This SuperSeries is composed of the SubSeries listed below.
Proteomic analysis of Medulloblastoma reveals functional biology with translational potential.
Sex, Specimen part
View SamplesThese gene expression microarrays were performed as part of a project aiming to integrate quantitative proteomic, gene expression and epigenetic data from the childhood brain tumor medulloblastoma.
Proteomic analysis of Medulloblastoma reveals functional biology with translational potential.
Sex, Specimen part
View SamplesCurrent prophylactic and therapeutic strategies targeting human influenza viruses include vaccines and antivirals. Given variable rates of vaccine efficacy and antiviral resistance, alternative strategies are urgently required to improve disease outcomes. Here we describe the use of HiSeq deep sequencing to analyze host gene expression in primary human alveolar epithelial type II (ATII) cells infected with highly pathogenic avian influenza H5N1 virus. We employed primary human ATII cells isolated from normal human lung tissue donated by patients that underwent lung resection. Human host gene expression following HPAI H5N1 virus (A/Chicken/Vietnam/0008/04) infection of primary ATII cells was analyzed using Illumina HiSeq deep sequencing. Overall design: Human non-tumor lung tissue samples were donated by three anonymous patients undergoing lung resection at Geelong Hospital, Barwon Health, Australia. The research protocols and human ethics were approved by the Human Ethics Committees of Deakin University, Barwon Health and the Commonwealth Scientific and Industrial Research Organisation (CSIRO). An informed consent was obtained from all tissue donors. All research were performed in accordance with the guidelines stated in the National Statement on Ethical Conduct in Human Research (2007). The sampling of normal lung tissue was confirmed by the Victorian Cancer Biobank, Australia.
Deep sequencing of primary human lung epithelial cells challenged with H5N1 influenza virus reveals a proviral role for CEACAM1.
Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Comparing Platforms for Messenger RNA Expression Profiling of Archival Formalin-Fixed, Paraffin-Embedded Tissues.
Specimen part, Disease
View SamplesTo study feasibility of gene expression profiling from FFPE tissues using NuGen amplified mRNA hybridized on Affymetrix GeneChip Human Gene 1.0 ST arrays, we designed a pilot study utilizing samples from prostate cancer cohort. We selected samples from large-scale epidemiologic studies and clinical trials representative of a wide variety of fixation times, block ages and block storage conditions.
Comparing Platforms for Messenger RNA Expression Profiling of Archival Formalin-Fixed, Paraffin-Embedded Tissues.
Specimen part
View SamplesTo study feasibility of gene expression profiling from FFPE tissues using NuGen amplified mRNA hybridized on Affymetrix GeneChip Human Gene 1.0 ST arrays, we designed a pilot study utilizing samples from prostate cancer cohort. We selected samples from large-scale epidemiologic studies and clinical trials representative of a wide variety of fixation times, block ages and block storage conditions.
Comparing Platforms for Messenger RNA Expression Profiling of Archival Formalin-Fixed, Paraffin-Embedded Tissues.
Disease
View SamplesBackground---For decades, plasma lipid levels have been known risk factors of atherosclerosis. Recently, inflammation has gained acceptance as a crucial event in the pathogenesis and development of atherosclerosis. A number of studies have provided some insights into the relationships between the two aspects of atherosclerosis: plasma lipids --- the risk factors, and circulating leukocytes --- the effectors of inflammation. In this study, we investigate the relationships between plasma lipids and leukocytes.
Identifying leukocyte gene expression patterns associated with plasma lipid levels in human subjects.
No sample metadata fields
View Samples- Gene expression changes linked to two step immortalization of human mammary epithelial cells (HMEC).
A lincRNA connected to cell mortality and epigenetically-silenced in most common human cancers.
Specimen part
View SamplesThe study aimed to identify role of OxyR during growth on different electron acceptors when E. coli are growing anaerobically.
Endogenous protein S-Nitrosylation in E. coli: regulation by OxyR.
No sample metadata fields
View SamplesAcetaminophen (APAP), a widely used analgesic and antipyretic that is considered to be relatively safe at recommended doses, is the leading cause of drug-induced liver failure in the United States. 3-Hydroxyacetanilide (AMAP), a regioisomer of acetaminophen is useful as a comparative tool for studying APAP-induced toxicity since it is non-toxic relative to APAP. TGF-alpha transgenic mouse hepatocytes were treated with both isomers to investigate mitogen-activated protein kinase cascades in order to differentiate their toxicological outcomes. Mitogen-activated protein kinase (MAPK) cascade expression and activation were measured using microarray and Bioplex technologies, respectively. APAP treatment led to c-Jun N-terminal kinase (JNK) activation, whereas AMAP treatment led to the activation of extracellular-signal-regulated protein kinase (ERK). The microarray data suggested APAP treatment may upregulate gene expression at multiple levels of the JNK cascade including a JNK-related scaffold protein. Expression data was related to phosphoprotein levels using the Bioplex system. APAP treatment led to a significant activation of JNK compared to its regioisomer. In contrast, microarray analysis of AMAP showed a slight upregulation of ERK gene activity. Furthermore, Bioplex data showed AMAP treatment led to significant ERK phosphorylation compared to APAP. Cell viability assays confirmed that APAP-induced activation of JNK was related to higher rates of cell death, whereas activation of ERK by AMAP may be cytoprotective.
Differential regulation of mitogen-activated protein kinase pathways by acetaminophen and its nonhepatotoxic regioisomer 3'-hydroxyacetanilide in TAMH cells.
Cell line
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