Patients exposed to a surgical safety checklist experience better postoperative outcomes, but this could simply reflect wider quality of care in hospitals where checklist use is routine.
C-Jun N-terminal kinase (JNK) is a pivotal MAPK (mitogen-activated protein kinase), which activated by ischemia brain injury and plays a fairly crucial function in cerebral ischemic injury. Emerging studies demonstrated that JNK-IN-8 (a JNK inhibitor with high specificity) regulates traumatic brain injury through controlling neuronal apoptosis and inflammation. However, the function of JNK-IN-8 in ischemic stroke and the mechanisms underlying of JNK-IN-8 about neuroprotection are not well understood. In this work, male rats were treated with JNK-IN-8 after transient middle cerebral artery occlusion, and then the modified improved neurological function score (mNSS), the foot-fault test (FFT), interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) levels were assessed. We found that JNK-IN-8-treated rats with MCAO exerted an observable melioration in space learning as tested by the improved mNSS, and showed sensorimotor functional recovery as measured by the FFT. JNK-IN-8 also played anti-inflammatory roles as indicated through decreased activation of microglia and decreased IL-6, IL-1β, and TNF-α expression. Furthermore, JNK-IN-8 suppressed the activation of JNK and nuclear factor-κB (NF-κB) signaling as indicated by the decreased level of phosphorylated-JNK and p65. All data demonstrate that JNK-IN-8 inhibits neuroinflammation and improved neurological function by inhibiting JNK/NF-κB and is a promising agent for the prevention of ischemic brain injury. K E Y W O R D S ischemia brain injury, JNK, JNK-IN-8
Ferroptosis is a new form of programmed cell death due to iron-dependent excess accumulation of lipid peroxides and differs from other programmed cell deaths in morphological and biochemical characteristics. The process of ferroptosis is precisely regulated by iron metabolism, lipid metabolism, amino acid metabolism, and numerous signaling pathways, and plays a complex role in many pathophysiological processes. Recent studies have found that ferroptosis is closely associated with the development and progression of many lung diseases, including acute lung injury, pulmonary ischemia-reperfusion injury, lung cancer, chronic obstructive pulmonary disease, and pulmonary fibrosis. Here, we present a review of the main regulatory mechanisms of ferroptosis and its research progress in the pathogenesis and treatment of lung diseases, with the aim of providing new ideas for basic and clinical research of lung-related diseases.
Glioblastoma (GBM) ranks the most common and aggressive primary brain malignant tumor worldwide. However, the survival rates of patients remain very poor. Therefore, molecular oncology of GBM are urgently needed. In this study, we performed an integrative analysis of DNA methylation and gene expression to identify key epigenetic genes in GBM. The methylation and gene expression of GBM patients in The Cancer Genome Atlas (TCGA) database were downloaded. After data preprocessing, we identified 4,881 differentially expressed genes (DEGs) between tumor and normal samples, including 1,111 upregulated and 3,770 downregulated genes. Then, we randomly separated all samples into training set (n = 69) and testing set (n = 69). We next obtained 11,269 survival-methylation sites by univariate and multivariate Cox regression analyses. In the correlation analysis, we defined 198 low promoter methylation with high gene expression as epigenetically induced (EI) genes and 111 high promoter methylation with low gene expression as epigenetically suppressed (ES) genes. Key markers including C1orf61 and FAM50B were selected with a Pearson correlation coefficient greater than 0.75. Further, we chose the 20 CpG methylation sites of above two genes in unsupervised clustering analysis using the Euclidean distance. We found that the prognosis of the hypomethylated group was significantly better than that in the hypermethylated group (log-rank test
p
-value = 0.011). Based on the validation in the TCGA testing set and GEO dataset, we validated the prognostic value of our signature (
p
-value = 0.02 in TCGA and 0.012 in GEO). In conclusion, our findings provided predictive and prognostic value as methylation-based biomarkers for the diagnosis and treatment of GBM.
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