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Saint Petersburg, Russia

Anisimov S.V.,Blood and Endocrinology Center
Advances in Gerontology | Year: 2012

Any spinal pathology is accompanied by a significant loss in the quality of life and a high disability rate. The rate of occurrence of spinal impairments increases with advancing age. Spinal impairments may be etiologically different and characterized by a wide range of significant and very diverse clinical symptoms. At the same time, the "lower back pain" (as well as the back pain) syndrome is the most common complaint. The main cause for the development of the syndrome is degenerative disc disease (DDD) of a nonspecific nature that leads to irreversible structural damage to intervertebral discs. Surgical DDD treatment methods, including those based on bone tissue autografting, are not radical; this compels researchers to search for alternative approaches. This review analyzes the principles of regenerative cellular and cell-replacement therapies that are based on the use of a variety of cell types, in the treatment of intervertebral pathologies and compares various cell substrates for these therapies. © Pleiades Publishing, Ltd., 2012. Source


Mikhaylov E.N.,Blood and Endocrinology Center | Bhagwandien R.,Electrophysiology Unit | Janse P.A.,Electrophysiology Unit | Theuns D.A.M.J.,Electrophysiology Unit | Szili-Torok T.,Electrophysiology Unit
Europace | Year: 2013

AimsCryoballoon ablation (CBA) is a well-used technique when performing pulmonary vein (PV) isolation in patients with paroxysmal atrial fibrillation (AF). Our aim is to describe incidence, characteristics, and clinical predictors for developing atrial tachycardias (ATs) after cryoballoon PV isolation in patients with paroxysmal AF.Methods and resultsThe study population consisted of 181 consecutive patients undergoing a first CBA. All patients received an event-recorder before cryoablation and transmitted daily electrocardiogram (ECG) during 1 month before ablation and 3 months after. Further follow-up consisted of 24 h Holter monitoring and ECG registration every 3 months and also in patients presenting with symptoms. A mean follow-up period was 497.9 ± 283.9 days, and 175 patients completed follow-up. In 14 (8%) patients regular ATs were registered. In multivariate logistic regression model, the following parameters were independently associated with ATs after ablation: an additional right PV, treatment with beta-blockers, and presence of AT on event-recording strips before ablation. Seven (4%) patients with registered AT underwent a redo procedure. In two (1.1%) patients ATs were originated in reconnected PVs. In other patients no left AT was induced. No macro re-entrant left AT was documented in any patient. During follow-up, after a redo ablation, no AT was registered.ConclusionThe incidence of left AT after CBA is low, and no left atrial macro re-entrant tachycardia was found. The following independent predictors of AT development have been identified: an additional right PV, regular AT registered before ablation, and the use of beta-blockers. © 2013 The Author. Source


Korostovtseva L.S.,Blood and Endocrinology Center
Medical science monitor : international medical journal of experimental and clinical research | Year: 2011

To assess the impact of obstructive sleep apnea-hypopnea syndrome (OSAHS) on prognosis and cardiovascular morbidity and mortality in relation to other major cardiovascular risk factors. This prospective study recruited 234 patients from an out-patient clinic. Based on the Berlin questionnaire, 147 patients (90 males, mean age 52.1 ± 10.4 years) with highly suspected sleep breathing disorders were included in the study. Based on cardiorespiratory monitoring, patients were divided into 2 groups: 42 patients without sleep breathing disorders (SBD), and 105 patients with OSAHS. Among these, 12 patients started CPAP therapy and formed the third group. The mean follow-up period was 46.4 ± 14.3 months. Event-free survival was lowest in the untreated OSAHS patients (log rank test 6.732, p = 0.035). In the non-adjusted regression model, OSAHS was also associated with a higher risk of cardiovascular events (OR = 8.557, 95% CI 1.142-64.131, p = 0.037). OSAHS patients demonstrated higher rates of hospitalization compared to the control group without SBD (OR 2.750, 95%CI 1.100-6.873, p = 0.04). OSAHS hypertensive patients, and in particular, according to our model, patients with severe OSAHS (AHI ≥ 30/h), are at higher risk of fatal and non-fatal cardiovascular events. Moreover, untreated OSAHS patients demonstrate higher rates of hospitalization caused by the onset or deterioration of cardiovascular disease. Source


Golovanova T.A.,RAS Sechenov Institute of Evolutionary Physiology and Biochemistry | Belostotskaya G.B.,Blood and Endocrinology Center
Cellular Transplantation and Tissue Engineering | Year: 2011

In mammalian heart, cardiac myocyte division ceases within the first week of postnatal life posing one of the most intriguing questions of evolution. Stimulation of cardiac myocyte proliferation during postnatal period would have profound impact on cardiac regeneration in humans. It has been shown that the primary culture of cardiac myocytes obtained from newborn rat could serve as an appropriate model for the investigation of the processes taking place in the heart during early postnatal ontogenesis. Similarly to the in vivo situation, the increased mitotic activity observed during the first 2-4 days after birth is diminished in cardiac myocyte culture within 4-5 days of culturing. Besides, 60% of cultured cells underwent mitotic division followed by increase in their volume which also closely resembles the process of cardiac myocyte hypertrophy in vivo. The cardiac myocyte volume was progressively increased during culturing and equaled to 819±68, 1532±212, and 3246±190 μm 3 on the 1 st, 3 rd, and 6 th day of culture, respectively. Furthermore, the rate of cardiac myocyte growth in culture was similar to the pattern of myocyte hypertrophy observed in the in vivo settings. Myocyte hypertrophy in culture was associated with the formation of polyploid and multinucleated, most commonly binucleated, cells which is generally analogous to the in vivo myocyte hypertrophy. The analysis of myocyte volume distribution suggested that during cultivation nearly 60% of cells are switched from hyperplasia to hypertrophy, stopping at the G 2/M boundary of the cell cycle. The results obtained indicate that cell growth patterns in primary cardiac myocyte culture share a lot of similarity with the in vivo cardiac myocyte growth. Primary cardiac myocyte culture is a valuable tool for investigation of the processes responsible for cessation of cardiac myocyte division in adult mammals. Source


Sonin D.L.,Medical College of Wisconsin | Sonin D.L.,Blood and Endocrinology Center | Wakatsuki T.,Invivosciences, Inc. | Routhu K.V.,Medical College of Wisconsin | And 4 more authors.
Journal of Cardiovascular Pharmacology and Therapeutics | Year: 2013

Purpose: Fibroblast activity promotes adverse left ventricular (LV) remodeling that underlies the development of ischemic cardiomyopathy. Transforming growth factor-b (TGF-b) is a potent stimulus for fibrosis, and the extracellular signal-regulated kinases(ERK) 1/2 pathway also contributes to the fibrotic response. The thrombin receptor, protease-activated receptor 1 (PAR1), has been shown to play an important role in the excessive fibrosis in different tissues. The aim of this study was to investigate the influence of a PAR1 inhibitor, SCH79797, on cardiac fibrosis, tissue stiffness and postinfarction remodeling, and effects of PAR1 inhibition on thrombin-induced TGF-b and (ERK) 1/2 activities in cardiac fibroblasts. Methods: We used a rat model of myocardial ischemia-reperfusion injury, isolated cardiac fibroblasts, and 3-dimensional (3D) cardiac tissue models fabricated to ascertain the contribution of PAR1 activation on cardiac fibrosis and LV remodeling. Results: The PAR1 inhibitor attenuated LV dilation and improved LV systolic function of the reperfused myocardium at 28 days. This improvement was associated with a nonsignificant decrease in scar size (%LV) from 23+% in the control group (n = 10) to 16%+5.5% in the treated group (n = 9; P = .052). In the short term, the PAR1 inhibitor did not rescue infarct size or LV systolic function after 3 days. The PAR1 inhibition abolished thrombin-mediated ERK1/2 phosphorylation, TGF-b and type I procollagen production, matrix metalloproteinase-2/9 activation, myofibroblasts transformation in vitro, and abrogated the remodeling of 3D tissues induced by chronic thrombin treatment. Conclusion: These studies suggest PAR1 inhibition initiated after ischemic injury attenuates adverse LV remodeling through late-stage antifibrotic events. © The Author(s) 2012. Source

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