This SuperSeries is composed of the SubSeries listed below.
In vitro analysis of tobramycin-treated Pseudomonas aeruginosa biofilms on cystic fibrosis-derived airway epithelial cells.
No sample metadata fields
View SamplesMicroarray analysis of the changes in transcript abundance in cell culture and shoot
Heterogeneity of the mitochondrial proteome for photosynthetic and non-photosynthetic Arabidopsis metabolism.
Specimen part
View SamplesWe grew Pseudomonas aeruginosa biofilms on CFBE41o- human airway cells in culture, and we treated these biofilms with tobramycin. Microarray analysis was performed to gain an understanding of the global transcriptional changes that occur during antibiotic treatment.
In vitro analysis of tobramycin-treated Pseudomonas aeruginosa biofilms on cystic fibrosis-derived airway epithelial cells.
No sample metadata fields
View SamplesDiploid and tetraploid budding yeast cell cultures were grown in YPD, at 30C, to O.D. approx. 0.5.
Genome-wide genetic analysis of polyploidy in yeast.
Sex
View SamplesIn the clinical setting, mutations in the CFTR gene enhance the inflammatory response to P. aeruginosa (PA01) infection, but measurements of the inflammatory response to pathogen stimulation by isolated airway epithelia can yield variable results. In this series, we exposed CFBE41o- cells over-expressing F508/F508 CFTR and CFBE41o- cells rescued with wt-CFTR to P. aeruginosa biofilms. P. aeruginosa elicited a more robust increase in cytokine and chemokine expression (e.g., IL-8, CXCL2, CXCL3, CXCR4 and TNF-) in CFBE-wt-CFTR cells compared to CFBE-F508-CFTR cells. These results demonstrate that CFBE41o- cells complemented with wt-CFTR mount a more robust inflammatory response to P. aeruginosa than CFBE41o- F508/F508-CFTR cells.
Does the F508-CFTR mutation induce a proinflammatory response in human airway epithelial cells?
Specimen part
View SamplesNZB/WF1 female mice spontaneously develop autoimmune lupus nephritis. Expression profiling of kidney tissue from (a) 12 week NZB/W F1 female mice defined as asymptomatic for lupus nephritis, (b) 36 and 42 week NZB/W F1 female mice defined as diseased/symptomatic for lupus nephritis and (c) 36 and 42 week NZB/W F1 female mice that are diseased/symptomatic for lupus nephritis and treated with Sirolimus was carried out. The goal of the study was to identify genes associated with lupus nephritis and modulated by Sirolimus, an inhibitor of mTOR. In addition, lupus nephritis genes resistant to Sirolimus therapy were also identfied
Mapping similarities in mTOR pathway perturbations in mouse lupus nephritis models and human lupus nephritis.
Sex, Specimen part, Disease, Treatment, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
MicroRNA and transcriptome analysis in periocular Sebaceous Gland Carcinoma.
Specimen part
View SamplesSamples were taken from patients undergoing cancer excision for pagetoid (wide) sebaceous gland carcinoma (SGC) and different individuals undergoing excision for nodular (local) SGC.
MicroRNA and transcriptome analysis in periocular Sebaceous Gland Carcinoma.
Specimen part
View SamplesSynovial fibroblasts in persistent inflammatory arthritis have been suggested to have parallels with cancer growth and wound healing, both of which involve a stereotypical serum response program. We tested the hypothesis that a serum response program can be used to classify diseased tissues, and investigated the serum response program in fibroblasts from multiple anatomical sites and two diseases. To test our hypothesis we utilized a bioinformatics approach to explore a publicly available microarray dataset including RA, OA and normal synovial tissue, then extended those findings in a new microarray dataset representing matched synovial, bone marrow and skin fibroblasts cultured from RA and OA patients undergoing arthroplasty. The classical fibroblast serum response program discretely classified RA, OA and normal synovial tissues. Analysis of low and high serum treated fibroblast microarray data revealed a hierarchy of control, with anatomical site the most powerful classifier followed by response to serum and then disease. In contrast to skin and bone marrow fibroblasts, exposure of synovial fibroblasts to serum led to convergence of RA and OA expression profiles. Pathway analysis revealed three inter-linked gene networks characterising OA synovial fibroblasts: Cell remodelling through insulin-like growth factors, differentiation and angiogenesis through 3 integrin, and regulation of apoptosis through CD44. We have demonstrated that Fibroblast serum response signatures define disease at the tissue level, and that an OA specific, serum dependent repression of genes involved in cell adhesion, extracellular matrix remodelling and apoptosis is a critical discriminator between cultured OA and RA synovial fibroblasts.
Stromal transcriptional profiles reveal hierarchies of anatomical site, serum response and disease and identify disease specific pathways.
Specimen part, Disease
View SamplesThis SuperSeries is composed of the SubSeries listed below.
MicroRNA profiling of the pubertal mouse mammary gland identifies miR-184 as a candidate breast tumour suppressor gene.
Sex, Age, Specimen part, Cell line
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