Рациональная антибиотикотерапия при лечении хронического декомпенсированного тонзиллита

Department of Otorhinolaryngology, Nicolae Testemitanu State Medical and Pharmaceutical University, Chisinau, Republic of MoldovaToday, as it has for the past several decades, tonsillitis is a current chronic problem mostly because of questionable treatment for this condition. Ideal treatment of chronic decompensated tonsillitis is tonsillectomy and antibiotics in the postoperative period. Classic conservative treatment of chronic tonsillitis includes local treatment, disinfectants and cleaning solutions. And while deepening systemic antibiotic therapy is compulsory, Sumamed is an antibiotic that can be successfully used to treat chronic decompensated tonsillitis. The type of antibiotics should be selected based on each patient’s individual situation, taking into account the patient’s bacteriological flora, previous antibiotic sensitivity of pathogenic flora, and the individual patient’s tolerance to the medication.Сегодня, также как и в течение многих предыдущих десятилетий, остается открыт вопрос о рациональном лечении хронического тонзиллита. Идеальное лечение хронического декомпенсированного тонзиллита остаётся тонзилэктомия и антибиотикотерапия в постоперационном периоде. Но, при этом всегда существуют пациенты, которым невозможно произвести тонзилэктомию, наличие противопоказаний, абсолютных или относительных, или отказ больного. Стандартное консервативное лечение включает в себя местное антисептическое лечение, витаминотерапия, а в периоды обострения − антибиотикотерапия. Выбор антибиотика должен проходить индивидуально, исходя из микробиологических исследований, чувствительности патогенной флоры и ранее использованных антибиотиков. Сумамед является антибиотиком, который может быть успешно использован в лечении хронического тонзиллита, как компенсированного, так и декомпенсированного

Physics of Solar Prominences: I - Spectral Diagnostics and Non-LTE Modelling

This review paper outlines background information and covers recent advances made via the analysis of spectra and images of prominence plasma and the increased sophistication of non-LTE (ie when there is a departure from Local Thermodynamic Equilibrium) radiative transfer models. We first describe the spectral inversion techniques that have been used to infer the plasma parameters important for the general properties of the prominence plasma in both its cool core and the hotter prominence-corona transition region. We also review studies devoted to the observation of bulk motions of the prominence plasma and to the determination of prominence mass. However, a simple inversion of spectroscopic data usually fails when the lines become optically thick at certain wavelengths. Therefore, complex non-LTE models become necessary. We thus present the basics of non-LTE radiative transfer theory and the associated multi-level radiative transfer problems. The main results of one- and two-dimensional models of the prominences and their fine-structures are presented. We then discuss the energy balance in various prominence models. Finally, we outline the outstanding observational and theoretical questions, and the directions for future progress in our understanding of solar prominences.Comment: 96 pages, 37 figures, Space Science Reviews. Some figures may have a better resolution in the published version. New version reflects minor changes brought after proof editin

Association Study of the β2-Adrenergic Receptor Gene Polymorphisms and Hypertension in the Northern Han Chinese

Background: The beta 2-adrenergic receptor (ADRB2) gene has been widely researched as a candidate gene for essential hypertension (EH), but no consensus has been reached in different ethnicities. The aim of the present study was to evaluate the possible association between the ADRB2 gene polymorphisms and the EH risk in the Northern Han Chinese population. Methodology/Principal Findings: This study included 747 hypertensive subjects and 390 healthy volunteers as control subjects in the Northern Han Chinese. Genotyping was performed to identify the C-47T, A46G and C79G polymorphisms of the ADRB2 gene. G allelic frequency of A46G polymorphism was significantly higher in hypertensive subjects (P = 0.011, OR = 1.287, 95% CI [1.059-1.565]) than that in controls. Significant association could also be found in dominant genetic model (GG+AG vs. AA, P = 0.006, OR = 1.497, 95% CI [1.121-1.998]), in homozygote comparison (GG vs. AA, P = 0.025, OR = 1.568, 95% CI [1.059-2.322]), and in additive genetic model (GG vs. AG vs. AA, P = 0.012, OR = 1.282, 95% CI [1.056-1.555]). Subgroup analyses performed by gender suggested that this association could be found in male, but not in female. Stratification analyses by obesity showed that A46G polymorphism was related to the prevalence of hypertension in the obese population (GG vs. AG vs. AA, P<0.001, OR = 1.645, 95% CI [1.258-2.151]). Significant interaction was found between A46G genotypes and body mass index on EH risk. No significant association could be found between C-47T or C79G polymorphism and EH risk. Linkage disequilibrium was detected between the C-47T, A46G and C79G polymorphisms. Haplotype analyses observed that the T-47-A46-C79 haplotype was a protective haplotype for EH, while the T-47-G46-C79 haplotype increased the risk. Conclusions/Significances: We revealed that the ADRB2 A46G polymorphism might increase the risk for EH in the Northern Han Chinese population.Multidisciplinary SciencesSCI(E)7ARTICLE4null

Effects of Mineralocorticoid Receptor Blockade and Statins on Kidney Injury Marker 1 (KIM-1) in Female Rats Receiving L-NAME and Angiotensin II

Kidney injury molecule-1 (KIM-1) is a biomarker of renal injury and a predictor of cardiovascular disease. Aldosterone, via activation of the mineralocorticoid receptor, is linked to cardiac and renal injury. However, the impact of mineralocorticoid receptor activation and blockade on KIM-1 is uncertain. We investigated whether renal KIM-1 is increased in a cardiorenal injury model induced by L-NAME/ANG II, and whether mineralocorticoid receptor blockade prevents the increase in KIM-1. Since statin use is associated with lower aldosterone, we also investigated whether administering eiSther a lipophilic statin (simvastatin) or a hydrophilic statin (pravastatin) prevents the increase in renal KIM-1. Female Wistar rats (8–10 week old), consuming a high salt diet (1.6% Na+), were randomized to the following conditions for 14 days: control; L-NAME (0.2 mg/mL in drinking water)/ANG II (225 ug/kg/day on days 12–14); L-NAME/ANG II + eplerenone (100 mg/kg/day p.o.); L-NAME/ANG II + pravastatin (20 mg/kg/day p.o.); L-NAME/ANG II + simvastatin (20 mg/kg/day p.o.). Groups treated with L-NAME/ANG II had significantly higher blood pressure, plasma and urine aldosterone, cardiac injury/stroke composite score, and renal KIM-1 than the control group. Both eplerenone and simvastatin reduced 24-h urinary KIM-1 (p = 0.0046, p = 0.031, respectively) and renal KIM-1 immunostaining (p = 0.004, p = 0.037, respectively). Eplerenone also reduced renal KIM-1 mRNA expression (p = 0.012) and cardiac injury/stroke composite score (p = 0.04). Pravastatin did not affect these damage markers. The 24-h urinary KIM-1, renal KIM-1 immunostaining, and renal KIM-1 mRNA expression correlated with cardiac injury/stroke composite score (p < 0.0001, Spearman ranked correlation = 0.69, 0.66, 0.59, respectively). In conclusion, L-NAME/ANG II increases renal KIM-1 and both eplerenone and simvastatin blunt this increase in renal KIM-1

Sensitivity of NOS-dependent vascular relaxation pathway to mineralocorticoid receptor blockade in caveolin-1-deficient mice

Endothelial caveolin-1 (cav-1) is an anchoring protein in plasma membrane caveolae where it binds endothelial nitric oxide synthase (eNOS) and limits its activation, particularly in animals fed a high salt (HS) diet. Cav-1 also interacts with steroid receptors such as the mineralocorticoid receptor (MR). To test the hypothesis that vascular reactivity is influenced by an interplay between MR and cav-1 during HS diet, we examined the effects of MR blockade on NOS-mediated vascular relaxation in normal and cav-1-deficient mice. Wild-type (WT) and cav-1 knockout mice (cav-1−/−) were fed for 14 days a HS (4% NaCl) diet with and without the MR antagonist eplerenone (Epl; 100 mg·kg−1·day−1). After systolic blood pressure (BP) was measured, the thoracic aorta was isolated for measurement of vascular reactivity, and the aorta and heart were used for measurement of eNOS and MR expression. BP was not different between WT + Epl and WT, but was higher in cav-1−/− + Epl than in cav-1−/− mice. Phenylephrine (Phe)-induced vascular contraction was less in cav-1−/− than WT, and significantly enhanced in cav-1−/− + Epl than in cav-1−/−, but not in WT + Epl compared with WT. Endothelium removal and NOS blockade by Nω-nitro-l-arginine methyl ester (l-NAME) enhanced Phe contraction in cav-1−/−, but not cav-1−/− + Epl. ACh-induced aortic relaxation was reduced in cav-1−/− + Epl versus cav-1−/−, but not in WT + Epl compared with WT. Endothelium removal, l-NAME, and the guanylate cyclase inhibitor ODQ abolished the large ACh-induced relaxation in cav-1−/− and the remaining relaxation in the cav-1−/− + Epl but had similar inhibitory effect in WT and WT + Epl. Real-time RT-PCR indicated decreased eNOS mRNA expression in the aorta and heart, and Western blots revealed decreased total eNOS in the heart of cav-1−/− + Epl compared with cav-1−/−. Vascular and cardiac MR expression was less in cav-1−/− than WT, but not in cav-1−/− + Epl compared with cav-1−/−. Plasma aldosterone (Aldo) was not different between WT and cav-1−/− mice nontreated or treated with Epl. Thus in cav-1 deficiency states and HS diet MR blockade is associated with increased BP, enhanced vasoconstriction, and decreased NOS-mediated vascular relaxation and eNOS expression. The data suggest that, in the absence of cav-1, MR activation plays a beneficial role in regulating eNOS expression/activity and, consequently, the vascular function during HS diet