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  • 1
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    Transmission phase lapse in the non-Hermitian Aharonov-Bohm interferometer near the spectral singularity (2015)
    American Physical Society (APS)
    Details
    Publication Date: 2015-01-27
    Description: Author(s): G. Zhang, X. Q. Li, X. Z. Zhang, and Z. Song We study the effect of PT -symmetric imaginary potentials embedded in the two arms of an Aharonov-Bohm interferometer on the transmission phase by finding an exact solution for a concrete tight-binding system. It is observed that the spectral singularity always occurs at k=±π/2 for a wide range of fl... [Phys. Rev. A 91, 012116] Published Mon Jan 26, 2015
    Keywords: Fundamental concepts
    Print ISSN: 1050-2947
    Electronic ISSN: 1094-1622
    Topics: Physics
    Published by American Physical Society (APS)
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  • 2
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    Non-Hermitian anisotropic XY model with intrinsic rotation-time-reversal symmetry (2013)
    American Physical Society (APS)
    Details
    Publication Date: 2013-01-17
    Description: Author(s): X. Z. Zhang and Z. Song We systematically study the non-Hermitian version of the one-dimensional anisotropic X Y model, which in its original form is a unique, exactly solvable, quantum spin model for understanding the quantum phase transition. The distinguishing features of this model are that it has a full real spectrum i... [Phys. Rev. A 87, 012114] Published Wed Jan 16, 2013
    Keywords: Fundamental concepts
    Print ISSN: 1050-2947
    Electronic ISSN: 1094-1622
    Topics: Physics
    Published by American Physical Society (APS)
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  • 3
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    Geometric phase and phase diagram for a non-Hermitian quantum XY model (2013)
    American Physical Society (APS)
    Details
    Publication Date: 2013-10-12
    Description: Author(s): X. Z. Zhang and Z. Song We study the geometric phase for the ground state of a generalized one-dimensional non-Hermitian quantum X Y model, which has transverse-field-dependent intrinsic rotation-time reversal symmetry. Based on the exact solution, this model is shown to have a full real spectrum in multiple regions for the... [Phys. Rev. A 88, 042108] Published Fri Oct 11, 2013
    Keywords: Fundamental concepts
    Print ISSN: 1050-2947
    Electronic ISSN: 1094-1622
    Topics: Physics
    Published by American Physical Society (APS)
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  • 4
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    Perfect state transfer in PT-symmetric non-Hermitian networks (2012)
    American Physical Society (APS)
    Details
    Publication Date: 2012-01-20
    Description: Author(s): X. Z. Zhang, L. Jin, and Z. Song We systematically study the parity- and time-reversal ( PT ) symmetric non-Hermitian version of a quantum network proposed in the paper of   Christandl et al. [ Phys. Rev. Lett. 92 187902 (2004) ]. The nature of this model shows that it is a paradigm to demonstrate the complex relationship between the... [Phys. Rev. A 85, 012106] Published Thu Jan 19, 2012
    Keywords: Fundamental concepts
    Print ISSN: 1050-2947
    Electronic ISSN: 1094-1622
    Topics: Physics
    Published by American Physical Society (APS)
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  • 5
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    Roles of PLC-beta2 and -beta3 and PI3Kgamma in chemoattractant-mediated signal transduction (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-11
    Description: The roles of phosphoinositide 3-kinase (PI3K) and phospholipase C (PLC) in chemoattractant-elicited responses were studied in mice lacking these key enzymes. PI3Kgamma was required for chemoattractant-induced production of phosphatidylinositol 3,4,5-trisphosphate [PtdIns (3,4,5)P3] and has an important role in chemoattractant-induced superoxide production and chemotaxis in mouse neutrophils and in production of T cell-independent antigen-specific antibodies composed of the immunoglobulin lambda light chain (TI-IglambdaL). The study of the mice lacking PLC-beta2 and -beta3 revealed that the PLC pathways have an important role in chemoattractant-mediated production of superoxide and regulation of protein kinases, but not chemotaxis. The PLC pathways also appear to inhibit the chemotactic activity induced by certain chemoattractants and to suppress TI-IglambdaL production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Z -- Jiang, H -- Xie, W -- Zhang, Z -- Smrcka, A V -- Wu, D -- New York, N.Y. -- Science. 2000 Feb 11;287(5455):1046-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Rochester, Rochester, NY 14642, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10669417" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology ; Chemokine CCL4 ; Chemotactic Factors/*pharmacology ; Chemotaxis, Leukocyte/*physiology ; Immunoglobulin lambda-Chains/biosynthesis ; Isoenzymes/*metabolism ; Macrophage Inflammatory Proteins/pharmacology ; Mice ; N-Formylmethionine Leucyl-Phenylalanine/pharmacology ; Neutrophil Infiltration ; Neutrophils/metabolism/*physiology ; Peritonitis/immunology ; Phosphatidylinositol 3-Kinases/*metabolism ; Phosphatidylinositol Phosphates/metabolism ; Phospholipase C beta ; Phosphorylation ; *Signal Transduction ; Skin Ulcer/pathology ; Superoxides/metabolism ; Type C Phospholipases/*metabolism
    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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  • 6
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    Severe fibronectin-deposit renal glomerular disease in mice lacking uteroglobin (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-05-30
    Description: Despite myriads of biological activities ascribed to uteroglobin (UG), a steroid-inducible secreted protein, its physiological functions are unknown. Mice in which the uteroglobin gene was disrupted had severe renal disease that was associated with massive glomerular deposition of predominantly multimeric fibronectin (Fn). The molecular mechanism that normally prevents Fn deposition appears to involve high-affinity binding of UG with Fn to form Fn-UG heteromers that counteract Fn self-aggregation, which is required for abnormal tissue deposition. Thus, UG is essential for maintaining normal renal function in mice, which raises the possibility that an analogous pathogenic mechanism may underlie genetic Fn-deposit human glomerular disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Z -- Kundu, G C -- Yuan, C J -- Ward, J M -- Lee, E J -- DeMayo, F -- Westphal, H -- Mukherjee, A B -- HL47620/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1997 May 30;276(5317):1408-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section on Developmental Genetics, Heritable Disorders Branch, National Institute of Child Health and Human Development (NICHD), National Insitutes of Health (NIH), Bethesda, MD 20892-1830, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9162006" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Crosses, Genetic ; Fibronectins/*metabolism ; Gene Targeting ; Humans ; Kidney Diseases/embryology/genetics/pathology ; *Kidney Glomerulus/embryology/metabolism/ultrastructure ; Mice ; Mice, Inbred C57BL ; Uteroglobin/deficiency/genetics/*physiology
    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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  • 7
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    A mechanically stabilized receptor-ligand flex-bond important in the vasculature (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-08-21
    Description: Haemostasis in the arteriolar circulation mediated by von Willebrand factor (VWF) binding to platelets is an example of an adhesive interaction that must withstand strong hydrodynamic forces acting on cells. VWF is a concatenated, multifunctional protein that has binding sites for platelets as well as subendothelial collagen. Binding of the A1 domain in VWF to the glycoprotein Ib alpha subunit (GPIbalpha) on the surface of platelets mediates crosslinking of platelets to one another and the formation of a platelet plug for arterioles. The importance of VWF is illustrated by its mutation in von Willebrand disease, a bleeding diathesis. Here, we describe a novel mechanochemical specialization of the A1-GPIbalpha bond for force-resistance. We have developed a method that enables, for the first time, repeated measurements of the binding and unbinding of a receptor and ligand in a single molecule (ReaLiSM). We demonstrate two states of the receptor-ligand bond, that is, a flex-bond. One state is seen at low force; a second state begins to engage at 10 pN with a approximately 20-fold longer lifetime and greater force resistance. The lifetimes of the two states, how force exponentiates lifetime, and the kinetics of switching between the two states are all measured. For the first time, single-molecule measurements on this system are in agreement with bulk phase measurements. The results have important implications not only for how platelets bound to VWF are able to resist force to plug arterioles, but also how increased flow activates platelet plug formation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4117310/" 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/PMC4117310/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Jongseong -- Zhang, Cheng-Zhong -- Zhang, Xiaohui -- Springer, Timothy A -- HL-48675/HL/NHLBI NIH HHS/ -- P01 HL048675/HL/NHLBI NIH HHS/ -- England -- Nature. 2010 Aug 19;466(7309):992-5. doi: 10.1038/nature09295.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immune Disease Institute, Children's Hospital Boston and Department of Pathology, Harvard Medical School, 3 Blackfan Circle, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20725043" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arterioles/cytology/*physiology ; Blood Coagulation/*physiology ; Blood Platelets/chemistry/cytology/*metabolism ; Cell Line ; Hemorheology ; Humans ; Kinetics ; Ligands ; Membrane Glycoproteins/chemistry/*metabolism ; Mice ; Models, Chemical ; Models, Molecular ; Platelet Glycoprotein GPIb-IX Complex ; Protein Binding ; Protein Structure, Tertiary ; Tensile Strength ; von Willebrand Factor/chemistry/*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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  • 8
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    The genomic landscapes of human breast and colorectal cancers (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-10-13
    Description: Human cancer is caused by the accumulation of mutations in oncogenes and tumor suppressor genes. To catalog the genetic changes that occur during tumorigenesis, we isolated DNA from 11 breast and 11 colorectal tumors and determined the sequences of the genes in the Reference Sequence database in these samples. Based on analysis of exons representing 20,857 transcripts from 18,191 genes, we conclude that the genomic landscapes of breast and colorectal cancers are composed of a handful of commonly mutated gene "mountains" and a much larger number of gene "hills" that are mutated at low frequency. We describe statistical and bioinformatic tools that may help identify mutations with a role in tumorigenesis. These results have implications for understanding the nature and heterogeneity of human cancers and for using personal genomics for tumor diagnosis and therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wood, Laura D -- Parsons, D Williams -- Jones, Sian -- Lin, Jimmy -- Sjoblom, Tobias -- Leary, Rebecca J -- Shen, Dong -- Boca, Simina M -- Barber, Thomas -- Ptak, Janine -- Silliman, Natalie -- Szabo, Steve -- Dezso, Zoltan -- Ustyanksky, Vadim -- Nikolskaya, Tatiana -- Nikolsky, Yuri -- Karchin, Rachel -- Wilson, Paul A -- Kaminker, Joshua S -- Zhang, Zemin -- Croshaw, Randal -- Willis, Joseph -- Dawson, Dawn -- Shipitsin, Michail -- Willson, James K V -- Sukumar, Saraswati -- Polyak, Kornelia -- Park, Ben Ho -- Pethiyagoda, Charit L -- Pant, P V Krishna -- Ballinger, Dennis G -- Sparks, Andrew B -- Hartigan, James -- Smith, Douglas R -- Suh, Erick -- Papadopoulos, Nickolas -- Buckhaults, Phillip -- Markowitz, Sanford D -- Parmigiani, Giovanni -- Kinzler, Kenneth W -- Velculescu, Victor E -- Vogelstein, Bert -- CA 43460/CA/NCI NIH HHS/ -- CA 57345/CA/NCI NIH HHS/ -- CA109274/CA/NCI NIH HHS/ -- CA112828/CA/NCI NIH HHS/ -- CA121113/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- GM070219/GM/NIGMS NIH HHS/ -- GM07309/GM/NIGMS NIH HHS/ -- P30-CA43703/CA/NCI NIH HHS/ -- RR017698/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 16;318(5853):1108-13. Epub 2007 Oct 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Center for Cancer Genetics and Therapeutics and Howard Hughes Medical Institute at Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17932254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/*genetics/metabolism ; Cell Line ; Chromosome Mapping ; Colorectal Neoplasms/*genetics/metabolism ; Computational Biology ; DNA, Neoplasm ; Databases, Genetic ; Genes, Neoplasm ; Genome, Human ; Humans ; Metabolic Networks and Pathways/genetics ; Mice ; Mutation ; Neoplasm Proteins/genetics/metabolism ; Sequence Analysis, DNA
    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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  • 9
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    A stress signaling pathway in adipose tissue regulates hepatic insulin resistance (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-06
    Description: A high-fat diet causes activation of the regulatory protein c-Jun NH2-terminal kinase 1 (JNK1) and triggers development of insulin resistance. JNK1 is therefore a potential target for therapeutic treatment of metabolic syndrome. We explored the mechanism of JNK1 signaling by engineering mice in which the Jnk1 gene was ablated selectively in adipose tissue. JNK1 deficiency in adipose tissue suppressed high-fat diet-induced insulin resistance in the liver. JNK1-dependent secretion of the inflammatory cytokine interleukin-6 by adipose tissue caused increased expression of liver SOCS3, a protein that induces hepatic insulin resistance. Thus, JNK1 activation in adipose tissue can cause insulin resistance in the liver.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2643026/" 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/PMC2643026/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sabio, Guadalupe -- Das, Madhumita -- Mora, Alfonso -- Zhang, Zhiyou -- Jun, John Y -- Ko, Hwi Jin -- Barrett, Tamera -- Kim, Jason K -- Davis, Roger J -- DK52530/DK/NIDDK NIH HHS/ -- R01 CA065861/CA/NCI NIH HHS/ -- R01 CA065861-14/CA/NCI NIH HHS/ -- R01 DK080756/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Dec 5;322(5907):1539-43. doi: 10.1126/science.1160794.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19056984" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/enzymology/*metabolism ; Adipose Tissue/enzymology/metabolism ; Animals ; Dietary Fats/administration & dosage ; Enzyme Activation ; Glucose/metabolism ; Insulin/metabolism ; Insulin Receptor Substrate Proteins/metabolism ; *Insulin Resistance ; Interleukin-6/administration & dosage/metabolism ; Liver/*metabolism ; MAP Kinase Signaling System ; Mice ; Mitogen-Activated Protein Kinase 8/deficiency/genetics/*metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt/metabolism ; *Signal Transduction ; *Stress, Physiological ; Suppressor of Cytokine Signaling Proteins/metabolism
    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
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    Antagonistic actions of Msx1 and Osr2 pattern mammalian teeth into a single row (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-03
    Description: Mammals have single-rowed dentitions, whereas many nonmammalian vertebrates have teeth in multiple rows. Neither the molecular mechanism regulating iterative tooth initiation nor that restricting mammalian tooth development in one row is known. We found that mice lacking the transcription factor odd-skipped related-2 (Osr2) develop supernumerary teeth lingual to their molars because of expansion of the odontogenic field. Osr2 was expressed in a lingual-to-buccal gradient and restricted expression of bone morphogenetic protein 4 (Bmp4), an essential odontogenic signal, in the developing tooth mesenchyme. Expansion of odontogenic field in Osr2-deficient mice required Msx1, a feedback activator of Bmp4 expression. These findings suggest that the Bmp4-Msx1 pathway propagates mesenchymal activation for sequential tooth induction and that spatial modulation of this pathway provides a mechanism for patterning vertebrate dentition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2650836/" 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/PMC2650836/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Zunyi -- Lan, Yu -- Chai, Yang -- Jiang, Rulang -- R01 DE013681/DE/NIDCR NIH HHS/ -- R01 DE013681-06/DE/NIDCR NIH HHS/ -- R01 DE013681-07/DE/NIDCR NIH HHS/ -- R01 DE013681-08/DE/NIDCR NIH HHS/ -- R01 DE013681-09/DE/NIDCR NIH HHS/ -- R01DE013681/DE/NIDCR NIH HHS/ -- T32DE007202/DE/NIDCR NIH HHS/ -- New York, N.Y. -- Science. 2009 Feb 27;323(5918):1232-4. doi: 10.1126/science.1167418.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Oral Biology and Department of Biomedical Genetics, University of Rochester Medical Center, Rochester, NY 14642, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19251632" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Morphogenetic Protein 4/metabolism ; Dentition ; Epithelium/embryology/metabolism ; Gene Expression ; Gene Expression Profiling ; MSX1 Transcription Factor/genetics/*metabolism ; Mesoderm/embryology/metabolism ; Mice ; Molar/embryology ; Morphogenesis ; Mutation ; *Odontogenesis ; Tooth Germ/embryology/metabolism ; Tooth, Supernumerary/*embryology ; Transcription Factors/genetics/*metabolism
    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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