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SNS Activity (sn + activity)
Selected AbstractsInfluence of Ohmic diffusion on the excitation and dynamics of MRIASTRONOMISCHE NACHRICHTEN, Issue 1 2010M.J. Korpi Abstract In this paper we make an effort to understand the interaction of turbulence generated by the magnetorotational instability (MRI) with turbulence from other sources, such as supernova explosions (SNe) in galactic disks. First we perform a linear stability analysis (LSA) of non-ideal MRI to derive the limiting value of Ohmic diffusion that is needed to inhibit the growth of the instability for different types of rotation laws. With the help of a simple analytical expression derived under first-order smoothing approximation (FOSA), an estimate of the limiting turbulence level and hence the turbulent diffusion needed to damp the MRI is derived. Secondly, we perform numerical simulations in local cubes of isothermal nonstratified gas with external forcing of varying strength to see whether the linear result holds for more complex systems. Purely hydrodynamic calculations with forcing, rotation and shear are made for reference purposes, and as expected, non-zero Reynolds stresses are found. In the magnetohydrodynamic calculations, therefore, the total stresses generated are a sum of the forcing and MRI contributions. To separate these contributions, we perform reference runs with MRI-stable shear profiles (angular velocity increasing outwards), which suggest that the MRI-generated stresses indeed become strongly suppressed as function of the forcing. The Maxwell to Reynolds stress ratio is observed to decrease by an order of magnitude as the turbulence level due to external forcing exceeds the predicted limiting value, which we interpret as a sign of MRI suppression. Finally, we apply these results to estimate the limiting radius inside of which the SN activity can suppress the MRI, arriving at a value of 14 kpc (© 2010 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim) [source] Effects of clonidine on diuretic response in ascitic patients with cirrhosis and activation of sympathetic nervous system,,HEPATOLOGY, Issue 4 2006Anne Lenaerts The effects of the addition of clonidine to diuretics on the mobilization of ascites in the short term (diuretic response and requirement of diuretics) and the long term (readmissions for tense ascites and requirement of diuretics) were examined in patients with cirrhosis and with increased sympathetic nervous system (SNS) activity. We also studied neurohormonal, hemodynamic effects and side effects of clonidine and diuretics. Patients were randomized to receive placebo (group1, n = 32) or clonidine (0.075 mg) twice daily (group 2, n = 32) for 3 months. After 8 days and for 10 days duration, spironolactone (200 mg/day) was added in both groups. After this period, the dosages of diuretics were individually increased until diuretic response. Responding patients were discharged and followed at the outpatient clinic. During the first hospitalization, the time needed for diuretic response was shorter in group 2 than in group 1. The mean requirement for diuretics was significantly higher in group 1 than in group 2, and the diuretic complications (hyperkalemia and renal impairment) were significantly lower in group 2. Clonidine induced a permanent decrease in SNS activity and delayed decrease in renin/aldosterone levels. During the follow-up, the time to the first readmission for tense ascites was shorter in group 1 than in group 2. Readmissions related to tense ascites or diuretic complications were significantly lower in group 2. The mean requirement for diuretics was significantly higher in group 1 than in group 2. In conclusion, the additional administration of clonidine to diuretics induced an earlier diuretic response associated with fewer diuretic requirements and complications. (HEPATOLOGY 2006;44:844,849.) [source] Neuropeptide Y and alpha-melanocyte-stimulating hormone: interaction in obesity and possible role in the development of hypertensionINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 9 2008M. Baltatzi Summary Aim:, Obesity and hypertension frequently coexist and both represent important risk factors for cardiovascular disease. The mechanisms implicated in the regulation of food intake have not been completely elucidated. Recent data suggests that peripheral and central neuropeptides play an important role in the maintenance of energy balance. More specifically, leptin, neuropeptide Y (NPY) and alpha-melanocyte-stimulating hormone (a-MSH) appear to be implicated in the pathogenesis of obesity and also contribute to the development of hypertension in obesity. Methods:, Analysis of the pertinent bibliography published in PubMed database. Results:, Leptin is produced in the adipose tissue directly correlated with fat tissue mass. Leptin acts on two distinct neural populations in the hypothalamus: the first expresses the orexigenic peptides NPY and agouti-related protein (AgRP), the second pro-opiomelanocortin (POMC). The activation of POMC neurons increases the production of the anorexigenic hormone a-MSH and inhibits the release of NPY and AgRP. In addition, the hypothalamus integrates the neuroendocrine systems with the autonomic nervous system and controls the activity of the latter. Stimulation of hypothalamic nuclei elicits sympathetic responses including blood pressure elevation. Both NPY and a-MSH appears to be implicated in the hypothalamic regulation of sympathetic nervous system (SNS) activity. Conclusion:, Alterations in leptin, NPY and a-MSH are frequently observed in obesity and might stimulate SNS activity, contributing to the development of hypertension in obese patients. These neuropeptides might provide a pathophysiologic link between excess weight and hypertension. However, more research is needed before the pharmacologic manipulation of these complex neuroendocrine systems can be applied in the treatment of obesity and hypertension. [source] Potential association between endogenous leptin and sympatho-vagal activities in young obese Japanese womenAMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 1 2003Tamaki Matsumoto Leptin is an adipocyte-derived hormone that decreases food intake and increases energy expenditure through the activation of the sympathetic nervous system (SNS). Notwithstanding recent intensive research, the underlying physiological mechanism of leptin as well as the etiology of obesity in humans remains elusive. The present study attempted to investigate the potential association between endogenous circulating leptin and sympatho-vagal activities in age- and height-matched obese and nonobese healthy young women. Plasma leptin concentrations were measured by radioimmunoassay. The autonomic nervous system activity was assessed during the resting condition by means of a recently devised power spectral analysis of heart rate variability, which serves to identify three separate frequency components, very low (VLO), low (LO), and high (HI). Plasma leptin concentrations were greater in the obese than in the control group (45.7 ± 5.89 vs. 11.2 ± 1.10 ng · ml,1, P < 0.01). As to the contribution of endogenous leptin to SNS activity, both the ratios of the VLO frequency component reflecting thermoregulatory sympathetic function and the global SNS index [(VLO + LO)/HI] to plasma leptin concentration were markedly reduced in the obese compared to the control group (VLO per leptin: 5.9 ± 1.39 vs. 37.8 ± 8.1 ms2 · ml · ng,1, P < 0.01; SNS index per leptin: 0.04 ± 0.008 vs. 0.33 ± 0.01 ml,,·,ng,1, P < 0.01). Additionally, a nonlinear regression analysis revealed that these ratios exponentially decreased as a function of body fat content (VLO per leptin r2 = 0.57, P < 0.01; SNS index per leptin r2 = 0.53, P < 0.01). Our data suggest that reduced sympathetic responsiveness to endogenous leptin production, implying peripheral leptin resistance, might be a pathophysiological feature of obesity in otherwise healthy young women. The findings regarding the association of leptin, body fat content, and SNS activity further indicate that the 30% of total body fat, which has been used as a criterion of obesity, might be a critical point at which leptin resistance is induced. Am. J. Hum. Biol. 15:8,15, 2003. © 2002 Wiley-Liss, Inc. [source] | ||||||||||