Lung donation after cardiac death (DCD), in contrast to donation after brain death (DBD), is a promising and increasingly common method to help relieve the shortage of donor organs. However, the pathogenetic consequences of retrieved lungs after DCD vs. DBD have not been clarified.
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Specimen part, Time
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Protein disulfide isomerase inhibition synergistically enhances the efficacy of sorafenib for hepatocellular carcinoma.
Specimen part, Cell line
View SamplesPhotoaging results from the damaging effects of long-term exposure to UV. It is characterized by deep wrinkle, but the mechanism is still lack. To better understand molecular events contributing to photoaging,
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Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Transition into inflammatory cancer-associated adipocytes in breast cancer microenvironment requires microRNA regulatory mechanism.
Specimen part, Cell line
View SamplesHuman UCB-MSCs showed donor-specific variation of therapeutic efficacy in improving LV systolic function, reducing infarct area, and preserving wall thickness after MI, even though there were no significant differences in MSC phenotypes. UCB-MSCs (M02) which showed better efficacy had better paracrine activity and unique gene expression profile than others.
N-cadherin determines individual variations in the therapeutic efficacy of human umbilical cord blood-derived mesenchymal stem cells in a rat model of myocardial infarction.
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View SamplesBackground: Identification of a lineage-specific marker plays a pivotal role in understanding developmental process and is necessary to isolate a certain cell type with high purity for therapeutic purposes. Here, we report a new cardiac-specific marker and demonstrate its functional significance in cardiac development.
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Specimen part, Time
View SamplesThe role of adipocytes in cancer microenvironment has gained focus during the recent years. However, the characteristics of the cancer-associated adipocytes (CAA) in human breast cancer tissues and the underlying regulatory mechanism are not clearly understood. We reviewed pathology specimens of breast cancer patients to understand the morphologic characteristics of CAA, and profiled the mRNA and miRNA expression of CAA by using indirect co-culture system in vitro.
No associated publication
Specimen part, Cell line
View SamplesThe concept of dedifferentiation of somatic cells into pluripotent stem cells has opened a new era in regenerative medicine. Viral transduction of defined factors has successfully achieved pluripotency derived from somatic cells. However, during the generation process of induced pluripotent stem (iPS) cells, genetic integration of certain factors may cause mutagenesis or tumorigenicity, which limits further application. Therefore, there is currently ongoing an extensive search for new methods such as transient gene delivery and oocyte-free and non-viral inducers like small molecules. Here we show that the transient delivery of embryonic stem (ES) cell-derived soluble proteins enables dedifferentiation of mouse adult somatic cells converting them into pluripotent stem cells without the introduction of certain transcription factors or genetic manipulation. During the dedifferentiation, global gene expression patterns and epigenetic status were converted from the somatic to the ES-equivalent status. Dedifferentiated somatic cells were morphologically, biologically and functionally indistinguishable from ES cells. Furthermore, the dedifferentiated cells possessed in vivo differentiation and development potential. Our results provide an alternative and safe strategy for dedifferentiation of somatic cells that can be used to facilitate pluripotent stem cell-based cell therapy.
Induction of pluripotent stem cells from adult somatic cells by protein-based reprogramming without genetic manipulation.
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View SamplesSorafenib is the only approved targeted drug for hepatocellular carcinoma (HCC), but its effect on patients survival gain is limited and varies over a wide range depending on patho-genetic conditions. Thus, enhancing the efficacy of sorafenib and finding a reliable predictive biomarker are crucuial to achieve efficient control of HCCs. In this study, we employed a systems approach by combining transcriptome analysis of the mRNA changes in HCC cell lines in response to sorafenib with network analysis to investigate the action and resistance mechanism of sorafenib. Gene ontology and gene set analysis revealed that proteotoxic stress and apoptosis modules are activated in the presence of sorafenib. Further analysis of the endoplasmic reticulum (ER) stress network model combined with in vitro experiments showed that introducing an additional stress by treating the orally active protein disulfide isomerase (PDI) inhibitor (PACMA 31) can synergistically increase the efficacy of sorafenib in vitro and in vivo, which was confirmed using a mouse xenograft model. We also found that HCC patients with high PDI expression show resistance to sorafenib and poor clinical outcomes, compared to the low PDI expression group. These results suggest that PDI is a promising therapeutic target for enhancing the efficacy of sorafenib and can also be a biomarker for predicting sorafenib responsiveness.
Protein disulfide isomerase inhibition synergistically enhances the efficacy of sorafenib for hepatocellular carcinoma.
Specimen part, Cell line
View SamplesSorafenib is the only approved targeted drug for hepatocellular carcinoma (HCC), but its effect on patients survival gain is limited and varies over a wide range depending on patho-genetic conditions. Thus, enhancing the efficacy of sorafenib and finding a reliable predictive biomarker are crucuial to achieve efficient control of HCCs. In this study, we employed a systems approach by combining transcriptome analysis of the mRNA changes in HCC cell lines in response to sorafenib with network analysis to investigate the action and resistance mechanism of sorafenib. Gene ontology and gene set analysis revealed that proteotoxic stress and apoptosis modules are activated in the presence of sorafenib. Further analysis of the endoplasmic reticulum (ER) stress network model combined with in vitro experiments showed that introducing an additional stress by treating the orally active protein disulfide isomerase (PDI) inhibitor (PACMA 31) can synergistically increase the efficacy of sorafenib in vitro and in vivo, which was confirmed using a mouse xenograft model. We also found that HCC patients with high PDI expression show resistance to sorafenib and poor clinical outcomes, compared to the low PDI expression group. These results suggest that PDI is a promising therapeutic target for enhancing the efficacy of sorafenib and can also be a biomarker for predicting sorafenib responsiveness.
Protein disulfide isomerase inhibition synergistically enhances the efficacy of sorafenib for hepatocellular carcinoma.
Specimen part, Cell line
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