The Impact of E-Management in improving the quality of public services Empirical study of CNAS

تهدف هذه الدراسة الى معرفة تصور الافراد العاملين في مؤسسة الصندوق الوطني للضمان الاجتماعي CNAS حول اثر استخدام الادارة الالكترونية في تحسين جودة الخدمة العمومية. وللحصول على معطيات كمية حقيقية تم توزيع استبيان على عينة من موظفي الصندوق لولاية بسكرة والبالغ عددها(36) موظفاً. توصلت هذه الدراسة إلى جملة من النتائج اهما: ان الادارة الالكترونية معمول بها بدرجة كبيرة في الصندوق الوطني للضمان الاجتماعيCNAS ، كما ان جودة الخدمة العمومية هي الأخرى سائدة بدرجة مرتفعة، تبين ايضا وجود أثر لاستخدام الإدارة الالكترونية بأبعادها المختلفة على جودة الخدمة العمومية في الصندوق الوطني للضمان الاجتماعي CNAS ، حيث فسرت الادارة الالكترونية ما مقداره 57.5 % من التغيرات الحاصلة في جودة الخدمة العمومية.We aim through this study to identify the perceptions of individuals working at the National Social Security Fund Foundation about the nature and the impact of the relationship between e-governance and the quality of public service, as well as the extent to which e-governance contributed to the improvement of the quality of the public service. A key tool designed to collect data was the identification of the sample. (36) Staff. The study produced a number of findings: The independent variable of e-governance is highly prevalent in the institution of the National Social Security Fund, the dependent variable of public service quality is highly prevalent in the same institution, and the moral impact of e-governance in its various dimensions on the quality of the public service in the institution of the National Social Security Fund, where e-administration has explained a 57.5% amount of changes in the quality of the public service

Effect of apoA-I on cholesterol release and apoE secretion in human mature adipocytes

<p>Abstract</p> <p>Background</p> <p>The risk of cardiovascular disease is inversely correlated to level of plasma HDL-c. Moreover, reverse cholesterol transport (RCT) from peripheral tissues to the liver is the most widely accepted mechanism linked to the anti-atherosclerotic activity of HDL. The apolipoprotein A-I (apoA-I) and the ABC transporters play a key role in this process.</p> <p>Adipose tissue constitutes the body's largest pool of free cholesterol. The adipose cell could therefore be regarded as a key factor in cholesterol homeostasis. The present study investigates the capacity of primary cultures of mature human adipocytes to release cholesterol and explores the relationships between apoA-I, ABCA1, and apoE as well as the signaling pathways that could be potentially involved.</p> <p>Results</p> <p>We demonstrate that apoA-I induces a strong increase in cholesterol release and apoE secretion from adipocytes, whereas it has no transcriptional effect on ABCA1 or apoE genes. Furthermore, brefeldin A (BFA), an intracellular trafficking inhibitor, reduces basal cholesterol and apoE secretion, but does not modify induction by apoA-I. The use of statins also demonstrates that apoA-I stimulated cholesterol release is independent of HMG-CoA reductase activation.</p> <p>Conclusion</p> <p>Our work highlights the fact that adipose tissue, and particularly adipocytes, may largely contribute to RCT <it>via </it>a mechanism specifically regulated within these cells. This further supports the argument that adipose tissue must be regarded as a major factor in the development of cardiovascular diseases, in particular atherosclerosis.</p

Signaling pathways involved in LPS induced TNFalpha production in human adipocytes

<p>Abstract</p> <p>Background</p> <p>The development of obesity has been linked to an inflammatory process, and the role of adipose tissue in the secretion of pro-inflammatory molecules such as IL-6 or TNFalpha has now been largely confirmed. Although TNFalpha secretion by adipose cells is probably induced, most notably by TLR ligands, the activation and secretion pathways of this cytokine are not yet entirely understood. Moreover, given that macrophagic infiltration is a characteristic of obesity, it is difficult to clearly establish the level of involvement of the different cellular types present within the adipose tissue during inflammation.</p> <p>Methods</p> <p>Primary cultures of human adipocytes and human peripheral blood mononuclear cells were used. Cells were treated with a pathogen-associated molecular pattern: LPS, with and without several kinase inhibitors. Western blot for p38 MAP Kinase was performed on cell lysates. TNFalpha mRNA was detected in cells by RT-PCR and TNFalpha protein was detected in supernatants by ELISA assays.</p> <p>Results</p> <p>We show for the first time that the production of TNFalpha in mature human adipocytes is mainly dependent upon two pathways: NFkappaB and p38 MAP Kinase. Moreover, we demonstrate that the PI3Kinase pathway is clearly involved in the first step of the LPS-pathway. Lastly, we show that adipocytes are able to secrete a large amount of TNFalpha compared to macrophages.</p> <p>Conclusion</p> <p>This study clearly demonstrates that the LPS induced activation pathway is an integral part of the inflammatory process linked to obesity, and that adipocytes are responsible for most of the secreted TNFalpha in inflamed adipose tissue, through TLR4 activation.</p

Effect of the Cannabinoid Receptor-1 antagonist SR141716A on human adipocyte inflammatory profile and differentiation

<p>Abstract</p> <p>Background</p> <p>Obesity is characterized by inflammation, caused by increase in proinflammatory cytokines, a key factor for the development of insulin resistance. SR141716A, a cannabinoid receptor 1 (CB1) antagonist, shows significant improvement in clinical status of obese/diabetic patients. Therefore, we studied the effect of SR141716A on human adipocyte inflammatory profile and differentiation.</p> <p>Methods</p> <p>Adipocytes were obtained from liposuction. Stromal vascular cells were extracted and differentiated into adipocytes. Media and cells were collected for secretory (ELISA) and expression analysis (qPCR). Triglyceride accumulation was observed using oil red-O staining. Cholesterol was assayed by a fluorometric method. 2-AG and anandamide were quantified using isotope dilution LC-MS. TLR-binding experiments have been conducted in HEK-Blue cells.</p> <p>Results</p> <p>In LPS-treated mature adipocytes, SR141716A was able to decrease the expression and secretion of TNF-a. This molecule has the same effect in LPS-induced IL-6 secretion, while IL-6 expression is not changed. Concerning MCP-1, the basal level is down-regulated by SR141716A, but not the LPS-induced level. This effect is not caused by a binding of the molecule to TLR4 (LPS receptor). Moreover, SR141716A restored adiponectin secretion to normal levels after LPS treatment. Lastly, no effect of SR141716A was detected on human pre-adipocyte differentiation, although the compound enhanced adiponectin gene expression, but not secretion, in differentiated pre-adipocytes.</p> <p>Conclusion</p> <p>We show for the first time that some clinical effects of SR141716A are probably directly related to its anti-inflammatory effect on mature adipocytes. This fact reinforces that adipose tissue is an important target in the development of tools to treat the metabolic syndrome.</p

Évaluation de l’exposition d’adipocytes humains sous-cutanés en culture aux acides linoléiques conjugués par une approche multi-omique

Conjugated linoleic acids are 18 carbones fatty acids members comprising a consecutive (conjugated) double bonds system with a various cis/trans geometry sequence, giving rise to at least 16 different isomers. Among those, the t10,c12 isomer has been reported to have anti-obesity properties. We evaluated the biological response of human primary adipose tissue cultured adipocytes to that CLA isomer, alone or present in a commercial mixture, using system biology approaches (primarily transcriptomics and metabolomics). We found that CLA changed the biological activity of at least 45 metabolic pathways at the genomic level, which transcriptional activities was associated to a parallelle metabolome adipocyte change (lipidome upmost) (r2value transcriptome/ metabolome of 0.89). In pairwise analysis, it appeared that 6 of these pathways at the genomic level were tightly associated to the metabolomic response, such as apoptosis, interleukine-6, proteasome, reticulum endoplasmic stress, transcription role of heterochromatine, cell proliferation through EGFR dependent tyrosine kinase, gamma-aminobutyrate receptor. This latter exhibited the most tightly relationship with the metabolome variations in multivariated analysis. One may infer that this pathway is the most targeted by CLA treatment. In conclusion, the implementation of a multi-omic global approach allowed the identification of a set of biological pathways at the genomic level associated to the metabolic balance of CLA-treated adipocytes. All of these pathways are related to insulin-resistance, metabolic syndrome and adipogenesis

Fatty acids do not pay the toll: effect of SFA and PUFA on human adipose tissue and mature adipocytes inflammation

<p>Abstract</p> <p>Background</p> <p>On the basis that high fat diet induces inflammation in adipose tissue, we wanted to test the effect of dietary saturated and polysunsaturated fatty acids on human adipose tissue and adipocytes inflammation. Moreover we wanted to determine if TLR2 and TLR4 are involved in this pathway.</p> <p>Methods</p> <p>Human adipose tissue and adipocytes primary cultures were treated with endotoxin-free BSA conjugated with SFA (lauric acid and palmitic acid - LA and PA) and PUFA (eicosapentaeneic acid, docosahexaenoic acid and oleic acid - EPA, DHA and OA) with or without LPS. Cytokines were then assayed by ELISA (TNF-alpha, IL-6 and MCP-1). In order to determine if TLR2 and TLR4 are activated by fatty acid (FA), we used HEK-Blue cells transfected by genes from TLR2 or TLR4 pathways associated with secreted alkaline phosphatase reporter gene.</p> <p>Results</p> <p>None of the FA tested in HEK-Blue cells were able to activate TLR2 or TLR4, which is concordant with the fact that after FA treatment, adipose tissue and adipocytes cytokines levels remain the same as controls. However, all the PUFA tested: DHA, EPA and to a lesser extent OA down-regulated TNF-alpha, IL-6 and MCP-1 secretion in human adipose tissue and adipocytes cultures.</p> <p>Conclusions</p> <p>This study first confirms that FA do not activate TLR2 and TLR4. Moreover by using endotoxin-free BSA, both SFA and PUFA tested were not proinflammatory in human adipose tissue and adipocytes model. More interestingly we showed that some PUFA exert an anti-inflammatory action in human adipose tissue and adipocytes model. These results are important since they clarify the relationship between dietary fatty acids and inflammation linked to obesity.</p