LEY 135-11 PDF

Transcript of Ley No. Quotation 1. Headline 2. Headline 3. Headline 4 $ Jueves 19 de julio Vol XCIII, No. Subtitle. Objeto y alcance de la ley – Free download as Powerpoint Presentation .ppt /.pptx), PDF File .pdf), Text File .txt) or view presentation slides. , enacted by the President of the Dominican Republic on 7 . “Ley de SIDA en República Dominicana: una apuesta por el retroceso.

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We therefore define a role for PDK1 in keratinocytes to maintain their homeostasis and prevent skin inflammation, and a model for studying complex pathogenesis of inflammatory skin diseases. Corroborating information could not be found among the sources consulted by the Research Directorate within the time constraints of this Response.

Inflammatory skin disease is caused by the interplay of skin barrier disruption and immune dysregulation. Statistical analysis For the two group comparisons, statistical differences were determined by unpaired two-tailed t-test. The original version of this document may be found on the offical website of the IRB at http: This Response is not, and does not purport to be, conclusive as to the merit of any particular claim for refugee protection.

OXCre mice Klinger et al. Ablation of PDK1 in pancreatic beta cells induces diabetes as a result of loss of beta cell mass.

Our results reveal that PDK1-signaling as a central regulatory pathway for keratinocyte homeostasis which prevents pathological immune infiltration and skin inflammation. Akt signaling in keratinocytes has been shown to induce their differentiation and survival O’Shaughnessy et al.

Please find below the list of sources consulted in researching this Information Request. The Journal of clinical investigation.

The skin of PDK1-CKO ely contained multiple alterations by histological anlaysis, including epidermal scales, hyperplasia, hyperkeratosis, loss of hair follicles and hypodermal fat, and increased dermal fibrosis, while the skin of PDK1-CHET mice remained healthy Figure 1c and Table S1.

The publisher’s final edited version of this article is available at J Invest Dermatol.

We did not observe inflammation in other organs lung, liver, kidney, gut Figure S1cindicating that the tissue target of disease pathology in PDK1-CKO mice was limited to skin. Together, these results reveal a role for PDK1 in keratinocyte function and integrity, and that PDK1-deficient keratinocytes can initiate disease development.

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The Journal of biological chemistry. Open in a separate window. We propose that the severe skin phenotypes induced by PDK1 ablation in keratinocytes may be due to dysregulation of multiple pathways e. Owens3, 4 Sankar Ghosh5 and Donna L. High-density genotyping study identifies four new susceptibility loci for atopic dermatitis. OXdirected gene ablation has been associated with potential manifestations in skin Cornish et al.

Disease was scored based on 4 aspects: PDK1 ablation in keratinocytes is sufficient for inducing skin infiltration and Th2 activation. Thymic OX40 expression discriminates cells undergoing strong responses to selection ligands. Correspondingly, mild epidermal hyperplasia and microabscess was observed in mice at 3 weeks of age but not at 10 days Figure S5bshowing that PDK1 ablation in keratinocytes is coincident with disease development.

Email this document Printable version. These BMT results indicate that the T cell-intrinsic impairments were not responsible for the severe skin disease and development of pathogenic skin-homing T cells observed in parent PDK1-CKO mice, and suggest that a non-hematopoietic cell may promote skin disease pathogenesis.

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Identification of 15 new psoriasis susceptibility loci highlights the role of innate immunity. The role of OXmediated co-stimulation in T-cell activation and survival. All mice were housed and bred in specific pathogen—free conditions in the Animal Barrier Facility at the Columbia University.

PDK1 is broadly expressed in many cell types including epithelial and hematopoietic lineages, and is important for embryonic development, cell growth, survival and metabolism Chen et al. Arrows indicate location of skin lesions.

In this study, we identify PDK1 as a molecular regulator of keratinocyte homeostasis and of the skin-immune interface, that when disrupted in vivo triggers severe skin pathology, systemic inflammation and morbidity.

Intraindividual genome expression analysis reveals a specific molecular signature of psoriasis and eczema. Disease scoring Disease was scored based on 4 aspects: Functional roles of Akt signaling in mouse skin tumorigenesis. T regulatory cells maintain intestinal homeostasis by suppressing gammadelta T cells.

Through a series of T cell transfers, bone marrow reconstitutions and crossing to lymphocyte-deficient backgrounds, we demonstrate that ablation of PDK1 in keratinocytes is the major driver of disease pathogenesis. UNHCR is not responsible for, nor does it necessarily endorse, its content. For bone marrow reconstitution experiments, bone marrow mononuclear cells isolated from the femurs and tibia of CD Akt-dependent Pp2a activity is required for epidermal ldy formation during late embryonic development.

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See other articles in PMC that cite the published article. The resultant mice PDK1-CKO spontaneously developed severe dermatitis, skin fibrosis and systemic Th2 immunity, succumbing by 11 weeks of age. Approximately people representing NGOs, government agencies and observers participated ibid. Remi Creusot and Damian Turner for critical review of this manuscript. These results indicate that PDK1 ablated keratinocytes can initiate disease in the context of a normal immune system.

PDK1-deficient keratinocytes exhibit intrinsic defects in expression of 1335-11 structural proteins including cytokeratin and loricrin, resulting in increased keratinocyte turnover, which in turn, triggers inflammation, T cell recruitment and immune-mediated destruction. For the two group comparisons, statistical differences were determined by unpaired two-tailed t-test. PDK1 regulates platelet activation and arterial thrombosis.

Ley No. by Carol Nelsys González Durán on Prezi

PDK1-CKO mice were born healthy; however, starting at 5 weeks of age, they developed severe, systemic dermatitis accompanied by hair loss and skin thickening Figure 1a. Minjun Yu1, 2 David M. Stat3 links activated keratinocytes and immunocytes required for development 13511 psoriasis in a novel transgenic mouse model.

Although the law prohibits the use of HIV testing to screen 1351-1, Human Rights Watch and Amnesty International reported that workers in various industries faced obligatory HIV testing in the workplace. The skin manifestations due to PDK1 ablation mimic different features of human skin diseases, with epidermal hyperplasia, reduced Krt10 and loricrin expression, barrier defects and skewed Th2 responses similar to AD, parakeratosis and thickening observed in psoriasis, and skin fibrosis and Th2 responses seen lfy scleroderma Chizzolini et al.