233 studies found
Patients with RA diagnosis according to 2010 ACR/EULAR criteria and who were prescribed for the first time a BP among the TNF inhibitors adalimumab, infliximab (original product or biosimilar), etanercept, the anti-CD20 antibody rituximab, or the anti-IL6R antibody tocilizumab (administered SC or intravenously) as first-line or second-line therapy were recruited from March 3, 2014 to June 21, 2016. Patients who were not naive for the biotherapy they were given in the study were excluded.
Study phase: recruitment. For more details, see http://www.aetionomy.eu/content/dam/scai/AETIONOMY/Dokumente/Aetionomy_Newsletter4_web.pdf
All baseline cohort parameters, clinical, conventional (knee x-ray and MRI and the robust biochemical markers), and novel markers (T2 relaxation MRI for cartilage collagen distribution, gagCEST MRI cartilage for proteoglycan content, knee CT/x-ray for bone shape and trabecular architecture, knee motion, and novel biochemical markers describing turnover of specific tissue component, as well as involvement of hand, hip and spine joint damage, hand joint inflammation, hip motion and shape and bo...
T cells from PBMCs isolated from patients and healthy controls were in vitro activated with anti-CD3 and anti-CD28 for 72 hours. After T cell activation, cells were harvested and RNA extracted for microarray analysis.
10 replicate T cell samples from SLE (Lupus) patients9 replicate T cell samples from healthy control (BC) subjects4 replicate Nitric Oxide (NOC-18) stimulated T cell samples from 4 of the control subjects4 replicate CD3/CD28 stimulated T cell samples from 4 of the control subjects
Whole blood from 33 female SLE patients and 16 matched controls from EA and AA ancestral backgrounds was analyzed through Affymetrix Gene 1.0 ST gene expression arrays and the data were further studied through Ingenuity Pathways Analysis for canonical pathway comparison. An independent replication cohort of more than 100 SLE patient samples and 30 controls was used to test the hypotheses generated by the microarray data, using qPCR to quantify gene expression.
Gene expression comparisons were made between: 1. asthmatics and healthy controls, and 2. Th2 high asthma and Th2 Low asthma/Healthy controls. The gene expression alterations most associated with asthma were then used in gene set enrichment analyses and gene signature development to compare this asthma dataset to COPD gene expression datasets.