35 research outputs found

    Comparative evaluation of the efficiency of the BG-Sentinel trap, CDC light trap and Mosquito-oviposition trap for the surveillance of vector mosquitoes

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    Distribution of the traps in the third week of each month. A. Liangtian (suburban area), B. Tonghe (urban area). Twelve each of BGS Traps, CDC Light Traps and MOTs were used to survey the mosquito density in Tonghe and Liangtian. (PDF 639 kb

    Century-Long Increasing Trend and Variability of Dissolved Organic Carbon Export from the Mississippi River Basin Driven by Natural and Anthropogenic Forcing

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    There has been considerable debate as to how natural forcing and anthropogenic activities alter the timing and magnitude of the delivery of dissolved organic carbon (DOC) to the coastal ocean, which has ramifications for the ocean carbon budget, land-ocean interactions, and coastal life. Here we present an analysis of DOC export from the Mississippi River to the Gulf of Mexico during 1901–2010 as influenced by changes in climate, land use and management practices, atmospheric CO2, and nitrogen deposition, through the integration of observational data with a coupled hydrologic/biogeochemical land model. Model simulations show that DOC export in the 2000s increased more than 40% since the 1900s. For the recent three decades (1981–2010), however, our simulated DOC export did not show a significant increasing trend, which is consistent with observations by U.S. Geological Survey. Our factorial analyses suggest that land use and land cover change, including land management practices (LMPs: i.e., fertilization, irrigation, tillage, etc.), were the dominant contributors to the century-scale trend of rising total riverine DOC export, followed by changes in atmospheric CO2, nitrogen deposition, and climate. Decadal and interannual variations of DOC export were largely attributed to year-to-year climatic variability and extreme flooding events, which have been exacerbated by human activity. LMPs show incremental contributions to DOC increase since the 1960s, indicating the importance of sustainable agricultural practices in coping with future environmental changes such as extreme flooding events. Compared to the observational-based estimate, the modeled DOC export was 20% higher, while DOC concentrations were slightly lower. Further refinements in model structure and input data sets should enable reductions in uncertainties in our prediction of century-long trends in DOC

    Climate Extremes Dominating Seasonal and Interannual Variations in Carbon Export from the Mississippi River Basinariations in Carbon Export from the Mississippi River Basin

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    Knowledge about the annual and seasonal patterns of organic and inorganic carbon (C) exports from the major rivers of the world to the coastal ocean is essential for our understanding and potential management of the global C budget so as to limit anthropogenic modification of global climate. Unfortunately our predictive understanding of what controls the timing, magnitude, and quality of C export is still rudimentary. Here we use a process-based coupled hydrologic/ecosystem biogeochemistry model (the Dynamic Land Ecosystem Model) to examine how climate variability and extreme events, changing land use, and atmospheric chemistry have affected the annual and seasonal patterns of C exports from the Mississippi River basin to the Gulf of Mexico. Our process-based simulations estimate that the average annual exports of dissolved organic C (DOC), particulate organic C (POC), and dissolved inorganic C (DIC) in the 2000s were 2.6 ± 0.4 Tg C yr−1, 3.4 ± 0.3 Tg C yr−1, and 18.8 ± 3.4 Tg C yr−1, respectively. Although land use change was the most important agent of change in C export over the past century, climate variability and extreme events (such as flooding and drought) were primarily responsible for seasonal and interannual variations in C export from the basin. The maximum seasonal export of DIC occurred in summer while for DOC and POC the maximum occurred in winter. Relative to the 10 year average (2001–2010), our modeling analysis indicates that the years of maximal and minimal C export cooccurred with wet and dry years (2008: 32% above average and 2006: 32% below average). Given Intergovernmental Panel on Climate Change-predicted changes in climate variability and the severity of rain events and droughts of wet and dry years for the remainder of the 21st century, our modeling results suggest major changes in the riverine link between the terrestrial and oceanic realms, which are likely to have a major impact on C delivery to the coastal ocean

    Relative contribution of risk factors for early-onset myopia in young Asian children

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    10.1167/iovs.15-16577Clinical and Epidemiologic Research56138101-8107GUSTO (Growing up towards Healthy Outcomes

    Analysis of the outward currents induced by metabolic inhibition

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    Astract: The aim of this work was to investigate whether the inward rectifying current Ik1 participates in the response of the myocardium to metabolic inhibition and to evaluate quantitatively the contribution of IK,ATP to the increase in outward current elicited by metabolic inhibition. The work was carried out on freshly isolated rabbit ventricular myocytes at room temperature using the patch clamp technique in the whole cell configuration. Steady-state currents (Iss) were measured at the end of 400 ms long pulses. The results showed that the current vs voltage relationship in control conditions varied with [K]o, 50 /µM Ba2+ abolished inward rectification of Iss and 30 µM glibenclamide had no effect on Iss in control conditions. This confirmed that the main component of Iss was Ik1 and that IK,ATP contribute to Iss in control. Metabolic inhibition with Carbonyl cyanide m-chlorophenylhydrazone (CCCP) induced a large time-independent, outward rectifying current which was reversible by washout even at a high concentration of 50 µM. This current was partially (about 45 to 50 %) inhibited by 30 µM glibenclamide. The blockade was time and voltage independent. Fifty micromolar Ba2+ also decreased the GLIB-insensitive component of the current induced by CCCP by about 40% at 0 mV and shifted the reversal potential from -72 to -54 mV. The conductance of this Ba2+ sensitive component at the reversal potential in the presence of CCCP and glibenclamide was higher than that at physiological [K]o in control conditions. Our data suggest that Ik1 was the main component of the CCCP induced current but that Ik1 was also involved in the response. Moreover, the Ik1 conductance seems to have changed and contributes to maintain the resting potential in response to metabolic inhibition. However, neither of these blockers alone nor even both together could not fully reverse the CCCP induced current at potential levels corresponding to the plateau whereas the same concentration of glibenclamide fully reversed the current elicited by a K-ATP channel opener, BRL-38277. The Ba2+ concentration that blocks Ik1 in control and partly inhibits the CCCP induced current had no significant effect on IK,ATP. However, a higher concentration of Ba2+ (100 µM) did partially block the BRL induced current without effect on reversal potential. Therefore, we conclude that Ik1 is the main component of Iss in control conditions and that IK,ATP does not contribute to it. Glibenclamide is a specifie blocker of the K-ATP channel and a low concentration of Ba2+ (50 µM) does not significantly inhibit K-ATP channels. IK,ATP and Ik1 contributed in the response to metabolic inhibition in rabbit ventricular myocytes. However, neither our work nor the work of others carried out in isolated cells could quantify the contributions of IK,ATP and Ik1 to the action potential shortening produced by metabolic inhibition with preservation of glycolysis. On the other hand, other current component(s) not yet identified should participate to fully explain the responses observed in isolated myocytes. || Résumé: Le but de ce travail était de vérifier si le courant à rectification entrante Ik1 participait à la réponse du myocarde à un stress métabolique et d'évaluer la contribution du courant IK,ATP courant sortant déclenché par l'inhibition métabolique. Le modèle expérimental était des myocytes ventriculaires de lapin et la méthode, celle du "patch clamp" en configuration cellule entière. En conditions témoins, la courbe courant voltage du courant au régime établi Iss (à la fin des "puises" de 400 ms de durée) variait en fonction du [K]o, la rectification entrante était abolie par 50 µM Ba2+, et le courant global était insensible à la glibenclamide. L'inhibiteur carbonyl-cyanure m-chlorophenylhydrazone (CCCP) a produit le développement d'un courant à rectification sortant. L'effet était réversible même à haute concentration de CCCP (50 µM). Ce courant était partiellement (45-50%) inhibé par la glibenclamide. La fraction insensible à la glibenclamide était encore réduite par 40% par exposition à 50 µM Ba2+. Le Ba2+ a aussi déplacé le potentiel l'inversion de -72 à -54 mV. La "slope conductance" du courant sensible au Ba2+ au niveau du potentiel d'inversion était plus grande que la valeur témoin en [K]o normal. Nos résultats suggèrent que le courant IK,ATP est la composante majeure du courant induit par l'inhibition métabolique mais que le courant Ik1 était aussi impliqué dans la réponse globale parce que sa conductance au niveau du potentiel de repos était augmentée. L'inhibition partielle du courant induite par CCCP par la glibenclamide et le barium n'était pas dû à un manque de spécificité de ces bloqueurs parce que la glibenclamide a aboli le courant déclanché par un activateur des canaux ATP sensibles tandis que le Ba2+ à faible concentration n'a eu aucun effet sur ce courant. A partir de nos données, nous atteignons les conclusions suivantes: 1. Iki est la composante la plus importante du courant de fonds en condition témoin; 2. Les canaux ATP sensibles sont bloqués par la concentration de glibenclamide employée dans cette étude mais ne sont pas affectés par une basse concentration de Ba2+; 3. les systèmes Ik-atp et Ik1 contribuent à la réponse à l'inhibition métabolique. La contribution de Ik1 explique le maintien du potentiel de repos malgré la perte de K+ cellulaire. A cause des limitations inhérentes aux méthodes employées, il est difficile d'extrapoler les résultats obtenus sur des myocytes isolés aux observations faites sur des préparations multicellulaires en conditions d'hypoxie modérée et préservation de la glycolise anaérobique qui ressemblent d'avantage à des conditions in vivo

    Analysis of the outward currents induced by metabolic inhibition

    No full text
    Astract: The aim of this work was to investigate whether the inward rectifying current Ik1 participates in the response of the myocardium to metabolic inhibition and to evaluate quantitatively the contribution of IK,ATP to the increase in outward current elicited by metabolic inhibition. The work was carried out on freshly isolated rabbit ventricular myocytes at room temperature using the patch clamp technique in the whole cell configuration. Steady-state currents (Iss) were measured at the end of 400 ms long pulses. The results showed that the current vs voltage relationship in control conditions varied with [K]o, 50 /µM Ba2+ abolished inward rectification of Iss and 30 µM glibenclamide had no effect on Iss in control conditions. This confirmed that the main component of Iss was Ik1 and that IK,ATP contribute to Iss in control. Metabolic inhibition with Carbonyl cyanide m-chlorophenylhydrazone (CCCP) induced a large time-independent, outward rectifying current which was reversible by washout even at a high concentration of 50 µM. This current was partially (about 45 to 50 %) inhibited by 30 µM glibenclamide. The blockade was time and voltage independent. Fifty micromolar Ba2+ also decreased the GLIB-insensitive component of the current induced by CCCP by about 40% at 0 mV and shifted the reversal potential from -72 to -54 mV. The conductance of this Ba2+ sensitive component at the reversal potential in the presence of CCCP and glibenclamide was higher than that at physiological [K]o in control conditions. Our data suggest that Ik1 was the main component of the CCCP induced current but that Ik1 was also involved in the response. Moreover, the Ik1 conductance seems to have changed and contributes to maintain the resting potential in response to metabolic inhibition. However, neither of these blockers alone nor even both together could not fully reverse the CCCP induced current at potential levels corresponding to the plateau whereas the same concentration of glibenclamide fully reversed the current elicited by a K-ATP channel opener, BRL-38277. The Ba2+ concentration that blocks Ik1 in control and partly inhibits the CCCP induced current had no significant effect on IK,ATP. However, a higher concentration of Ba2+ (100 µM) did partially block the BRL induced current without effect on reversal potential. Therefore, we conclude that Ik1 is the main component of Iss in control conditions and that IK,ATP does not contribute to it. Glibenclamide is a specifie blocker of the K-ATP channel and a low concentration of Ba2+ (50 µM) does not significantly inhibit K-ATP channels. IK,ATP and Ik1 contributed in the response to metabolic inhibition in rabbit ventricular myocytes. However, neither our work nor the work of others carried out in isolated cells could quantify the contributions of IK,ATP and Ik1 to the action potential shortening produced by metabolic inhibition with preservation of glycolysis. On the other hand, other current component(s) not yet identified should participate to fully explain the responses observed in isolated myocytes. || Résumé: Le but de ce travail était de vérifier si le courant à rectification entrante Ik1 participait à la réponse du myocarde à un stress métabolique et d'évaluer la contribution du courant IK,ATP courant sortant déclenché par l'inhibition métabolique. Le modèle expérimental était des myocytes ventriculaires de lapin et la méthode, celle du "patch clamp" en configuration cellule entière. En conditions témoins, la courbe courant voltage du courant au régime établi Iss (à la fin des "puises" de 400 ms de durée) variait en fonction du [K]o, la rectification entrante était abolie par 50 µM Ba2+, et le courant global était insensible à la glibenclamide. L'inhibiteur carbonyl-cyanure m-chlorophenylhydrazone (CCCP) a produit le développement d'un courant à rectification sortant. L'effet était réversible même à haute concentration de CCCP (50 µM). Ce courant était partiellement (45-50%) inhibé par la glibenclamide. La fraction insensible à la glibenclamide était encore réduite par 40% par exposition à 50 µM Ba2+. Le Ba2+ a aussi déplacé le potentiel l'inversion de -72 à -54 mV. La "slope conductance" du courant sensible au Ba2+ au niveau du potentiel d'inversion était plus grande que la valeur témoin en [K]o normal. Nos résultats suggèrent que le courant IK,ATP est la composante majeure du courant induit par l'inhibition métabolique mais que le courant Ik1 était aussi impliqué dans la réponse globale parce que sa conductance au niveau du potentiel de repos était augmentée. L'inhibition partielle du courant induite par CCCP par la glibenclamide et le barium n'était pas dû à un manque de spécificité de ces bloqueurs parce que la glibenclamide a aboli le courant déclanché par un activateur des canaux ATP sensibles tandis que le Ba2+ à faible concentration n'a eu aucun effet sur ce courant. A partir de nos données, nous atteignons les conclusions suivantes: 1. Iki est la composante la plus importante du courant de fonds en condition témoin; 2. Les canaux ATP sensibles sont bloqués par la concentration de glibenclamide employée dans cette étude mais ne sont pas affectés par une basse concentration de Ba2+; 3. les systèmes Ik-atp et Ik1 contribuent à la réponse à l'inhibition métabolique. La contribution de Ik1 explique le maintien du potentiel de repos malgré la perte de K+ cellulaire. A cause des limitations inhérentes aux méthodes employées, il est difficile d'extrapoler les résultats obtenus sur des myocytes isolés aux observations faites sur des préparations multicellulaires en conditions d'hypoxie modérée et préservation de la glycolise anaérobique qui ressemblent d'avantage à des conditions in vivo

    Physiological and anatomical changes in two rapeseed (Brassica napus L.) genotypes under drought stress conditions

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    Understanding the mechanisms of drought resistance in crop species is crucial for the selection and breeding of tolerant rapeseed (Brassica napus L.) varieties. The present study aimed to assess the physiological and anatomical responses of two rapeseed genotypes, P287 (drought-tolerant) and T88 (drought-sensitive) under three intensities of drought stress. All physiological and anatomical parameters related to drought acclimation were significantly altered in both genotypes under stress conditions. At the fourth-leaf stage, the relative water content, chlorophyll content, protein content, malondialdehyde content, and the activities of peroxidase and catalase in P287 were significantly higher than those in T88, particularly under severe drought conditions. After rehydration, all physiological indexes recovered rapidly, especially in P287. In addition, under drought stress, compared with T88, P287 had thicker palisade tissue, thinner spongy tissue, higher ratio of chloroplast length to chloroplast width, higher stomatal density and stomatal closure rate. Overall, the interaction between physiological and anatomical features improved the drought tolerance of P287 under drought stress conditions
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