Although surgical resection is the primary means of curing both primary and metastatic lung cancers, about 80% of lung cancers cannot be removed by surgery. As most patients with unresectable lung cancer receive only limited benefits from traditional radiotherapy and chemotherapy, many new local treatment methods have emerged, including local ablation therapy. The Minimally Invasive and Comprehensive Treatment of Lung Cancer Branch, Professional Committee of Minimally Invasive Treatment of Cancer of the Chinese Anti-Cancer Association has organized multidisciplinary experts to develop guidelines for this treatment modality. These guidelines aim at standardizing thermal ablation procedures and criteria for selecting treatment candidates and assessing outcomes; and for preventing and managing post-ablation complications.
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Background:Sevoflurane as a widely used inhalational general anesthetic that also has a cardioprotective role in hypoxiareoxygenation (H/R) injury. This study aimed to investigate the effects of microRNA-107 (miR-107) on sevoflurane postconditioning (SpostC) in H9C2 embryonic rat cardiomyocytes and to use bioinformatics analysis to identify the molecular basis of cardioprotection from sevoflurane in human cardiac tissue.
Material/Methods:The STRADA gene was identified from the Gene Expression Omnibus (GEO) database. H9C2 embryonic rat cardiomyocytes were cultured with sevoflurane. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were used to measure the mRNA expression and protein expression of STRADA and miR-107 in H9C2 cells. TargetScanHuman version 7.2 was used to identify the target gene of miR-107 and to predict the STRADA 3'-UTR binding site of miR-107. The dual-luciferase reporter assay measured the relative luciferase activity. The cell proliferation rate and cell apoptosis were measured using the MTT assay and flow cytometry, respectively.
Results:H/R injury in H9C2 cells following SpostC resulted in increased expression of miR-107 and reduced expression of STRADA. Specific binding of miR-107 was identified to STRADA 3'-UTR. Upregulation of the miR-107 in SpostC H/R injured H9C2 cells promoted cell proliferation, reduced cell apoptosis, and downregulating the protein expression of caspase-3. STRADA overexpression reduced the effects of a miR-107 mimic on SpostC.
Conclusions:SpostC reduced H/R injury in H9C2 embryonic rat cardiomyocytes by targeting the STRADA gene and by upregulating the expression of microRNA-107.
Chronic morphine administration has been shown to change the expression of extracellular signal-regulated kinase (ERK), which is a molecule known to play an important role in homeostatic adaptations caused by addictive drugs. In the present study, we investigated the expression of ERK messenger ribonucleic acid (mRNA) of the prefrontal cortex (PFC), nucleus accumbens (NAc), hippocampus, and caudate putamen (CPu) in morphine-induced conditioned place preference (CPP) by real-time reverse transcriptase polymerase chain reaction (real-time PCR). CPP was established by alternate morphine (10 mg/kg) injections, extinguished after a 10-day extinction training, and reinstated by a priming injection of morphine (10 mg/kg). During three phases of morphine-induced CPP, the expression levels of ERK1 and ERK2 mRNA were altered in various brain regions. In the PFC, the expression levels of ERK1 and ERK2 mRNA were increased after chronic morphine injection (p=0.003, p=0.000), and did not return to the basal level after extinction training (p=0.025, p=0.000), but decreased after a priming injection (p=0.000, p=0.000). In the CPu, ERK1 mRNA had an abrupt increase following a priming injection (p=0.000). Different from other brain regions, the expression levels of ERK1 and ERK2 mRNA were decreased in three phases of morphine-induced CPP in the hippocampus (ERK1: p=0.000, p=0.040, p=0.000; ERK2: p=0.000, p=0.000, p=0.000, respectively). These results suggest region-specific changes of ERK1 and ERK2 mRNA expression during morphine-induced CPP.
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