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  • American Society of Hematology  (9)
  • American Geophysical Union  (8)
  • American Chemical Society (ACS)  (4)
  • Public Library of Science  (4)
  • Nature Publishing Group (NPG)  (3)
  • Geological Society London
  • 2010-2014  (27)
  • 2000-2004  (1)
  • 1
    Publication Date: 2012-04-13
    Description: Energy & Fuels DOI: 10.1021/ef300515q
    Print ISSN: 0887-0624
    Electronic ISSN: 1520-5029
    Topics: Chemistry and Pharmacology , Energy, Environment Protection, Nuclear Power Engineering , Process Engineering, Biotechnology, Nutrition Technology
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  • 2
    Publication Date: 2012-03-03
    Description: Energy & Fuels DOI: 10.1021/ef201853k
    Print ISSN: 0887-0624
    Electronic ISSN: 1520-5029
    Topics: Chemistry and Pharmacology , Energy, Environment Protection, Nuclear Power Engineering , Process Engineering, Biotechnology, Nutrition Technology
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  • 3
    Publication Date: 2014-01-15
    Description: Energy & Fuels DOI: 10.1021/ef402057w
    Print ISSN: 0887-0624
    Electronic ISSN: 1520-5029
    Topics: Chemistry and Pharmacology , Energy, Environment Protection, Nuclear Power Engineering , Process Engineering, Biotechnology, Nutrition Technology
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  • 4
    Publication Date: 2012-01-18
    Description: Energy & Fuels DOI: 10.1021/ef201551m
    Print ISSN: 0887-0624
    Electronic ISSN: 1520-5029
    Topics: Chemistry and Pharmacology , Energy, Environment Protection, Nuclear Power Engineering , Process Engineering, Biotechnology, Nutrition Technology
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  • 5
    Publication Date: 2010-07-31
    Description: Small (〈200 nucleotide) RNA (sRNA) profiling of human cells using various technologies demonstrates unexpected complexity of sRNAs with hundreds of thousands of sRNA species present. Genetic and in vitro studies show that these RNAs are not merely degradation products of longer transcripts but could indeed have a function. Furthermore, profiling of RNAs, including the sRNAs, can reveal not only novel transcripts, but also make clear predictions about the existence and properties of novel biochemical pathways operating in a cell. For example, sRNA profiling in human cells indicated the existence of an unknown capping mechanism operating on cleaved RNA, a biochemical component of which was later identified. Here we show that human cells contain a novel type of sRNA that has non-genomically encoded 5' poly(U) tails. The presence of these RNAs at the termini of genes, specifically at the very 3' ends of known mRNAs, strongly argues for the presence of a yet uncharacterized endogenous biochemical pathway in cells that can copy RNA. We show that this pathway can operate on multiple genes, with specific enrichment towards transcript-encoding components of the translational machinery. Finally, we show that genes are also flanked by sense, 3' polyadenylated sRNAs that are likely to be capped.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058539/" 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/PMC3058539/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kapranov, Philipp -- Ozsolak, Fatih -- Kim, Sang Woo -- Foissac, Sylvain -- Lipson, Doron -- Hart, Chris -- Roels, Steve -- Borel, Christelle -- Antonarakis, Stylianos E -- Monaghan, A Paula -- John, Bino -- Milos, Patrice M -- GM079756/GM/NIGMS NIH HHS/ -- MH60774/MH/NIMH NIH HHS/ -- R01 GM079756/GM/NIGMS NIH HHS/ -- R01 GM079756-01A1/GM/NIGMS NIH HHS/ -- R01 GM079756-02/GM/NIGMS NIH HHS/ -- R01 GM079756-03/GM/NIGMS NIH HHS/ -- R01 HG005230/HG/NHGRI NIH HHS/ -- England -- Nature. 2010 Jul 29;466(7306):642-6. doi: 10.1038/nature09190.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Helicos BioSciences Corporation, 1 Kendall Sq. Ste B7301 Cambridge, Massachusetts 02139-1671, USA. philippk08@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20671709" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Genes/*genetics ; HeLa Cells ; Humans ; Models, Genetic ; Nucleotides/genetics ; Poly A/genetics/metabolism ; Poly U/genetics/metabolism ; RNA/biosynthesis/*classification/genetics/*metabolism ; RNA, Antisense/classification/genetics/metabolism ; Templates, Genetic
    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: 2011-11-18
    Description: Legumes (Fabaceae or Leguminosae) are unique among cultivated plants for their ability to carry out endosymbiotic nitrogen fixation with rhizobial bacteria, a process that takes place in a specialized structure known as the nodule. Legumes belong to one of the two main groups of eurosids, the Fabidae, which includes most species capable of endosymbiotic nitrogen fixation. Legumes comprise several evolutionary lineages derived from a common ancestor 60 million years ago (Myr ago). Papilionoids are the largest clade, dating nearly to the origin of legumes and containing most cultivated species. Medicago truncatula is a long-established model for the study of legume biology. Here we describe the draft sequence of the M. truncatula euchromatin based on a recently completed BAC assembly supplemented with Illumina shotgun sequence, together capturing approximately 94% of all M. truncatula genes. A whole-genome duplication (WGD) approximately 58 Myr ago had a major role in shaping the M. truncatula genome and thereby contributed to the evolution of endosymbiotic nitrogen fixation. Subsequent to the WGD, the M. truncatula genome experienced higher levels of rearrangement than two other sequenced legumes, Glycine max and Lotus japonicus. M. truncatula is a close relative of alfalfa (Medicago sativa), a widely cultivated crop with limited genomics tools and complex autotetraploid genetics. As such, the M. truncatula genome sequence provides significant opportunities to expand alfalfa's genomic toolbox.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3272368/" 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/PMC3272368/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Young, Nevin D -- Debelle, Frederic -- Oldroyd, Giles E D -- Geurts, Rene -- Cannon, Steven B -- Udvardi, Michael K -- Benedito, Vagner A -- Mayer, Klaus F X -- Gouzy, Jerome -- Schoof, Heiko -- Van de Peer, Yves -- Proost, Sebastian -- Cook, Douglas R -- Meyers, Blake C -- Spannagl, Manuel -- Cheung, Foo -- De Mita, Stephane -- Krishnakumar, Vivek -- Gundlach, Heidrun -- Zhou, Shiguo -- Mudge, Joann -- Bharti, Arvind K -- Murray, Jeremy D -- Naoumkina, Marina A -- Rosen, Benjamin -- Silverstein, Kevin A T -- Tang, Haibao -- Rombauts, Stephane -- Zhao, Patrick X -- Zhou, Peng -- Barbe, Valerie -- Bardou, Philippe -- Bechner, Michael -- Bellec, Arnaud -- Berger, Anne -- Berges, Helene -- Bidwell, Shelby -- Bisseling, Ton -- Choisne, Nathalie -- Couloux, Arnaud -- Denny, Roxanne -- Deshpande, Shweta -- Dai, Xinbin -- Doyle, Jeff J -- Dudez, Anne-Marie -- Farmer, Andrew D -- Fouteau, Stephanie -- Franken, Carolien -- Gibelin, Chrystel -- Gish, John -- Goldstein, Steven -- Gonzalez, Alvaro J -- Green, Pamela J -- Hallab, Asis -- Hartog, Marijke -- Hua, Axin -- Humphray, Sean J -- Jeong, Dong-Hoon -- Jing, Yi -- Jocker, Anika -- Kenton, Steve M -- Kim, Dong-Jin -- Klee, Kathrin -- Lai, Hongshing -- Lang, Chunting -- Lin, Shaoping -- Macmil, Simone L -- Magdelenat, Ghislaine -- Matthews, Lucy -- McCorrison, Jamison -- Monaghan, Erin L -- Mun, Jeong-Hwan -- Najar, Fares Z -- Nicholson, Christine -- Noirot, Celine -- O'Bleness, Majesta -- Paule, Charles R -- Poulain, Julie -- Prion, Florent -- Qin, Baifang -- Qu, Chunmei -- Retzel, Ernest F -- Riddle, Claire -- Sallet, Erika -- Samain, Sylvie -- Samson, Nicolas -- Sanders, Iryna -- Saurat, Olivier -- Scarpelli, Claude -- Schiex, Thomas -- Segurens, Beatrice -- Severin, Andrew J -- Sherrier, D Janine -- Shi, Ruihua -- Sims, Sarah -- Singer, Susan R -- Sinharoy, Senjuti -- Sterck, Lieven -- Viollet, Agnes -- Wang, Bing-Bing -- Wang, Keqin -- Wang, Mingyi -- Wang, Xiaohong -- Warfsmann, Jens -- Weissenbach, Jean -- White, Doug D -- White, Jim D -- Wiley, Graham B -- Wincker, Patrick -- Xing, Yanbo -- Yang, Limei -- Yao, Ziyun -- Ying, Fu -- Zhai, Jixian -- Zhou, Liping -- Zuber, Antoine -- Denarie, Jean -- Dixon, Richard A -- May, Gregory D -- Schwartz, David C -- Rogers, Jane -- Quetier, Francis -- Town, Christopher D -- Roe, Bruce A -- BB/G023832/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBS/B/11524/Biotechnology and Biological Sciences Research Council/United Kingdom -- England -- Nature. 2011 Nov 16;480(7378):520-4. doi: 10.1038/nature10625.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Plant Pathology, University of Minnesota, St Paul, Minnesota 55108, USA. neviny@umn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22089132" target="_blank"〉PubMed〈/a〉
    Keywords: *Biological Evolution ; *Genome, Plant ; Medicago truncatula/*genetics/*microbiology ; Molecular Sequence Data ; Nitrogen Fixation/genetics ; Rhizobium/*physiology ; Soybeans/genetics ; *Symbiosis ; Synteny ; Vitis/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: 2011-07-01
    Description: Rett's syndrome (RTT) is an X-chromosome-linked autism spectrum disorder caused by loss of function of the transcription factor methyl-CpG-binding protein 2 (MeCP2). Although MeCP2 is expressed in most tissues, loss of MeCP2 expression results primarily in neurological symptoms. Earlier studies suggested the idea that RTT is due exclusively to loss of MeCP2 function in neurons. Although defective neurons clearly underlie the aberrant behaviours, we and others showed recently that the loss of MECP2 from glia negatively influences neurons in a non-cell-autonomous fashion. Here we show that in globally MeCP2-deficient mice, re-expression of Mecp2 preferentially in astrocytes significantly improved locomotion and anxiety levels, restored respiratory abnormalities to a normal pattern, and greatly prolonged lifespan compared to globally null mice. Furthermore, restoration of MeCP2 in the mutant astrocytes exerted a non-cell-autonomous positive effect on mutant neurons in vivo, restoring normal dendritic morphology and increasing levels of the excitatory glutamate transporter VGLUT1. Our study shows that glia, like neurons, are integral components of the neuropathology of RTT, and supports the targeting of glia as a strategy for improving the associated symptoms.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3268776/" 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/PMC3268776/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lioy, Daniel T -- Garg, Saurabh K -- Monaghan, Caitlin E -- Raber, Jacob -- Foust, Kevin D -- Kaspar, Brian K -- Hirrlinger, Petra G -- Kirchhoff, Frank -- Bissonnette, John M -- Ballas, Nurit -- Mandel, Gail -- P30 NS061800/NS/NINDS NIH HHS/ -- R01 HD056503/HD/NICHD NIH HHS/ -- R01 HD056503-03/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Jun 29;475(7357):497-500. doi: 10.1038/nature10214.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute, Oregon Health and Science University, Portland, Oregon 97239, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21716289" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anxiety/metabolism ; Astrocytes/metabolism ; Behavior, Animal ; Disease Progression ; Female ; Gene Expression Regulation ; Male ; Methyl-CpG-Binding Protein 2/deficiency/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Motor Activity ; Neuroglia/*metabolism/pathology ; Neurons/metabolism ; Rett Syndrome/*genetics/*metabolism/physiopathology ; Vesicular Glutamate Transport Protein 1/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2011-11-18
    Description: Abstract 1840 Introduction: The IMiD® immunomodulatory drugs lenalidomide (LEN) and pomalidomide (POM) yield high response rates in patients with multiple myeloma (MM). However, the use of IMiDs is associated with neutropenia and thrombocytopenia. It has been shown before that IMiDs down-regulate the transcription factor PU.1/SPI1 leading to maturational arrest of granulocytes with accumulation of immature myeloid precursors and subsequent neutropenia (Blood. 2010; 115:605-614). However, the mechanism underlying the development of thrombocytopenia is unclear. Methods and Results: Here, we investigated the effects of IMiDs on megakaryopoiesis. In megakaryocytic colony formation assays IMiDs significantly (p
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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  • 9
    Publication Date: 2011-11-18
    Description: Abstract 2885 Introduction: Lenalidomide (LEN) is structurally similar to thalidomide and induces high response rates in multiple myeloma (MM). Recently several randomized trials (IFM 2005–02, CALGB 100104) have shown that LEN maintenance given after autologous stem cell transplant (ASCT) in newly diagnosed MM patients resulted in significant prolongation of the progression-free survival. Unfortunately in both trials an increased rate of second cancers with a high concern for the development of MDS/AML was observed. Therefore the goal of this study was to evaluate the bone marrow and corresponding cytogenetic data of patients treated with LEN alone or in combination for early signs of MDS. Methods: To investigate the role of ASCT and alkylators such as bendamustine in combination with LEN in the development of MDS we evaluated We evaluated 110 bone marrow specimens (aspirate smears and biopsy) and the corresponding peripheral blood films and cytogenetic studies, including classical and myeloma-related FISH studies, in 40 MM patients. Review of morphology and cytogenetic studies were performed independently of each other. Results: In the LD alone arm, 5 out of 14 (36%) patients showed mild, non-specific erythropoietic and megakaryopoietic dyspoiesis pre-treatment. Those changes were also found in 6 of 14 (43%) and 4 of 6 (67%) of patients after 6–9 cycles and at further follow up (median follow up 14 months; range 12–28.5), respectively. One patient developed MDS 13 months after start of treatment that was characterized by frank megakaryocytic dysplasia, ring sideroblasts and an abnormal clone 46, XX, t(4;11)(q31;p15)[3]/46, XX[18]. This patient had no karyotypic abnormalities related to MDS prior to treatment. In patients treated with LEN for 4 cycles followed by ASCT (LD+ASCT), 1 of 16 patients (6%) showed mild megakaryocytic dyspoiesis pretreatment. Mild megakaryocytic dyspoiesis was present in 2 of 17 (12%) and 3 of 16 (19%) patients after 4 cycles of LEN and at 3 months post ASCT, respectively. At further follow up in 8 patients (median 12.5 months, range: 10–22), dysmegakaryopoietic signs were no longer detected. Only one patient was found to have a potentially significant clonal cytogenetic abnormality post LD+ASCT that could not be attributed to myeloma – 46, XY, t(2;17)(p23;q11.2)[2]/46, XY[17]. The t(2;17) persisted in the subsequent bone marrow evaluation, but was no longer present in the next evaluation. In relapsed and heavily pretreated MM patients (median 3 prior treatments; range 2–9) receiving BLD, 5 of 7 patients (71%) showed mild non-specific dyspoiesis prior to treatment involving either erythroid, megakaryocytic or granulocytic lineages. Mild non-specific erythropoietic and/or megakaryopoietic dyspoiesis was found in 7 of 8 (88%) and 2 of 4 (50%) of patients at end of treatment and at further follow up (median 14.5 months; range 12–23), respectively. Overall, frank morphologic dysplasia was not detected in any patient except the one (from LD alone) who developed MDS. Conclusion: In summary the careful longitudinal reevaluation of 110 bone marrow samples and corresponding cytogenetic studies treated with LEN alone, in combination with ASCT or bendamustine did not show increased signs of early or overt MDS. It is of note that many MM patients showed mild dyspoiesis even before treatment. The development of MDS in one patient (2.5%) suggests that longer follow up is needed for all patients. To our knowledge this is the first study that re-evaluated longitudinal bone marrow samples for early signs of MDS before clinical symptoms are overt. Disclosures: Lentzsch: Celgene Corp: Consultancy, Research Funding; Onyx: Consultancy; Genzyme: Consultancy; prIME Oncology: Honoraria; Imedex: Honoraria; Clinical Care Options: Honoraria.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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  • 10
    Publication Date: 2014-08-21
    Description: Key PointsEstablishing HSC transplantation and assay methods for the axolotl. Axolotl sites of hematopoiesis are the spleen and liver.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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