77 research outputs found

    Social orientation of banks

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    The influence of the bank's orientation on clients and the quality of the services provided on the financial efficiency of the commercial institution (sales volume, profitability, cost reduction) was studied. The development of online banking and Internet banking is considered. The relationship between the profitability of the bank and the level of customercentricity is proved. World experience has been compared and generalized, and country specificity has been singled out in different regions of the world. The dependence between the degree of customer satisfaction and their subsequent loyalty to the bank was studied. Prospective directions of expansion of the market of banking services are outlined, and also changes in the psychology of the client that took place due to scientific and technological progress are noted. The basic directions of increase of efficiency of work of the bank personnel are allocated

    Endothelial NOS (NOS3) impairs myocardial function in developing sepsis

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    Endothelial nitric oxide synthase (NOS)3-derived nitric oxide (NO) modulates inotropic response and diastolic interval for optimal cardiac performance under non-inflammatory conditions. In sepsis, excessive NO production plays a key role in severe hypotension and myocardial dysfunction. We aimed to determine the role of NOS3 on myocardial performance, NO production, and time course of sepsis development. NOS3(−/−) and C57BL/6 wildtype mice were rendered septic by cecum ligation and puncture (CLP). Cardiac function was analyzed by serial echocardiography, in vivo pressure and isolated heart measurements. Cardiac output (CO) increased to 160 % of baseline at 10 h after sepsis induction followed by a decline to 63 % of baseline after 18 h in wildtype mice. CO was unaltered in septic NOS3(−/−) mice. Despite the hyperdynamic state, cardiac function and mean arterial pressure were impaired in septic wildtype as early as 6 h post CLP. At 12 h, cardiac function in septic wildtype was refractory to catecholamines in vivo and respective isolated hearts showed impaired pressure development and limited coronary flow reserve. Hemodynamics remained stable in NOS3(−/−) mice leading to significant survival benefit. Unselective NOS inhibition in septic NOS3(−/−) mice diminished this survival benefit. Plasma NO(x)- and local myocardial NO(x)- and NO levels (via NO spin trapping) demonstrated enhanced NO(x)- and bioactive NO levels in septic wildtype as compared to NOS3(−/−) mice. Significant contribution by inducible NOS (NOS2) during this early phase of sepsis was excluded. Our data suggest that NOS3 relevantly contributes to bioactive NO pool in developing sepsis resulting in impaired cardiac contractility. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s00395-013-0330-8) contains supplementary material, which is available to authorized users

    Повышение эффективности управления расчетами с персоналом по оплате труда посредством внедрения электронного документооборота

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    В данной статье рассмотрены понятие документооборота, его роль на предприятии, взаимодействие бухгалтерии с другими предприятиями через документооборот, а также проблемы, возникающие при взаимодействии, понятие системы электронного документооборота, преимущества и недостатки электронного документооборота

    Desmoglein 2 mutant mice develop cardiac fibrosis and dilation

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    Desmosomes are cell–cell adhesion sites and part of the intercalated discs, which couple adjacent cardiomyocytes. The connection is formed by the extracellular domains of desmosomal cadherins that are also linked to the cytoskeleton on the cytoplasmic side. To examine the contribution of the desmosomal cadherin desmoglein 2 to cardiomyocyte adhesion and cardiac function, mutant mice were prepared lacking a part of the extracellular adhesive domain of desmoglein 2. Most live born mutant mice presented normal overall cardiac morphology at 2 weeks. Some animals, however, displayed extensive fibrotic lesions. Later on, mutants developed ventricular dilation leading to cardiac insufficiency and eventually premature death. Upon histological examination, cardiomyocyte death by calcifying necrosis and replacement by fibrous tissue were observed. Fibrotic lesions were highly proliferative in 2-week-old mutants, whereas the fibrotic lesions of older mutants showed little proliferation indicating the completion of local muscle replacement by scar tissue. Disease progression correlated with increased mRNA expression of c-myc, ANF, BNF, CTGF and GDF15, which are markers for cardiac stress, remodeling and heart failure. Taken together, the desmoglein 2-mutant mice display features of dilative cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy, an inherited human heart disease with pronounced fibrosis and ventricular arrhythmias that has been linked to mutations in desmosomal proteins including desmoglein 2
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