Inflammatory stimuli clearly contribute to lung cancer development and progression, but the underlying pathogenic mechanisms are not fully understood. We found that the proinflammatory cytokine IL-1b is dramatically elevated in the serum of patients with non-small cell lung cancer (NSCLC). In vitro studies showed that IL-1b promoted the proliferation and migration of NSCLC cells. Mechanistically, IL-1b acted through the COX2-HIF1a pathway to repress the expression of microRNA-101 (miR-101), a microRNA with an established role in tumor suppression. Lin28B was identified as critical effector target of miR-101 with its repression of Lin28B, a critical aspect of tumor suppression. Overall, IL-1b upregulated Lin28B by downregulating miR-101. Interestingly, cyclooxygenase-2 inhibition by aspirin or celecoxib abrogated IL-1b-mediated repression of miR-101 and IL-1b-mediated activation of Lin28B along with their stimulatory effects on NSCLC cell proliferation and migration. Together, our findings defined an IL-1b-miR-101-Lin28B pathway as a novel regulatory axis of pathogenic inflammatory signaling in NSCLC. Cancer Res; 74(17); 4720-30. Ó2014 AACR.

Ferroptosis is an important form of myocardial cell death in myocardial ischemia-reperfusion injury (MIRI). Naringenin (NAR), as a flavonoid, has a significant advantage in improving MIRI. But the regulatory effect and mechanism of NAR on ferroptosis in MIRI have not been reported. After the rats were given NAR and induced to form myocardial ischemia-reperfusion (MI/R) injury, Tetrazolium chloride (TTC) staining was used to detect the myocardial infarction area of rats, and Hematoxylin-eosin (H&E) staining was used to detect myocardial injury. The markers of tissue inflammation were detected by ELISA. Serum creatine kinase Serum creatin kinase (CPK), Lactate dehydrogenase (LDH), and lipid peroxide (LPO) and oxidative stress related levels were measured. In addition, iron detection kits were used to detect total iron and Fe 2+ levels in cardiac tissues, and western blot was used to detect the expression of ferroptosis-related proteins and the expression of nuclear factor-erythroid factor 2-related factor 2 (Nrf2) and glutathione peroxidase 4 (GPX4). At the cellular level, H9C2 cardiomyocytes were induced by hypoxia/reoxygenation (H/R), and ferroptosis inducer Erastin was administered to detect cell viability, ferroptosis-related indicators, oxidative stress related indicators, and expressions of Nrf2 and GPX4, to explore the mechanisms involved. NAR alleviated MI/R-induced pathological damage, inflammation and lipid peroxidation in myocardial tissue of rats. NAR adjusted the NRF2 /System xc – /GPX4 axis and improved ferroptosis. At the cellular level, ferroptosis inducer Erastin reversed the protective effect of NAR on H/R-induced H9C2 cardiomyocytes. In conclusion, NAR can alleviate MIRI by regulating the Nrf2/System xc-/GPX4 axis to inhibit ferroptosis.

Background: Spontaneous intraventricular hemorrhage is an infrequent but severe complication of hemorrhagic stroke. The conventional treatment of intraventricular hemorrhage consists of ventricular drainage or surgical evacuation, but neither of them is encouraged. The objective of this article is to compare different surgical procedures in order to evaluate a method of minimally invasive treatment for intraventricular hemorrhage. Methods: Neuroendoscopy was applied to treat 22 cases of intraventricular hemorrhage. Twenty cases of the same disease that were treated by external ventricular drainage were taken as a control and comparison. Results: All patients were followed up for 2 months. In the neuroendoscopy group, according to the Glasgow outcome scale, the result was excellent in 5 cases, good in 9, fair in 4, poor in 2 and death in 2. In the external ventricular drainage group, the result was excellent in 1 case, good in 5, fair in 7, poor in 5 and death in 2. More patients in the neuroendoscopy group showed good recovery after 2 months of surgery (p < 0.05). The difference in mortality rate between the 2 groups was not statistically significant (p > 0.05). Conclusions: Neuroendoscopic neurosurgery for intraventricular hemorrhage offers better surgical treatment because it is characterized by visualized manipulation, effective hemorrhage evacuation and excellent postoperative outcomes.

Deep brain stimulation (DBS) is an established treatment for patients with Parkinson’s disease (PD). Sleep disorders are common complications of PD and affected by subthalamic DBS treatment. To achieve more precise neuromodulation, chronic sleep monitoring and closed-loop DBS toward sleep-wake cycles could potentially be utilized. Local field potential (LFP) signals that are sensed by the DBS electrode could be processed as primary feedback signals. This is the first study to systematically investigate the sleep-stage classification based on LFPs in subthalamic nucleus (STN). With our newly developed recording and transmission system, STN-LFPs were collected from 12 PD patients during wakefulness and nocturnal polysomnography sleep monitoring at one month after DBS implantation. Automatic sleep-stage classification models were built with robust and interpretable machine learning methods (support vector machine and decision tree). The accuracy, sensitivity, selectivity, and specificity of the classification reached high values (above 90% at most measures) at group and individual levels. Features extracted in alpha (8–13 Hz), beta (13–35 Hz), and gamma (35–50 Hz) bands were found to contribute the most to the classification. These results will directly guide the engineering development of implantable sleep monitoring and closed-loop DBS and pave the way for a better understanding of the STN-LFP sleep patterns.