We analyzed three clinical parameters with gene expression data from 122 liver tissues. Six healthy samples were used in validation.
Predictive model for inflammation grades of chronic hepatitis B: Large-scale analysis of clinical parameters and gene expressions.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
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Age, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
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Specimen part, Cell line, Treatment
View SamplesThe retina is often subjected to tractional forces in a variety of conditions, for instance, pathological myopia, proliferative vitreoretinopathy. As the predominant glial element in the sensory retina, Muller cells are responsible for the homeostatic and metabolic support of retinal neurons and active players in virtually all forms of retinal injury and disease. Besides, Muller cells span the entire retinal thickness, extending from the inner to the outer limiting membranes, with cell bodies located in the inner nuclear layer and lateral processes expanding into the plexiform layers of the tissue. Because of this unique morphology, Muller cells can sense even minute changes in the retinal structure because of the mechanical stretching of their long processes or side branches. Thus, its reasonable to infer that Muller cells also participate in ocular diseases when the retina is overstretched. In this study, we aim to investigate the whole genome regulation of Muller cells under mechanical stretching, which may help in excluding possible molecular mechanisms that would account for many retinal diseases in which the retina is often subjected to mechanical forces.
Gene expression changes under cyclic mechanical stretching in rat retinal glial (Müller) cells.
Specimen part, Treatment, Time
View SamplesCancers located adjacent to adipose tissues often show intrinsic and acquired resistance to antiangiogenic therapy. The resistance is developed potentially via tumor cell metabolic paradigm shift.
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Specimen part
View SamplesDNA damage response (DDR) plays pivotal roles in maintaining genome integrity and stability. An effective DDR requires the involvement of hundreds of genes that compose a complicated network. To identify novel genes involved in DDR, we screened a genome-wide Schizosaccharomyces pombe (S. pombe) haploid deletion library against six different DNA damage reagents. We identified 52 genes that were actively involved in DDR. Among the 52 genes, 20 genes were linked to DDR for the first time.
Identification of novel genes involved in DNA damage response by screening a genome-wide Schizosaccharomyces pombe deletion library.
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View SamplesMicroarray-dependent transcriptional analysis of interferon stimulated genes treated with different kind of interferon subtypes in HBV-infected PHH.
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Specimen part, Treatment
View SamplesHuman monocyte THP-1 cells obtained from ATCC were cultured in RPMI 1640 (Invitrogen, Carlsbad, CA) containing 10% FBS and supplemented with 10 mM Hepes (Gibco BRL). THP-1 was differentiated into macrophages by 24-h incubation with 160 nM phorbol 12-myristate 13-acetate (PMA; Sigma, St. Louis, MO) followed by 24-h incubation in RPMI medium. Macrophages were further polarized to M1 macrophages by incubation with 10 pg/ml of lipopolysaccharide (LPS; Sigma) and 20 ng/ml of interferon (IFN)- (R&D Systems, MN) and are referred to as M(LPS+IFN-) cells. M2 macrophages were obtained by incubation with 20 ng/ml of interleukin (IL)-4 (R&D Systems) and are referred to as M(IL4) cells. To test the represented polarization marker of PMA differentiated-THP-1 macrophages stimulated with 20 ng ml(-1) IFN + 10 pg ml(-1) LPS and 20 ng ml(-1) IL-4, which are known to influence macrophage polarization in vetro into the M1 and M2 state, respectively.
No associated publication
Specimen part
View SamplesCancers located adjacent to adipose tissues often show intrinsic and acquired resistance to antiangiogenic therapy. The resistance is developed potentially via tumor cell metabolic paradigm shift.
No associated publication
Specimen part
View SamplesMolecular mechanisms underlying the cancer stroma in metastasis is largely unknown. Here we show that cancer-associated fibroblasts (CAFs) produce high levels of IL-33 that acted on tumor-associated macrophages (TAMs) to induce the M1 to M2 transition. Genome profiling of metastasis-related genes in the IL-33-stimulated TAMs showed a > 200-fold increase of metalloproteinase 9 (MMP9). Signaling analysis demonstrated the IL-33-ST2-NFkB-MMP9-laminin pathway that mediates cancer metastasis. In mouse and human fibroblast-rich pancreatic cancers, genetic deletion of IL-33, ST2 and MMP9 markedly blocked metastasis. Pharmacological inhibition of NFkB and MMP9 also blocked cancer metastasis. Deletion of IL-33, ST2 and MMP9 restored laminin, a key basement membrane component associated to tumor microvessels. Together, our data provide novel mechanistic insights on the IL-33-NFkB-MMP9-laminin axis that mediates the CAF-TAM-committed cancer metastasis. Thus, targeting the CAF-TAM-vessel interaction provides an outstanding therapeutic opportunity for cancer treatment.
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Cell line
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