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 Rep├║blica Dominicana: una apuesta por el retroceso.

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Inflammatory skin diseases such as atopic dermatitis AD and psoriasis involve immune-mediated and skin-intrinsic defects with each disease having specific immune signatures and skin pathology Bergboer et al.

Skin histology revealed skin scale formation, hyperkeratosis, epidermal hyperplasia and fibrosis Figure 2c and Table S1. The role of OXmediated co-stimulation in T-cell activation and survival. Many workers or patients found to have the disease were not hired, were fired from their jobs, or were denied adequate health care. We used a series of T cell transfers, bone marrow reconstitutions and crossings to lymphocyte-deficient backgrounds to identify the respective roles of PDK1 ablation in each cell type.

Phosphoinositide dependent kinase-1 PDK1 is a key signaling molecule downstream of the phosphatidylinositol 3-kinase PI-3 kinase pathway and is a master regulator of multiple kinases in cells of epithelial and hematopoietic lineages. Through a series of T cell transfers, bone marrow reconstitutions and crossing to lymphocyte-deficient backgrounds, we demonstrate that ablation of PDK1 in keratinocytes initiates disease pathogenesis, that is further exacerbated by T cell-mediated immune responses.

Ablation of PDK1 in pancreatic beta cells induces diabetes as a result of loss of beta cell mass. Pathogenic role for skin macrophages in a mouse model of keratinocyte-induced psoriasis-like skin inflammation.

Abstract Phosphoinositide dependent kinase-1 PDK1 is a key signaling molecule downstream of the phosphatidylinositol 3-kinase PI-3 kinase pathway and is a master regulator of multiple kinases in cells of epithelial and hematopoietic lineages. 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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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. Akt activation induces epidermal hyperplasia and proliferation of epidermal progenitors.

PDK1 ablation in keratinocytes is sufficient for inducing skin infiltration and Th2 activation. Stat3 links activated keratinocytes and immunocytes required for development of psoriasis in a novel transgenic mouse model.

PDK1-deficient keratinocytes exhibit intrinsic defects in expression of key structural proteins including cytokeratin and loricrin, resulting in increased keratinocyte turnover, which in turn, triggers inflammation, T cell recruitment and immune-mediated destruction.

Corroborating information could not be found among the sources consulted by the Research Directorate within the time constraints of this Response.

Our results reveal PDK1 as a central regulator of keratinocyte homeostasis which prevents skin immune infiltration and inflammation. For the two group comparisons, statistical differences were determined by unpaired two-tailed t-test.

The report also indicates that the number of people receiving antiretroviral treatment as of December was leu, ibid. Email this document Printable version. Severe liver degeneration in mice lacking the IkappaB kinase 2 gene.

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OXdirected gene ablation has been associated with potential manifestations in skin Cornish et al. This Response was prepared after researching publicly accessible information currently available to the Research Directorate within time constraints.

This increased turnover of PDK1-deficient keratinocytes was not associated with overt cell death, based on lack of cleaved Caspase3 staining Figure S7. All primer sequences are in supplementary Table S2. Thus, immune-mediated defects appear secondary to disease initiation.

The skin of PDK1-CKO mice with advanced disease contained lesions with epidermal damage, resulting in loss of skin barrier integrity, as shown by dye penetration Figure S1c. Many inmates could not attend their monthly appointments” ibid.

Support Center Support Center. 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.

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The models presented here which separate skin-intrinsic and immune-mediated bases of complex skin phenotypes, as well as their combined effects, can be of important clinical relevance for designing targeted therapies for treating inflammatory skin syndromes.

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This Response is not, and does not purport to be, conclusive as to the merit of any particular claim for refugee protection. Mouse models targeting keratinocyte signaling can lead to development of skin pathology and immune activation with features of key inflammatory skin diseases Sano et al. Genome-wide association studies GWAS have identified genes involved in skin barrier integrity and immune regulation Ellinghaus et al.

Owens3, 4 Sankar Ghosh5 and Donna L. Farber 1, 5, 6. PDK1-CKO mice were born healthy; however, starting at 5 weeks of age, they developed severe, 153-11 dermatitis accompanied by hair loss and skin thickening Figure 1a. T regulatory cells maintain intestinal homeostasis by suppressing gammadelta T cells. We investigated whether PDK1 ablation in epidermal cells affected its turnover. Our results reveal that PDK1-signaling as a central regulatory pathway for keratinocyte homeostasis which prevents pathological immune infiltration and skin inflammation.

The Journal of clinical investigation. Information on government and international support services was scarce among the sources consulted by the Research Directorate within the time constraints of this 1351-1. Arrows indicate location of skin lesions. Approximately people representing NGOs, government agencies and observers participated ibid. UNHCR is not responsible for, nor does it necessarily endorse, its content. Remi Creusot and Damian Turner for critical review of this manuscript.