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  • 1
    Publication Date: 2013-02-16
    Description: Author(s): X. Qian, D. A. Dwyer, R. D. McKeown, P. Vogel, W. Wang, and C. Zhang Determination of the neutrino mass hierarchy using a reactor neutrino experiment at ∼60  km is analyzed. Such a measurement is challenging due to the finite detector resolution, the absolute energy scale calibration, and the degeneracies caused by current experimental uncertainty of | Δ m 32 2 |. The sta... [Phys. Rev. D 87, 033005] Published Fri Feb 15, 2013
    Keywords: Electroweak interactions
    Print ISSN: 0556-2821
    Electronic ISSN: 1089-4918
    Topics: Physics
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  • 2
    Publication Date: 2012-07-11
    Description: REPRESSOR OF SILENCING 1 (ROS1) is a DNA demethylation enzyme that was previously identified during a genetic screen for the silencing of both RD29A-LUC and 35S-NPTII transgenes on a T-DNA construct. Here we performed a genetic screen to identify additional mutants in which the 35S-NPTII transgene is silenced. We identified several alleles of ros1 and of the following components of the RNA-directed DNA methylation (RdDM) pathway: NRPD1 (the largest subunit of polymerase IV), RDR2, NRPE1 (the largest subunit of polymerase V), NRPD2, AGO4, and DMS3. Our results show that the silencing of 35S-NPTII in the RdDM pathway mutants is due to the reduced expression of ROS1 in the mutants. We also identified a putative histone acetyltransferase (ROS4) from the genetic screen. The acetyltransferase contains a PHD-finger domain that binds to unmethylated histone H3K4. The mutation in ROS4 led to reduction of H3K18 and H3K23 acetylation levels. We show that the silencing of 35S-NPTII and some transposable element genes was released by the ddm1 mutation but that this also required ROS4. Our study identifies a unique antisilencing factor, and reveals that the RdDM pathway has an antisilencing function due to its role in maintaining ROS1 expression.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 3
    Publication Date: 2011-03-23
    Description: Golgi-localized nucleotide sugar transporters (NSTs) are considered essential for the biosynthesis of wall polysaccharides and glycoproteins based on their characteristic transport of a large number of nucleotide sugars to the Golgi lumen. The lack of NST mutants in plants has prevented evaluation of this hypothesis in plants. A previously undescribed Golgi NST mutant, brittle culm14 (bc14), displays reduced mechanical strength caused by decreased cellulose content and altered wall structure, and exhibits abnormalities in plant development. Map-based cloning revealed that all of the observed mutant phenotypes result from a missense mutation in a putative NST gene, Oryza sativa Nucleotide Sugar Transporter1 (OsNST1). OsNST1 was identified as a Golgi-localized transporter by analysis of a fluorescence-tagged OsNST1 expressed in rice protoplast cells and demonstration of UDP-glucose transport activity via uptake assays in yeast. Compositional sugar analyses in total and fractionated wall residues of wild-type and bc14 culms showed a deficiency in the synthesis of glucoconjugated polysaccharides in bc14, indicating that OsNST1 supplies the glucosyl substrate for the formation of matrix polysaccharides, and thereby modulates cellulose biosynthesis. OsNST1 is ubiquitously expressed, with high expression in mechanical tissues. The inferior mechanical strength and abnormal development of bc14 plants suggest that OsNST1 has pleiotropic effects on cell wall biosynthesis and plant growth. Identification of OsNST1 has improved our understanding of how cell wall polysaccharide synthesis is regulated by Golgi NSTs in plants.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 4
    Publication Date: 2012-03-28
    Description: Antibiotic resistance is a worldwide public health concern. Conjugative transfer between closely related strains or species of bacteria is an important method for the horizontal transfer of multidrug-resistance genes. The extent to which nanomaterials are able to cause an increase in antibiotic resistance by the regulation of the conjugative transfer of antibiotic-resistance genes in bacteria, especially across genera, is still unknown. Here we show that nanomaterials in water can significantly promote the horizontal conjugative transfer of multidrug-resistance genes mediated by the RP4, RK2, and pCF10 plasmids. Nanoalumina can promote the conjugative transfer of the RP4 plasmid from Escherichia coli to Salmonella spp. by up to 200-fold compared with untreated cells. We also explored the mechanisms behind this phenomenon and demonstrate that nanoalumina is able to induce oxidative stress, damage bacterial cell membranes, enhance the expression of mating pair formation genes and DNA transfer and replication genes, and depress the expression of global regulatory genes that regulate the conjugative transfer of RP4. These findings are important in assessing the risk of nanomaterials to the environment, particularly from water and wastewater treatment systems, and in the estimation of the effect of manufacture and use of nanomaterials on the environment.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 5
    Publication Date: 2011-08-11
    Description: Author(s): X. Qian et al. (Jefferson Lab Hall A Collaboration) We report the first measurement of target single spin asymmetries in the semi-inclusive 3 He(e,e ′ π ± )X reaction on a transversely polarized target. The experiment, conducted at Jefferson Lab using a 5.9 GeV electron beam, covers a range of 0.16〈 x 〈0.35 with 1.4〈 Q 2 〈2.7  GeV 2 . The Collins and... [Phys. Rev. Lett. 107, 072003] Published Wed Aug 10, 2011
    Keywords: Elementary Particles and Fields
    Print ISSN: 0031-9007
    Electronic ISSN: 1079-7114
    Topics: Physics
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  • 6
    Publication Date: 2014-12-05
    Description: A novel biomarker Linc00974 interacting with KRT19 promotes proliferation and metastasis in hepatocellular carcinoma Cell Death and Disease 5, e1549 (December 2014). doi:10.1038/cddis.2014.518 Authors: J Tang, H Zhuo, X Zhang, R Jiang, J Ji, L Deng, X Qian, F Zhang & B Sun
    Electronic ISSN: 2041-4889
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 7
    Publication Date: 2015-03-20
    Description: Author(s): M. Bass, M. Bishai, D. Cherdack, M. Diwan, Z. Djurcic, J. Hernandez, B. Lundberg, V. Paolone, X. Qian, R. Rameika, L. Whitehead, R. J. Wilson, E. Worcester, and G. Zeller Next-generation long-baseline electron neutrino appearance experiments will seek to discover CP violation, determine the mass hierarchy and resolve the θ 23 octant. In light of the recent precision measurements of θ 13 , we consider the sensitivity of these measurements in a study to determine the opti... [Phys. Rev. D 91, 052015] Published Thu Mar 19, 2015
    Keywords: Particle Experiment
    Print ISSN: 0556-2821
    Electronic ISSN: 1089-4918
    Topics: Physics
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  • 8
    Publication Date: 2010-01-08
    Description: The ability to silence the activity of genetically specified neurons in a temporally precise fashion would provide the opportunity to investigate the causal role of specific cell classes in neural computations, behaviours and pathologies. Here we show that members of the class of light-driven outward proton pumps can mediate powerful, safe, multiple-colour silencing of neural activity. The gene archaerhodopsin-3 (Arch) from Halorubrum sodomense enables near-100% silencing of neurons in the awake brain when virally expressed in the mouse cortex and illuminated with yellow light. Arch mediates currents of several hundred picoamps at low light powers, and supports neural silencing currents approaching 900 pA at light powers easily achievable in vivo. Furthermore, Arch spontaneously recovers from light-dependent inactivation, unlike light-driven chloride pumps that enter long-lasting inactive states in response to light. These properties of Arch are appropriate to mediate the optical silencing of significant brain volumes over behaviourally relevant timescales. Arch function in neurons is well tolerated because pH excursions created by Arch illumination are minimized by self-limiting mechanisms to levels comparable to those mediated by channelrhodopsins or natural spike firing. To highlight how proton pump ecological and genomic diversity may support new innovation, we show that the blue-green light-drivable proton pump from the fungus Leptosphaeria maculans (Mac) can, when expressed in neurons, enable neural silencing by blue light, thus enabling alongside other developed reagents the potential for independent silencing of two neural populations by blue versus red light. Light-driven proton pumps thus represent a high-performance and extremely versatile class of 'optogenetic' voltage and ion modulator, which will broadly enable new neuroscientific, biological, neurological and psychiatric investigations.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2939492/" 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/PMC2939492/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chow, Brian Y -- Han, Xue -- Dobry, Allison S -- Qian, Xiaofeng -- Chuong, Amy S -- Li, Mingjie -- Henninger, Michael A -- Belfort, Gabriel M -- Lin, Yingxi -- Monahan, Patrick E -- Boyden, Edward S -- 1K99MH085944/MH/NIMH NIH HHS/ -- DP2 OD002002/OD/NIH HHS/ -- DP2 OD002002-01/OD/NIH HHS/ -- K99 MH085944/MH/NIMH NIH HHS/ -- K99 MH085944-01/MH/NIMH NIH HHS/ -- England -- Nature. 2010 Jan 7;463(7277):98-102. doi: 10.1038/nature08652.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The MIT Media Laboratory, Synthetic Neurobiology Group, and Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20054397" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/radiation effects ; Animals ; Ascomycota/metabolism/radiation effects ; Color ; Electric Conductivity ; Euryarchaeota/metabolism/radiation effects ; Genetic Engineering/*methods ; Hydrogen-Ion Concentration ; Mice ; Molecular Sequence Data ; Neocortex/cytology/physiology/radiation effects ; Neurons/*metabolism/*radiation effects ; Proton Pumps/classification/genetics/*metabolism/*radiation effects ; Rhodopsins, Microbial/antagonists & inhibitors/genetics/metabolism/radiation ; effects ; Wakefulness
    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: 2011-03-19
    Description: Decreased cardiac contractility is a central feature of systolic heart failure. Existing drugs increase cardiac contractility indirectly through signaling cascades but are limited by their mechanism-related adverse effects. To avoid these limitations, we previously developed omecamtiv mecarbil, a small-molecule, direct activator of cardiac myosin. Here, we show that it binds to the myosin catalytic domain and operates by an allosteric mechanism to increase the transition rate of myosin into the strongly actin-bound force-generating state. Paradoxically, it inhibits adenosine 5'-triphosphate turnover in the absence of actin, which suggests that it stabilizes an actin-bound conformation of myosin. In animal models, omecamtiv mecarbil increases cardiac function by increasing the duration of ejection without changing the rates of contraction. Cardiac myosin activation may provide a new therapeutic approach for systolic heart failure.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4090309/" 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/PMC4090309/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malik, Fady I -- Hartman, James J -- Elias, Kathleen A -- Morgan, Bradley P -- Rodriguez, Hector -- Brejc, Katjusa -- Anderson, Robert L -- Sueoka, Sandra H -- Lee, Kenneth H -- Finer, Jeffrey T -- Sakowicz, Roman -- Baliga, Ramesh -- Cox, David R -- Garard, Marc -- Godinez, Guillermo -- Kawas, Raja -- Kraynack, Erica -- Lenzi, David -- Lu, Pu Ping -- Muci, Alexander -- Niu, Congrong -- Qian, Xiangping -- Pierce, Daniel W -- Pokrovskii, Maria -- Suehiro, Ion -- Sylvester, Sheila -- Tochimoto, Todd -- Valdez, Corey -- Wang, Wenyue -- Katori, Tatsuo -- Kass, David A -- Shen, You-Tang -- Vatner, Stephen F -- Morgans, David J -- 1-R43-HL-66647-1/HL/NHLBI NIH HHS/ -- R01 HL106511/HL/NHLBI NIH HHS/ -- R43 HL066647/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2011 Mar 18;331(6023):1439-43. doi: 10.1126/science.1200113.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Preclinical Research and Development, Cytokinetics, Inc., South San Francisco, CA 94080, USA. fmalik@cytokinetics.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21415352" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/metabolism ; Actins/metabolism ; Adenosine Triphosphatases/metabolism ; Adenosine Triphosphate/metabolism ; Adrenergic beta-Agonists/pharmacology ; Allosteric Regulation ; Animals ; Binding Sites ; Calcium/metabolism ; Cardiac Myosins/chemistry/*metabolism ; Cardiac Output/drug effects ; Dogs ; Female ; Heart Failure, Systolic/*drug therapy/physiopathology ; Isoproterenol/pharmacology ; Male ; Myocardial Contraction/*drug effects ; Myocytes, Cardiac/*drug effects/physiology ; Phosphates/metabolism ; Protein Binding ; Protein Conformation ; Protein Isoforms/chemistry/metabolism ; Rats ; Rats, Sprague-Dawley ; Urea/*analogs & derivatives/chemistry/metabolism/pharmacology ; Ventricular Function, Left/drug effects
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2014-12-17
    Description: Quantum spin Hall (QSH) effect materials feature edge states that are topologically protected from backscattering. However, the small band gap in materials that have been identified as QSH insulators limits applications. We use first-principles calculations to predict a class of large-gap QSH insulators in two-dimensional transition metal dichalcogenides with 1T' structure, namely, 1T'-MX2 with M = (tungsten or molybdenum) and X = (tellurium, selenium, or sulfur). A structural distortion causes an intrinsic band inversion between chalcogenide-p and metal-d bands. Additionally, spin-orbit coupling opens a gap that is tunable by vertical electric field and strain. We propose a topological field effect transistor made of van der Waals heterostructures of 1T'-MX2 and two-dimensional dielectric layers that can be rapidly switched off by electric field through a topological phase transition instead of carrier depletion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Qian, Xiaofeng -- Liu, Junwei -- Fu, Liang -- Li, Ju -- New York, N.Y. -- Science. 2014 Dec 12;346(6215):1344-7. doi: 10.1126/science.1256815. Epub 2014 Nov 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Nuclear Science and Engineering and Department of Materials Science and Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. ; Department of Physics, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. ; Department of Physics, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. liangfu@mit.edu liju@mit.edu. ; Department of Nuclear Science and Engineering and Department of Materials Science and Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. liangfu@mit.edu liju@mit.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25504715" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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