Institution
University of Nevada, Reno
Education•Reno, Nevada, United States•
About: University of Nevada, Reno is a education organization based out in Reno, Nevada, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 13561 authors who have published 28217 publications receiving 882002 citations. The organization is also known as: University of Nevada & Nevada State University.
Papers published on a yearly basis
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TL;DR: The current state of knowledge on the role of ROS-induced oxidative stress in altering the genetic and epigenetic involvement during human carcinogenesis is reviewed.
Abstract: Cancer is a multistage and complex process characterized by molecular alterations that underlie all three phases of its development: (i) initiation, (ii) promotion and (iii) progression. Some of these molecular events include alterations in gene expression that are regulated by both genetic and epigenetic mechanisms. On the other hand, "oxidative stress" implies a cellular state where ROS production exceeds the cell's ability to metabolize them resulting in excessive accumulation of ROS that overwhelms cellular defenses. Such state has been shown to regulate both genetic and epigenetic cascades underlying altered gene expression in human disease including cancer. Throughout this manuscript, we review the current state of knowledge on the role of ROS-induced oxidative stress in altering the genetic and epigenetic involvement during human carcinogenesis.
476 citations
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TL;DR: Multineuron patch-clamp recordings in the ferret medial prefrontal cortex showed a heterogeneity of synapses interconnecting distinct subnetworks of different pyramidal cells, which could amplify recurrent interactions between pyramides and support persistent activity in the prefrontal cortex.
Abstract: The prefrontal cortex is specially adapted to generate persistent activity that outlasts stimuli and is resistant to distractors, presumed to be the basis of working memory. The pyramidal network that supports this activity is unknown. Multineuron patch-clamp recordings in the ferret medial prefrontal cortex showed a heterogeneity of synapses interconnecting distinct subnetworks of different pyramidal cells. One subnetwork was similar to the pyramidal network commonly found in primary sensory areas, consisting of accommodating pyramidal cells interconnected with depressing synapses. The other subnetwork contained complex pyramidal cells with dual apical dendrites displaying nonaccommodating discharge patterns; these cells were hyper-reciprocally connected with facilitating synapses displaying pronounced synaptic augmentation and post-tetanic potentiation. These cellular, synaptic and network properties could amplify recurrent interactions between pyramidal neurons and support persistent activity in the prefrontal cortex.
474 citations
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University of Colorado Boulder1, ETH Zurich2, Universidad Autónoma del Estado de Morelos3, Paul Scherrer Institute4, University of Reading5, University of Wisconsin-Madison6, Montana State University7, Texas A&M University8, Saint Louis University9, Brookhaven National Laboratory10, Pacific Northwest National Laboratory11, University of Arkansas12, University of Nevada, Reno13, Massachusetts Institute of Technology14
TL;DR: In this article, an analysis of high resolution OA spectra was performed at the T0 urban supersite in Mexico City with a High-Resolution Time-of-Flight Aerosol Mass Spectrometer (HR-ToF-AMS) and complementary instrumentation.
Abstract: . Submicron aerosol was analyzed during the MILAGRO field campaign in March 2006 at the T0 urban supersite in Mexico City with a High-Resolution Time-of-Flight Aerosol Mass Spectrometer (HR-ToF-AMS) and complementary instrumentation. Mass concentrations, diurnal cycles, and size distributions of inorganic and organic species are similar to results from the CENICA supersite in April 2003 with organic aerosol (OA) comprising about half of the fine PM mass. Positive Matrix Factorization (PMF) analysis of the high resolution OA spectra identified three major components: chemically-reduced urban primary emissions (hydrocarbon-like OA, HOA), oxygenated OA (OOA, mostly secondary OA or SOA), and biomass burning OA (BBOA) that correlates with levoglucosan and acetonitrile. BBOA includes several very large plumes from regional fires and likely also some refuse burning. A fourth OA component is a small local nitrogen-containing reduced OA component (LOA) which accounts for 9% of the OA mass but one third of the organic nitrogen, likely as amines. OOA accounts for almost half of the OA on average, consistent with previous observations. OA apportionment results from PMF-AMS are compared to the PM2.5 chemical mass balance of organic molecular markers (CMB-OMM, from GC/MS analysis of filters). Results from both methods are overall consistent. Both assign the major components of OA to primary urban, biomass burning/woodsmoke, and secondary sources at similar magnitudes. The 2006 Mexico City emissions inventory underestimates the urban primary PM2.5 emissions by a factor of ~4, and it is ~16 times lower than afternoon concentrations when secondary species are included. Additionally, the forest fire contribution is at least an order-of-magnitude larger than in the inventory.
472 citations
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TL;DR: In this article, the authors reviewed relevant literature which deals with various manifestations of energy absorption of composites from the nano to the macro-scale, with emphasis on the nano-scale.
472 citations
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TL;DR: The established mechanisms by which oxidative stress and environmental stressors regulate the apoptotic machinery are reviewed with the aim of underscore the relevance of apoptosis as a component in environmental toxicity and human disease progression.
Abstract: Apoptosis is an evolutionary conserved homeostatic process involved in distinct physiological processes including organ and tissue morphogenesis, development and senescence. Its deregulation is also known to participate in the etiology of several human diseases including cancer, neurodegenerative and autoimmune disorders. Environmental stressors (cytotoxic agents, pollutants or toxicants) are well known to induce apoptotic cell death and to contribute to a variety of pathological conditions. Oxidative stress seems to be the central element in the regulation of the apoptotic pathways triggered by environmental stressors. In this work, we review the established mechanisms by which oxidative stress and environmental stressors regulate the apoptotic machinery with the aim to underscore the relevance of apoptosis as a component in environmental toxicity and human disease progression.
470 citations
Authors
Showing all 13726 results
Name | H-index | Papers | Citations |
---|---|---|---|
Robert Langer | 281 | 2324 | 326306 |
Thomas C. Südhof | 191 | 653 | 118007 |
David W. Johnson | 160 | 2714 | 140778 |
Menachem Elimelech | 157 | 547 | 95285 |
Jeffrey L. Cummings | 148 | 833 | 116067 |
Bing Zhang | 121 | 1194 | 56980 |
Arturo Casadevall | 120 | 980 | 55001 |
Mark H. Ellisman | 117 | 637 | 55289 |
Thomas G. Ksiazek | 113 | 398 | 46108 |
Anthony G. Fane | 112 | 565 | 40904 |
Leonardo M. Fabbri | 109 | 566 | 60838 |
Gary H. Lyman | 108 | 694 | 52469 |
Steven C. Hayes | 106 | 450 | 51556 |
Stephen P. Long | 103 | 384 | 46119 |
Gary Cutter | 103 | 737 | 40507 |