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  • 1
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    Predicting the existence of a 2.9 GeV Df_{0}(980) molecular state (2013)
    American Physical Society (APS)
    Details
    Publication Date: 2013-02-21
    Description: Author(s): A. Martínez Torres, K. P. Khemchandani, M. Nielsen, and F. S. Navarra A D -like meson resonance with mass around 2.9 GeV has been found in the D K K ̅ system using two independent and different model calculations based on (1) QCD sum rules and (2) solution of Fadeev equations with input interactions obtained from effective field theories built by considering both ... [Phys. Rev. D 87, 034025] Published Wed Feb 20, 2013
    Keywords: Strong interactions & Lattice methods
    Print ISSN: 0556-2821
    Electronic ISSN: 1089-4918
    Topics: Physics
    Published by American Physical Society (APS)
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  • 2
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    Negative parity Λ and Σ resonances coupled to pseudoscalar and vector mesons (2012)
    American Physical Society (APS)
    Details
    Publication Date: 2012-06-13
    Description: Author(s): K. P. Khemchandani, A. Martínez Torres, H. Nagahiro, and A. Hosaka An exploration of the dynamically generated Λ and Σ resonances has been made in the vector meson-baryon (VB) systems coupled to pseudoscalar meson-baryon (PB) channels. The VB interactions are obtained from the Lagrangians written within the hidden local symmetry which, in addition to Yukawa-type ve... [Phys. Rev. D 85, 114020] Published Tue Jun 12, 2012
    Keywords: Strong interactions & Lattice methods
    Print ISSN: 0556-2821
    Electronic ISSN: 1089-4918
    Topics: Physics
    Published by American Physical Society (APS)
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  • 3
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    Coupling vector and pseudoscalar mesons to study baryon resonances (2011)
    American Physical Society (APS)
    Details
    Publication Date: 2011-11-16
    Description: Author(s): K. P. Khemchandani, A. Martínez Torres, H. Kaneko, H. Nagahiro, and A. Hosaka [Phys. Rev. D 84, 094018] Published Tue Nov 15, 2011
    Keywords: Strong interactions & Lattice methods
    Print ISSN: 0556-2821
    Electronic ISSN: 1089-4918
    Topics: Physics
    Published by American Physical Society (APS)
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  • 4
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    Theoretical support for the π(1300) and the recently claimed f_{0}(1790) as molecular resonances (2011)
    American Physical Society (APS)
    Details
    Publication Date: 2011-10-18
    Description: Author(s): A. Martínez Torres, K. P. Khemchandani, D. Jido, and A. Hosaka [Phys. Rev. D 84, 074027] Published Mon Oct 17, 2011
    Keywords: Strong interactions & Lattice methods
    Print ISSN: 0556-2821
    Electronic ISSN: 1089-4918
    Topics: Physics
    Published by American Physical Society (APS)
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  • 5
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    Soft gluon emission off a heavy quark revisited (2012)
    American Physical Society (APS)
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    Publication Date: 2012-03-17
    Description: Author(s): Raktim Abir, Carsten Greiner, Mauricio Martinez, Munshi G. Mustafa, and Jan Uphoff An improved generalized suppression factor for gluon emission off a heavy quark is derived within perturbative QCD, which is valid for the full range of rapidity of the radiated gluon and also has no restriction on the scaled mass of the quark with its energy. In the appropriate limit, it correctly ... [Phys. Rev. D 85, 054012] Published Fri Mar 16, 2012
    Keywords: Strong interactions & Lattice methods
    Print ISSN: 0556-2821
    Electronic ISSN: 1089-4918
    Topics: Physics
    Published by American Physical Society (APS)
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  • 6
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    KD, ηD_{s} interaction in finite volume and the D_{s*0}(2317) resonance (2012)
    American Physical Society (APS)
    Details
    Publication Date: 2012-01-26
    Description: Author(s): A. Martínez Torres, L. R. Dai, C. Koren, D. Jido, and E. Oset An SU(4) extrapolation of the chiral unitary theory in coupled channels done to study the scalar mesons in the charm sector is extended to produce results in finite volume. The theory in the infinite volume produces dynamically the D s * 0 (2317) resonance by means of the coupled channels K D , η D s . Energ... [Phys. Rev. D 85, 014027] Published Wed Jan 25, 2012
    Keywords: Strong interactions & Lattice methods
    Print ISSN: 0556-2821
    Electronic ISSN: 1089-4918
    Topics: Physics
    Published by American Physical Society (APS)
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  • 7
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    Chemical genetics of Plasmodium falciparum (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-05-21
    Description: Malaria caused by Plasmodium falciparum is a disease that is responsible for 880,000 deaths per year worldwide. Vaccine development has proved difficult and resistance has emerged for most antimalarial drugs. To discover new antimalarial chemotypes, we have used a phenotypic forward chemical genetic approach to assay 309,474 chemicals. Here we disclose structures and biological activity of the entire library-many of which showed potent in vitro activity against drug-resistant P. falciparum strains-and detailed profiling of 172 representative candidates. A reverse chemical genetic study identified 19 new inhibitors of 4 validated drug targets and 15 novel binders among 61 malarial proteins. Phylochemogenetic profiling in several organisms revealed similarities between Toxoplasma gondii and mammalian cell lines and dissimilarities between P. falciparum and related protozoans. One exemplar compound displayed efficacy in a murine model. Our findings provide the scientific community with new starting points for malaria drug discovery.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874979/" 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/PMC2874979/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guiguemde, W Armand -- Shelat, Anang A -- Bouck, David -- Duffy, Sandra -- Crowther, Gregory J -- Davis, Paul H -- Smithson, David C -- Connelly, Michele -- Clark, Julie -- Zhu, Fangyi -- Jimenez-Diaz, Maria B -- Martinez, Maria S -- Wilson, Emily B -- Tripathi, Abhai K -- Gut, Jiri -- Sharlow, Elizabeth R -- Bathurst, Ian -- El Mazouni, Farah -- Fowble, Joseph W -- Forquer, Isaac -- McGinley, Paula L -- Castro, Steve -- Angulo-Barturen, Inigo -- Ferrer, Santiago -- Rosenthal, Philip J -- Derisi, Joseph L -- Sullivan, David J -- Lazo, John S -- Roos, David S -- Riscoe, Michael K -- Phillips, Margaret A -- Rathod, Pradipsinh K -- Van Voorhis, Wesley C -- Avery, Vicky M -- Guy, R Kiplin -- AI045774/AI/NIAID NIH HHS/ -- AI053680/AI/NIAID NIH HHS/ -- AI067921/AI/NIAID NIH HHS/ -- AI075517/AI/NIAID NIH HHS/ -- AI075594/AI/NIAID NIH HHS/ -- AI080625/AI/NIAID NIH HHS/ -- AI082617/AI/NIAID NIH HHS/ -- AI28724/AI/NIAID NIH HHS/ -- AI35707/AI/NIAID NIH HHS/ -- AI53862/AI/NIAID NIH HHS/ -- AI772682/AI/NIAID NIH HHS/ -- CA78039/CA/NCI NIH HHS/ -- F32 AI077268/AI/NIAID NIH HHS/ -- F32 AI077268-03/AI/NIAID NIH HHS/ -- P01 AI035707/AI/NIAID NIH HHS/ -- P01 AI035707-140007/AI/NIAID NIH HHS/ -- P01 CA078039-10/CA/NCI NIH HHS/ -- P41 RR001614/RR/NCRR NIH HHS/ -- P41 RR001614-246970/RR/NCRR NIH HHS/ -- R01 AI045774/AI/NIAID NIH HHS/ -- R01 AI045774-09/AI/NIAID NIH HHS/ -- R37 AI028724/AI/NIAID NIH HHS/ -- R37 AI028724-17/AI/NIAID NIH HHS/ -- R56 AI082617/AI/NIAID NIH HHS/ -- R56 AI082617-01/AI/NIAID NIH HHS/ -- U01 AI053862/AI/NIAID NIH HHS/ -- U01 AI053862-05/AI/NIAID NIH HHS/ -- U01 AI075594-03/AI/NIAID NIH HHS/ -- UL1 TR000005/TR/NCATS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 May 20;465(7296):311-5. doi: 10.1038/nature09099.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemical Biology and Therapeutics, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20485428" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antimalarials/*analysis/isolation & purification/*pharmacology ; Cell Line ; *Drug Discovery ; Drug Evaluation, Preclinical ; Drug Resistance/drug effects ; Drug Therapy, Combination ; Erythrocytes/drug effects/parasitology ; Humans ; Malaria, Falciparum/drug therapy/parasitology ; Mice ; Phenotype ; Phylogeny ; Plasmodium falciparum/*drug effects/*genetics/metabolism ; Reproducibility of Results ; Small Molecule Libraries/chemistry/pharmacology
    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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    Asymmetric segregation of polarized antigen on B cell division shapes presentation capacity (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-28
    Description: During the activation of humoral immune responses, B cells acquire antigen for subsequent presentation to cognate T cells. Here we show that after mouse B cells accumulate antigen, it is maintained in a polarized distribution for extended periods in vivo. Using high-throughput imaging flow cytometry, we observed that this polarization is preserved during B cell division, promoting asymmetric antigen segregation among progeny. Antigen inheritance correlates with the ability of progeny to activate T cells: Daughter cells receiving larger antigen stores exhibit a prolonged capacity to present antigen, which renders them more effective in competing for T cell help. The generation of progeny with differential capacities for antigen presentation may have implications for somatic hypermutation and class switching during affinity maturation and as B cells commit to effector cell fates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thaunat, Olivier -- Granja, Aitor G -- Barral, Patricia -- Filby, Andrew -- Montaner, Beatriz -- Collinson, Lucy -- Martinez-Martin, Nuria -- Harwood, Naomi E -- Bruckbauer, Andreas -- Batista, Facundo D -- Cancer Research UK/United Kingdom -- New York, N.Y. -- Science. 2012 Jan 27;335(6067):475-9. doi: 10.1126/science.1214100.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lymphocyte Interaction Laboratory, London Research Institute, Cancer Research UK, 44 Lincoln's Inn Fields, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22282815" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigen Presentation ; Antigens/*analysis/*immunology ; B-Lymphocytes/cytology/*immunology ; Cell Division ; Cell Proliferation ; Cells, Cultured ; Coculture Techniques ; Computer Simulation ; Flow Cytometry ; *Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Models, Immunological ; Muramidase/analysis/immunology ; T-Lymphocytes/*immunology
    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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    Interactions between cancer stem cells and their niche govern metastatic colonization (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-12-14
    Description: Metastatic growth in distant organs is the major cause of cancer mortality. The development of metastasis is a multistage process with several rate-limiting steps. Although dissemination of tumour cells seems to be an early and frequent event, the successful initiation of metastatic growth, a process termed 'metastatic colonization', is inefficient for many cancer types and is accomplished only by a minority of cancer cells that reach distant sites. Prevalent target sites are characteristic of many tumour entities, suggesting that inadequate support by distant tissues contributes to the inefficiency of the metastatic process. Here we show that a small population of cancer stem cells is critical for metastatic colonization, that is, the initial expansion of cancer cells at the secondary site, and that stromal niche signals are crucial to this expansion process. We find that periostin (POSTN), a component of the extracellular matrix, is expressed by fibroblasts in the normal tissue and in the stroma of the primary tumour. Infiltrating tumour cells need to induce stromal POSTN expression in the secondary target organ (in this case lung) to initiate colonization. POSTN is required to allow cancer stem cell maintenance, and blocking its function prevents metastasis. POSTN recruits Wnt ligands and thereby increases Wnt signalling in cancer stem cells. We suggest that the education of stromal cells by infiltrating tumour cells is an important step in metastatic colonization and that preventing de novo niche formation may be a novel strategy for the treatment of metastatic disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malanchi, Ilaria -- Santamaria-Martinez, Albert -- Susanto, Evelyn -- Peng, Hong -- Lehr, Hans-Anton -- Delaloye, Jean-Francois -- Huelsken, Joerg -- England -- Nature. 2011 Dec 7;481(7379):85-9. doi: 10.1038/nature10694.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ecole Polytechnique Federale de Lausanne, Swiss Institute for Experimental Cancer Research and National Center of Competence in Research Molecular Oncology, 1015 Lausanne, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22158103" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/pathology ; Cell Adhesion Molecules/genetics/metabolism ; Female ; Lung Neoplasms/secondary ; Mice ; Mice, Inbred C57BL ; Neoplasm Metastasis/*pathology ; Neoplastic Stem Cells/metabolism/*pathology ; Stem Cell Niche/*physiology ; Stromal Cells/metabolism ; Wnt Signaling Pathway
    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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  • 10
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    CLP1 links tRNA metabolism to progressive motor-neuron loss (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-03-12
    Description: CLP1 was the first mammalian RNA kinase to be identified. However, determining its in vivo function has been elusive. Here we generated kinase-dead Clp1 (Clp1(K/K)) mice that show a progressive loss of spinal motor neurons associated with axonal degeneration in the peripheral nerves and denervation of neuromuscular junctions, resulting in impaired motor function, muscle weakness, paralysis and fatal respiratory failure. Transgenic rescue experiments show that CLP1 functions in motor neurons. Mechanistically, loss of CLP1 activity results in accumulation of a novel set of small RNA fragments, derived from aberrant processing of tyrosine pre-transfer RNA. These tRNA fragments sensitize cells to oxidative-stress-induced p53 (also known as TRP53) activation and p53-dependent cell death. Genetic inactivation of p53 rescues Clp1(K/K) mice from the motor neuron loss, muscle denervation and respiratory failure. Our experiments uncover a mechanistic link between tRNA processing, formation of a new RNA species and progressive loss of lower motor neurons regulated by p53.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3674495/" 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/PMC3674495/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanada, Toshikatsu -- Weitzer, Stefan -- Mair, Barbara -- Bernreuther, Christian -- Wainger, Brian J -- Ichida, Justin -- Hanada, Reiko -- Orthofer, Michael -- Cronin, Shane J -- Komnenovic, Vukoslav -- Minis, Adi -- Sato, Fuminori -- Mimata, Hiromitsu -- Yoshimura, Akihiko -- Tamir, Ido -- Rainer, Johannes -- Kofler, Reinhard -- Yaron, Avraham -- Eggan, Kevin C -- Woolf, Clifford J -- Glatzel, Markus -- Herbst, Ruth -- Martinez, Javier -- Penninger, Josef M -- K99NS077435-01A1/NS/NINDS NIH HHS/ -- NS038253/NS/NINDS NIH HHS/ -- P 19223/Austrian Science Fund FWF/Austria -- P 21667/Austrian Science Fund FWF/Austria -- R00 NS077435/NS/NINDS NIH HHS/ -- R01 NS038253/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Mar 28;495(7442):474-80. doi: 10.1038/nature11923. Epub 2013 Mar 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉IMBA, Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Vienna 1030, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23474986" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis ; Animals ; Animals, Newborn ; Axons/metabolism/pathology ; Cell Death ; Diaphragm/innervation ; Embryo Loss ; Embryo, Mammalian/metabolism/pathology ; Exons/genetics ; Female ; Fibroblasts ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Motor Neurons/*metabolism/*pathology ; Muscular Atrophy, Spinal ; Neuromuscular Diseases/metabolism/pathology ; Oxidative Stress ; RNA Processing, Post-Transcriptional ; RNA, Transfer, Tyr/genetics/*metabolism ; Respiration ; Spinal Nerves/cytology ; Transcription Factors/deficiency/*metabolism ; Tumor Suppressor Protein p53/metabolism ; Tyrosine/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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