Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28417535_1.fastq.gz | Fastqsanger.gz | |||
| SRR28417535_2.fastq.gz | Fastqsanger.gz |
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Project description:Bare-metal (BMS) and drug-eluting stents (DES) were implanted in pig coronary arteries with an overstretch during coronary angioplasty under optical coherence tomography guidance. Arteries subjected to plain old balloon angioplasty (POBA) alone served as controls. Stented/balloon dilated segments were harvested 1, 3, 7, 14 and 28 days post-intervention for proteomics analysis. At day 28 all stented arteries showed a neointima formation covering the stent struts. The evolved neointima was separated from the media and analysed in a separate proteomics analysis. In total, 31 samples were analysed for the media by LC-MS/MS (n=3 BMS/DES at each time-point 1, 3, 7 and 28 days; n=4 POBA early [day1-day3] and n=3 POBA late [day 14 - day28]). For the neointima a total of 14 samples were analysed (n=7 BMS, n=7 DES at 28 days) including the neointima of arteries of a second cohort with 4 samples each for BMS and DES day 28. The neointima samples were run in duplicates.
2017-11-24 | PXD005726 | Pride
Project description:BMS oral microbiome
| PRJEB75198 | ENA
Project description:Human breast cancer cell line MCF-7 is usually sensitive to chemotherapy drug BMS-554417, an insulin receptor (IR) and insulin-like growth factor receptor (IGFR) inhibitor. However, through step-wise increase in BMS-554417 doses in culture media, we were able able to screen and select a single MCF-7 clone that is BMS-554417 resistant. It is cross resistant to BMS-536924. This new line of MCF-7 cells was named as MCF-7R4. The transcriptome profiling of both MCF-7 and MCF-7R4 was performed using Affymetrix HG-U133 plus2.0 GeneChip arrays. Five replicates of MCF-7 and five replicates of MCF-7R4 were profiled.
2009-11-05 | E-GEOD-18912 | biostudies-arrayexpress
Project description:Human breast cancer cell line MCF-7 is usually sensitive to chemotherapy drug BMS-554417, an insulin receptor (IR) and insulin-like growth factor receptor (IGFR) inhibitor. However, through step-wise increase in BMS-554417 doses in culture media, we were able able to screen and select a single MCF-7 clone that is BMS-554417 resistant. It is cross resistant to BMS-536924. This new line of MCF-7 cells was named as MCF-7R4. The transcriptome profiling of both MCF-7 and MCF-7R4 was performed using Affymetrix HG-U133 plus2.0 GeneChip arrays.
2009-11-06 | GSE18912 | GEO
Project description:Aims: Congenital heart defect (CHD) account for 25% of all human congenital abnormalities. Very few CHD-causing genes have been identified so far; so, to discover further genes we performed a global transcriptome analysis in mouse models of CHD. Methods and results: By the use of a retinoic acid competitive antagonist (BMS-189453) we caused CHD, thymic abnormalities and neural tube defects in mouse newborns. Transposition of great arteries was the prevalent cardiac defect observed (61%). Recently we were able to partially rescue this abnormal phenotype by oral administration of folic acid. Now we have performed a microarray analysis in mouse embryos (8.5 dpc) treated with BMS-189453 alone and with BMS-189453 plus folic acid (FA). On the basis of microarray and QRT-PCR results, we deeper analysed Hif1α because of its down-regulation in BMS-treated embryos vs WT and its increased expression level in BMS+FA treated embryos compared to BMS-treated ones. Immunofluorescence experiments confirmed the under-expression of Hif1α protein in BMS-treated embryos compared to WT and BMS+FA treated ones and moreover demonstrated that at 8.5 dpc Hif1α is mainly expressed in the embryo’s heart. Conclusion: We propose that Hif1α down-regulation by blocking retinoic acid binding, may contribute to the development of the cardiac defects of mouse newborns. In line with our hypothesis, when Hif1α expression level is restored (by supplementation of folic acid) a decrement of CHD is found. At the best of our knowledge this is the first report that link retinoic acid metabolism to Hif1α regulation and the development of TGA 2 samples w/ 2 dye-swaps
2010-09-20 | E-GEOD-19012 | biostudies-arrayexpress
Project description:Aims: Congenital heart defect (CHD) account for 25% of all human congenital abnormalities. Very few CHD-causing genes have been identified so far; so, to discover further genes we performed a global transcriptome analysis in mouse models of CHD. Methods and results: By the use of a retinoic acid competitive antagonist (BMS-189453) we caused CHD, thymic abnormalities and neural tube defects in mouse newborns. Transposition of great arteries was the prevalent cardiac defect observed (61%). Recently we were able to partially rescue this abnormal phenotype by oral administration of folic acid. Now we have performed a microarray analysis in mouse embryos (8.5 dpc) treated with BMS-189453 alone and with BMS-189453 plus folic acid (FA). On the basis of microarray and QRT-PCR results, we deeper analysed Hif1α because of its down-regulation in BMS-treated embryos vs WT and its increased expression level in BMS+FA treated embryos compared to BMS-treated ones. Immunofluorescence experiments confirmed the under-expression of Hif1α protein in BMS-treated embryos compared to WT and BMS+FA treated ones and moreover demonstrated that at 8.5 dpc Hif1α is mainly expressed in the embryo's heart. Conclusion: We propose that Hif1α down-regulation by blocking retinoic acid binding, may contribute to the development of the cardiac defects of mouse newborns. In line with our hypothesis, when Hif1α expression level is restored (by supplementation of folic acid) a decrement of CHD is found. At the best of our knowledge this is the first report that link retinoic acid metabolism to Hif1α regulation and the development of TGA
2010-09-20 | GSE19012 | GEO
Project description:Purpose: To identify the aberrant long non-coding RNA (lncRNA) and explore the predictive value of lncRNA on the risk of brain metastases (BMs) for patients with limited-stage small cell lung cancer (SCLC). Patients and Methods: We executed an array of lncRNA and mRNA chip assays on peripheral blood mononuclear cells of SCLC patients with BM comparing to others without BMs to identify the lncRNAs relating to BMs. Then validation was conducted in clinical data to confirm the relationship of lncRNAs and BMs furtherly. We estimated the cumulative incidence of BMs using the Kaplan-Meier method and differences between the groups were analyzed using the log-rank test. Results: The expression of 67 lncRNAs (27 up, 40 down) and 47 mRNAs (20 up, 27 down) were different significantly in BM groups comparing to the group without BMs (fold change ≥ 2.0, p value ≤0.05) which were found by lncRNA and mRNA chip assays initially. Four lncRNAs were verified by qRT-PCR to confirm the accuracy of the microarray data and then the results of 11 pairs of patients (11 patients with BMs, while 11 patients without BMs) showed that low expression of LncRNA XR_429159.1 was the high-risk factor of BM. Further clinical data showed that the BM incidence of 25 patients with low level LncRNA XR_429159.1 was 31% at 1-year, and that was 14.3% in the 18 patients with high level LncRNA XR_429159.1, p = 0.035. Conclusion: Our present study identified that low expression of lncRNA XR_429159.1 was the high-risk factor of BM in patients with limited-stage SCLC.
2021-04-16 | GSE161968 | GEO
Project description:breast cancer. Combined IGF and estrogen-targeted therapy may improve the benefit of hormonal therapy alone. We employed a postmenopausal model of estrogen-dependent breast cancer in vitro and in vivo using the aromatase-expressing MCF-7/AC-1cells. Using this model, we investigated the anti-tumor effects of the dual IGF-1R/InsR tyrosine kinase inhibitor, BMS-754807 alone and in combination with letrozole or tamoxifen in vivo. We used microarrays to compare gene expression changes of MCF7 breast xenograft treated with either BMS754807, or Tamoxifen or Letrozole alone; or Tamoxifen or Letrozole in combination with BMS754807 for 28 days Breast xenograft MCF7 bearing mice treated with either BMS754807, or Tamoxifen or Letrozole alone; or Tamoxifen or Letrozole in combination with BMS754807 for 28 days. RNA were extracted from tumors and hybridizedon Affymetrix microarrays to compare gene expression changes
2011-11-02 | E-GEOD-33366 | biostudies-arrayexpress
Project description:Three types of BMs from adult human eyes, the inner limiting membrane, the retinal vascular BMs and the lens capsule, were isolated for analysis by 1D-SDS-PAGE and LC-MS/MS.
2014-07-16 | PXD001025 | Pride
Project description:An unanticipated complication of the use of bare metal stents in percutaneous transluminal coronary angioplasty is in-stent restenosis resulting in >50% late lumen diameter loss in treated patients. In an effort to reduce in-stent restenosis, drug eluting stents containing the immunosuppressant sirolimus or zotarolimus have recently been developed. We report here the molecular response of arterial tissue to the implanting of these drug-eluting stents. Gene expression profiling was performed on 4 artery segments surrounding bare metal stents (BMS), 4 artery segments surrounding sirolimus-eluting stents (SES), and 4 artery segments surrounding zotarolimus-eluting stents (ZES) implanted into porcine animal models for 28 days.
2011-04-22 | E-GEOD-28781 | biostudies-arrayexpress