Institution
University of Texas Medical Branch
Education•Galveston, Texas, United States•
About: University of Texas Medical Branch is a education organization based out in Galveston, Texas, United States. It is known for research contribution in the topics: Population & Virus. The organization has 22033 authors who have published 38268 publications receiving 1517502 citations. The organization is also known as: The University of Texas Medical Branch at Galveston & UTMB.
Topics: Population, Virus, Poison control, Immune system, Receptor
Papers published on a yearly basis
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University of Oxford1, University of Birmingham2, University of São Paulo3, Oswaldo Cruz Foundation4, Fred Hutchinson Cancer Research Center5, University of Washington6, Evandro Chagas Institute7, Pasteur Institute8, Ontario Institute for Cancer Research9, University of Nottingham10, Scripps Research Institute11, University of California, San Francisco12, Mexican Social Security Institute13, National Autonomous University of Mexico14, Paul Ehrlich Institute15, University of Pittsburgh16, Colorado State University17, University Hospital Heidelberg18, State University of Feira de Santana19, Federal University of Amazonas20, Federal University of Tocantins21, University of Sydney22, University of Edinburgh23, National Institutes of Health24, University of Texas Medical Branch25
TL;DR: The origin and epidemic history of ZIKV in Brazil and the Americas remain poorly understood, despite the value of this information for interpreting observed trends in reported microcephaly and other birth defects as mentioned in this paper.
Abstract: Transmission of Zika virus (ZIKV) in the Americas was first confirmed in May 2015 in northeast Brazil. Brazil has had the highest number of reported ZIKV cases worldwide (more than 200,000 by 24 December 2016) and the most cases associated with microcephaly and other birth defects (2,366 confirmed by 31 December 2016). Since the initial detection of ZIKV in Brazil, more than 45 countries in the Americas have reported local ZIKV transmission, with 24 of these reporting severe ZIKV-associated disease. However, the origin and epidemic history of ZIKV in Brazil and the Americas remain poorly understood, despite the value of this information for interpreting observed trends in reported microcephaly. Here we address this issue by generating 54 complete or partial ZIKV genomes, mostly from Brazil, and reporting data generated by a mobile genomics laboratory that travelled across northeast Brazil in 2016. One sequence represents the earliest confirmed ZIKV infection in Brazil. Analyses of viral genomes with ecological and epidemiological data yield an estimate that ZIKV was present in northeast Brazil by February 2014 and is likely to have disseminated from there, nationally and internationally, before the first detection of ZIKV in the Americas. Estimated dates for the international spread of ZIKV from Brazil indicate the duration of pre-detection cryptic transmission in recipient regions. The role of northeast Brazil in the establishment of ZIKV in the Americas is further supported by geographic analysis of ZIKV transmission potential and by estimates of the basic reproduction number of the virus.
470 citations
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TL;DR: In this article, the authors examined antigen-specific B-cell responses in peripheral blood and draining lymph nodes in 14 individuals who had received 2-doses of BNT162b2, an mRNA-based vaccine that encodes the full-length SARS-CoV-2 spike (S) gene1.
Abstract: SARS-CoV-2 mRNA-based vaccines are about 95% effective in preventing COVID-191–5. The dynamics of antibody-secreting plasmablasts and germinal centre B cells induced by these vaccines in humans remain unclear. Here we examined antigen-specific B cell responses in peripheral blood (n = 41) and draining lymph nodes in 14 individuals who had received 2 doses of BNT162b2, an mRNA-based vaccine that encodes the full-length SARS-CoV-2 spike (S) gene1. Circulating IgG- and IgA-secreting plasmablasts that target the S protein peaked one week after the second immunization and then declined, becoming undetectable three weeks later. These plasmablast responses preceded maximal levels of serum anti-S binding and neutralizing antibodies to an early circulating SARS-CoV-2 strain as well as emerging variants, especially in individuals who had previously been infected with SARS-CoV-2 (who produced the most robust serological responses). By examining fine needle aspirates of draining axillary lymph nodes, we identified germinal centre B cells that bound S protein in all participants who were sampled after primary immunization. High frequencies of S-binding germinal centre B cells and plasmablasts were sustained in these draining lymph nodes for at least 12 weeks after the booster immunization. S-binding monoclonal antibodies derived from germinal centre B cells predominantly targeted the receptor-binding domain of the S protein, and fewer clones bound to the N-terminal domain or to epitopes shared with the S proteins of the human betacoronaviruses OC43 and HKU1. These latter cross-reactive B cell clones had higher levels of somatic hypermutation as compared to those that recognized only the SARS-CoV-2 S protein, which suggests a memory B cell origin. Our studies demonstrate that SARS-CoV-2 mRNA-based vaccination of humans induces a persistent germinal centre B cell response, which enables the generation of robust humoral immunity. Analysis of antigen-specific B cells in lymph nodes of individuals vaccinated with BNT162b2 reveals lasting germinal centre responses, explaining the robust humoral immunity induced by SARS-CoV-2 mRNA-based vaccines.
470 citations
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TL;DR: Constitutive expression of viral proteins leads to common pathologic features of hepatitis C in the absence of specific anti-viral immune responses, while additional low level expression of nonstructural proteins increases the risk of cancer.
469 citations
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TL;DR: A functional role for PKCα is identified as a functional Bcl2 kinase that can enhance cell resistance to antileukemic chemotherapy and suggest a novel target for antileukesmic strategies.
469 citations
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TL;DR: Data indicate that the residue in position 104 helps to define the geometry of the hydrophobic substrate-binding site, and may also influence activity by interacting with residues directly involved in substrate binding.
Abstract: Glutathione S-transferase P1-1 isoforms, differing in a single amino acid residue (Ile104 or Val104), have been previously identified in human placenta [Ahmad, H., Wilson, D. E., Fritz, R. R., Singh, S. V., Medh, R. D., Nagle, G. T., Awasthi, Y. C. & Kurosky, A. (1990) Arch. Biochem. Biophys. 278, 398-408]. In the present report, the enzymic properties of these two proteins are compared. [I104]glutathione S-transferase P1-1 has been expressed from its cDNA in Escherichia coli and purified to homogeneity by affinity chromatography; the cDNA has been mutated to replace Ile104 by Val104, and [V104]glutathione S-transferase P1-1 was expressed and isolated as described for [I104]glutathione S-transferase P1-1. The two enzymes differed in their specific activity and affinity for electrophilic substrates (KM values for 1-chloro-2,4-dinitrobenzene were 0.8 mM and 3.0 mM for [I-104]glutathione S-transferase P1-1 and [V-104]glutathione S-transferase P1-1, respectively), but were identical in their affinity for glutathione. In addition, the two enzymes were distinguishable by their heat stability, with half-lives at 45 degrees C of 19 min and 51 min, respectively. The resistance to heat denaturation was differentially modulated by the presence of substrates. These data, in conjunction with molecular modeling, indicate that the residue in position 104 helps to define the geometry of the hydrophobic substrate-binding site, and may also influence activity by interacting with residues directly involved in substrate binding.
469 citations
Authors
Showing all 22143 results
Name | H-index | Papers | Citations |
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Stuart H. Orkin | 186 | 715 | 112182 |
Eric R. Kandel | 184 | 603 | 113560 |
John C. Morris | 183 | 1441 | 168413 |
Joseph Biederman | 179 | 1012 | 117440 |
Richard A. Gibbs | 172 | 889 | 249708 |
Timothy A. Springer | 167 | 669 | 122421 |
Gabriel N. Hortobagyi | 166 | 1374 | 104845 |
Roberto Romero | 151 | 1516 | 108321 |
Charles B. Nemeroff | 149 | 979 | 90426 |
Peter J. Schwartz | 147 | 647 | 107695 |
Clifford J. Woolf | 141 | 509 | 86164 |
Thomas J. Smith | 140 | 1775 | 113919 |
Edward C. Holmes | 138 | 824 | 85748 |
Jun Lu | 135 | 1526 | 99767 |
Henry T. Lynch | 133 | 925 | 86270 |