Construction of pain prediction model for patients undergoing hepatic arterial chemoembolization.

OBJECTIVE: To construct a predictive model for pain in patients undergoing hepatic arterial chemoembolization (TACE) in interventional operating room. METHODS: Through literature review and expert interviews, a questionnaire was prepared for the assessment of pain factors in patients with hepatic arterial chemoembolization. A prospective cohort study was used to select 228 patients with hepatic arterial chemoembolization in a tertiary and first-class hospital. The data of the patients in the pain group and the non-pain group were compared, and a rapid screening prediction model was constructed by univariate analysis and logistic regression analysis, and its prediction effect was tested. RESULTS: Tumor size, liver cancer stage, and chemoembolization with drug-loaded microspheres and pirarubicin hydrochloride (THP) mixed with lipiodol were independent predictors of pain in patients after hepatic arterial chemoembolization. Finally, the pain prediction model after TACE was obtained. The results of Hosmer-Lemeshow test showed that the model fit was good (χ2 = 13.540, p = 0.095). The area under the receiver operating characteristic curve was 0.798, p < 0.001. CONCLUSION: The rapid screening and prediction model of pain in patients undergoing hepatic arterial chemoembolization has certain efficacy, which is helpful for clinical screening of patients with high risk of pain, and can provide reference for predictive pain management decision-making.

LncRNA MALAT1 Promotes OGD-Induced Apoptosis of Brain Microvascular Endothelial Cells by Sponging miR-126 to Repress PI3K/Akt Signaling Pathway.

Ischemic stroke (IS) is a common disease that seriously endangers human health. Patients with IS present with increased death of brain microvascular endothelial cells (BMECs). MALAT1 is found to be upregulated in IS patients. However, the function of MALAT1 in IS pathogenesis still remains unclear. This study aimed to investigate the role of MALAT1 in IS in vitro model and the related molecular mechanisms. The expressions of MALAT1 and miR-126 were detected by qPCR. The in vitro IS model was established by treating BMECs with oxygen-glucose deprivation (OGD). Cell viability and cell apoptosis were assessed by MTT assay and flow cytometry, respectively. Luciferase assay was conducted to examine the interplay between MALAT1 and miR-126. Western blotting was used to determine the protein levels of apoptosis-associated proteins (e.g. caspase 3, Bax and Bcl-2) and PI3K/Akt pathway-related proteins (e.g. PI3K, Akt, p-PI3K, p-Akt). OGD induced upregulation of MALAT1 and downregulation of miR-126 in HBMECs. MALAT1 knockdown promoted the proliferation of HBMECs and reduced the proportion of apoptotic HBMECs by regulating the expression of apoptosis-related proteins. MALAT1 targeted and negatively regulated miR-126 expression. Overexpression of miR-126 activated the PI3K/Akt pathway, which in turn affected the proliferation and apoptosis of HBMECs. MALAT1 negatively regulated PI3K/Akt pathway. MALAT1 inhibited the proliferation and induced the apoptosis of OGD-induced HBMECs through suppressing PI3K/AKT pathway by sponging miR-126, providing a potential therapeutic target for IS.

Overexpressed HspB6 Underlines a Novel Inhibitory Role in Kainic Acid-Induced Epileptic Seizure in Rats by Activating the cAMP-PKA Pathway.

Epilepsy is a commonly occurring neurological disease that has a large impact on the patient's daily life. Phosphorylation of heat shock protein B6 (HspB6) has been reported to protect the central nervous system. In this investigation, we explored whether HspB6 played a positive effect on epilepsy with the involvement of the cyclic adenosine monophosphate-protein kinase A (cAMP-PKA) pathway. The epileptic seizure was induced in rats by intraperitoneal injection of kainic acid (KA). The extent of HspB6 phosphorylation and expressions of HspB6, PKA, and inflammatory factors TNF-α, IL-1ß, and IL-6 were quantified along with neuronal apoptosis. To further understand the regulatory mechanism of the HspB6 in the hippocampus, we altered the expression and the extent of HspB6 phosphorylation to see whether the cAMP-PKA pathway was inactivated or not in hippocampal neurons of rats post KA. Results showed that HspB6 was poorly expressed, resulting in the inactivation of the cAMP-PKA pathway in rats post KA, as well as an aggravated inflammatory response and hippocampal neuronal apoptosis. HspB6 overexpression and the cAMP-PKA pathway activation decreased the expression of inflammatory factors and inhibited hippocampal neuronal apoptosis. Additionally, HspB6 phosphorylation further augments the inhibitory effects of HspB6 on the inflammatory response and hippocampal neuronal apoptosis. The cAMP-PKA pathway activation was found to result in increased HspB6 phosphorylation. HspB6 decreased apoptosis signal-regulating kinase 1 (ASK1) expression to inhibit inflammatory response and hippocampal neuronal apoptosis. Collectively, our findings demonstrate that activation of the cAMP-PKA pathway induces overexpression and partial phosphorylation of HspB6 lead to the inhibition of ASK1 expression. This in turn protects rats against epilepsy and provides a potential approach to prevent the onset of epileptic seizure in a clinical setting.

Prognostic factors in older patients with advanced non-small cell lung cancer in China.

AIMS AND BACKGROUND: The human life expectancy and the incidence of lung cancer have increased dramatically in recent years. As a result, there is a high demand for the management of older patients with advanced non-small cell lung cancer (NSCLC) in clinical practice. The purpose of this study is to evaluate the prognostic factors in ≥65-year-old patients with advanced NSCLC in China. METHOD: This study involved a retrospective review of 78 ≥65-year-old patients with a diagnosis of NSCLC and at an advanced stage of disease, defined as stage IIIB or IV. All patients were followed up for a 3-year interval to determine the survival rates. Clinical data including gender, smoking history, comorbidities, performance status (PS), histological differentiation, disease stage, treatment and overall survival were recorded. The log-rank test was used to calculate survival rates. Multivariate Cox regression analysis was performed to determine independent prognostic factors. RESULTS: The 1-year, 2-year and 3-year survival rates of the 78 patients were 44.9%, 23.1% and 9.0%, respectively. In univariate analysis by the log-rank test, the 3-year survival rate was significantly associated with PS (P <0.01), disease stage (P <0.01) and chemotherapy treatment (P <0.01). The results of multivariate Cox regression analysis confirmed that PS and disease stage were independent prognostic factors. CONCLUSION: The 3-year survival rate in ≥65-year-old patients with advanced NSCLC was significantly associated with PS, disease stage and chemotherapy. PS and disease stage were independent prognostic factors. Older patients with advanced NSCLC in China might benefit from chemotherapy.