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  • 1
    Electronic Resource
    Electronic Resource
    Temporal Variation in Concentrations of Heavy Metals in Marine Sediments
    Amsterdam : Elsevier
    Estuarine, Coastal and Shelf Science 38 (1994), S. 271-282 
    Details
    ISSN: 0272-7714
    Keywords: New South Wales coast ; heavy metals ; sampling methods ; sediments ; temporal variations
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Geography , Geosciences
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1006/ecss.1994.1018
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Effects of copper on the faunas of marine soft-sediments: An experimental field study (1996)
    Springer
    Marine biology 125 (1996), S. 199-213 
    Details
    ISSN: 1432-1793
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Although laboratory experimental studies have shown that copper is toxic to marine organisms at concentrations found in contaminated sediments, there is little unequivocal evidence of undesirable ecological effects in the field, other than at extreme concentrations. We describe a study in Botany Bay, New South Wales, Australia, in which the concentrations of copper in marine sediments were experimentally enhanced. Changes in the abundance and taxonomic composition of the fauna of copper-treated sediments relative to those of two control treatments were monitored over a period of six months. Univariate (ANOVA) and multivariate (non-metric multidimensional scaling, MDS) analyses of the changes in the fauna showed that increased concentrations of copper (140 to 1200 μg g-1 compared with background concentrations of 29 to 40 μg g-1) had an impact on the fauna. The nature of the response varied among taxa. For example, in some taxa, numbers of individuals decreased through time relative to controls, whereas the abundance of another taxon remained fairly constant through time in the copper treatment while numbers of control individuals increased. Differences in the changes of the faunas through time among the control and copper treatments were not always consistent among replicate experimental units 5 m apart, nor were they consistent between replicate experimental sites 100 m apart. The magnitudes of the changes in the faunas caused by the copper treatment are considered in the context of the magnitude of previously measured “natural” temporal variation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00350774
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    Paper (German National Licenses)
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  • 3
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    Chronic deficit in nitric oxide elicits oxidative stress and augments T-type calcium-channel contribution to vascular tone of rodent arteries and arterioles (2013)
    Oxford University Press
    Details
    Publication Date: 2013-05-18
    Description: Aims As cardiovascular disease is characterized by reduced nitric oxide bioavailability, our aim was to determine the impact of this change on the mechanism underlying vascular tone of pressurized arteries in vitro and in vivo . Methods and results We used pressurized cerebral and mesenteric arteries in vitro and skeletal muscle arterioles in vivo to study the contribution of L-type (1 µmol/L nifedipine) and T-type (1 µmol/L mibefradil, 3 µmol/L NNC 55–0396) calcium channels to vascular tone, following acute or chronic inhibition of nitric oxide. Acute inhibition with l -NAME (10 µmol/L) significantly increased the T-type, but not the L-type, channel contribution to vascular tone in vitro and in vivo, and altered the smooth muscle expression of the Ca v 3.1 and Ca v 3.2 T-type channels. In pressurized mesenteric arteries of Ca v 3.1ko and Ca v 3.2ko mice, acutely treated with l -NAME, the contribution of T-type channels relative to L-type channels was significantly reduced, compared with arteries from wild-type mice . Chronic l -NAME treatment (40 mg/kg/day; 14–18 days) increased blood pressure, vascular superoxide, and the contribution of T-type channels to vascular tone in vivo . The latter was reversed by acute scavenging of superoxide with tempol (1 mmol/L), or inhibition of NADPH oxidase with apocynin (500 µmol/L) or DPI (5 µmol/L). Conclusion We conclude that nitric oxide deficit produces a significant increase in the contribution of Ca v 3.1 and Ca v 3.2 T-type calcium channels to vascular tone, by regulating the bioavailability of reactive oxygen species produced by NADPH oxidase. Our data provide evidence for a novel causal link between nitric oxide deficit, oxidative stress, and T-type calcium channel function.
    Print ISSN: 0008-6363
    Electronic ISSN: 1755-3245
    Topics: Medicine
    Published by Oxford University Press
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  • 4
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    Serotonin availability in rat colon is reduced during a Western diet model of obesity (2012)
    The American Physiological Society (APS)
    Details
    Publication Date: 2012-08-02
    Description: Constipation and slowed transit are associated with diet-induced obesity, although the mechanisms by which this occurs are unclear. Enterochromaffin (EC) cells within the intestinal epithelium respond to mechanical stimulation with the release of serotonin [5-hydroxytryptamine (5-HT)], which promotes transit. Thus our aim was to characterize 5-HT availability in the rat colon of a physiologically relevant model of diet-induced obesity. EC cell numbers were determined immunohistochemically in chow-fed (CF) and Western diet-fed (WD) rats, while electrochemical methods were used to measure mechanically evoked (peak) and steady-state (SS) 5-HT levels. Fluoxetine was used to block the 5-HT reuptake transporter (SERT), and the levels of mRNA for tryptophan hydroxylase 1 and SERT were determined by quantitative PCR, and SERT protein was determined by Western blot. In WD rats, there was a significant decrease in the total number of EC cells per crypt (0.86 ± 0.06 and 0.71 ± 0.05 in CF and WD, respectively), which was supported by a reduction in the levels of 5-HT in WD rats (2.9 ± 1.0 and 10.5 ± 2.6 μM at SS and peak, respectively) compared with CF rats (7.3 ± 0.4 and 18.4 ± 3.4 μM at SS and peak, respectively). SERT-dependent uptake of 5-HT was unchanged, which was supported by a lack of change in SERT protein levels. In WD rats, there was no change in tryptophan hydroxylase 1 mRNA but an increase in SERT mRNA. In conclusion, our data show that foods typical of a WD are associated with decreased 5-HT availability in rat colon. Decreased 5-HT availability is driven primarily by a reduction in the numbers and/or 5-HT content of EC cells, which are likely to be associated with decreased intestinal motility in vivo.
    Print ISSN: 0193-1857
    Electronic ISSN: 1522-1547
    Topics: Medicine
    Published by The American Physiological Society (APS)
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  • 5
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    Dietary obesity increases NO and inhibits BKCa-mediated, endothelium-dependent dilation in rat cremaster muscle artery: association with caveolins and caveolae (2012)
    The American Physiological Society (APS)
    Details
    Publication Date: 2012-06-16
    Description: Obesity is a risk factor for hypertension and other vascular disease. The aim of this study was to examine the effect of diet-induced obesity on endothelium-dependent dilation of rat cremaster muscle arterioles. Male Sprague-Dawley rats (213 ± 1 g) were fed a cafeteria-style high-fat or control diet for 16–20 wk. Control rats weighed 558 ± 7 g compared with obese rats 762 ± 12 g ( n = 52–56; P 〈 0.05). Diet-induced obesity had no effect on acetylcholine (ACh)-induced dilation of isolated, pressurized (70 mmHg) arterioles, but sodium nitroprusside (SNP)-induced vasodilation was enhanced. ACh-induced dilation of arterioles from control rats was abolished by a combination of the K Ca blockers apamin, 1-[(2-chlorophenyl)diphenylmethyl]-1H-pyrazole (TRAM-34), and iberiotoxin (IBTX; all 0.1 μmol/l), with no apparent role for nitric oxide (NO). In arterioles from obese rats, however, IBTX had no effect on responses to ACh while the NO synthase (NOS)/guanylate cyclase inhibitors N -nitro- l -arginine methyl ester ( l -NAME; 100 μmol/l)/1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 10 μmol/l) partially inhibited ACh-induced dilation. Furthermore, NOS activity (but not endothelial NOS expression) was increased in arteries from obese rats. l -NAME/ODQ alone or removal of the endothelium constricted arterioles from obese but not control rats. Expression of caveolin-1 and -2 oligomers (but not monomers or caveolin-3) was increased in arterioles from obese rats. The number of caveolae was reduced in the endothelium of arteries, and caveolae density was increased at the ends of smooth muscle cells from obese rats. Diet-induced obesity abolished the contribution of large-conductance Ca 2+ -activated K + channel to ACh-mediated endothelium-dependent dilation of rat cremaster muscle arterioles, while increasing NOS activity and inducing an NO-dependent component.
    Print ISSN: 0363-6135
    Electronic ISSN: 1522-1539
    Topics: Medicine
    Published by The American Physiological Society (APS)
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  • 6
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    Loss of Functional Endothelial Connexin40 Results in Exercise-Induced Hypertension in Mice [Endothelial Dysfunction] (2015)
    American Heart Association (AHA)
    Details
    Publication Date: 2015-02-12
    Description: During activity, coordinated vasodilation of microcirculatory networks with upstream supply vessels increases blood flow to skeletal and cardiac muscles and reduces peripheral resistance. Endothelial dysfunction in humans attenuates activity-dependent vasodilation, resulting in exercise-induced hypertension in otherwise normotensive individuals. Underpinning activity-dependent hyperemia is an ascending vasodilation in which the endothelial gap junction protein, connexin (Cx)40, plays an essential role. Because exercise-induced hypertension is proposed as a forerunner to clinical hypertension, we hypothesized that endothelial disruption of Cx40 function in mice may create an animal model of this condition. To this end, we created mice in which a mutant Cx40T152A was expressed alongside wildtype Cx40 selectively in the endothelium. Expression of the Cx40T152A transgene in Xenopus oocytes and mouse coronary endothelial cells in vitro impaired both electric and chemical conductance and acted as a dominant-negative against wildtype Cx40, Cx43, and Cx45, but not Cx37. Endothelial expression of Cx40T152A in Cx40T152ATg mice attenuated ascending vasodilation, without effect on radial coupling through myoendothelial gap junctions. Using radiotelemetry, Cx40T152ATg mice showed an activity-dependent increase in blood pressure, which was significantly greater than in wildtype mice, but significantly less than in chronically hypertensive, Cx40knockout mice. The increase in heart rate with activity was also greater than in wildtype or Cx40knockout mice. We conclude that the endothelial Cx40T152A mutation attenuates activity-dependent vasodilation, producing a model of exercise-induced hypertension. These data highlight the importance of endothelial coupling through Cx40 in regulating blood pressure during activity.
    Keywords: Animal models of human disease, Peripheral vascular disease, Endothelium/vascular type/nitric oxide
    Print ISSN: 0194-911X
    Topics: Medicine
    Published by American Heart Association (AHA)
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