Recent studies have provided considerable evidence to support the hypothesis that tumor stroma plays a crucial role in the induction of immune tolerance to human cancers. Here, we investigated the contribution of reactive stromal tumor-associated fibroblasts (TAFs) and microvessels to the immunosuppressive factor indoleamine 2,3-dioxygenase (IDO) expression in the ESCC microenvironment. The immunohistochemical (IHC) analyses demonstrated a significant increased densities of TAFs and microvessels in the ESCC stroma, double IHCs showed that these increased TAFs and microvessels were with a high proliferation activity. Further IHC examinations revealed that increased expression of IDO were frequently observed in the stromal cells with TAF morphology and microvessels. Double immunofluorescence examinations confirmed the colocalization of IDO positive cells with SMA-alpha positive TAFs and CD34 positive endothelial cells in the ESCC stroma. Our current findings strongly suggest that the activated stromal TAFs and endothelial cells of microvessels contribute to the expression of IDO and then the orchestration of immunosuppressive microenvironment.

ObjectivesTo identify differential protein expression pattern associated with polycystic ovary syndrome (PCOS).MethodsTwenty women were recruited for the study, ten with PCOS as a test group and ten without PCOS as a control group. Differential in-gel electrophoresis (DIGE) analysis and mass spectroscopy were employed to identify proteins that were differentially expressed between the PCOS and normal ovaries. The differentially expressed proteins were further validated by western blot (WB) and immunohistochemistry (IHC).ResultsDIGE analysis revealed eighteen differentially expressed proteins in the PCOS ovaries of which thirteen were upregulated, and five downregulated. WB and IHC confirmed the differential expression of membrane-associated progesterone receptor component 1 (PGRMC1), retinol-binding protein 1 (RBP1), heat shock protein 90B1, calmodulin 1, annexin A6, and tropomyosin 2. Also, WB analysis revealed significantly (P<0.05) higher expression of PGRMC1 and RBP1 in PCOS ovaries as compared to the normal ovaries. The differential expression of the proteins was also validated by IHC.ConclusionsThe present study identified novel differentially expressed proteins in the ovarian tissues of women with PCOS that can serve as potential biomarkers for the diagnosis and development of novel therapeutics for the treatment of PCOS using molecular interventions.

Summary Introduction Myocardial ischemia/reperfusion injury (myocardial I/R injury) has a high disability rate and mortality. Novel treatments for myocardial I/R injury are necessary. Aim In order to explore the protective effect of hydromorphine on myocardial I/R injury, we illuminate the underlying mechanism of the protective effect. Results Hydromorphine significantly reduced myocardial infarct size (IFN/AAR), CKMB (Creatine Kinase MB) and TN‐T (Troponin T) release, and improved cardiac function compared with I/R group. However, these advantageous effects were partly suppressed in the presence of hydromorphine. Myocardial I/R injury significantly decreased the phosphorylation of Akt and eNOS, and down‐regulated total nitric oxide and nitrotyrosine content, while these inhibitory effects were partly abolished by hydromorphine. Conversely, the activated effects of hydromorphine on the phosphorylation of Akt and eNOS, and NO release were totally reversed by LY294002, which, used individually, show the same influence on reperfusion injury. Conclusions These findings suggest that hydromorphine postconditioning may protect isolated rat heart against reperfusion injury via activating P13K/Akt/eNOS signaling.

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