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  • 1
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    Flexible conformable hydrophobized surfaces for turbulent flow drag reduction (2015)
    Springer Nature
    Details
    Publication Date: 2015-05-16
    Description: In recent years extensive work has been focused onto using superhydrophobic surfaces for drag reduction applications. Superhydrophobic surfaces retain a gas layer, called a plastron, when submerged underwater in the Cassie-Baxter state with water in contact with the tops of surface roughness features. In this state the plastron allows slip to occur across the surface which results in a drag reduction. In this work we report flexible and relatively large area superhydrophobic surfaces produced using two different methods: Large roughness features were created by electrodeposition on copper meshes; Small roughness features were created by embedding carbon nanoparticles (soot) into Polydimethylsiloxane (PDMS). Both samples were made into cylinders with a diameter under 12 mm. To characterize the samples, scanning electron microscope (SEM) images and confocal microscope images were taken. The confocal microscope images were taken with each sample submerged in water to show the extent of the plastron. The hydrophobized electrodeposited copper mesh cylinders showed drag reductions of up to 32% when comparing the superhydrophobic state with a wetted out state. The soot covered cylinders achieved a 30% drag reduction when comparing the superhydrophobic state to a plain cylinder. These results were obtained for turbulent flows with Reynolds numbers 10,000 to 32,500. Scientific Reports 5 doi: 10.1038/srep10267
    Electronic ISSN: 2045-2322
    Topics: Natural Sciences in General
    Published by Springer Nature
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  • 2
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    Genetics and genomics in wildlife studies: Implications for ecology, evolution, and conservation biology (2012)
    Wiley
    In: BioEssays
    Details
    Publication Date: 2012-03-04
    Print ISSN: 0265-9247
    Electronic ISSN: 1521-1878
    Topics: Biology , Medicine
    Published by Wiley
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  • 3
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    Germline selection shapes human mitochondrial DNA diversity (2019)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2019
    Description: 〈p〉Approximately 2.4% of the human mitochondrial DNA (mtDNA) genome exhibits common homoplasmic genetic variation. We analyzed 12,975 whole-genome sequences to show that 45.1% of individuals from 1526 mother–offspring pairs harbor a mixed population of mtDNA (heteroplasmy), but the propensity for maternal transmission differs across the mitochondrial genome. Over one generation, we observed selection both for and against variants in specific genomic regions; known variants were more likely to be transmitted than previously unknown variants. However, new heteroplasmies were more likely to match the nuclear genetic ancestry as opposed to the ancestry of the mitochondrial genome on which the mutations occurred, validating our findings in 40,325 individuals. Thus, human mtDNA at the population level is shaped by selective forces within the female germ line under nuclear genetic control, which ensures consistency between the two independent genetic lineages.〈/p〉
    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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  • 4
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    Full wave analysis of EM wave propagation over terrain using the Improved Tabulated Interaction Method (2015)
    Wiley
    Details
    Publication Date: 2015-03-12
    Description: This paper proposes extending the forward-scattering based Tabulated Interaction Method (TIM) Brennan and Cullen [1998a] for computing electromagnetic wave propagation over terrain profiles to one incorporating back-scattering. The proposed method uses a common set of basis functions in conjunction with a “matching technique” to produce a linear system with much fewer unknowns than that created using pulse basis functions and therefore provides a very efficient and accurate method. The original TIM Brennan and Cullen [1998a] is shown to be a special case of the proposed method whereby the lower triangular portion of the reduced system is retained and solved. The proposed method is compared with the recently proposed Characteristic Basis Function Method (CBFM) Prakash and Mittra [2003] with which it shares several features. The complexity and numerical analysis demonstrates that the proposed method has an extremely low computational complexity and storage.
    Print ISSN: 0048-6604
    Electronic ISSN: 1944-799X
    Topics: Geosciences , Physics
    Published by Wiley on behalf of American Geophysical Union (AGU).
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  • 5
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    The IRF5-TNPO3 association with systemic lupus erythematosus has two components that other autoimmune disorders variably share (2014)
    Kottyan, L. C., Zoller, E. E., Bene, J., Lu, X., Kelly, J. A., Rupert, A. M., Lessard, C. J., Vaughn, S. E., Marion, M., Weirauch, M. T., Namjou, B., Adler, A., Rasmussen, A., Glenn, S., Montgomery, C. G., Hirschfield, G. M., Xie, G., Coltescu, C., Amos, C., Li, H., Ice, J. A., Nath, S. K., Mariette, X., Bowman, S., for UK Primary Sjogren's Syndrome Registry, Rischmueller, M., Lester, S., Brun, J. G., Goransson, L. G., Harboe, E., Omdal, R., Cunninghame-Graham, D. S., Vyse, T., Miceli-Richard, C., Brennan, M. T., Lessard, J. A., Wahren-Herlenius, M., Kvarnstrom, M., Illei, G. G., Witte, T., Jonsson, R., Eriksson, P., Nordmark, G., Ng, W.-F., for UK Primary Sjogren's Syndrome Registry, Anaya, J.-M., Rhodus, N. L., Segal, B. M., Merrill, J. T., James, J. A., Guthridge, J. M., Hal Scofield, R., Alarcon-Riquelme, M., Bae, S.-C., Boackle, S. A., Criswell, L. A., Gilkeson, G., Kamen, D. L., Jacob, C. O., Kimberly, R., Brown, E., Edberg, J., Alarcon, G. S., Reveille, J. D., Vila, L. M., Petri, M., Ramsey-Goldman, R., Freedman, B. I., Niewold, T., Stevens, A. M., Tsao, B. P., Ying, J., Mayes, M. D., Gorlova, O. Y., Wakeland, W., Radstake, T., Martin, E., Martin, J., Siminovitch, K., Moser Sivils, K. L., Gaffney, P. M., Langefeld, C. D., Harley, J. B., Kaufman, K. M.
    Oxford University Press
    Details
    Publication Date: 2014-12-24
    Description: Exploiting genotyping, DNA sequencing, imputation and trans-ancestral mapping, we used Bayesian and frequentist approaches to model the IRF5 – TNPO3 locus association, now implicated in two immunotherapies and seven autoimmune diseases. Specifically, in systemic lupus erythematosus (SLE), we resolved separate associations in the IRF5 promoter (all ancestries) and with an extended European haplotype. We captured 3230 IRF5 – TNPO3 high-quality, common variants across 5 ethnicities in 8395 SLE cases and 7367 controls. The genetic effect from the IRF5 promoter can be explained by any one of four variants in 5.7 kb ( P -value meta = 6 x 10 –49 ; OR = 1.38–1.97). The second genetic effect spanned an 85.5-kb, 24-variant haplotype that included the genes IRF5 and TNPO3 ( P -values EU = 10 –27 –10 –32 , OR = 1.7–1.81). Many variants at the IRF5 locus with previously assigned biological function are not members of either final credible set of potential causal variants identified herein. In addition to the known biologically functional variants, we demonstrated that the risk allele of rs4728142, a variant in the promoter among the lowest frequentist probability and highest Bayesian posterior probability, was correlated with IRF5 expression and differentially binds the transcription factor ZBTB3. Our analytical strategy provides a novel framework for future studies aimed at dissecting etiological genetic effects. Finally, both SLE elements of the statistical model appear to operate in Sjögren's syndrome and systemic sclerosis whereas only the IRF5–TNPO3 gene-spanning haplotype is associated with primary biliary cirrhosis, demonstrating the nuance of similarity and difference in autoimmune disease risk mechanisms at IRF5 – TNPO3 .
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 6
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    p53 and Pten control neural and glioma stem/progenitor cell renewal and differentiation (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-10-25
    Description: Glioblastoma (GBM) is a highly lethal brain tumour presenting as one of two subtypes with distinct clinical histories and molecular profiles. The primary GBM subtype presents acutely as a high-grade disease that typically harbours mutations in EGFR, PTEN and INK4A/ARF (also known as CDKN2A), and the secondary GBM subtype evolves from the slow progression of a low-grade disease that classically possesses PDGF and TP53 events. Here we show that concomitant central nervous system (CNS)-specific deletion of p53 and Pten in the mouse CNS generates a penetrant acute-onset high-grade malignant glioma phenotype with notable clinical, pathological and molecular resemblance to primary GBM in humans. This genetic observation prompted TP53 and PTEN mutational analysis in human primary GBM, demonstrating unexpectedly frequent inactivating mutations of TP53 as well as the expected PTEN mutations. Integrated transcriptomic profiling, in silico promoter analysis and functional studies of murine neural stem cells (NSCs) established that dual, but not singular, inactivation of p53 and Pten promotes an undifferentiated state with high renewal potential and drives increased Myc protein levels and its associated signature. Functional studies validated increased Myc activity as a potent contributor to the impaired differentiation and enhanced renewal of NSCs doubly null for p53 and Pten (p53(-/-) Pten(-/-)) as well as tumour neurospheres (TNSs) derived from this model. Myc also serves to maintain robust tumorigenic potential of p53(-/-) Pten(-/-) TNSs. These murine modelling studies, together with confirmatory transcriptomic/promoter studies in human primary GBM, validate a pathogenetic role of a common tumour suppressor mutation profile in human primary GBM and establish Myc as an important target for cooperative actions of p53 and Pten in the regulation of normal and malignant stem/progenitor cell differentiation, self-renewal and tumorigenic potential.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4051433/" 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/PMC4051433/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zheng, Hongwu -- Ying, Haoqiang -- Yan, Haiyan -- Kimmelman, Alec C -- Hiller, David J -- Chen, An-Jou -- Perry, Samuel R -- Tonon, Giovanni -- Chu, Gerald C -- Ding, Zhihu -- Stommel, Jayne M -- Dunn, Katherine L -- Wiedemeyer, Ruprecht -- You, Mingjian J -- Brennan, Cameron -- Wang, Y Alan -- Ligon, Keith L -- Wong, Wing H -- Chin, Lynda -- DePinho, Ronald A -- 5P01CA95616/CA/NCI NIH HHS/ -- P01 CA095616/CA/NCI NIH HHS/ -- P01 CA095616-01A19003/CA/NCI NIH HHS/ -- R01 CA099041/CA/NCI NIH HHS/ -- R01 CA099041-05/CA/NCI NIH HHS/ -- R01CA99041/CA/NCI NIH HHS/ -- U01 CA84313/CA/NCI NIH HHS/ -- England -- Nature. 2008 Oct 23;455(7216):1129-33. doi: 10.1038/nature07443.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18948956" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Neoplasms/genetics/*pathology ; *Cell Differentiation ; Cell Proliferation ; Gene Expression Regulation ; Glioblastoma/genetics/pathology ; Glioma/genetics/*pathology ; Humans ; Immunohistochemistry ; Mice ; Neoplastic Stem Cells/metabolism/*pathology ; Neurons/metabolism/*pathology ; PTEN Phosphohydrolase/genetics/*metabolism ; Proto-Oncogene Proteins c-myc/genetics/metabolism ; Tumor Suppressor Protein p53/genetics/*metabolism
    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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  • 7
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    Glioblastoma stem-like cells give rise to tumour endothelium (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-11-26
    Description: Glioblastoma (GBM) is among the most aggressive of human cancers. A key feature of GBMs is the extensive network of abnormal vasculature characterized by glomeruloid structures and endothelial hyperplasia. Yet the mechanisms of angiogenesis and the origin of tumour endothelial cells remain poorly defined. Here we demonstrate that a subpopulation of endothelial cells within glioblastomas harbour the same somatic mutations identified within tumour cells, such as amplification of EGFR and chromosome 7. We additionally demonstrate that the stem-cell-like CD133(+) fraction includes a subset of vascular endothelial-cadherin (CD144)-expressing cells that show characteristics of endothelial progenitors capable of maturation into endothelial cells. Extensive in vitro and in vivo lineage analyses, including single cell clonal studies, further show that a subpopulation of the CD133(+) stem-like cell fraction is multipotent and capable of differentiation along tumour and endothelial lineages, possibly via an intermediate CD133(+)/CD144(+) progenitor cell. The findings are supported by genetic studies of specific exons selected from The Cancer Genome Atlas, quantitative FISH and comparative genomic hybridization data that demonstrate identical genomic profiles in the CD133(+) tumour cells, their endothelial progenitor derivatives and mature endothelium. Exposure to the clinical anti-angiogenesis agent bevacizumab or to a gamma-secretase inhibitor as well as knockdown shRNA studies demonstrate that blocking VEGF or silencing VEGFR2 inhibits the maturation of tumour endothelial progenitors into endothelium but not the differentiation of CD133(+) cells into endothelial progenitors, whereas gamma-secretase inhibition or NOTCH1 silencing blocks the transition into endothelial progenitors. These data may provide new perspectives on the mechanisms of failure of anti-angiogenesis inhibitors currently in use. The lineage plasticity and capacity to generate tumour vasculature of the putative cancer stem cells within glioblastoma are novel findings that provide new insight into the biology of gliomas and the definition of cancer stemness, as well as the mechanisms of tumour neo-angiogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Rong -- Chadalavada, Kalyani -- Wilshire, Jennifer -- Kowalik, Urszula -- Hovinga, Koos E -- Geber, Adam -- Fligelman, Boris -- Leversha, Margaret -- Brennan, Cameron -- Tabar, Viviane -- England -- Nature. 2010 Dec 9;468(7325):829-33. doi: 10.1038/nature09624. Epub 2010 Nov 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurosurgery, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21102433" target="_blank"〉PubMed〈/a〉
    Keywords: Amyloid Precursor Protein Secretases/antagonists & inhibitors ; Animals ; Antibodies, Monoclonal/pharmacology ; Antibodies, Monoclonal, Humanized ; Antigens, CD/metabolism ; Bevacizumab ; Cadherins/deficiency/metabolism ; *Cell Differentiation ; Cell Line, Tumor ; Cell Lineage ; Chromosome Aberrations ; Coculture Techniques ; Endothelial Cells/metabolism/*pathology ; Female ; Glioblastoma/*blood supply/genetics/*pathology ; Glycoproteins/metabolism ; Humans ; In Situ Hybridization, Fluorescence ; Integrin beta4/metabolism ; Male ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Neovascularization, Pathologic/*pathology ; Neural Stem Cells/metabolism/*pathology ; Peptides/metabolism ; Receptor, Notch1/deficiency/genetics ; Vascular Endothelial Growth Factor A/antagonists & inhibitors
    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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    Extrageniculate vision in hemianopic humans: saccade inhibition by signals in the blind field (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-10-05
    Description: The functional competence of extrageniculate visual pathways in hemianopic humans was demonstrated by showing that distractor signals in the blind half of the visual field could inhibit saccades toward targets in the intact visual field. This inhibitory effect of unseen distractors in patients occurred only when distractors were presented in the temporal half of the visual field, was specific to oculomotor responses, and did not occur in normal subjects. These results show that a peripheral visual signal activates retinotectal pathways to prime the oculomotor system and that these pathways can mediate orienting behavior in hemianopic humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rafal, R -- Smith, J -- Krantz, J -- Cohen, A -- Brennan, C -- MH 41544/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1990 Oct 5;250(4977):118-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Clinical Neurosciences, Brown University, Providence, RI 02908.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2218503" target="_blank"〉PubMed〈/a〉
    Keywords: Analysis of Variance ; Brain/anatomy & histology/*physiopathology/radiography ; Hemianopsia/*physiopathology/radiography ; Humans ; Reference Values ; *Saccades ; Scotoma/physiopathology ; Tomography, X-Ray Computed ; *Vision, Ocular ; *Visual Fields
    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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  • 9
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    Coactivation of receptor tyrosine kinases affects the response of tumor cells to targeted therapies (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-18
    Description: Targeted therapies that inhibit receptor tyrosine kinases (RTKs) and the downstream phosphatidylinositol 3-kinase (PI3K) signaling pathway have shown promising anticancer activity, but their efficacy in the brain tumor glioblastoma multiforme (GBM) and other solid tumors has been modest. We hypothesized that multiple RTKs are coactivated in these tumors and that redundant inputs drive and maintain downstream signaling, thereby limiting the efficacy of therapies targeting single RTKs. Tumor cell lines, xenotransplants, and primary tumors indeed show multiple concomitantly activated RTKs. Combinations of RTK inhibitors and/or RNA interference, but not single agents, decreased signaling, cell survival, and anchorage-independent growth even in glioma cells deficient in PTEN, a frequently inactivated inhibitor of PI3K. Thus, effective GBM therapy may require combined regimens targeting multiple RTKs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stommel, Jayne M -- Kimmelman, Alec C -- Ying, Haoqiang -- Nabioullin, Roustem -- Ponugoti, Aditya H -- Wiedemeyer, Ruprecht -- Stegh, Alexander H -- Bradner, James E -- Ligon, Keith L -- Brennan, Cameron -- Chin, Lynda -- DePinho, Ronald A -- 5P01CA95616/CA/NCI NIH HHS/ -- R01CA99041/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 Oct 12;318(5848):287-90. Epub 2007 Sep 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17872411" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Agents/*pharmacology ; Antineoplastic Combined Chemotherapy Protocols/pharmacology/therapeutic use ; Brain Neoplasms/drug therapy/*enzymology ; Cell Line, Tumor ; Cell Survival ; Enzyme Activation ; Erlotinib Hydrochloride ; Glioblastoma/drug therapy/*enzymology ; Humans ; Indoles/pharmacology ; PTEN Phosphohydrolase/genetics/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Piperazines/pharmacology ; Protein Kinase Inhibitors/*pharmacology ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-met ; Quinazolines/pharmacology ; Receptor Protein-Tyrosine Kinases/antagonists & inhibitors/*metabolism ; Receptor, Epidermal Growth Factor/antagonists & inhibitors/metabolism ; Receptors, Growth Factor/metabolism ; Signal Transduction ; Sulfonamides/pharmacology
    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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  • 10
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    Corrigendum: Passenger deletions generate therapeutic vulnerabilities in cancer (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-07-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muller, Florian -- Colla, Simona -- Aquilanti, Elisa -- Manzo, Veronica E -- Genovese, Giannicola -- Lee, Jaclyn -- Eisenson, Daniel -- Narurkar, Rujuta -- Deng, Pingna -- Nezi, Luigi -- Lee, Michelle -- Hu, Baoli -- Hu, Jian -- Sahin, Ergun -- Ong, Derrick -- Fletcher-Sananikone, Eliot -- Ho, Dennis -- Kwong, Lawrence -- Brennan, Cameron -- Wang, Y Alan -- Chin, Lynda -- DePinho, Ronald A -- England -- Nature. 2015 Sep 10;525(7568):278. doi: 10.1038/nature14609. Epub 2015 Jul 8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26153864" target="_blank"〉PubMed〈/a〉
    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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