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Dependent Effects (dependent + effects)
Selected AbstractsTime Dependent Effects of Glucocorticoids on Adrenocorticotropin Secretion of Rat Pituitaries Ex-vivoJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 1 2000R. BRUNS Different glucocorticoids have been compared with respect to the inhibition of corticotropin-releasing factor (CRF)-mediated adrenocorticotropin (ACTH) secretion from pituitary fragments of the rat. The influence of time of exposure to glucocorticoids and glucocorticoid concentration has been investigated. CRF-stimulated ACTH secretion of perifused rat pituitary fragments was measured by a chemiluminescence immunoassay. ACTH secretion was monitored over three days. Inhibition of CRF-stimulated ACTH secretion by glucocorticoids was quantified by the area under the curve of CRF-stimulated ACTH secretion over baseline. Concentrations needed to inhibit ACTH secretion decreased with the receptor affinities of the glucocorticoids as follows: fluticasone propionate; receptor affinity 1800, concentration 10,8 M; budesonide, 935 and 3,2.5 times 10,8 M; flunisolide, 478 and 5 times 10,7 M; prednisolone, 10 and 10,6 M. CRF-stimulated secretion was inhibited by glucocorticoids after incubation for 1 min at concentrations between 10,8 and 10,6 M. The same absolute quantity of the glucocorticoids produced no inhibition when incubation was prolonged to 50 min or when a lower concentration was used. Immediately after the perifusion stimulation of ACTH secretion was observed. The results suggest the possibility of minimizing the side effects of glucocorticoids by prolonging drug release. [source] Environmental effects on recruitment and productivity of Japanese sardine Sardinops melanostictus and chub mackerel Scomber japonicus with recommendations for managementFISHERIES OCEANOGRAPHY, Issue 4 2005AKIHIKO YATSU Abstract We compared a wide range of environmental data with measures of recruitment and stock production for Japanese sardine Sardinops melanostictus and chub mackerel Scomber japonicus to examine factors potentially responsible for fishery regimes (periods of high or low recruitment and productivity). Environmental factors fall into two groups based on principal component analyses. The first principal component group was determined by the Pacific Decadal Oscillation Index and was dominated by variables associated with the Southern Oscillation Index and Kuroshio Sverdrup transport. The second was led by the Arctic Oscillation and dominated by variables associated with Kuroshio geostrophic transport. Instantaneous surplus production rates (ISPR) and log recruitment residuals (LNRR) changed within several years of environmental regime shifts and then stabilized due, we hypothesize, to rapid changes in carrying capacity and relaxation of density dependent effects. Like ISPR, LNRR appears more useful than fluctuation in commercial catch data for identifying the onset of fishery regime shifts. The extended Ricker models indicate spawning stock biomass and sea surface temperatures (SST) affect recruitment of sardine while spawning stock biomass, SST and sardine biomass affect recruitment of chub mackerel. Environmental conditions were favorable for sardine during 1969,87 and unfavorable during 1951,67 and after 1988. There were apparent shifts from favorable to unfavorable conditions for chub mackerel during 1976,77 and 1985,88, and from unfavorable to favorable during 1969,70 and 1988,92. Environmental effects on recruitment and surplus production are important but fishing effects are also influential. For example, chub mackerel may have shifted into a new favorable fishery regime in 1992 if fishing mortality had been lower. We suggest that managers consider to shift fishing effort in response to the changing stock productivity, and protect strong year classes by which we may detect new favorable regimes. [source] Nutrient dependent effects of consumer identity and diversity on freshwater ecosystem functionFRESHWATER BIOLOGY, Issue 1 2008ANDREW R. DZIALOWSKI Summary 1. Over the past decade, ecologists have tried to determine how changes in species composition and diversity affect ecosystem structure and function. Until recently, the majority of these studies have been conducted in terrestrial ecosystems and have not taken into account environmental variability. The purpose of this research was to determine how species identity and diversity in the freshwater zooplankton affected biomass of algae and zooplankton at two levels of nutrient enrichment. 2. Several species of cladocerans were grown alone and together in microcosms at both ambient and raised phosphorus concentrations to determine if the effects of consumer identity and diversity were nutrient dependent. 3. Total zooplankton biomass was greater, while algal biomass was lower, in mixed culture than in monoculture. The effects of zooplankton diversity on algal biomass, however, were only observed at raised phosphorus concentrations, suggesting that diversity effects were nutrient dependent. Specifically, diversity effects appeared to be related with biological mechanisms such as complementarity in resource use and/or facilitation. 4. More diverse communities of zooplankton appear to be better able to control algae than single species of zooplankton at high nutrient concentrations; therefore, zooplankton diversity may provide a buffer against eutrophication in freshwater ecosystems. [source] PTH-dependent adenylyl cyclase activation in SaOS-2 cells: Passage dependent effects on G protein interactionsJOURNAL OF CELLULAR PHYSIOLOGY, Issue 1 2002Hong Gao Parathyroid hormone (PTH) sensitive adenylyl cyclase activity (ACA) in SaOS-2 cells varies as a function of cell passage. In early passage (EP) cells (<,6), ACA in response to PTH and forskolin (FOR) was relatively low and equivalent, whereas in late passage (LP) cells (>,22), PTH exceeded FOR dependent ACA. Potential biochemical mechanisms for this passage dependent change in ACA were considered. In EP, prolonged exposure to pertussis toxin (PT) markedly enhanced ACA activity in response to PTH, Isoproterenol and Gpp(NH)p, whereas ACA in response to FOR was decreased. In contrast, the identical treatment of LP with PT diminished all ACA in response to PTH, Gpp(NH)p, and FOR. The dose dependent effects of PT on subsequent [32P]ADP-ribosylation of its substrates, GTPase activity, as well as FOR-dependent ACA, were equivalent in EP and LP. The relative amounts of G,i and G,s proteins, as determined both by Western blot, PT and cholera toxin (CT) dependent [32P]ADP-ribosylation, were quantitatively similar in EP and LP. Western blot levels of G,s and G,i proteins were not influenced by prior exposure to PT. Both PT and CT dependent [32P]ADP-ribosylation were dose-dependently decreased following exposure to PT. However, the PT-dependent decline in CT-dependent [32P]ADP-ribosylation occurred with enhanced sensitivity in LP. The protein synthesis inhibitor cycloheximide partially reversed the PT associated decrease in FOR dependent ACA in EP. In contrast, cycloheximide completely reversed the PT associated decrease in FOR and as well as PTH dependent ACA in LP. G,s activity, revealed by cyc, reconstitution, was not altered either by cell passage or exposure to PT. The results suggest that the coupling between the components of the complex may be pivotally important in the differential responsiveness of early and late passage SaOS-2 cells to PTH. J. Cell. Physiol. 193: 10,18, 2002. © 2002 Wiley-Liss, Inc. [source] Role of the nitric oxide/cyclic GMP pathway and extracellular environment in the nitric oxide donor-induced increase in dopamine secretion from PC12 cells: a microdialysis in vitro studyJOURNAL OF NEUROCHEMISTRY, Issue 6 2003Pier Andrea Serra Abstract In vitro microdialysis was used to investigate the mechanism of nitric oxide (NO) donor-induced changes in dopamine (DA) secretion from PC12 cells. Infusion of the NO-donor S-nitroso- N -acetylpenicillamine (SNAP, 1.0 mm) induced a long-lasting increase in DA and 3-methoxytyramine (3-MT) dialysate concentrations. SNAP-induced increases were inhibited either by pre-infusion of the soluble guanylate cyclase (sGC) inhibitor 1H-[1,2,4] oxadiazolo[4,3]quinoxalin-1-one (ODQ, 0.1 mm) or by Ca2+ omission. Ca2+ re-introduction restored SNAP effects. SNAP-induced increases in DA + 3-MT were unaffected by co-infusion of the l -type Ca2+ channel inhibitor nifedipine. The NO-donor (+/,)-(E)-4-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexenamide (NOR-3, 1.0 mm) induced a short-lasting decrease in dialysate DA + 3-MT. Ascorbic acid (0.2 mm) co-infusion allowed NOR-3 to increase dialysate DA + 3-MT. ODQ pre-infusion inhibited NOR-3 + ascorbic acid-induced DA + 3-MT increases. Infusion of high K+ (75 mm) induced a 2.5-fold increase in dialysate DA + 3-MT. The increase was abolished by NOR-3 co-infusion. Conversely, co-infusion of ascorbic acid (0.2 mm) with NOR-3 + high K+ restored high K+ effects. Co-infusion of nifedipine inhibited high K+ -induced DA + 3-MT increases. These results suggest that activation of the NO/sGC/cyclic GMP pathway may be the underlying mechanism of extracellular Ca2+ -dependent effects of exogenous NO on DA secretion from PC12 cells. Extracellular Ca2+ entry may occur through nifedipine-insensitive channels. NO effects and DA concentrations in dialysates largely depend on both the timing of NO generation and the extracellular environment in which NO is generated. [source] Uncoupling of intestinal mitochondrial oxidative phosphorylation and inhibition of cyclooxygenase are required for the development of NSAID-enteropathy in the ratALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 5 2000Somasundaram Background: The pathogenesis of NSAID-induced gastrointestinal damage is believed to involve a nonprostaglandin dependent effect as well as prostaglandin dependent effects. One suggestion is that the nonprostaglandin mechanism involves uncoupling of mitochondrial oxidative phosphorylation. Aims: To assess the role of uncoupling of mitochondrial oxidative phosphorylation in the pathogenesis of small intestinal damage in the rat. Methods: We compared key pathophysiologic events in the small bowel following (i) dinitrophenol, an uncoupling agent (ii) parenteral aspirin, to inhibit cyclooxygenase without causing a ,topical' effect and (iii) the two together, using (iv) indomethacin as a positive control. Results: Dinitrophenol altered intestinal mitochondrial morphology, increased intestinal permeability and caused inflammation without affecting gastric permeability or intestinal prostanoid levels. Parenteral aspirin decreased mucosal prostanoids without affecting intestinal mitochondria in vivo, gastric or intestinal permeability. Aspirin caused no inflammation or ulcers. When dinitrophenol and aspirin were given together the changes in intestinal mitochondrial morphology, permeability, inflammation and prostanoid levels and the macro- and microscopic appearances of intestinal ulcers were similar to indomethacin. Conclusions: These studies allow dissociation of the contribution and consequences of uncoupling of mitochondrial oxidative phosphorylation and cyclooxygenase inhibition in the pathophysiology of NSAID enteropathy. While uncoupling of enterocyte mitochondrial oxidative phosphorylation leads to increased intestinal permeability and low grade inflammation, concurrent decreases in mucosal prostanoids appear to be important in the development of ulcers. [source] | |||||||||||||