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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Please find below the list of sources consulted in researching this Information Request. Farber 1, 5, 6. Information on government and international support services was scarce among the sources consulted by the Research Directorate within the time constraints of this Response.
This Response is not, and does not purport to be, conclusive as to the merit of any particular claim for refugee protection. The role of OXmediated co-stimulation in T-cell activation and survival. The skin of PDK1-CKO 135-111 with advanced disease contained lesions with epidermal damage, resulting in loss of skin barrier integrity, as shown by dye penetration Figure S1c. Keratinocyte-specific Pten deficiency results in epidermal hyperplasia, accelerated hair follicle morphogenesis and tumor formation.
The Journal of clinical investigation. Author manuscript; available in Leu May 1. 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, lry suggest that a non-hematopoietic cell may promote skin disease pathogenesis. Akt activation induces epidermal hyperplasia and proliferation of epidermal progenitors. Disease was scored based on 4 aspects: 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 in scleroderma Chizzolini et al.
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.
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Minjun Yu1, 2 David M. Skin histology revealed skin scale formation, hyperkeratosis, epidermal hyperplasia and fibrosis Figure 2c and Table S1.
The physiological role of PDK1 in regulating skin and immune homeostasis is not known. The resultant mice PDK1-CKO spontaneously developed severe dermatitis, skin fibrosis and systemic Th2 immunity, succumbing by 11 pey of age.
F and an Arthritis Foundation fellowship awarded to M. These results indicate that PDK1 ablated keratinocytes leu initiate disease in the context of a normal immune system. Our results reveal PDK1 as a central regulator of keratinocyte homeostasis which prevents skin immune infiltration and inflammation. Ablation of PDK1 in pancreatic beta cells induces diabetes as a result of loss of beta cell mass.
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.
This skin barrier defect was observed in mice with severe disease at wks of age and not in infant mice Figure S1c. PDK1 ablation in keratinocytes is sufficient for inducing skin infiltration and Th2 activation. 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 13-11 fibrosis, while the skin of PDK1-CHET mice remained healthy Figure 1c and Table S1.
Lley investigated whether PDK1 ablation in epidermal cells affected its turnover. For bone marrow reconstitution experiments, bone marrow mononuclear cells isolated from the femurs and tibia of CD 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.
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.
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. Psoriasis-like skin disease and arthritis caused by inducible epidermal deletion of Jun proteins.
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. Akt signaling in keratinocytes has been shown to induce their differentiation and survival O’Shaughnessy et al. The resultant PDK1-CKO mice are born healthy but gradually develop severe inflammatory skin disease, with systemic Th2-mediated inflammation, skin thickening and fibrosis.
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.
Fibrosis and immune dysregulation in systemic sclerosis.
Tissue specific deletion of inhibitor of kappa B kinase 2 with OXCre reveals the unanticipated expression from the OX40 locus in skin epidermis. Thursday, 27 December The report also indicates that the number of people receiving antiretroviral treatment as of December was 23, ibid. This Response was prepared after 135-111 publicly accessible information currently available to the Research Directorate within time constraints. 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: