H. All (h + all)

Distribution by Scientific Domains


Selected Abstracts


How to model shallow water-table depth variations: the case of the Kervidy-Naizin catchment, France

HYDROLOGICAL PROCESSES, Issue 4 2005
Jérôme Molénat
Abstract The aim of this work is threefold: (1) to identify the main characteristics of water-table variations from observations in the Kervidy-Naizin catchment, a small catchment located in western France; (2) to confront these characteristics with the assumptions of the Topmodel concepts; and (3) to analyse how relaxation of the assumptions could improve the simulation of distributed water-table depth. A network of piezometers was installed in the Kervidy-Naizin catchment and the water-table depth was recorded every 15 min in each piezometer from 1997 to 2000. From these observations, the Kervidy-Naizin groundwater appears to be characteristic of shallow groundwaters of catchments underlain by crystalline bedrock, in view of the strong relation between water distribution and topography in the bottom land of the hillslopes. However, from midslope to summit, the water table can attain a depth of many metres, it does not parallel the topographic surface and it remains very responsive to rainfall. In particular, hydraulic gradients vary with time and are not equivalent to the soil surface slope. These characteristics call into question some assumptions that are used to model shallow lateral subsurface flow in saturated conditions. We investigate the performance of three models (Topmodel, a kinematic model and a diffusive model) in simulating the hourly distributed water-table depths along one of the hillslope transects, as well as the hourly stream discharge. For each model, two sets of parameters are identified following a Monte Carlo procedure applied to a simulation period of 2649 h. The performance of each model with each of the two parameter sets is evaluated over a test period of 2158 h. All three models, and hence their underlying assumptions, appear to reproduce adequately the stream discharge variations and water-table depths in bottom lands at the foot of the hillslope. To simulate the groundwater depth distribution over the whole hillslope, the steady-state assumption (Topmodel) is quite constraining and leads to unacceptable water-table depths in midslope and summit areas. Once this assumption is relaxed (kinematic model), the water-table simulation is improved. A subsequent relaxation of the hydraulic gradient (diffusive model) further improves water-table simulations in the summit area, while still yielding realistic water-table depths in the bottom land. Copyright © 2004 John Wiley & Sons, Ltd. [source]


Up-Regulation of Cell Surface Insulin Receptor by Protein Kinase C-, in Adrenal Chromaffin Cells

JOURNAL OF NEUROCHEMISTRY, Issue 2 2000
Involvement of Transcriptional, Translational Events
Our previous study showed that treatment of cultured bovine adrenal chromaffin cells with phorbol 12, 13-dibutyrate (PDBu) or 12- O -tetradecanoylphorbol 13-acetate (TPA) caused a rapid (<15 min) and persistent (>15 h) translocation of both conventional (c) protein kinase C-, (PKC-,) and novel PKC-, (but not atypical PKC-,) from cytosol to membranes, whereas thymeleatoxin (TMX) increased the similar but selective membrane association of only cPKC-,. In the present study, chronic (,12 h) treatment of chromaffin cells with PDBu raised cell surface 125I-insulin binding without altering the KD value ; it developed in a concentration (EC50 = 1.9 nM)-and time (t1/2 = 14.6 h)-dependent manner, reaching its maximum 115% increase at 48 h. Either TPA (30 nM) or TMX (EC50 = 6.4 nM) also increased 125I-insulin binding by 97 or 88%, whereas the biologically inactive 4,-TPA had no effect. The increasing effect of PDBu (30 nM for 24 h) on 125I-insulin binding was significantly blocked, even when H7, an inhibitor of PKC, was added at 8 h after the initiation of PDBu treatment. Concurrent treatment with brefeldin A, an inhibitor of vesicular transport from the trans -Golgi network, cycloheximide, an inhibitor of protein synthesis, or 5,6-dichlorobenzimidazole riboside, an inhibitor of RNA synthesis, abolished the PDBu-induced increment of 125I-insulin binding. Western blot analysis, using antibody against the ,-subunit of the insulin receptor, showed that treatment with PDBu (30 nM) or TMX (EC50 = 2.3 nM) increased levels of insulin receptor precursor (~190 kDa ; t1/2 = 7.1 h) and insulin receptor ,-subunit (t1/2 = 15.4 h), causing their almost maximum 52 and 59% rises, respectively, at 24 h. Northern blot analysis revealed that PDBu or TMX increased levels of insulin receptor mRNAs by ~35% as soon as 3 h, producing its monophasic peak ~76% increases at 24 h. All of these increasing effects of PDBu and TMX on 125I-insulin binding and insulin receptor ,-subunit and insulin receptor mRNA levels were entirely prevented by simultaneous treatment with Gö6976, a selective inhibitor of cPKC. These results suggest that long-term activation of cPKC-, up-regulates the density of the cell surface insulin receptor via transcriptional/translational events. [source]


Synthesis and properties of conjugated polymers containing 3,9- and 2,9-linked carbazole units in the main chain

JOURNAL OF POLYMER SCIENCE (IN TWO SECTIONS), Issue 14 2009
Kosaku Tamura
Abstract Novel conjugated polymers containing 3,9- or 2,9-linked carbazole units in the main chain were synthesized by the polycondensation of ethynyl- and iodo-substituted 9-arylenecarbazolylene monomers, and their optical and electrical properties were studied. Polymers with weight-average molecular weights of 3400,12,000 were obtained in 76,99% yields by the Sonogashira coupling polycondensation in piperidine or tetrahydrofuran (THF)/piperidine at 30 °C for 48 h. All the 3,9-linked polymers absorbed light around 300 nm. The para -phenylene-linked polymer also absorbed light around 350 nm, while meta -phenylene-linked one did not. The 3,9-linked polymers absorbed light at a wavelength longer than the 2,9-linked one. The polymers emitted blue fluorescence with high quantum yields (0.21,0.78) upon excitation at the absorption maxima. The polymers were oxidized around 0.6 V, and reduced around 0.5 V. Poly(1) showed the dark conductivity of 3.7 × 10,11 S/cm (103 V/cm). © 2009 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 47: 3506,3517, 2009 [source]


Sputum eosinophilia: an early marker of bronchial response to occupational agents

ALLERGY, Issue 5 2009
O. Vandenplas
Background:, False-negative responses to specific inhalation challenge (SIC) with occupational agents may occur. We explored whether assessing changes in sputum cell counts would help improve the identification of bronchial reactivity to occupational agents during SICs. Methods:, The predictive value of the changes in sputum cell counts after a negative FEV1 response to a first challenge exposure to an occupational agent was determined using the changes in airway calibre observed during repeated challenges as the ,gold standard'. The study included 68 subjects investigated for work-related asthma in a tertiary centre. After a control day, the subjects were challenged with the suspected occupational agent(s) for up to 2 h. All subjects who did not show an asthmatic reaction were re-challenged on the following day. Additional challenges were proposed to those who demonstrated a , 2% increase in sputum eosinophils or an increase in nonspecific bronchial hyperresponsiveness to histamine after the second challenge day. Results:, Six of the 35 subjects without changes in FEV1 on the first challenge developed an asthmatic reaction on subsequent challenges. ROC analysis revealed that a >3% increase in sputum eosinophils at the end of the first challenge day was the most accurate parameter for predicting the development of an asthmatic response on subsequent challenges with a sensitivity of 67% and a specificity of 97%. Conclusions:, An increase in sputum eosinophils is an early marker of specific bronchial reactivity to occupational agents, which may help to identify subjects who will develop an asthmatic reaction only after repeated exposure. [source]


Mechanisms involved in the early increase of serotonin contraction evoked by endotoxin in rat middle cerebral arteries

BRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2003
Raquel Hernanz
The present study investigated the mechanisms involved in the increased 5-hydroxytryptamine (5-HT) vasoconstriction observed in rat middle cerebral arteries exposed in vitro to lipopolysaccharide (LPS, 10 ,g ml,1) for 1,5 h. Functional, immunohistochemical and Western blot analysis and superoxide anion measurements by ethidium fluorescence were performed. LPS exposure increased 5-HT (10 ,M) vasoconstriction only during the first 4 h. In contrast to control tissue, indomethacin (10 ,M), the COX-2 inhibitor NS 398 (10 ,M), the TXA2/PGH2 receptor antagonist SQ 29,548 (1 ,M) and the TXA2 synthase inhibitor furegrelate (1 ,M) reduced 5-HT contraction of LPS-treated arteries from hour one. The iNOS inhibitor aminoguanidine (0.1 mM) increased 5-HT contraction from hour three of LPS incubation. The superoxide anion scavenger superoxide dismutase (SOD, 100 U ml,1) and the H2O2 scavenger catalase (1000 U ml,1), as well as the respective inhibitors of NAD(P)H oxidase and xanthine oxidase, apocynin (0.3 mM) and allopurinol (0.3 mM), reduced 5-HT contraction after LPS incubation. LPS induced an increase in superoxide anion levels that was abolished by PEG-SOD. Subthreshold concentrations of the TXA2 analogue U 46619, xanthine/xanthine oxidase and H2O2 potentiated, whereas those of sodium nitroprusside inhibited, the 5-HT contraction. COX-2 expression was increased at 1 and 5 h of LPS incubation, while that of iNOS, Cu/Zn-SOD and Mn-SOD was only increased after 5 h. All the three vascular layers expressed COX-2 and Cu/Zn-SOD. iNOS expression was detected in the endothelium and adventitia after LPS. In conclusion, increased production of TXA2 from COX-2, superoxide anion and H2O2 enhanced vasoconstriction to 5-HT during the first few hours of LPS exposure; iNOS and SOD expression counteracted that increase at 5 h. These changes can contribute to the disturbance of cerebral blood flow in endotoxic shock. British Journal of Pharmacology (2003) 140, 671,680. doi:10.1038/sj.bjp.0705501 [source]