Integrative analysis of circRNA networks in postoperative cognitive dysfunction.

OBJECTIVE: In the quest to decipher the molecular intricacies of Postoperative Cognitive Dysfunction (POCD), this study focused on circular RNA (circRNA) and their regulatory networks. MATERIALS AND METHODS: Analyzing the Gene Expression Omnibus Series (GSE) 147277 dataset, we pinpointed 10 differentially expressed circRNAs linked to POCD. RESULTS: The ensuing competing endogenous RNA (ceRNA) network, featuring pivotal players like Homo sapiens(hsa)_circ_0003424 and hsa-miR-193b-5p, provided a comprehensive understanding of the molecular players at play in POCD. CONCLUSION: Additionally, the Protein-Protein Interaction (PPI) network spotlighted 10 core Hub genes, including phosphatase and tensin homolog (PTEN) and signal transducer and activator of transcription 3(STAT3), shedding light on potential therapeutic targets.

Dexmedetomidine improves postoperative neurocognitive disorder after cardiopulmonary bypass in rats.

PURPOSE: To investigate whether dexmedetomidine can improve postoperative neurocognitive function after cardiopulmonary bypass in rats. METHODS: A total of 45 male Sprague Dawley (SD) rats were randomly divided into sham group, control group, and dexmedetomidine (Dex) group. The rats in the sham group received skin excision and blood vessel ligation treatment, rats in the control group received cardiopulmonary bypass (CPB), and rats in the Dex group received CPB and Dex treatment. Morris water maze test and open-field tests were used to evaluate the rats' cognition. The expression of inflammatory mediators in the rats' central and peripheral regions, Aß and Tau in the hippocampus and prefrontal cortex, and apoptosis in brain tissue were measured. RESULTS: The CPB model rats were found to have significantly decreased cognitive function, increased expression of caspase-3 and Bax in the prefrontal cortex and hippocampus DG, increased apoptosis and activated microglia, and increased plasma levels of TNF-α, IL-6, and TNF-α. Dexmedetomidine reduced apoptosis in the prefrontal cortex and hippocampus DG region of rats, decreased the expression of caspase-3 and bax, inhibited microglia activation in the prefrontal cortex and hippocampus DG region of rats, and decreased the plasma levels of IL-ß, IL-6, and TNF-α. CONCLUSIONS: Dexmedetomidine plays a neuroprotective role by inhibiting inflammation, apoptosis, and microglia activation in the prefrontal cortex and hippocampal DG region, and attenuates the cognitive deficit identified in the control group.

Tumor-Associated Fibroblasts and Microvessels Contribute to the Expression of Immunosuppressive Factor Indoleamine 2, 3-Dioxygenase in Human Esophageal Cancers.

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.

Hydromorphine postconditioning protects isolated rat heart against ischemia-reperfusion injury via activating P13K/Akt/eNOS signaling.

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.

Proteomic Profiling for Identification of Novel Biomarkers Differentially Expressed in Human Ovaries from Polycystic Ovary Syndrome Patients.

OBJECTIVES: To identify differential protein expression pattern associated with polycystic ovary syndrome (PCOS). METHODS: Twenty 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). RESULTS: DIGE 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. CONCLUSIONS: The 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.