497/HG/NHGRI NIH HHS/ -- U41HG007497/HG/NHGRI NIH HHS/ -- WT085532/Z/08/Z/Wellcome Trust/United Kingdom -- WT104947/Z/14/Z/Wellcome Trust/United Kingdom -- England -- Nature. 2015 Oct 1;526(7571):75-81. doi: 10.1038/nature15394.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genome Sciences, University of Washington, 3720 15th Avenue NE, Seattle, Washington 98195-5065, USA. ; European Molecular Biology Laboratory (EMBL), Genome Biology Unit, Meyerhofstrasse 1, 69117 Heidelberg, Germany. ; Institute for Genome Sciences, University of Maryland School of Medicine, 801 W Baltimore Street, Baltimore, Maryland 21201, USA. ; Department of Genetics, Harvard Medical School, Boston, 25 Shattuck Street, Boston, Massachusetts 02115, USA. ; Program in Medical and Population Genetics, Broad Institute of MIT and Harvard, 415 Main Street, Cambridge, Massachusetts 02142, USA. ; Department of Health Sciences Research, Center for Individualized Medicine, Mayo Clinic, 200 First Street SW, Rochester, Minnesota 55905, USA. ; Howard Hughes Medical Institute, University of Washington, Seattle, Washington 98195, USA. ; Program in Computational Biology and Bioinformatics, Yale University, BASS 432 &437, 266 Whitney Avenue, New Haven, Connecticut 06520, USA. ; Department of Molecular Biophysics and Biochemistry, School of Medicine, Yale University, 266 Whitney Avenue, New Haven, Connecticut 06520, USA. ; The Genome Institute, Washington University School of Medicine, 4444 Forest Park Avenue, St Louis, Missouri 63108, USA. ; Department of Genetics, Washington University in St Louis, 4444 Forest Park Avenue, St Louis, Missouri 63108, USA. ; Department of Biostatistics and Center for Statistical Genetics, University of Michigan, 1415 Washington Heights, Ann Arbor, Michigan 48109, USA. ; Human Genetics Center, School of Public Health, The University of Texas Health Science Center at Houston, 1200 Pressler St., Houston, Texas 77030, USA. ; Department of Biological Sciences, Louisiana State University, 202 Life Sciences Building, Baton Rouge, Louisiana 70803, USA. ; The Jackson Laboratory for Genomic Medicine, 10 Discovery 263 Farmington Avenue, Farmington, Connecticut 06030, USA. ; Department of Bioinformatics and Genomics, University of North Carolina at Charlotte, 9201 University City Blvd., Charlotte, North Carolina 28223, USA. ; European Molecular Biology Laboratory, European Bioinformatics Institute (EMBL-EBI), Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SD, UK. ; Integrated Graduate Program in Physical and Engineering Biology, Yale University, New Haven, Connecticut 06520, USA. ; Department of Computational Medicine &Bioinformatics, University of Michigan, 500 S. State Street, Ann Arbor, Michigan 48109, USA. ; The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA. ; The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK. ; Department of Biology, Boston College, 355 Higgins Hall, 140 Commonwealth Avenue, Chestnut Hill, Massachusetts 02467, USA. ; Department of Genetics, Albert Einstein College of Medicine, 1301 Morris Park Avenue, Bronx, New York 10461, USA. ; Bina Technologies, Roche Sequencing, 555 Twin Dolphin Drive, Redwood City, California 94065, USA. ; Cancer Program, Broad Institute of MIT and Harvard, 415 Main Street, Cambridge, Massachusetts 02142, USA. ; Department of Computer Engineering, Bilkent University, 06800 Ankara, Turkey. ; University of California San Diego (UCSD), 9500 Gilman Drive, La Jolla, California 92093, USA. ; National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland 20892 USA. ; Department of Medicine, Washington University in St Louis, 4444 Forest Park Avenue, St Louis, Missouri 63108, USA. ; Siteman Cancer Center, 660 South Euclid Avenue, St Louis, Missouri 63110, USA. ; Department of Human Genetics, University of Michigan, 1241 Catherine Street, Ann Arbor, Michigan 48109, USA. ; Molecular Epidemiology, Leiden University Medical Center, Leiden 2300RA, The Netherlands. ; Baylor College of Medicine, 1 Baylor Plaza, Houston, Texas 77030, USA. ; The Department of Physiology and Biophysics and the HRH Prince Alwaleed Bin Talal Bin Abdulaziz Alsaud Institute for Computational Biomedicine, 1305 York Avenue, Weill Cornell Medical College, New York, New York 10065, USA. ; The Feil Family Brain and Mind Research Institute, 413 East 69th St, Weill Cornell Medical College, New York, New York 10065, USA. ; University of Oxford, 1 South Parks Road, Oxford OX3 9DS, UK. ; Department of Medical Genetics, Center for Molecular Medicine, University Medical Center Utrecht, Utrecht, 3584 CG, The Netherlands. ; Department of Genetics and Genomic Sciences, Icahn School of Medicine, New York School of Natural Sciences, 1428 Madison Avenue, New York, New York 10029, USA. ; Institute for Virus Research, Kyoto University, 53 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan. ; Center for Biomarker Research and Precision Medicine, Virginia Commonwealth University, 1112 East Clay Street, McGuire Hall, Richmond, Virginia 23298-0581, USA. ; Zentrum fur Molekulare Biologie, University of Heidelberg, Im Neuenheimer Feld 282, 69120 Heidelberg, Germany. ; Department of Computer Science, Yale University, 51 Prospect Street, New Haven, Connecticut 06511, USA. ; Department of Graduate Studies - Life Sciences, Ewha Womans University, Ewhayeodae-gil, Seodaemun-gu, Seoul 120-750, South Korea.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26432246" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Genetic Predisposition to Disease ; Genetic Variation/*genetics ; Genetics, Medical ; Genetics, Population ; Genome, Human/*genetics ; Genome-Wide Association Study ; Genomics ; Genotype ; Haplotypes/genetics ; Homozygote ; Humans ; Molecular Sequence Data ; Mutation Rate ; *Physical Chromosome Mapping ; Polymorphism, Single Nucleotide/genetics ; Quantitative Trait Loci/genetics ; Sequence Analysis, DNA ; Sequence Deletion/genetics
    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: 2016-04-21
    Description: New methods and strategies for the direct functionalization of C-H bonds are beginning to reshape the field of retrosynthetic analysis, affecting the synthesis of natural products, medicines and materials. The oxidation of allylic systems has played a prominent role in this context as possibly the most widely applied C-H functionalization, owing to the utility of enones and allylic alcohols as versatile intermediates, and their prevalence in natural and unnatural materials. Allylic oxidations have featured in hundreds of syntheses, including some natural product syntheses regarded as "classics". Despite many attempts to improve the efficiency and practicality of this transformation, the majority of conditions still use highly toxic reagents (based around toxic elements such as chromium or selenium) or expensive catalysts (such as palladium or rhodium). These requirements are problematic in industrial settings; currently, no scalable and sustainable solution to allylic oxidation exists. This oxidation strategy is therefore rarely used for large-scale synthetic applications, limiting the adoption of this retrosynthetic strategy by industrial scientists. Here we describe an electrochemical C-H oxidation strategy that exhibits broad substrate scope, operational simplicity and high chemoselectivity. It uses inexpensive and readily available materials, and represents a scalable allylic C-H oxidation (demonstrated on 100 grams), enabling the adoption of this C-H oxidation strategy in large-scale industrial settings without substantial environmental impact.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4860034/" 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/PMC4860034/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Horn, Evan J -- Rosen, Brandon R -- Chen, Yong -- Tang, Jiaze -- Chen, Ke -- Eastgate, Martin D -- Baran, Phil S -- GM-097444/GM/NIGMS NIH HHS/ -- R01 GM073949/GM/NIGMS NIH HHS/ -- R01 GM097444/GM/NIGMS NIH HHS/ -- England -- Nature. 2016 May 5;533(7601):77-81. doi: 10.1038/nature17431. Epub 2016 Apr 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, The Scripps Research Institute, La Jolla, California 92037, USA. ; Asymchem Life Science (Tianjin), Tianjin Economic-Technological Development Zone, Tianjin 300457, China. ; Chemical Development, Bristol-Myers Squibb, New Brunswick, New Jersey 08903, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27096371" target="_blank"〉PubMed〈/a〉
    Keywords: Allyl Compounds/chemistry ; Biological Products/chemical synthesis/chemistry ; Carbon/*chemistry ; *Chemistry Techniques, Synthetic ; Electrochemistry ; Green Chemistry Technology ; Hydrogen/*chemistry ; Oxidants/*chemistry ; Oxidation-Reduction ; Substrate Specificity
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2018-12-04
    Description: Gastrointestinal stromal tumors (GIST) are the most prevalent mesenchymal tumors of the digestive tract. To investigate the association of imatinib mesylate plasma concentration with adverse drug reactions (ADRs) and influences of genetic polymorphisms on ADRs in GIST patients taking imatinib, a cohort of GIST patients consecutively treated with imatinib were included in the observational study. Clinical, pathologic and genotype information was recorded at enrollment and blood samples were collected at time as design. The plasma concentration of the imatinib was detected by LC-MS/MS. A questionnaire was used to evaluate the ADRs at each visit. SNPs in 13 genes were analyzed for a possible association with ADRs. The mean plasma trough concentration of 129 patients taking imatinib was 1.45 ± 0.79 μg/ml, average peak concentration was 2.63 ± 1.07 μg/ml. The imatinib concentration in patients treated with 600 mg/day was significantly higher than other dosage groups ( P 〈 0.05). The ADRs were mostly mild. Edema, vomiting, and fatigue were significantly correlated with imatinib concentration ( P 〈 0.05). Mutations of IL13 rs1800925 and CXCL14 rs7716492 were related with the incidence of leukopenia and rash in our research, separately ( P 〈 0.05). We confirmed that with the increase of imatinib concentration, the incidence of edema, vomiting, and fatigue rises as well. Mutations of IL13 rs1800925 and CXCL14 rs7716492 may be the promising biomarkers to predict the ADRs of imatinib. The results of the study are of guiding significance for the use of imatinib in patients with GIST.
    Print ISSN: 1535-7163
    Electronic ISSN: 1538-8514
    Topics: Medicine
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  • 9
    Publication Date: 2018-12-11
    Description: Cryptosporidium is an important opportunistic intestinal pathogen for immunocompromised individuals and a common cause of diarrhea in young children in developing countries. Gastrointestinal epithelial cells play a central role in activating and orchestrating host immune responses against Cryptosporidium infection, but underlying molecular mechanisms are not fully understood. We report in this paper that C. parvum infection causes significant alterations in long noncoding RNA (lncRNA) expression profiles in murine intestinal epithelial cells. Transcription of a panel of lncRNA genes, including NR_045064 , in infected cells is controlled by the NF-B signaling. Functionally, inhibition of NR_045064 induction increases parasite burden in intestinal epithelial cells. Induction of NR_045064 enhances the transcription of selected defense genes in host cells following C. parvum infection. Epigenetic histone modifications are involved in NR_045064-mediated transcription of associated defense genes in infected host cells. Moreover, the p300/MLL-associated chromatin remodeling is involved in NR_045064-mediated transcription of associated defense genes in intestinal epithelial cells following C. parvum infection. Expression of NR_045064 and associated genes is also identified in intestinal epithelium in C57BL/6J mice following phosphorothioate oligodeoxynucleotide or LPS stimulation. Our data demonstrate that lncRNAs, such as NR_045064, play a role in regulating epithelial defense against microbial infection.
    Print ISSN: 0022-1767
    Electronic ISSN: 1550-6606
    Topics: Medicine
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  • 10
    Publication Date: 2011-02-05
    Description: Genomic structural variants (SVs) are abundant in humans, differing from other forms of variation in extent, origin and functional impact. Despite progress in SV characterization, the nucleotide resolution architecture of most SVs remains unknown. We constructed a map of unbalanced SVs (that is, copy number variants) based on whole genome DNA sequencing data from 185 human genomes, integrating evidence from complementary SV discovery approaches with extensive experimental validations. Our map encompassed 22,025 deletions and 6,000 additional SVs, including insertions and tandem duplications. Most SVs (53%) were mapped to nucleotide resolution, which facilitated analysing their origin and functional impact. We examined numerous whole and partial gene deletions with a genotyping approach and observed a depletion of gene disruptions amongst high frequency deletions. Furthermore, we observed differences in the size spectra of SVs originating from distinct formation mechanisms, and constructed a map of SV hotspots formed by common mechanisms. Our analytical framework and SV map serves as a resource for sequencing-based association studies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3077050/" 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/PMC3077050/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mills, Ryan E -- Walter, Klaudia -- Stewart, Chip -- Handsaker, Robert E -- Chen, Ken -- Alkan, Can -- Abyzov, Alexej -- Yoon, Seungtai Chris -- Ye, Kai -- Cheetham, R Keira -- Chinwalla, Asif -- Conrad, Donald F -- Fu, Yutao -- Grubert, Fabian -- Hajirasouliha, Iman -- Hormozdiari, Fereydoun -- Iakoucheva, Lilia M -- Iqbal, Zamin -- Kang, Shuli -- Kidd, Jeffrey M -- Konkel, Miriam K -- Korn, Joshua -- Khurana, Ekta -- Kural, Deniz -- Lam, Hugo Y K -- Leng, Jing -- Li, Ruiqiang -- Li, Yingrui -- Lin, Chang-Yun -- Luo, Ruibang -- Mu, Xinmeng Jasmine -- Nemesh, James -- Peckham, Heather E -- Rausch, Tobias -- Scally, Aylwyn -- Shi, Xinghua -- Stromberg, Michael P -- Stutz, Adrian M -- Urban, Alexander Eckehart -- Walker, Jerilyn A -- Wu, Jiantao -- Zhang, Yujun -- Zhang, Zhengdong D -- Batzer, Mark A -- Ding, Li -- Marth, Gabor T -- McVean, Gil -- Sebat, Jonathan -- Snyder, Michael -- Wang, Jun -- Ye, Kenny -- Eichler, Evan E -- Gerstein, Mark B -- Hurles, Matthew E -- Lee, Charles -- McCarroll, Steven A -- Korbel, Jan O -- 1000 Genomes Project -- 062023/Wellcome Trust/United Kingdom -- 077009/Wellcome Trust/United Kingdom -- 077014/Wellcome Trust/United Kingdom -- 077192/Wellcome Trust/United Kingdom -- 085532/Wellcome Trust/United Kingdom -- G0701805/Medical Research Council/United Kingdom -- G1000758/Medical Research Council/United Kingdom -- P01 HG004120/HG/NHGRI NIH HHS/ -- P41 HG004221/HG/NHGRI NIH HHS/ -- P41 HG004221-01/HG/NHGRI NIH HHS/ -- P41 HG004221-02/HG/NHGRI NIH HHS/ -- P41 HG004221-03/HG/NHGRI NIH HHS/ -- P41 HG004221-03S1/HG/NHGRI NIH HHS/ -- P41 HG004221-03S2/HG/NHGRI NIH HHS/ -- P41 HG004221-03S3/HG/NHGRI NIH HHS/ -- R01 GM059290/GM/NIGMS NIH HHS/ -- R01 GM081533/GM/NIGMS NIH HHS/ -- R01 GM081533-01A1/GM/NIGMS NIH HHS/ -- R01 GM081533-02/GM/NIGMS NIH HHS/ -- R01 GM081533-03/GM/NIGMS NIH HHS/ -- R01 GM081533-04/GM/NIGMS NIH HHS/ -- R01 GM59290/GM/NIGMS NIH HHS/ -- R01 HG004719/HG/NHGRI NIH HHS/ -- R01 HG004719-01/HG/NHGRI NIH HHS/ -- R01 HG004719-02/HG/NHGRI NIH HHS/ -- R01 HG004719-02S1/HG/NHGRI NIH HHS/ -- R01 HG004719-03/HG/NHGRI NIH HHS/ -- R01 HG004719-04/HG/NHGRI NIH HHS/ -- R01 MH091350/MH/NIMH NIH HHS/ -- RC2 HG005552/HG/NHGRI NIH HHS/ -- RC2 HG005552-01/HG/NHGRI NIH HHS/ -- RC2 HG005552-02/HG/NHGRI NIH HHS/ -- U01 HG005209/HG/NHGRI NIH HHS/ -- U01 HG005209-01/HG/NHGRI NIH HHS/ -- U01 HG005209-02/HG/NHGRI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Feb 3;470(7332):59-65. doi: 10.1038/nature09708.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21293372" target="_blank"〉PubMed〈/a〉
    Keywords: DNA Copy Number Variations/*genetics ; Gene Duplication/genetics ; Genetic Predisposition to Disease/genetics ; *Genetics, Population ; Genome, Human/*genetics ; *Genomics ; Genotype ; Humans ; Mutagenesis, Insertional/genetics ; Reproducibility of Results ; Sequence Analysis, DNA ; Sequence Deletion/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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