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Institution

University of Massachusetts Medical School

EducationWorcester, 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.


Papers
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Journal ArticleDOI
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

Journal ArticleDOI
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

Journal ArticleDOI
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

Journal ArticleDOI
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

Journal ArticleDOI
01 Jun 2008-Chest
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

NameH-indexPapersCitations
Michael Karin236704226485
Richard A. Flavell2311328205119
Robert M. Califf1961561167961
Eric J. Topol1931373151025
Joan Massagué189408149951
Stuart H. Orkin186715112182
Ramachandran S. Vasan1721100138108
Mark Gerstein168751149578
David R. Jacobs1651262113892
Bruce L. Miller1631153115975
Yuh Nung Jan16246074818
Christopher J. O'Donnell159869126278
David W. Bates1591239116698
Adi F. Gazdar157776104116
John E. Morley154137797021
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202341
2022241
20212,038
20201,960
20191,734
20181,653