Transcription profiling of peripheral blood from patients with carotid artery stenosis
ABSTRACT: Identification of novel pathophysiological mechanisms of carotid artery disease at systemic level by studying the gene expression profile of peripheral blood of affected patients with respect to control subjects.
Project description:We performed two different pools for the 10 AAA patients (n=5 AAA patients in pool A and n=5 AAA patients in pool B) and two different pools for the 10 healthy subjects (n=5 controls in pool C and n=5 controls in pool D). Two replicates of the two microarray experiments were made. Experiment 1: AAA pool A Cy3 labeled vs control pool C Cy5 labeled AAA pool A Cy5 labeled vs control pool C Cy3 labeled (dye swap); Experiment 2: AAA pool B Cy3 labeled vs control pool D Cy5 labeled AAA pool B Cy5 labeled vs control pool D Cy3 labeled (dye swap).
Project description:The purpose of this study was to assess the impact of sex on gene expression in LV of AS patients at the time of AVR. LV samples of men (n = 9; age: 75 ± 8 y) and women (n = 10; age: 72 ± 9 y) undergoing AVR were used for RNA isolation. Genome-wide expression profiling was performed using the Affymetrix platform and the data were analyzed with R and Bioconductor. Diseased samples were compared with LV samples of men (n = 10; age: 56 ± 4 y) and women (n = 8; age: 56 ± 5 y) with no apparent cardiovascular disorder.
Project description:Patients with the diffuse avascular form of Systemic Sclerosis (SSc) and healthy controls (N) were used as sources of microvascular endothelial cells (MVEC). MVEC were obtained from biopsies of involved skin of the hands in 6 SSc patients and from 6 healthy patients undergoing surgery for traumatic events at the hands. The controls were matched by age and sex to the SSc cases. All patients fulfilled the American College of Rheumatology criteria for SSc, as well as the criteria for the diffuse form of the disease.
Project description:In this study we aimed to identify the molecular pathways modified by the false positive genotoxins Quercetin, 8-Hydroxyquinoline and 17beta-Estradiol that may explain their in vitro genotoxic and their in vivo non-genotoxic effects, by combining in vitro transcriptomics with phenotypic data. The effects of the false positive genotoxins were compared to the effects of the true genotoxins Benzo[a]pyrene and Aflatoxin B1 and the non-genotoxins 2,3,7,8-Tetrachlorodibenzodioxin, Cyclosporin A and Ampicillin C. <br><br>A custom CDF for use with the processed data file is available on the FTP site for this experiment.
Project description:Disproportionate short stature refers to a heterogeneous group of hereditary disorders, which are classified according to their mode of inheritance, their clinical skeletal and non-skeletal manifestations, and their radiological characteristics. In the present study, we report on a novel autosomal recessive osteocutaneous disorder that we termed short stature-onychodysplasia-facial dysmorphism-hypotrichosis (SOFT) syndrome. we identified a homozygous point mutation (p.L171P) in POC1A (Centriolar Protein Homolog A). The mutation affects a highly conserved amino acid residue and is predicted to interfere with protein function. To gain insight into the pathomechanisms underlying the deleterious effect of the causative mutation, we compared transcription profiles of patient and control fibroblasts.
Project description:Wild type (C57BL/6J) mice were divided in control (W), leptin-treated (E) and pair-fed (F). Obese (ob/ob) mice were divided in control (O), leptin-treated (L) and pair-fed (P). Control (W and O) and pair-fed animals (F and P) received vehicle (PBS), while E and L groups were intraperitoneally administrated with leptin for 28 days. Control (W and O) and leptin-treated (E and L) groups were provided with water and food ad libitum with, while daily food intake of pair fed (F and P) groups were matched to the amount eaten by the leptin-treated groups (E and L) the day before to discriminate the inhibitory effect of leptin on appetite.
Project description:Recent findings have challenged the prevailing histology- or imaging-based definition of the “vulnerable plaque”. To investigate molecular characteristics associated with “clinical instability” of atherosclerosis, we performed a proteomics comparison of the vascular extracellular matrix and associated molecules in human carotid endarterectomy specimens from symptomatic versus asymptomatic patients. The proteomics data were integrated with gene expression profiling and an analysis of protein secretion by lipid-loaded human vascular smooth muscle cells. The molecular signature of plaques from symptomatic patients identified by proteomics and at least one of the other two approaches comprised matrix metalloproteinase-9, chitinase-3-like protein 1, S100A8/S100A9, cathepsin B, fibronectin and galectin-3-binding protein. These biomarker candidates were measured in 685 subjects of the Bruneck Study and found to significantly predict the progression to advanced atherosclerosis (as assessed by repeated carotid ultrasound) and the incidence of cardiovascular disease over a 10-year follow-up period, highlighting the strength of tissue-based proteomics for biomarker discovery.
Project description:We have used normal, tumoral and pure stromal whole tissue samples, and cells lines in order to identify new markers of prostate cancer.<br>The normal, tumoral and stromal tissue were obtained from patients diagnosed with prostate adenocarcinoma.<br>
Project description:The integration of different omics technologies has already been shown in several in vivo studies to offer a complementary insight into cellular responses of toxic processes. We therefore hypothesize that the combining of transcriptomics and metabonomics data may improve the understanding of molecular mechanisms underlying non-genotoxic carcinogenicity in vitro. To test this hypothesis, the human hepatocarcinoma cell line HepG2 was exposed to the well known environmental pollutant TCDD. <br><br>A custom CDF file is available on the FTP site for this experiment (in file E-MEXP-2817.additional.zip) for use with the normalized data file for this experiment.