393 research outputs found
Atmospheric Balloon Studies : A Collaboration Between Minority and Traditional Undergraduate and Graduate Institutions
The Minority University Consortium for Earth and Space Sciences (MUCESS), a collaboration among diverse minority institutions dedicated to increasing the number of underrepresented students pursuing professional and research careers in Earth and Atmospheric Science and Space Science, were informed that they had been funded by NSF for a faculty and student research opportunity in atmospheric science. Among the institutions only Medgar Evers College, City University of New York had a prior program in ozone monitoring and a bachelor's degree in environmental science. The funding provided an opportunity to strengthen the initial team with the addition of G. Morris, Valparaiso University and B. Lefer, University of Houston as both had an ongoing ozone research program. The grant enabled MEC to continue their activities and the University of Houston-Downtown to increase the number of launches per year. South Carolina State University is able to strengthen their support system and incorporate the activities into both their academic and outreach programs. The opportunity to partner with G. Morris and B. Lefer will enable the institutions to expand their ozonesonde launches to include both tropospheric and stratospheric ozone distribution and transport. Faculty student workshops will be an integral part of the program as the activity will increase the scientific knowledge of the participants. The program provides an opportunity for minority students to pursue studies in the geosciences and develop the skills and knowledge to pursue graduate degrees in the discipline.</p
Simplified or not simplified? The different guises of mediated English at the European Parliament
In this article we describe a framework for the corpus-based comparative investigation of interpreting and translation, illustrating it through a study of simplification across different modes of language production and across different language pairs. We rely on EPTIC, a corpus featuring plenary speeches at the European Parliament in their interpreted and translated versions, aligned to each other and to their source texts in EnglishItalian and EnglishFrench. Aiming to shed light on lexical simplification in different mediation modes, we compare interpretations and translations to each other and to comparable original speeches and their edited written versions. Specifically, we compare lexical features (lexical density, type-token ratio, core vocabulary and list head coverage) in interpreting and translation into English from French and Italian, both in a monolingual comparable perspective and an intermodal perspective. Our results do not unconditionally support the simplification hypothesis: lexical simplification is observed in mediated English, but is found to be greater when the source language is French, and in interpretations rather than translations. We conclude that this feature is contingent on both the mediation mode and the source languages involved, and that the influence of the latter seems to be stronger than that of the former
Word-formation in translated language: The impact of language-pair specific features and genre variation
Corpus-based studies in the field of word-formation have looked at translated language with the aim of (i) assessing the role of the source language (SL) in the overuse of certain derivational affixes in the target language (TL) and (ii) examining translationrelated, SL- and TL-independent trends such as the normalization of creative lexis. However, two aspects of the word-formation features of translated language remain underresearched: (i) language-pair specific properties which lead to a marked decrease in the use of certain word-forming devices in the target texts compared to their source texts (here referred to as ‘language-pair specific morphological decrease’) and (ii) the genre-sensitivity of word-forming devices in translated language. To examine these two aspects, we report on a corpus-based case study of the French translation of the English un- and in-prefixes. The translation data makes it possible to identify the following language-pair-related factors which are responsible for morphological decrease in French target texts: morphological productivity, diverging polysemy and partial phraseological equivalence. The study also shows that morphological decrease is significantly more frequent in fiction than in news, thereby indicating that genre also plays a major role in shaping the word-formation features of translated language
Notices biographiques
Notices biographiques de J.-J. Baude, A. Billiard, A. Bixio, A. Bouchené-Lefer, P. Boudet, J. Boulatignier, J. Boulay de la Meurthe, H. Boulay de la Meurthe, F. Carteret, H. Carteret, P. de Chasseloup-Laubat, Ch. Dunoyer de Segonzac, E. Janvier, F. de Jouvencel, A. P. É. Landrin, C. Lanyer, A. Legrand, Ch. Lesseps, L. Macarel, Ch. Maillard, A. Marchand, J.-L. B. O’Donnel, Ch. Paravey, A. Pons de l’Hérault, C. A. H. de Préval, J.-Ch. Rivet, G. E. Rousseau de Saint-Aignan, A. A. Stourm, J. S. Tournouër, É. Vincens, A. Vivien de Goubert</p
Global knockout of ROMK potassium channel worsens cardiac ischemia-reperfusion injury but cardiomyocyte-specific knockout does not: Implications for the identity of mitoKATP
The renal-outer-medullary‐potassium (ROMK) channel, mutated in Bartter's syndrome, regulates ion exchange in kidney, but its extra-renal functions remain unknown. Additionally, ROMK was postulated to be the pore-forming subunit of the mitochondrial ATP-sensitive K+ channel (mitoKATP), a mediator of cardioprotection. Using global and cardiomyocyte-specific knockout mice (ROMK-GKO and ROMK-CKO respectively), we characterize the effects of ROMK knockout on mitochondrial ion handling, the response to pharmacological KATP channel modulators, and ischemia/reperfusion (I/R) injury. Mitochondria from ROMK-GKO hearts exhibited a lower threshold for Ca2+-triggered permeability transition pore (mPTP) opening but normal matrix volume changes during oxidative phosphorylation. Isolated perfused ROMK-GKO hearts exhibited impaired functional recovery and increased infarct size when I/R was preceded by an ischemic preconditioning (IPC) protocol. Because ROMK-GKO mice exhibited severe renal defects and cardiac remodeling, we further characterized ROMK-CKO hearts to avoid confounding systemic effects. Mitochondria from ROMK-CKO hearts had unchanged matrix volume responses during oxidative phosphorylation and still swelled upon addition of a mitoKATP opener, but exhibited a lower threshold for mPTP opening, similar to GKO mitochondria. Nevertheless, I/R induced damage was not exacerbated in ROMK-CKO hearts, either ex vivo or in vivo. Lastly, we examined the response of ROMK-CKO hearts to ex vivo I/R injury with or without IPC and found that IPC still protected these hearts, suggesting that cardiomyocyte ROMK does not participate significantly in the cardioprotective pathway elicited by IPC. Collectively, our findings from these novel strains of mice suggest that cardiomyocyte ROMK is not a central mediator of mitoKATP function, although it can affect mPTP activation threshold
Diurnal tracking of anthropogenic CO2 emissions in the Los Angeles basin megacity during spring 2010
abstract: Attributing observed CO2 variations to human or natural cause is critical to deducing and tracking emissions from observations. We have used in situ CO2, CO, and planetary boundary layer height (PBLH) measurements recorded during the CalNex-LA (CARB et al., 2008) ground campaign of 15 May-15 June 2010, in Pasadena, CA, to deduce the diurnally varying anthropogenic component of observed CO2 in the megacity of Los Angeles (LA). This affordable and simple technique, validated by carbon isotope observations and WRF-STILT (Weather Research and Forecasting model - Stochastic Time-Inverted Lagrangian Transport model) predictions, is shown to robustly attribute observed CO2 variation to anthropogenic or biogenic origin over the entire diurnal cycle. During CalNex-LA, local fossil fuel combustion contributed up to similar to 50% of the observed CO2 enhancement overnight, and similar to 100% of the enhancement near midday. This suggests that sufficiently accurate total column CO2 observations recorded near midday, such as those from the GOSAT or OCO-2 satellites, can potentially be used to track anthropogenic emissions from the LA megacity.As published at http://www.atmos-chem-phys.net/13/4359/2013
Effects of NO synthase inhibitors on the synovial microcirculation in the mouse knee joint
Production of nitric oxide by the inducible NO synthase (iNOS) is known to be enhanced in chronic joint inflammation and osteoarthritis as well as aseptic loosening of joint prostheses. Initial studies yielded promising results after inhibition of the nitric oxide synthase (NOS). However, the effect of NOS inhibition has not been studied at the site of the primary function of NO, the microcirculation of the synovium in vivo. Using our recently developed model for the in vivo study of synovial microcirculation in the mouse knee joint, the effects of selective versus nonselective inhibition of iNOS were investigated by means of intravital fluorescence microscopy. After resection of the patella tendon, the synovial fatty tissue was exposed for intravital microscopy. Diameter of arterioles, functional capillary density (FCD), diameter of venules, venular red blood cell velocity and leukocyte-endothelial cell interaction were quantitatively analyzed before, and 10 and 60 min after intravenous injection of NOS inhibitors {[}selective iNOS inhibitor N-iminoethyl-L-lysine (L-NIL), and nonselective NOS inhibitor N-G-nitro-L-arginine methyl ester (L-NAME)]. Our results demonstrate that L-NAME causes a significant decrease in the arteriolar diameter and FCD associated with an increase in the leukocyte accumulation in the synovium in vivo. In contrast, L-NIL neither altered the microhemodynamics nor the leukocyte-endothelial cell interaction in the synovium, indicating its potential use for selective inhibition of iNOS in joint inflammation. Using our method, further studies will provide new insights into the unknown effect of NOS inhibition on the synovial microvasculature in inflammatory joint disease in vivo. Copyright (C) 1999 S. Karger AG, Basel
Tumor Necrosis Factor-α Contributes to Ischemia- and Reperfusion-Induced Endothelial Activation in Isolated Hearts
During myocardial reperfusion, polymorphonuclear neutrophil (PMN) adhesion involving the intercellular adhesion molecule-1 (ICAM-1) may lead to aggravation and prolongation of reperfusion injury. We studied the role of early tumor necrosis factor-α (TNF-α) cleavage and nuclear factor-κB (NF-κB) activation on ICAM-1 expression and venular adhesion of PMN in isolated hearts after ischemia (15 minutes) and reperfusion (30 to 480 minutes). NF-κB activation (electromobility shift assay) was found after 30 minutes of reperfusion and up to 240 minutes. ICAM-1 mRNA, assessed by Northern blot, increased during the same interval. Functional effect of newly synthesized adhesion molecules was found by quantification (in situ fluorescence microscopy) of PMN, given as bolus after ischemia, which became adherent to small coronary venules (10 to 50 mm in diameter). After 480 minutes of reperfusion, ICAM-1–dependent PMN adhesion increased 2.5-fold compared with PMN adhesion obtained during acute reperfusion. To study the influence of NF-κB on PMN adhesion, we inhibited NF-κB activation by transfection of NF-κB decoy oligonucleotides into isolated hearts using HJV-liposomes. Decoy NF-κB but not control oligonucleotides blocked ICAM-1 upregulation and inhibited the subacute increase in PMN adhesion. Similar effects were obtained using BB 1101 (10 μg), an inhibitor of TNF-α cleavage enzyme. These data suggest that ischemia and reperfusion in isolated hearts cause liberation of TNF-α, activation of NF-κB, and upregulation of ICAM-1, an adhesion molecule involved in inflammatory response after ischemia and reperfusion
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