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Ideally, the results from models operating at different scales should agree in trend direction and magnitude of impacts under climate change. However, this implies that the sensitivity to climate variability and climate change is comparable for impact models designed for either scale. In this study, we compare hydrological changes simulated by 9 global and 9 regional hydrological models (HM) for 11 large river basins in all continents under reference and scenario conditions. The foci are on model validation runs, sensitivity of annual discharge to climate variability in the reference period, and sensitivity of the long-term average monthly seasonal dynamics to climate change. One major result is that the global models, mostly not calibrated against observations, often show a considerable bias in mean monthly discharge, whereas regional models show a better reproduction of reference conditions. However, the sensitivity of the two HM ensembles to climate variability is in general similar. The simulated climate change impacts in terms of long-term average monthly dynamics evaluated for HM ensemble medians and spreads show that the medians are to a certain extent comparable in some cases, but have distinct differences in other cases, and the spreads related to global models are mostly notably larger. Summarizing, this implies that global HMs are useful tools when looking at large-scale impacts of climate change and variability. Whenever impacts for a specific river basin or region are of interest, e.g. for complex water management applications, the regional-scale models calibrated and validated against observed discharge should be used. [ABSTRACT FROM AUTHOR]

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Copyright of Gefaesschirurgie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The article discusses on the pyrethroids that are acting on the axons in the peripheral and central nervous system of mammals and insects, which the neurotoxic effect is determined by the opening of the Na channel. In addition, it also evokes the nerve action associated with hyperactivity, tremor, ataxia, convulsions and paralysis. Moreover, the ester pyrethroids are rapidly detoxified in humans by hydrolysis, oxidation, and conjugation in which after the oral, inhalative or dermal intake, both acid and alcohol moieties of the pyrethroids are metabolized into carboxylic acids.

Applications of high-resolution gas chromatography and high-resolution mass spectrometry (GC-MS) for identification and quantitation of trace amounts of pyrethroid metabolites in human urine samples are demonstrated. The method covers the pyrethroid metabolites cis- and trans-3-(2,2-dichlorovinyl)-2,2-dimethyl-cyclopropane carboxylic acid ( cis- and trans-DCCA), cis-3-(2,2-dibromovinyl)-2,2-dimethylcyclopropane carboxylic acid ( cis-DBCA), 4-fluoro-3-phenoxybenzoic acid (FPBA), and 3-phenoxybenzoic acid (3-PBA). After acid-induced hydrolysis of urine samples and exhaustive solvent extraction, a carbodiimide-coupled esterification of the free carboxylic acids with hexafluoroisopropanol (HFIP) is applied. Identification of the derivatives formed is achieved by low-resolution electron-impact mass spectrometry (EIMS) using an ion-trap detector. Quantitation was by capillary gas chromatography—high-resolution mass spectrometry using negative chemical ionization (GC-NCIMS). 2-Phenoxybenzoic acid (2-PBA) served as internal standard. The limits of detection for cis- and trans-DCCA, cis-DBCA, FPBA and 3-PBA were 0.03 μg L−1 or below. The applicability of the presented method was tested on urine samples of persons exposed to low levels of pyrethroids. [ABSTRACT FROM AUTHOR]

Spontaneous electrical activity of oxytocin-secreting neurones in the rat supraoptic nucleus is depressed by the mu-opiate receptor agonist morphine, leading to a reduction in plasma oxytocin concentration. In the present experiments, the electrical activity of single neurones was recorded from the supraoptic nucleus of urethane-anaesthetized rats. For 5 days prior to the experiments the rats had received a continuous infusion of either morphine or vehicle into a lateral cerebral ventricle; this regimen of morphine treatment results in tolerance to, and dependence upon, morphine in the central mechanisms controlling oxytocin secretion. Intravenous injection of the specific kappa- opioid agonist U50,488 at low doses resulted in small but significant increases in the electrical discharge activity of some putative oxytocin neurones in both morphine-treated and morphine- naive rats. At higher doses, the kappa-agonist consistently inhibited almost all cells tested. Morphine-treated rats, despite showing tolerance to morphine itself, showed no cross-tolerance to the inhibitory actions of U50,488 upon the oxytocin system. In separate experiments both morphine and U50,488 were effective in inhibiting supraoptic neuronal activation evoked by stimulation of the region anterior and ventral to the third ventricle, and activation following systemic injection of cholecystokinin, suggesting that both opioids act upon the final common pathway - the oxytocin neurone itself. [ABSTRACT FROM AUTHOR]

We investigated the effects of intracerebroventricular (i.c.v.) pertussis toxin upon the sensitivity of supraoptic oxytocin neurones to intravenous morphine (1-5000 μg/kg) in urethane-anaesthetized rats. The maximal inhibitory capacity of morphine was diminished by prior administration of pertussis toxin. Some cells were tested with both morphine and with the kappa-opioid agonist U50,488 (1-5000 μg/kg): U50,488-induced inhibition of firing rate was apparently unimpaired by pertussis toxin pre-treatment. The opioid inhibition of firing rate seen in the absence of and after pertussis toxin pretreatment was naloxone-reversible. Thus a pertussis toxin-sensitive G protein may mediate the inhibitory action of morphine upon supraoptic putative oxytocin neurones or inputs to them. [ABSTRACT FROM AUTHOR]

Studies performed in conscious female rats confirmed that iv injection of cholecystokinin octapeptide (CCK; 20µ/kg) increased the circulating concentration of oxytocin but not that of vasopressin, and confirmed that the stimulation of oxytocin release was markedly facilitated after iv administration of naloxone (1mg/kg), indicating attenuation of oxytocin release by endogenous opioids. To investigate the site of action of the endogenous opioids, the electrical activity of putative oxytocin neurones in the supraoptic nucleus was recorded in urethaneanaesthetised female rats. Oxytocin neurones responded to CCK injection with an increase in firing rate lasting 5-15 min, but this response was not facilitated by prior injection of naloxone. The results suggest that the opioid influence upon CCK-induced oxytocin release operates at the level of the neurosecretory terminals in the neurohypophysis rather than centrally. Since CCK does not elevate vasopressin release, it appears unlikely that dynorphin, the opioid peptide co-existing with vasopressin, is responsible in these circumstances for the cross-inhibition of oxytocin release. It is suggested that products of proenkephalin A, the met-enkephalin precursor present in the supraoptic nucleus and in the neurohypophysis itself, may be active in the regulation of oxytocin release. [ABSTRACT FROM AUTHOR]

When electrical stimuli are applied to the neural stalk of the pituitary, oxytocin, vasopressin, and probably several opioid peptides also contained in nerve terminals in the gland are released: one action of the released opioids appears to be to inhibit oxytocin release by an action that has been likened to pre-synaptic inhibition. Thus, when Clarke et al. (1979) stimulated the neural stalk following intravenous injection of the opioid antagonist naloxone, they observed that the evoked oxytocin release was potentiated. In the present study we confirm this result and show that oxytocin release evoked by stimulation of the supraoptic nucleus is similarly potentiated by naloxone. This finding is consistent with the hypothesis that the opioid responsible for inhibition of oxytocin release coexists with either oxytocin or vasopressin. We further report that the specific δ-receptor antagonist ICI 174864 does not potentiate oxytocin release either in vivo or in vitro. Thus, it seems unlikely that the enkephalins, putative δ-receptor agonists present in neurohypophysial fibres, are the opioids responsible for the observed inhibition of oxytocin release. [ABSTRACT FROM AUTHOR]

Magnocellular neurones of the supraoptic and paraventricular nuclei display a complex waveform when recorded extracellularly. The present work has examined the possible reasons for the complexity of this waveform by making extracellular recordings from antidromically identified neurones in the anaesthetized rat and extra- and intracellular recordings from similar neurones in the hypothalamic slice preparation, where external solutions can be changed. In extracellularly recorded units, action potentials had two positive going components. The first of these was abolished by tetrodotoxin. The second, slower component was abolished when external Ca concentration was lowered, but enhanced in magnitude and duration when Ba was placed in the external medium. The second component was sensitive to electrode movement and was not observed to the same degree when intracellular recordings were made. In light of these observations and the known morphology of these neurones, it is suggested that the magnocellular neurone action potential is comprised of a fast Na-dependent component and a slower component dependent on Ca entry which may originate from a part of the cell other than the soma. The most likely site for this Ca component to occur is at the cell dendrite. [ABSTRACT FROM AUTHOR]

In Brattleboro rats, many more supraoptic neurones are baroresponsive than in normal rats. This may reflect the more widespread noradrenergic innervation of the supraoptic nucleus in Brattleboro rats. If so, the present data suggest that baroreceptor influences on vasopressin secretion are mediated by a noradrenergic pathway and that the altered responsiveness reflects the altered innervation. [ABSTRACT FROM AUTHOR]

Antidromically identified neurones were recorded from the supraoptic neucleus of urethane-anaesthetised rats. In test periods of about 10 min, each recorded action potential was followed 1 ms later by a shock to the neural stalk. In phasically firing cells, this stimulation consistently modified the observed firing pattern: burst length was shortened but intraburst activity was unchanged. The stimulation invaded most supraoptic neurones antidromically, but antidromic spikes evoked in the recorded neurone were extinguished by collision. Thus, the observed changes in firing pattern were probably the consequence of interaction between the recorded unit and other neurones projecting to the neural stalk - most probably other supraoptic neurones. The behaviour of continuously firing supraoptic neurones was studied following single shocks and following trains of shocks. The results suggest that the widely reported evidence for recurrent inhibition in the rat supraoptic nucleus has been misinterpreted, and that inhibition cannot be demonstrated in most supraoptic neurones following single shocks to the neural stalk. However, the experiments using trains of shocks produced evidence consistent with a complex interaction between magnocellular neurosecretory cells involving both excitation and inhibition. [ABSTRACT FROM AUTHOR]

Scala tympani of the guinea pig was perfused with artificial perilymph containing putative transmitter substances. Single auditory nerve fibre activity was recorded during these perfusions and the responses of these fibres were studied using computer-controlled routines. Acetylcholine significantly inhibited tone-induced responses of a large proportion of the fibres tested. Glutamate appeared to be a potent depolarising agent when applied in concentrations between 2 and 10 mM. Noradrenaline did not affect tone-induced activity, but inhibited the spontaneous activity of some fibres. The results support the view that acetylcholine is the transmitter at synapses of the olivocochlear bundle, and that glutamate may be involved in the afferent synapse. The data do not support the hypothesis that noradrenaline is the afferent transmitter. [ABSTRACT FROM AUTHOR]

The article presents a study which compares the frequency of complains reported by Pest Control Operators (PCOs) exposed to pyrethroids with a control group of unexposed subjects. In order to compare, a group of 22 male (PCOs) aged 23 to 59 years and 20 unexposed men aged 26 to 54 years were investigated. Those who belong with the PCOs group were handling pyrethroids on a daily basis; they were exposed to cyfluthrin, permethrin, deltamethrin, and cypermethrin. On the other hand, the members of the control group had no contact to pyrethroids at work or at home. At the end of a week's investigation, all subjects were interviewed and had physical and neurological investigations. As a result, it was concluded that those exposed to pyrethroids complain more as far as their health are concern.

CORRECTION TO:: British Journal of Cancer 2003; 89 (S1), S9-S11 doi:10.1038/sj.bjc.6601078 [ABSTRACT FROM AUTHOR]

Raising the K concentration in scala tympani of the guinea-pig cochlea generally caused a substantial increase in the spontaneous firing rate of single auditory nerve fibres. This effect was not accompanied by any observed reduction in the threshold sensitivity of these fibres. These findings cast doubt on current theories of cochlear transduction. [ABSTRACT FROM AUTHOR]