Forecast, observation and modelling of a deep stratospheric intrusion event over Europe

A wide range of measurements was carried out in central and southeastern Europe within the framework of the EU-project STACCATO (Influence of Stratosphere-Troposphere Exchange in a Changing Climate on Atmospheric Transport and Oxidation Capacity) with the principle goal to create a comprehensive data set on stratospheric air intrusions into the troposphere along a rather frequently observed pathway over central Europe from the North Sea to the Mediterranean Sea. The measurements were based on predictions by suitable quasi-operational trajectory calculations using ECMWF forecast data. A predicted deep Stratosphere to Troposphere Transport (STT) event, encountered during the STACCATO period on 20-21 June 2001, could be followed by the measurements network almost from its inception. Observations provide evidence that the intrusion affected large parts of central and southeastern Europe. Especially, the ozone lidar observations on 20-21 June 2001 at Garmisch-Partenkirchen, Germany captured the evolution of two marked tongues of high ozone with the first one reaching almost a height of 2 km, thus providing an excellent data set for model intercomparisons and validation. In addition, for the first time to our knowledge concurrent measurements of the cosmogenic radionuclides <sup>10</sup>Be and <sup>7</sup>Be and their ratio <sup>10</sup>Be/<sup>7</sup>Be are presented together as stratospheric tracers in a case study of a stratospheric intrusion. The ozone tracer columns calculated with the FLEXPART model were found to be in good agreement with water vapour satellite images, capturing the evolution of the observed dry streamers of stratospheric origin. Furthermore, the time-height cross section of ozone tracer simulated with FLEXPART over Garmisch-Partenkirchen captures with many details the evolution of the two observed high-ozone filaments measured with the IFU lidar, thus demonstrating the considerable progress in model simulations. Finally, the modelled ozone (operationally available since October 1999) from the ECMWF (European Centre for Medium-Range Weather Forecasts) atmospheric model is shown to be in very good agreement with the observations during this case study, which provides the first successful validation of a chemical tracer that is used operationally in a weather forecast model. This suggests that coupling chemistry and weather forecast models may significantly improve both weather and chemical forecasts in the future

Dynamical restriction for a growing neck due to mass parameters in a dinuclear system

Mass parameters for collective variables of a dinuclear system and strongly deformed mononucleus are microscopically formulated with the linear response theory making use of the width of single particle states and the fluctuation-dissipation theorem. For the relative motion of the nuclei and for the degree of freedom describing the neck between the nuclei, we calculate mass parameters with basis states of the adiabatic and diabatic two-center shell model. Microscopical mass parameters are found larger than the ones obtained with the hydrodynamical model and give a strong hindrance for a melting of the dinuclear system along the internuclear distance into a compound system. Therefore, the dinuclear system lives a long time enough comparable to the reaction time for fusion by nucleon transfer. Consequences of this effect for the complete fusion process are discussed.Comment: 22 pages, 7 figures, submitted to Nucl.Phys.

Renal and Blood Pressure Response to a High-Salt Diet in Mice With Reduced Global Expression of the Glucocorticoid Receptor

Salt-sensitive hypertension is common in glucocorticoid excess. Glucocorticoid resistance also presents with hypercortisolemia and hypertension but the relationship between salt intake and blood pressure (BP) is not well defined. GRβgeo/+ mice have global glucocorticoid receptor (GR) haploinsufficiency and increased BP. Here we examined the effect of high salt diet on BP, salt excretion and renal blood flow in GRβgeo/+mice. Basal BP was ∼10 mmHg higher in male GRβgeo/+ mice than in GR+/+ littermates. This modest increase was amplified by ∼10 mmHg following a high-salt diet in GRβgeo/+ mice. High salt reduced urinary aldosterone excretion but increased renal mineralocorticoid receptor expression in both genotypes. Corticosterone, and to a lesser extent deoxycorticosterone, excretion was increased in GRβgeo/+ mice following a high-salt challenge, consistent with enhanced 24 h production. GR+/+ mice increased fractional sodium excretion and reduced renal vascular resistance during the high salt challenge, retaining neutral sodium balance. In contrast, sodium excretion and renal vascular resistance did not adapt to high salt in GRβgeo/+ mice, resulting in transient sodium retention and sustained hypertension. With high-salt diet, Slc12a3 and Scnn1a mRNAs were higher in GRβgeo/+ than controls, and this was reflected in an exaggerated natriuretic response to thiazide and benzamil, inhibitors of NCC and ENaC, respectively. Reduction in GR expression causes salt-sensitivity and an adaptive failure of the renal vasculature and tubule, most likely reflecting sustained mineralocorticoid receptor activation. This provides a mechanistic basis to understand the hypertension associated with loss-of-function polymorphisms in GR in the context of habitually high salt intake

Glucocorticoids and renal sodium transport:implications for hypertension and salt-sensitivity

The clinical manifestations of glucocorticoid excess include central obesity, hyperglycaemia, dyslipidaemia, electrolyte abnormalities and hypertension. A century on from Cushing's original case study, these cardinal features are prevalent in industrialized nations. Hypertension is the major modifiable risk factor for cardiovascular and renal disease and reflects underlying abnormalities of Na(+) homeostasis. Aldosterone is a master regulator of renal Na(+) transport but here we argue that glucocorticoids are also influential, particularly during moderate excess. The hypothalamic–pituitary–adrenal axis can affect renal Na(+) homeostasis on multiple levels, systemically by increasing mineralocorticoid synthesis and locally by actions on both the mineralocorticoid and glucocorticoid receptors, both of which are expressed in the kidney. The kidney also expresses both of the 11β-hydroxysteroid dehydrogenase (11βHSD) enzymes. The intrarenal generation of active glucocorticoid by 11βHSD1 stimulates Na(+) reabsorption; failure to downregulate the enzyme during adaption to high dietary salt causes salt-sensitive hypertension. The deactivation of glucocorticoid by 11βHSD2 underpins the regulatory dominance for Na(+) transport of mineralocorticoids and defines the ‘aldosterone-sensitive distal nephron’. In summary, glucocorticoids can stimulate renal transport processes conventionally attributed to the renin–angiotensin–aldosterone system. Importantly, Na(+) and volume homeostasis do not exert negative feedback on the hypothalamic–pituitary–adrenal axis. These actions are therefore clinically relevant and may contribute to the pathogenesis of hypertension in conditions associated with elevated glucocorticoid levels, such as the metabolic syndrome and chronic stress

Effects of thyromimetic drugs on aldosterone-dependent sodium transport in the toad bladder.

Aldosterone increases transepithelial Na+ transport in the urinary bladder of Bufo marinus. The response is characterized by 3 distinct phases: 1) a lag period of about 60 min, ii) an initial phase (early response) of about 2 hr during which Na+ transport increases rapidly and transepithelial electrical resistance falls, and iii) a late phase (late response) of about 4 to 6 hr during which Na+ transport still increases significantly but with very little change in resistance. Triiodothyronine (T3, 6 nM) added either 2 or 18 hr before aldosterone selectively antagonizes the late response. T3 per se (up to 6 nM) has no effect on base-line Na+ transport. The antagonist activity of T3 is only apparent after a latent period of about 6 to 8 hr. It is not rapidly reversible after a 4-hr washout of the hormone. The effects appear to be selective for thyromimetic drugs since reverse T3 (rT3) is inactive and isopropyldiiodothyronine (isoT2) is more active than T3. The relative activity of these analogs corresponds to their relative affinity for T3 nuclear binding sites which we have previously described. Our data suggest that T3 might control the expression of aldosterone by regulating gene expression, e.g. by the induction of specific proteins, which in turn will inhibit the late mineralocorticoid response, without interaction with the early response

Control of transepithelial Na+ transport and Na-K-ATPase by oxytocin and aldosterone.

Short- and long-term effect of oxytocin on Na+ transport and Na-K-ATPase biosynthesis in the toad bladder, and the potential interaction of this hormone with aldosterone have been studied, leading to the following observations. An early Na+ transport response (oxytocin, 50 mU/ml) peaked at 10-15 min of hormone addition. At maximal stimulation a three- to fourfold increase in Na+ transport was observed, a sustained Na+ transport response (about two-fold control base line) was observed as long as the hormone was present in the medium and for up to 20 h of incubation. Pretreatment for 30 min with actinomycin D (2 micrograms/ml) did not inhibit the early response, but significantly impaired the sustained response, suggesting that de novo protein synthesis was required. The simultaneous addition of the two hormones led within 60 min to a marked potentiation of the action on Na+ transport. This synergism could be mimicked by exogenous cyclic adenosine monophosphate (cAMP). Oxytocin alone (18 h exposure, 50 mU/ml) increased the relative rate of synthesis of both alpha and beta subunits of Na-K-ATPase (1.9- and 1.6-fold, respectively; P less than 0.05), whereas aldosterone (80 nM) increased the relative rate of synthesis of the same subunits (2.6- and 2.2-fold, respectively; P less than 0.02). Finally, in contrast to what was observed at the physiological level, the interaction of oxytocin and aldosterone did not lead to a similar potentiation at the biochemical level, i.e., induction of Na-K-ATPase biosynthesis (2.7- and 2.9-fold, for alpha and beta subunits, respectively; P less than 0.025)