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L. M. Nath

Bio: L. M. Nath is an academic researcher from University of Dhaka. The author has contributed to research in topics: Pion & Nucleon. The author has an hindex of 8, co-authored 22 publications receiving 421 citations. Previous affiliations of L. M. Nath include International Centre for Theoretical Physics & International Centre for Genetic Engineering and Biotechnology.

Papers
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Journal ArticleDOI
05 Mar 2010-Cell
TL;DR: A genome-wide siRNA screen to identify host factors that regulated pathogen load in human macrophages infected with a virulent strain of Mycobacterium tuberculosis identified 275 molecules that were all found to functionally associate with each other through a dense network of interactions.

328 citations

Journal ArticleDOI
TL;DR: In this paper, a field theory model for photoproduction of pions at low energy is presented, and the free parameters in the theory representing the off-mass-shell effects of the spin-3/2 particles are fixed on the basis of theoretical considerations.
Abstract: Presented in this paper is a field theory model for photoproduction of pions at low energy. In particular, it is shown that certain interaction terms, which were previously considered to be essential in order to explain the experimental situation corresponding to the spin-3/2 resonances, are really unnecessary and that the presence of these terms are not justifiable from the theoretical point of view. Further, the free parameters in the theory representing the off-mass-shell effects of the spin-3/2 particles are fixed on the basis of theoretical considerations.

18 citations

Journal ArticleDOI
TL;DR: In this paper, the parity-violating effects in the (quasi)elastic scattering of longitudinally polarized electrons from spin-textonehalf{} targets are discussed in the framework of the unified guage theories of weak and electromagnetic interactions.
Abstract: Parity-violating effects in the (quasi)elastic scattering of longitudinally polarized electrons from spin-\textonehalf{} targets are discussed in the framework of the unified guage theories of weak and electromagnetic interactions. In particular, the $R\ensuremath{-}L$ asymmetry in electroproduction of the $\ensuremath{\Delta}(1232)$ is studied in considerable detail, taking into account the full spin-$\frac{3}{2}$ structure of this resonance. Our results are valid for all values of $E$ and the entire range of ${Q}^{2}$. Numerical predictions are given for the standard Weinberg-Salam model at several energies of the electron beam.

13 citations

Journal ArticleDOI
TL;DR: In this article, it was shown that the spin 2 field equations are consistent with the subsidiary conditions, irrespective of the value of the parameter A. The covariant commutation relations for the free field do not depend on the parameters A, but the propagators do.

12 citations

Journal ArticleDOI
TL;DR: In this paper, the Yang-Feldman formalism was used to obtain the condition for the anticommutator between a spin-$\frac{3}{2}$ field and its Hermitian conjugate to be positive definite.
Abstract: The electrodynamics of spin-$\frac{3}{2}$ particles is discussed in this paper. In particular, the spin-$\frac{3}{2}$ field in the presence of the minimal electromagnetic interaction is quantized by using the Yang-Feldman formalism. The Hamiltonian for this system is obtained explicitly and the commutation relations derived in this paper are shown to be consistent with Heisenberg's equations of motion. In this formalism, the condition for the anticommutator between a spin-$\frac{3}{2}$ field and its Hermitian conjugate to be positive definite is simple to formulate.

11 citations


Cited by
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Journal ArticleDOI
Luke Jostins1, Stephan Ripke2, Rinse K. Weersma3, Richard H. Duerr4, Dermot P.B. McGovern5, Ken Y. Hui6, James Lee7, L. Philip Schumm8, Yashoda Sharma6, Carl A. Anderson1, Jonah Essers9, Mitja Mitrovic3, Kaida Ning6, Isabelle Cleynen10, Emilie Theatre11, Sarah L. Spain12, Soumya Raychaudhuri9, Philippe Goyette13, Zhi Wei14, Clara Abraham6, Jean-Paul Achkar15, Tariq Ahmad16, Leila Amininejad17, Ashwin N. Ananthakrishnan9, Vibeke Andersen18, Jane M. Andrews19, Leonard Baidoo4, Tobias Balschun20, Peter A. Bampton21, Alain Bitton22, Gabrielle Boucher13, Stephan Brand23, Carsten Büning24, Ariella Cohain25, Sven Cichon26, Mauro D'Amato27, Dirk De Jong3, Kathy L Devaney9, Marla Dubinsky5, Cathryn Edwards28, David Ellinghaus20, Lynnette R. Ferguson29, Denis Franchimont17, Karin Fransen3, Richard B. Gearry30, Michel Georges11, Christian Gieger, Jürgen Glas22, Talin Haritunians5, Ailsa Hart31, Christopher J. Hawkey32, Matija Hedl6, Xinli Hu9, Tom H. Karlsen33, Limas Kupčinskas34, Subra Kugathasan35, Anna Latiano36, Debby Laukens37, Ian C. Lawrance38, Charlie W. Lees39, Edouard Louis11, Gillian Mahy40, John C. Mansfield41, Angharad R. Morgan29, Craig Mowat42, William G. Newman43, Orazio Palmieri36, Cyriel Y. Ponsioen44, Uroš Potočnik45, Natalie J. Prescott6, Miguel Regueiro4, Jerome I. Rotter5, Richard K Russell46, Jeremy D. Sanderson47, Miquel Sans, Jack Satsangi39, Stefan Schreiber20, Lisa A. Simms48, Jurgita Sventoraityte34, Stephan R. Targan, Kent D. Taylor5, Mark Tremelling49, Hein W. Verspaget50, Martine De Vos37, Cisca Wijmenga3, David C. Wilson39, Juliane Winkelmann51, Ramnik J. Xavier9, Sebastian Zeissig20, Bin Zhang25, Clarence K. Zhang6, Hongyu Zhao6, Mark S. Silverberg52, Vito Annese, Hakon Hakonarson53, Steven R. Brant54, Graham L. Radford-Smith55, Christopher G. Mathew12, John D. Rioux13, Eric E. Schadt25, Mark J. Daly2, Andre Franke20, Miles Parkes7, Severine Vermeire10, Jeffrey C. Barrett1, Judy H. Cho6 
Wellcome Trust Sanger Institute1, Broad Institute2, University of Groningen3, University of Pittsburgh4, Cedars-Sinai Medical Center5, Yale University6, University of Cambridge7, University of Chicago8, Harvard University9, Katholieke Universiteit Leuven10, University of Liège11, King's College London12, Université de Montréal13, New Jersey Institute of Technology14, Cleveland Clinic15, Peninsula College of Medicine and Dentistry16, Université libre de Bruxelles17, Aarhus University18, University of Adelaide19, University of Kiel20, Flinders University21, McGill University22, Ludwig Maximilian University of Munich23, Charité24, Icahn School of Medicine at Mount Sinai25, University of Bonn26, Karolinska Institutet27, Torbay Hospital28, University of Auckland29, Christchurch Hospital30, Imperial College London31, Queen's University32, University of Oslo33, Lithuanian University of Health Sciences34, Emory University35, Casa Sollievo della Sofferenza36, Ghent University37, University of Western Australia38, University of Edinburgh39, Queensland Health40, Newcastle University41, University of Dundee42, University of Manchester43, University of Amsterdam44, University of Maribor45, Royal Hospital for Sick Children46, Guy's and St Thomas' NHS Foundation Trust47, QIMR Berghofer Medical Research Institute48, Norfolk and Norwich University Hospital49, Leiden University50, Technische Universität München51, University of Toronto52, University of Pennsylvania53, Johns Hopkins University54, University of Queensland55
01 Nov 2012-Nature
TL;DR: A meta-analysis of Crohn’s disease and ulcerative colitis genome-wide association scans is undertaken, followed by extensive validation of significant findings, with a combined total of more than 75,000 cases and controls.
Abstract: Crohn's disease and ulcerative colitis, the two common forms of inflammatory bowel disease (IBD), affect over 2.5 million people of European ancestry, with rising prevalence in other populations. Genome-wide association studies and subsequent meta-analyses of these two diseases as separate phenotypes have implicated previously unsuspected mechanisms, such as autophagy, in their pathogenesis and showed that some IBD loci are shared with other inflammatory diseases. Here we expand on the knowledge of relevant pathways by undertaking a meta-analysis of Crohn's disease and ulcerative colitis genome-wide association scans, followed by extensive validation of significant findings, with a combined total of more than 75,000 cases and controls. We identify 71 new associations, for a total of 163 IBD loci, that meet genome-wide significance thresholds. Most loci contribute to both phenotypes, and both directional (consistently favouring one allele over the course of human history) and balancing (favouring the retention of both alleles within populations) selection effects are evident. Many IBD loci are also implicated in other immune-mediated disorders, most notably with ankylosing spondylitis and psoriasis. We also observe considerable overlap between susceptibility loci for IBD and mycobacterial infection. Gene co-expression network analysis emphasizes this relationship, with pathways shared between host responses to mycobacteria and those predisposing to IBD.

4,094 citations

Journal ArticleDOI
20 Jan 2011-Nature
TL;DR: A crucial role is revealed for the autophagy pathway and proteins in immunity and inflammation, and they balance the beneficial and detrimental effects of immunity andinflammation, and thereby may protect against infectious, autoimmune and inflammatory diseases.
Abstract: Autophagy is an essential, homeostatic process by which cells break down their own components. Perhaps the most primordial function of this lysosomal degradation pathway is adaptation to nutrient deprivation. However, in complex multicellular organisms, the core molecular machinery of autophagy - the 'autophagy proteins' - orchestrates diverse aspects of cellular and organismal responses to other dangerous stimuli such as infection. Recent developments reveal a crucial role for the autophagy pathway and proteins in immunity and inflammation. They balance the beneficial and detrimental effects of immunity and inflammation, and thereby may protect against infectious, autoimmune and inflammatory diseases.

2,757 citations

Journal ArticleDOI
TL;DR: An overview of the mechanisms and regulation of autophagy, the role of this pathway in disease and strategies for therapeutic modulation is provided.
Abstract: The lysosomal degradation pathway known as autophagy has an essential homeostatic role in controlling the quality of the cytoplasm. However, this pathway has also been implicated in the pathology of an array of human disorders. Here, Rubinsztein and colleagues provide an overview of the mechanisms and regulation of autophagy, discuss the role of this pathway in disease and highlight potential strategies for therapeutic modulation.

1,292 citations

Journal ArticleDOI
Anil Koul1, Eric Arnoult1, Nacer Lounis1, Jerome Guillemont1, Koen Andries1 
27 Jan 2011-Nature
TL;DR: In this review, innovations in TB drug discovery and evolving strategies to bring newer agents more quickly to patients are discussed.
Abstract: Tuberculosis (TB) is more prevalent in the world today than at any other time in human history Mycobacterium tuberculosis, the pathogen responsible for TB, uses diverse strategies to survive in a variety of host lesions and to evade immune surveillance A key question is how robust are our approaches to discovering new TB drugs, and what measures could be taken to reduce the long and protracted clinical development of new drugs The emergence of multi-drug-resistant strains of M tuberculosis makes the discovery of new molecular scaffolds a priority, and the current situation even necessitates the re-engineering and repositioning of some old drug families to achieve effective control Whatever the strategy used, success will depend largely on our proper understanding of the complex interactions between the pathogen and its human host In this review, we discuss innovations in TB drug discovery and evolving strategies to bring newer agents more quickly to patients

953 citations

Journal ArticleDOI
17 Aug 2012-Cell
TL;DR: It is shown that phagosomal permeabilization mediated by the bacterial ESX-1 secretion system allows cytosolic components of the ubiquitin-mediated autophagy pathway access to Phagosomal M. tuberculosis infection and indicates a major role for this autophagic pathway in resistance to M.culosis.

649 citations