Institution
Rutgers University
Education•New Brunswick, New Jersey, United States•
About: Rutgers University is a education organization based out in New Brunswick, New Jersey, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 68736 authors who have published 159418 publications receiving 6713860 citations. The organization is also known as: Rutgers, The State University of New Jersey & Rutgers.
Topics: Population, Poison control, Health care, Cancer, Galaxy
Papers published on a yearly basis
Papers
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TL;DR: It is shown that subinhibitory concentrations of aminoglycoside antibiotics induce biofilm formation in P. aeruginosa and Escherichia coli, and the molecular basis of this response includes alterations in the level of c-di-GMP.
Abstract: Biofilms are adherent aggregates of bacterial cells that form on biotic and abiotic surfaces, including human tissues. Biofilms resist antibiotic treatment and contribute to bacterial persistence in chronic infections. Hence, the elucidation of the mechanisms by which biofilms are formed may assist in the treatment of chronic infections, such as Pseudomonas aeruginosa in the airways of patients with cystic fibrosis. Here we show that subinhibitory concentrations of aminoglycoside antibiotics induce biofilm formation in P. aeruginosa and Escherichia coli. In P. aeruginosa, a gene, which we designated aminoglycoside response regulator (arr), was essential for this induction and contributed to biofilm-specific aminoglycoside resistance. The arr gene is predicted to encode an inner-membrane phosphodiesterase whose substrate is cyclic di-guanosine monophosphate (c-di-GMP)-a bacterial second messenger that regulates cell surface adhesiveness. We found that membranes from arr mutants had diminished c-di-GMP phosphodiesterase activity, and P. aeruginosa cells with a mutation changing a predicted catalytic residue of Arr were defective in their biofilm response to tobramycin. Furthermore, tobramycin-inducible biofilm formation was inhibited by exogenous GTP, which is known to inhibit c-di-GMP phosphodiesterase activity. Our results demonstrate that biofilm formation can be a specific, defensive reaction to the presence of antibiotics, and indicate that the molecular basis of this response includes alterations in the level of c-di-GMP.
1,172 citations
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TL;DR: Animal models of PD have yielded some insights into the molecular pathways of neuronal degeneration and highlighted previously unknown mechanisms by which oxidative stress contributes to PD, but therapeutic attempts to target the general state of oxidative stress in clinical trials have failed to demonstrate an impact on disease progression.
Abstract: Oxidative stress plays an important role in the degeneration of dopaminergic neurons in Parkinson's disease (PD). Disruptions in the physiologic maintenance of the redox potential in neurons interfere with several biological processes, ultimately leading to cell death. Evidence has been developed for oxidative and nitrative damage to key cellular components in the PD substantia nigra. A number of sources and mechanisms for the generation of reactive oxygen species (ROS) are recognized including the metabolism of dopamine itself, mitochondrial dysfunction, iron, neuroinflammatory cells, calcium, and aging. PD causing gene products including DJ-1, PINK1, parkin, alpha-synuclein and LRRK2 also impact in complex ways mitochondrial function leading to exacerbation of ROS generation and susceptibility to oxidative stress. Additionally, cellular homeostatic processes including the ubiquitin-proteasome system and mitophagy are impacted by oxidative stress. It is apparent that the interplay between these various mechanisms contributes to neurodegeneration in PD as a feed forward scenario where primary insults lead to oxidative stress, which damages key cellular pathogenetic proteins that in turn cause more ROS production. Animal models of PD have yielded some insights into the molecular pathways of neuronal degeneration and highlighted previously unknown mechanisms by which oxidative stress contributes to PD. However, therapeutic attempts to target the general state of oxidative stress in clinical trials have failed to demonstrate an impact on disease progression. Recent knowledge gained about the specific mechanisms related to PD gene products that modulate ROS production and the response of neurons to stress may provide targeted new approaches towards neuroprotection.
1,171 citations
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15 Mar 2008TL;DR: The sections in this article are==================PRECI and the standard isotherm concept as mentioned in this paper, the BET method, the standard isotope concept, and an assessment of porosity.
Abstract: The sections in this article are
Introduction
Physisorption of Gases
Determination of Surface Area
The BET Method
The Standard Isotherm Concept
Assessment of Porosity
Capillary Condensation and the Kelvin Equation
Adsorption Hysteresis
Microporosity
Micropore Analysis: Dubinin's Theory of Micropore Filling
Micropore Analysis: Empirical Methods
Other Methods for Micropore Pore Size Analysis
Application of Density Functional Theory
Adsorption at the Liquid–Solid Interface
Adsorption from Solution
Heat of Immersion
Mercury Porosimetry
General Conclusions
Keywords:
physisorption;
pore size;
mercury porosimetry;
heat of immersion
1,170 citations
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TL;DR: It is found that the level of subsidiary R&D depends on MNE group‐level and subsidiary‐level characteristics as well as locational factors, and that MNEs that grow through acquisition have more inter‐subsidiary R &D diversity.
Abstract: The determinants of R&D intensity differ between subsidiaries in a multinational enterprise (MNE). Previous literature suggests that whether a subsidiary achieves a competence-creating output mandate depends on the qualities of its location. R&D strategies in competence-creating subsidiaries are supply-driven while those in purely competence-exploiting subsidiaries are demand-driven. Using data on U.K. subsidiaries of non-U.K. MNEs, we find that the level of subsidiary R&D depends on MNE group-level and subsidiary-level characteristics as well as locational factors. The R&D of mandated subsidiaries rises with acquisition, but for non-mandated subsidiaries R&D falls upon acquisition. MNEs that grow through acquisition have more inter-subsidiary R&D diversity. Copyright © 2005 John Wiley & Sons, Ltd.
1,170 citations
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TL;DR: The robust, consistent and inducible nature of the ChR2 mice represents a significant advance over previous lines, and the Arch-ER2 and eNpHR3.0 mice are to the authors' knowledge the first demonstration of successful conditional transgenic optogenetic silencing.
Abstract: Cell type-specific expression of optogenetic molecules allows temporally precise manipulation of targeted neuronal activity. Here we present a toolbox of four knock-in mouse lines engineered for strong, Cre-dependent expression of channelrhodopsins ChR2-tdTomato and ChR2-EYFP, halorhodopsin eNpHR3.0 and archaerhodopsin Arch-ER2. All four transgenes mediated Cre-dependent, robust activation or silencing of cortical pyramidal neurons in vitro and in vivo upon light stimulation, with ChR2-EYFP and Arch-ER2 demonstrating light sensitivity approaching that of in utero or virally transduced neurons. We further show specific photoactivation of parvalbumin-positive interneurons in behaving ChR2-EYFP reporter mice. The robust, consistent and inducible nature of our ChR2 mice represents a significant advance over previous lines, and the Arch-ER2 and eNpHR3.0 mice are to our knowledge the first demonstration of successful conditional transgenic optogenetic silencing. When combined with the hundreds of available Cre driver lines, this optimized toolbox of reporter mice will enable widespread investigations of neural circuit function with unprecedented reliability and accuracy.
1,168 citations
Authors
Showing all 69437 results
Name | H-index | Papers | Citations |
---|---|---|---|
Salim Yusuf | 231 | 1439 | 252912 |
Daniel Levy | 212 | 933 | 194778 |
Eugene V. Koonin | 199 | 1063 | 175111 |
Eric Boerwinkle | 183 | 1321 | 170971 |
David L. Kaplan | 177 | 1944 | 146082 |
Derek R. Lovley | 168 | 582 | 95315 |
Mark Gerstein | 168 | 751 | 149578 |
Gang Chen | 167 | 3372 | 149819 |
Hongfang Liu | 166 | 2356 | 156290 |
Robert Stone | 160 | 1756 | 167901 |
Mark E. Cooper | 158 | 1463 | 124887 |
Michael B. Sporn | 157 | 559 | 94605 |
Cumrun Vafa | 157 | 509 | 88515 |
Wolfgang Wagner | 156 | 2342 | 123391 |
David M. Sabatini | 155 | 413 | 135833 |