<?xml version="1.0" encoding="ASCII"?>
<biogps><data><item key="owner">ArrayExpress Uploader</item><item key="pop_total">0</item><item key="id">3285</item><item key="factors"><item><item key="GSM405507"><item key="INDIVIDUAL">Patient 0002</item><item key="CONDITION">atopic dermatitis (AD)</item></item></item><item><item key="GSM405508"><item key="INDIVIDUAL">Patient 0004</item><item key="CONDITION">atopic dermatitis (AD)</item></item></item><item><item key="GSM405509"><item key="INDIVIDUAL">Patient 0005</item><item key="CONDITION">atopic dermatitis (AD)</item></item></item><item><item key="GSM405510"><item key="INDIVIDUAL">Patient 0006</item><item key="CONDITION">atopic dermatitis (AD)</item></item></item><item><item key="GSM4055"><item key="INDIVIDUAL">Patient 0007</item><item key="CONDITION">atopic dermatitis (AD)</item></item></item><item><item key="GSM405512"><item key="INDIVIDUAL">Patient 0008</item><item key="CONDITION">atopic dermatitis (AD)</item></item></item><item><item key="GSM405513"><item key="INDIVIDUAL">Patient 0009</item><item key="CONDITION">atopic dermatitis (AD)</item></item></item><item><item key="GSM405514"><item key="INDIVIDUAL">Patient 0010</item><item key="CONDITION">atopic dermatitis (AD)</item></item></item><item><item key="GSM405515"><item key="INDIVIDUAL">Patient 0011</item><item key="CONDITION">atopic dermatitis (AD)</item></item></item><item><item key="GSM40553"><item key="INDIVIDUAL">Patient 1</item><item key="CONDITION">normal</item></item></item><item><item key="GSM405532"><item key="INDIVIDUAL">Patient 2</item><item key="CONDITION">normal</item></item></item><item><item key="GSM405533"><item key="INDIVIDUAL">Patient 3</item><item key="CONDITION">normal</item></item></item><item><item key="GSM405534"><item key="INDIVIDUAL">Patient 4</item><item key="CONDITION">normal</item></item></item><item><item key="GSM405535"><item key="INDIVIDUAL">Patient 5</item><item key="CONDITION">normal</item></item></item><item><item key="GSM405536"><item key="INDIVIDUAL">Patient 6</item><item key="CONDITION">normal</item></item></item><item><item key="GSM405537"><item key="INDIVIDUAL">Patient 7</item><item key="CONDITION">normal</item></item></item><item><item key="GSM405538"><item key="INDIVIDUAL">Patient 8</item><item key="CONDITION">normal</item></item></item><item><item key="GSM405539"><item key="INDIVIDUAL">Patient 10</item><item key="CONDITION">normal</item></item></item></item><item key="ownerprofile_id">arrayexpress_sid</item><item key="platform">4</item><item key="summary_wrapped">In this study we used genomic profiling to characterize differences in expression of genes related to epidermal growth/differentiation...</item><item key="pubmed_id">20004782</item><item key="geo_gse_id">E-GEOD-16161</item><item key="owner_profile">/profile/8773/arrayexpressuploader</item><item key="factor_count">2</item><item key="sample_count">18</item><item key="tags"><item>atopic dermatitis</item><item>dendritic</item><item>dermatitis</item><item>psoriasis</item><item>skin</item></item><item key="lastmodified">Dec.12, 2014</item><item key="is_default">False</item><item key="geo_id_plat">E-GEOD-16161_A-AFFY-44</item><item key="slug">broad-defects-in-epidermal-cornification-in-atopic</item><item key="geo_gds_id"/><item key="name">Broad defects in epidermal cornification in atopic dermatitis (AD) identified through genomic analysis</item><item key="created">Sep.12, 2014</item><item key="summary">In this study we used genomic profiling to characterize differences in expression of genes related to epidermal growth/differentiation and inflammatory circuits in skin lesions of psoriasis and atopic dermatitis (AD), comparing expression values to normal skin. Skin biopsies were collected from 9 patients with chronic atopic dermatitis, 15 psoriasis patients, and 9 healthy volunteers.  Keywords: Genetic-pathology Psoriasis and AD are common inflammatory skin diseases which share important features, including: 1) large infiltrates of T-cells and inflammatory dendritic cells in skin lesions, 2) immune activation with up-regulated expression of many cytokines, chemokines, and inflammatory molecules 3) marked epidermal hyperplasia in chronic diseased skin and 4) defective barrier function with increased transepidermal water loss (TEWL), which reflects underlying alterations in keratinocyte differentiation. Using genomic profiling we provide a comprehensive comparison of chronic psoriasis and AD skin lesions as compared with normal skin.</item><item key="source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-16161</item><item key="species">human</item><item key="sample_source">http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-16161/samples/</item></data></biogps>
