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Vikas Pareek

Bio: Vikas Pareek is an academic researcher from National Brain Research Centre. The author has contributed to research in topics: Furin & Pathogenesis. The author has an hindex of 9, co-authored 41 publications receiving 356 citations. Previous affiliations of Vikas Pareek include Indian Institute of Technology Gandhinagar.
Topics: Furin, Pathogenesis, Genome, Proteases, Virus

Papers
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Journal ArticleDOI
TL;DR: An extensive overview of the role of reactive oxygen species (ROS)-induced oxidative stress and its fatal effects on brain after TBI is provided.
Abstract: Background & objective Traumatic Brain Injury (TBI) is one of the major causes of mortality and morbidity worldwide. It represents mild, moderate and severe effects of physical assault to brain which may cause sequential, primary or secondary ramifications. Primary injury can be due to the first physical hit, blow or jolt to one of the brain compartments. The primary injury is then followed by secondary injury which leads to biochemical, cellular, and physiological changes like blood brain barrier disruption, inflammation, excitotoxicity, necrosis, apoptosis, mitochondrial dysfunction and generation of oxidative stress. Apart from this, there is also an immediate increase in glutamate at the synapses following severe TBI. Excessive glutamate at synapses in turn activates corresponding NMDA and AMPA receptors that facilitate excessive calcium influx into the neuronal cells. This leads to the generation of oxidative stress which further leads to mitochondrial dysfunction, lipid peroxidation and oxidation of proteins and DNA. As a consequence, neuronal cell death takes place and ultimately people start facing some serious disabilies. Conclusion In the present review we provide extensive overview of the role of reactive oxygen species (ROS)-induced oxidative stress and its fatal effects on brain after TBI.

162 citations

Journal ArticleDOI
Michael P. Milham, Christopher I. Petkov, Daniel S. Margulies, Charles E. Schroeder, Michele A. Basso, Pascal Belin, Damien A. Fair, Andrew S. Fox, Sabine Kastner, Rogier B. Mars, Adam Messinger, Colline Poirier, Wim Vanduffel, David C. Van Essen, Ashkan Alvand, Yannick Becker, Suliann Ben Hamed, Austin Benn, Clémentine Bodin, Susann Boretius, Bastien Cagna, Olivier Coulon, Sherif Hamdy El-Gohary, Henry C. Evrard1, Stephanie J. Forkel, Patrick Friedrich, Sean Froudist-Walsh, Eduardo A. Garza-Villarreal, Yang Gao, Alessandro Gozzi, Antoine Grigis, Renée Hartig1, Takuya Hayashi, Katja Heuer, Henrietta Howells, Dirk Jan Ardesch, Béchir Jarraya, Wendy Jarrett, Hank P. Jedema, Igor Kagan, Clare Kelly, Henry Kennedy, P. Christiaan Klink, Sze Chai Kwok, Robert Leech, Xiaojin Liu, Christopher R. Madan, Wasana Madushanka, Piotr Majka, Ann-Marie Mallon, Kevin Marche, Adrien Meguerditchian, Ravi S. Menon, Hugo Merchant, Anna S. Mitchell, Karl-Heinz Nenning, Aki Nikolaidis, Michael Ortiz-Rios, Marco Pagani, Vikas Pareek, Mark J. Prescott, Emmanuel Procyk, Reza Rajimehr, Ioana-Sabina Rautu, Amir Raz, Anna W. Roe, Román Rossi-Pool, Lea Roumazeilles, Tomoko Sakai, Jerome Sallet, Pamela Garcia-Saldivar, Chika Sato, Stephen J. Sawiak, Marike Schiffer, Caspar M. Schwiedrzik, Jakob Seidlitz, Julien Sein, Zhi-ming Shen, Amir Shmuel, Afonso C. Silva, Luciano Simone, Nikoloz Sirmpilatze, Julia Sliwa, Jonathan Smallwood, Jordy Tasserie, Michel Thiebaut de Schotten, Roberto Toro, Régis Trapeau, Lynn Uhrig, Julien Vezoli, Zheng Wang, Sara Wells, Bella Williams, Ting Xu, Augix Guohua Xu, Essa Yacoub, Ming Zhan, Lei Ai, Céline Amiez, Fabien Balezeau, Mark G. Baxter, Erwin L. A. Blezer, Thomas Brochier, Aihua Chen, Paula L. Croxson, Christienne G. Damatac, Stanislas Dehaene, Stefan Everling, Lazar Fleysher, Winrich A. Freiwald, Timothy D. Griffiths, Carole Guedj, Fadila Hadj-Bouziane, Noam Harel, Bassem Hiba, Benjamin Jung, Bonhwang Koo, Kevin N. Laland, David A. Leopold, Patrik Lindenfors, Martine Meunier, Kelvin Mok, John H. Morrison, Jennifer Nacef, Jamie Nagy, Mark A. Pinsk, Simon M. Reader, Pieter R. Roelfsema, David A. Rudko, Matthew F. S. Rushworth, Brian E. Russ, Michael C. Schmid, Elinor L. Sullivan, Alexander Thiele, Orlin S. Todorov, Doris Y. Tsao, Leslie G. Ungerleider, Charles R.E. Wilson, Frank Q. Ye, Wilbert Zarco, Yong-di Zhou 
19 Feb 2020-Neuron
TL;DR: Inspired by an open data-sharing initiative, the global community recently met and, in this article, breaks through obstacles to define its ambitions.

85 citations

Journal ArticleDOI
TL;DR: Investigators provided robust evidence that SARS‐CoV‐2‐specific virulence factors may have an impact on viral infectivity and transmissibility and disease severity as well as the development of immunity against the infection, including response to the vaccines.
Abstract: The paucity of knowledge about severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-specific virulence factors has greatly hampered the therapeutic management of patients with coronavirus disease 2019 (COVID-19). Recently, a cluster of studies appeared, which presented empirical evidence for SARS-CoV-2-specific virulence factors that can explain key elements of COVID-19 pathology. These studies unravel multiple structural and nonstructural specifics of SARS-CoV-2, such as a unique FURIN cleavage site, papain-like protease (SCoV2-PLpro), ORF3b and nonstructural proteins, and dynamic conformational changes in the structure of spike protein during host cell fusion, which give it an edge in infectivity and virulence over previous coronaviruses causing pandemics. Investigators provided robust evidence that SARS-CoV-2-specific virulence factors may have an impact on viral infectivity and transmissibility and disease severity as well as the development of immunity against the infection, including response to the vaccines. In this article, we are presenting a summarized account of the newly reported studies.

52 citations

Journal ArticleDOI
TL;DR: This work proposes a SARS-CoV-2 cell entry receptor ACE2 based mechanism for vascular thrombosis in COVID-19 patients, which is based on the circumstantial evidence present in the literature.

49 citations

Journal ArticleDOI
TL;DR: This review article has discussed the possible routes of SARS‐CoV‐2 brain entry based on the emerging evidence for this virus, and that available for other betacoronaviruses in literature.
Abstract: Manifestation of neurological symptoms in certain patients of coronavirus disease-2019 (COVID-19) has warranted for their virus-induced etiogenesis. SARS-CoV-2, the causative agent of COVID-19, belongs to the genus of betacoronaviruses which also includes SARS-CoV-1 and MERS-CoV; causative agents for severe acute respiratory syndrome (SARS) in 2002 and Middle East respiratory syndrome (MERS) in 2012, respectively. Studies demonstrating the neural invasion of SARS-CoV-2 in vivo are still scarce, although such characteristics of certain other betacoronaviruses are well demonstrated in the literature. Based on the recent evidence for the presence of SARS-CoV-2 host cell entry receptors in specific components of the human nervous and vascular tissue, a neural (olfactory and/or vagal), and a hematogenous-crossing the blood-brain barrier, routes have been proposed. The neurological symptoms in COVID-19 may also arise as a consequence of the "cytokine storm" (characteristically present in severe disease) induced neuroinflammation, or co-morbidities. There is also a possibility that, there may be multiple routes of SARS-CoV-2 entry into the brain, or multiple mechanisms can be involved in the pathogenesis of the neurological symptoms. In this review article, we have discussed the possible routes of SARS-CoV-2 brain entry based on the emerging evidence for this virus, and that available for other betacoronaviruses in literature.

41 citations


Cited by
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DOI
01 Jan 2020

1,967 citations

Dissertation
01 Jan 2006

273 citations

Journal Article
TL;DR: In this paper, the authors used a mouse model of cytomegalovirus infection to show that, like T cells, NK cells bearing the virus-specific Ly49H receptor proliferate 100fold in the spleen and 1,000-fold in liver after infection.
Abstract: In an adaptive immune response, naive T cells proliferate during infection and generate long-lived memory cells that undergo secondary expansion after a repeat encounter with the same pathogen. Although natural killer (NK) cells have traditionally been classified as cells of the innate immune system, they share many similarities with cytotoxic T lymphocytes. We use a mouse model of cytomegalovirus infection to show that, like T cells, NK cells bearing the virus-specific Ly49H receptor proliferate 100-fold in the spleen and 1,000-fold in the liver after infection. After a contraction phase, Ly49H-positive NK cells reside in lymphoid and non-lymphoid organs for several months. These self-renewing 'memory' NK cells rapidly degranulate and produce cytokines on reactivation. Adoptive transfer of these NK cells into naive animals followed by viral challenge results in a robust secondary expansion and protective immunity. These findings reveal properties of NK cells that were previously attributed only to cells of the adaptive immune system.

194 citations

01 Sep 2020
TL;DR: There is currently no evidence for intrauterine infection caused by vertical transmission in women who develop COVID-19 pneumonia in late pregnancy, according to this small group of cases.
Abstract: Summary Background Previous studies on the pneumonia outbreak caused by the 2019 novel coronavirus disease (COVID-19) were based on information from the general population. Limited data are available for pregnant women with COVID-19 pneumonia. This study aimed to evaluate the clinical characteristics of COVID-19 in pregnancy and the intrauterine vertical transmission potential of COVID-19 infection. Methods Clinical records, laboratory results, and chest CT scans were retrospectively reviewed for nine pregnant women with laboratory-confirmed COVID-19 pneumonia (ie, with maternal throat swab samples that were positive for severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2]) who were admitted to Zhongnan Hospital of Wuhan University, Wuhan, China, from Jan 20 to Jan 31, 2020. Evidence of intrauterine vertical transmission was assessed by testing for the presence of SARS-CoV-2 in amniotic fluid, cord blood, and neonatal throat swab samples. Breastmilk samples were also collected and tested from patients after the first lactation. Findings All nine patients had a caesarean section in their third trimester. Seven patients presented with a fever. Other symptoms, including cough (in four of nine patients), myalgia (in three), sore throat (in two), and malaise (in two), were also observed. Fetal distress was monitored in two cases. Five of nine patients had lymphopenia ( Interpretation The clinical characteristics of COVID-19 pneumonia in pregnant women were similar to those reported for non-pregnant adult patients who developed COVID-19 pneumonia. Findings from this small group of cases suggest that there is currently no evidence for intrauterine infection caused by vertical transmission in women who develop COVID-19 pneumonia in late pregnancy. Funding Hubei Science and Technology Plan, Wuhan University Medical Development Plan.

181 citations

01 Jan 2020
TL;DR: This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record.
Abstract: This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

155 citations