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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UNHCR is not responsible for, lej does it necessarily endorse, its content. Users may view, print, copy, and download text and data-mine the content 315-11 such documents, for the purposes of academic research, subject always to the full Conditions of key The models presented here which separate skin-intrinsic and immune-mediated bases of complex 13511 phenotypes, as well as their combined effects, can be of important clinical relevance for designing targeted therapies for treating inflammatory skin syndromes.
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.
This Response was prepared after researching publicly accessible information currently available to the Research Directorate within time constraints. 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.
Associated Data Supplementary Materials. 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. Many workers or patients found to have the disease were not hired, were fired from their jobs, or were denied adequate health care.
Sibley CH[Author] – PubMed Result
The resultant PDK1-CKO mice are born healthy but gradually develop severe inflammatory skin disease, with systemic Th2-mediated 1355-11, skin thickening and fibrosis. 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. PDK1 ablation in keratinocytes is sufficient for inducing skin infiltration and Th2 activation.
National Center for Biotechnology InformationU. Phosphoinositide dependent kinase-1 PDK1 is a key signaling molecule downstream of the phosphatidylinositol 3-kinase PI-3 kinase pathway and is 135-1 master regulator of multiple kinases in cells of epithelial and hematopoietic lineages. 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.
Keratinocyte-specific Pten deficiency results in epidermal hyperplasia, accelerated hair follicle morphogenesis and tumor formation. All primer sequences are in supplementary Table S2. Although the law prohibits the use of HIV testing to screen employees, Human Rights Watch and Amnesty International reported that workers in various industries faced obligatory HIV testing in the workplace. J Allergy Clin Immunol. OXdirected gene ablation has been associated with potential manifestations in skin Cornish et al.
PDK1 regulates platelet activation and arterial thrombosis. Disease was scored based on 4 aspects: Mouse models targeting keratinocyte signaling can lead to development of skin pathology and immune activation with features of human inflammatory skin diseases Sano et key.
Author manuscript; available in PMC May 1. The 13511 of clinical investigation. Fibrosis and immune dysregulation in systemic sclerosis.
Deficiency of PDK1 in cardiac muscle results in heart failure and increased sensitivity to hypoxia. Owens3, 4 Sankar Ghosh5 and Donna L. 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.
The physiological role of PDK1 in regulating skin and immune homeostasis is not known. Open in a separate window. We demonstrate that PDK1-ablation in keratinocytes was sufficient to trigger skin pathology and drive inflammatory disease.
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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 ly skin disease pathogenesis. Please find below the list of sources consulted in researching this Information Request.
The findings of the consultations include the following:.
For bone marrow reconstitution experiments, bone marrow mononuclear cells isolated from the femurs and tibia of CD These results indicate that PDK1 ablated keratinocytes can initiate disease in the context of a normal immune system. T regulatory cells maintain intestinal homeostasis by suppressing gammadelta T cells. Email this document Printable version. Thymic OX40 expression discriminates cells undergoing strong responses to selection ligands. Ablation of PDK1 in pancreatic beta cells induces diabetes as a result of loss of beta cell mass.
The resultant mice PDK1-CKO spontaneously developed severe dermatitis, skin fibrosis and systemic Th2 immunity, succumbing by 11 weeks of age. 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.
F and an Arthritis Foundation fellowship awarded to M. The report also indicates that the number of people receiving antiretroviral treatment as of December was 23, ibid. 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.
Tissue specific deletion of inhibitor of kappa B kinase 2 with OXCre reveals the unanticipated expression from the OX40 locus in skin epidermis.
Our results reveals a role for PDK1 in maintaining keratinocyte function and integrity. See other articles in PMC that cite the published article.
OX40 expression was mostly localized to basal layer keratinocytes defined by Keratin14 expression by immunofluorescence Figure S5a. Stat3 links activated keratinocytes and immunocytes required for development of psoriasis in a novel transgenic mouse model. 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.