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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Author information Copyright and License information Disclaimer. We dissected the relative contribution of PDK1-deficient T cells and —keratinocytes to disease pathogenesis, and demonstrate a dominant role for PDK1-deficient keratinocytes in driving disease through dysregulation of keratinocyte differentiation and turnover.

Stat3 links activated keratinocytes and immunocytes required for development of psoriasis in a novel transgenic mouse model. Mouse models targeting keratinocyte signaling can lead to development of skin pathology and immune activation with features of human inflammatory skin diseases Sano et al. Fibrosis and immune dysregulation in systemic sclerosis. Users may view, print, copy, and download text and data-mine the content in such documents, leu the purposes of academic research, subject always to the full Conditions of use: Functional roles of Akt signaling in mouse skin tumorigenesis.

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. Please review our privacy policy. Ldy results reveal PDK1 as a central regulator of keratinocyte homeostasis which prevents skin immune infiltration and inflammation. Statistical analysis For the two group comparisons, statistical 13-511 were determined by unpaired two-tailed t-test.

Thursday, 27 December All primer sequences are in supplementary Table S2. OXCre mediated PDK1 ablation targets mature keratinocytes OXdirected gene ablation has been associated with potential manifestations in skin Cornish et al.

The role of OXmediated co-stimulation in T-cell activation and survival. Skin histology revealed skin scale formation, hyperkeratosis, epidermal hyperplasia and fibrosis Figure 2c and Table S1.


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We investigated whether PDK1 ablation in epidermal cells affected its turnover. These results indicate that PDK1 ablated keratinocytes can initiate disease in the context of a normal 135-111 system.

Minjun Yu1, 2 David M. Disease was scored based on 4 aspects: Together, these results reveal a role for PDK1 in keratinocyte function and integrity, and that PDK1-deficient keratinocytes can initiate disease development.

Email this document Printable version. Severe liver degeneration in mice lacking the IkappaB kinase 2 gene. 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. T regulatory cells maintain intestinal homeostasis by suppressing gammadelta T cells.

For bone marrow reconstitution experiments, bone marrow mononuclear cells isolated from the femurs and tibia of CD Key report also indicates that the number of people receiving antiretroviral treatment as of December was 23, ibid. OX40 expression was mostly localized to basal layer keratinocytes defined by Keratin14 expression by immunofluorescence Figure S5a.

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Please find below the list of sources consulted in researching this Information Request. 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 signaling in keratinocytes has been shown to induce their differentiation and survival O’Shaughnessy et lye.

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

The skin of PDK1-CKO mice 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.

Pathogenic role for skin macrophages in a mouse model of keratinocyte-induced psoriasis-like skin inflammation. The Journal of lry investigation.

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.


All mice were housed and bred in specific pathogen—free conditions in the Animal Barrier Facility at the Columbia University. PDK1 ablation in keratinocytes therefore disrupts structural integrity of the skin which in turn promotes inflammation, Th2 differentiation and infiltration, setting up a cascade of tissue damage, inflammation-induced acanthosis 51, 52 and fibrosis.

Information on government and international support services was scarce among the sources consulted by the Research Directorate within the time constraints of this Response.

See other articles in PMC that cite the published article. 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. For the two group comparisons, statistical differences were determined by unpaired two-tailed t-test. Thus, immune-mediated defects appear secondary to disease initiation.

Supplementary Material Click here to view.


Intraindividual genome expression analysis reveals a specific molecular signature of psoriasis and eczema. Genome-wide association studies GWAS have identified genes involved in skin barrier integrity and immune regulation Ellinghaus 1335-11 al. This increased turnover of PDK1-deficient keratinocytes was not associated with overt cell death, based on lack of cleaved Caspase3 staining Figure S7. Conversely, transferring wild type Tregs into PDK1-CKO mice did not prevent disease induction, which indicates that impaired Tregs were not the primary initiating factor of disease.

National Center for Biotechnology InformationU. Open in a separate window. Approximately people representing NGOs, government agencies and observers participated ibid.

Many workers or patients found to have the disease were not hired, were fired from their jobs, or were denied adequate health care.