Methodology of assessment of population satisfaction with the quality of medical service based on the adaptive polling technologyn

This article covers the problem of assessment of patient satisfaction as a parameter of the quality of medical service. The existing methods of assessment of patients' attitude to a medical institution, their benefits and disadvantages are considered. The methodology for the calculation of the satisfaction coefficient is proposed, which can be the basis for the application of the technology (depending on the type and amount of medical care received by the patient) of adaptive polling and analysis of the information received

ИССЛЕДОВАНИЕ ВОЗДЕЙСТВИЯ АПОЛЯРНЫХ РЕАГЕНТОВ НА ТЕКУЧЕСТЬ ВОДОУГОЛЬНЫХ СУСПЕНЗИЙ

В последнее время возник интерес к поведению водоугольных суспензий в связи с поиском альтернативных видов энергоресурсов [1-4]. Повышенный интерес к водо угольному топливу вызван ростом цен на нефть и нефтепродукты и ограниченностью запасов этого сырья. Водоугольные смеси широко изучаются в различных странах мира, так как они могут заменить и традиционное пылевидное топливо, перед которым имеют ряд существенных преимуществ. Особенности горения водоугольного топлива позволяют относить его к разряду экологически чистых видов топлива. При сжигании угля в виде водоугольной суспензии увеличивается скорость выгорания углерода, снижаются выбросы вредных веществ в атмосферу и образование оксидов азота

Simulation of the furnace of the boiler P-49 in the package of applied programs fire 3D

The combustion of solid low-grade fuel in LTV-boiler furnaces is a pressing research questions currently. The aim of this work is the creation of a computational grid model LTV-furnace to calculate the package of applied programs FIRE 3D. The study created a model LTV-furnace. The model tested on brown coal from the Nazarovo Deposit. The resulting distribution of temperatures and velocities has proved the performance of the model

Corporate Culture of Contemporary Research University in Search of Complementarity of Humanitarian and Commercial Principles in Education (Russian Context)

Background: In the paper the formation of world-class research universities is analysed. The paper studies the history of the research university, prerequisites of its appearance, formation and its development toward modern research university. The modern research university is being cautiously viewed nowadays. The crisis of the university is its reality. The question of the corporate culture formation is now considered to be a topical matter in connection with globalization process, Methods: The authors implemented comparative analysis by comparing Humboldt's model of the research university and the modern one. Results: The comparison is made in regard to the idea of university, its criteria and mission. Special emphasis is laid on the analysis and comparison of corporate culture systems. Conclusions: Corporate culture is a novel criterion of the classical university that has recently arisen in the information society and now characterizes the university in a complementary way: on the one hand, as a competitive market entity, and on the other hand, as a guardian of its traditional, historically formed humanitarian criteria, ideas and mission. The following conclusion has been reached: the updated parameters have the identical form to those found by W. von Humboldt, only essence has changed

Genome-wide comparison between IL-17 and combined TNF-alpha/IL-17 induced genes in primary murine hepatocytes

<p>Abstract</p> <p>Background</p> <p>Cytokines such as TNF-alpha and IL-1beta are known for their contribution to inflammatory processes in liver. In contrast, the cytokine IL-17 has not yet been assigned a role in liver diseases. IL-17 can cooperate with TNF-alpha to induce a synergistic response on several target genes in different cell lines, but no data exist for primary hepatocytes. To enhance our knowledge on the impact of IL-17 alone and combined with TNF-alpha in primary murine hepatocytes a comprehensive microarray study was designed. IL-1beta was included as this cytokine is suggested to act in a similar manner as the combination of TNF-alpha and IL-17, especially with respect to its role in mRNA stabilization.</p> <p>Results</p> <p>The present microarray analysis demonstrates that primary murine hepatocytes responded to IL-17 stimulation by upregulation of chemokines and genes, which are functionally responsible to increase and sustain inflammation. Cxcl2, Nfkbiz and Zc3h12a were strongly induced, whereas the majority of the genes were only very moderately up-regulated. Promoter analysis revealed involvement of NF-kappaB in the activation of many genes. Combined stimulation of TNF-alpha/IL-17 resulted in enhanced induction of gene expression, but significantly synergistic effects could be applied only to a few genes, such as Nfkbiz, Cxcl2, Zc3h12 and Steap4. Comparison of the gene expression profile obtained after stimulation of TNF-alpha/IL-17 versus IL-1beta proposed an "IL-1beta-like effect" of the latter cytokine combination. Moreover, evidence was provided that modulation of mRNA stability may be a major mechanism by which IL-17 regulates gene expression in primary hepatocytes. This assumption was exemplarily proven for Nfkbiz mRNA for the first time in hepatocytes. Our studies also suggest that RNA stability can partially be correlated to the existence of AU rich elements, but further mechanisms like the RNase activity of the up-regulated Zc3h12a have to be considered.</p> <p>Conclusions</p> <p>Our microarray analysis gives new insights in IL-17 induced gene expression in primary hepatocytes highlighting the crosstalk with the NF-kappaB signaling pathway. Gene expression profile suggests IL-17 alone and in concert with TNF-alpha a role in sustaining liver inflammatory processes. IL-17 might exceed this function by RNA stabilization.</p

Ahmet Ferdi

Suat Derviş'in Yeni Şark'ta tefrika edilen Ahmet Ferdi adlı romanıTelif hakları nedeniyle romanın tam metni verilememiştir

IL-1β and TNFα Differentially Influence NF-κB Activity and FasL-Induced Apoptosis in Primary Murine Hepatocytes During LPS-Induced Inflammation

Macrophage-derived cytokines largely influence the behavior of hepatocytes during an inflammatory response. We previously reported that both TNFα and IL-1β, which are released by macrophages upon LPS stimulation, affect Fas ligand (FasL)-induced apoptotic signaling. Whereas TNFα preincubation leads to elevated levels of caspase-3 activity and cell death, pretreatment with IL-1β induces increased caspase-3 activity but keeps cells alive. We now report that IL-1β and TNFα differentially influence NF-κB activity resulting in a differential upregulation of target genes, which may contribute to the distinct effects on cell viability. A reduced NF-κB activation model was established to further investigate the molecular mechanisms which determine the distinct cell fate decisions after IL-1β and TNFα stimulation. To study this aspect in a more physiological setting, we used supernatants from LPS-stimulated bone marrow-derived macrophages (BMDMs). The treatment of hepatocytes with the BMDM supernatant, which contains both IL-1β and TNFα, sensitized to FasL-induced caspase-3 activation and cell death. However, when TNFα action was blocked by neutralizing antibodies, cell viability after stimulation with the BMDM supernatant and FasL increased as compared to single FasL stimulation. This indicates the important role of TNFα in the sensitization of apoptosis in hepatocytes. These results give first insights into the complex interplay between macrophages and hepatocytes which may influence life/death decisions of hepatocytes during an inflammatory reaction of the liver in response to a bacterial infection

Influenza A Virus Inhibits Type I IFN Signaling via NF-κB-Dependent Induction of SOCS-3 Expression

The type I interferon (IFN) system is a first line of defense against viral infections. Viruses have developed various mechanisms to counteract this response. So far, the interferon antagonistic activity of influenza A viruses was mainly observed on the level of IFNβ gene induction via action of the viral non-structural protein 1 (NS1). Here we present data indicating that influenza A viruses not only suppress IFNβ gene induction but also inhibit type I IFN signaling through a mechanism involving induction of the suppressor of cytokine signaling-3 (SOCS-3) protein. Our study was based on the observation that in cells that were infected with influenza A virus and subsequently stimulated with IFNα/β, phosphorylation of the signal transducer and activator of transcription protein 1 (STAT1) was strongly reduced. This impaired STAT1 activation was not due to the action of viral proteins but rather appeared to be induced by accumulation of viral 5′ triphosphate RNA in the cell. SOCS proteins are potent endogenous inhibitors of Janus kinase (JAK)/STAT signaling. Closer examination revealed that SOCS-3 but not SOCS-1 mRNA levels increase in an RNA- and nuclear factor kappa B (NF-κB)-dependent but type I IFN-independent manner early in the viral replication cycle. This direct viral induction of SOCS-3 mRNA and protein expression appears to be relevant for suppression of the antiviral response since in SOCS-3 deficient cells a sustained phosphorylation of STAT1 correlated with elevated expression of type I IFN-dependent genes. As a consequence, progeny virus titers were reduced in SOCS-3 deficient cells or in cells were SOCS-3 expression was knocked-down by siRNA. These data provide the first evidence that influenza A viruses suppress type I IFN signaling on the level of JAK/STAT activation. The inhibitory effect is at least in part due to the induction of SOCS-3 gene expression, which results in an impaired antiviral response