Institution
University of Massachusetts Medical School
Education•Worcester, Massachusetts, United States•
About: University of Massachusetts Medical School is a education organization based out in Worcester, Massachusetts, United States. It is known for research contribution in the topics: Population & Health care. The organization has 16161 authors who have published 31822 publications receiving 1909739 citations. The organization is also known as: UMass Medical School.
Topics: Population, Health care, Immune system, Gene, Signal transduction
Papers published on a yearly basis
Papers
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TL;DR: Simulations based on concentrations and kinetic parameters of GLUT1 and −3 in BBB endothelial cells, astrocytes, and neurons, along with the corresponding kinetic properties of the MCTs, have successfully modeled brain glucose and lactate levels as well as lactate transients in response to neuronal stimulation.
Abstract: Glucose is the obligate energetic fuel for the mammalian brain, and most studies of cerebral energy metabolism assume that the majority of cerebral glucose utilization fuels neuronal activity via oxidative metabolism, both in the basal and activated state. Glucose transporter (GLUT) proteins deliver glucose from the circulation to the brain: GLUT1 in the microvascular endothelial cells of the blood-brain barrier (BBB) and glia; GLUT3 in neurons. Lactate, the glycolytic product of glucose metabolism, is transported into and out of neural cells by the monocarboxylate transporters (MCT): MCT1 in the BBB and astrocytes and MCT2 in neurons. The proposal of the astrocyte-neuron lactate shuttle hypothesis suggested that astrocytes play the primary role in cerebral glucose utilization and generate lactate for neuronal energetics, especially during activation. Since the identification of the GLUTs and MCTs in brain, much has been learned about their transport properties, that is capacity and affinity for substrate, which must be considered in any model of cerebral glucose uptake and utilization. Using concentrations and kinetic parameters of GLUT1 and -3 in BBB endothelial cells, astrocytes, and neurons, along with the corresponding kinetic properties of the MCTs, we have successfully modeled brain glucose and lactate levels as well as lactate transients in response to neuronal stimulation. Simulations based on these parameters suggest that glucose readily diffuses through the basal lamina and interstitium to neurons, which are primarily responsible for glucose uptake, metabolism, and the generation of the lactate transients observed on neuronal activation.
716 citations
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TL;DR: The full range of antiviral functions of CD4+ T cells are reviewed, discussing the activities of these cells in helping other lymphocytes and in inducing innate immune responses, as well as their direct antiviral roles.
Abstract: Viral pathogens often induce strong effector CD4(+) T cell responses that are best known for their ability to help B cell and CD8(+) T cell responses. However, recent studies have uncovered additional roles for CD4(+) T cells, some of which are independent of other lymphocytes, and have described previously unappreciated functions for memory CD4(+) T cells in immunity to viruses. Here, we review the full range of antiviral functions of CD4(+) T cells, discussing the activities of these cells in helping other lymphocytes and in inducing innate immune responses, as well as their direct antiviral roles. We suggest that all of these functions of CD4(+) T cells are integrated to provide highly effective immune protection against viral pathogens.
714 citations
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TL;DR: It is confirmed that disrupted miRNA pairing, not changes in PHB protein sequence, causes the developmental defects in phb‐d mutants, supporting a model in which this region of the silencing RNA nucleates pairing to its target.
Abstract: MicroRNAs (miRNAs) are B22-nucleotide noncoding RNAs that can regulate gene expression by directing mRNA degradation or inhibiting productive translation. Dominant mutations in PHABULOSA (PHB )a ndPHAVOLUTA (PHV) map to a miR165/166 complementary site and impair miRNA-guided cleavage of these mRNAs in vitro. Here, we confirm that disrupted miRNA pairing, not changes in PHB protein sequence, causes the developmental defects in phb-d mutants. In planta, disrupting miRNA pairing near the center of the miRNA complementary site had far milder developmental consequences than more distal mismatches. These differences correlated with differences in miRNA-directed cleavage efficiency in vitro, where mismatch scanning revealed more tolerance for mismatches at the center and 3 0 end of the miRNA compared to mismatches to the miRNA 5 0 region. In this respect, miR165/ 166 resembles animal miRNAs in its pairing requirements. Pairing to the 5 0 portion of the small silencing RNA appears crucial regardless of the mode of post-transcriptional repression or whether it occurs in plants or animals, supporting a model in which this region of the silencing RNA nucleates pairing to its target.
714 citations
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New England Biolabs1, New York State Department of Health2, Columbia University3, Wayne State University4, University of Basel5, University of Toledo6, University of Edinburgh7, University of Alabama8, University of Portsmouth9, Moscow State University10, University of Illinois at Chicago11, University of Bristol12, University of Rochester13, Duke University14, University of Sheffield15, Vilnius University16, University of Giessen17, University of Copenhagen18, Hungarian Academy of Sciences19, North Carolina State University20, University of Tokyo21, Humboldt University of Berlin22, Brookhaven National Laboratory23, University of Massachusetts Medical School24, National Institutes of Health25, Indian Institute of Science26, University of Warsaw27, University of California, Santa Barbara28, State Research Center of Virology and Biotechnology VECTOR29, University of Oregon30, The Chinese University of Hong Kong31, University of Maryland, College Park32, Fred Hutchinson Cancer Research Center33, University of Wisconsin-Madison34, University of Nebraska–Lincoln35, University of Lisbon36
TL;DR: In this article, a nomenclature for restriction endonucleases, DNA methyltransferases, homing endon nucleases and related genes and gene products is described.
Abstract: A nomenclature is described for restriction endonucleases, DNA methyltransferases, homing endonucleases and related genes and gene products. It provides explicit categories for the many different Type II enzymes now identified and provides a system for naming the putative genes found by sequence analysis of microbial genomes.
710 citations
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TL;DR: Within this chapter, the majority of recommendations are separate for neonates and children, reflecting the significant differences in epidemiology of thrombosis and safety and efficacy of therapy in these two populations.
708 citations
Authors
Showing all 16331 results
Name | H-index | Papers | Citations |
---|---|---|---|
Michael Karin | 236 | 704 | 226485 |
Richard A. Flavell | 231 | 1328 | 205119 |
Robert M. Califf | 196 | 1561 | 167961 |
Eric J. Topol | 193 | 1373 | 151025 |
Joan Massagué | 189 | 408 | 149951 |
Stuart H. Orkin | 186 | 715 | 112182 |
Ramachandran S. Vasan | 172 | 1100 | 138108 |
Mark Gerstein | 168 | 751 | 149578 |
David R. Jacobs | 165 | 1262 | 113892 |
Bruce L. Miller | 163 | 1153 | 115975 |
Yuh Nung Jan | 162 | 460 | 74818 |
Christopher J. O'Donnell | 159 | 869 | 126278 |
David W. Bates | 159 | 1239 | 116698 |
Adi F. Gazdar | 157 | 776 | 104116 |
John E. Morley | 154 | 1377 | 97021 |