Problem-based learning (PBL), a pedagogical approach, is widely accepted in medical education. Manipulated by many factors, the internal motivation of learner is the most crucial determinant that affects the nature of the outcome, in which the influences of critical thinking (CT) remained elusive. One hundred two third-year undergraduate medical students at Peking University were involved in this study. A Chinese version of the Critical Thinking Disposition Inventory (CTDI-CV) was used to assess the CT disposition, and the performance scores of students in PBL tutorials were compiled. A parametric bivariate correlation analysis was performed between the students’ CT scores and their PBL average scores. The PBL scores were compared between the strong and weak CT disposition groups using independent t-test. The analysis of numerical data was conducted using SPSS 16.0. CT disposition of third-year undergraduate medical students at Peking University was at a positive level, with an average score of 297.72. The total CT scores had a positive correlation with the scores of the PBL performance and its five dimensions significantly. In the majority, students with Strong-CT disposition obtained higher scores in PBL tutorials compared with students with Weak-CT disposition. The performance of these two groups was significantly different in the Late-Half but not in the Early-Half PBL tutorials. Furthermore, a significant improvement was observed in the students with strong CT but not weak CT dispositions. CT disposition positively correlates to a students’ PBL performance. Students with stronger CT dispositions perform better in the PBL process and obtain higher scores. Our work suggested that the open-mindedness of the CT disposition is the primary factor that determines the improvement of the preparation dimensions in the PBL process.

As a novel type of non-coding RNAs, covalently closed circular RNAs (circRNAs) are ubiquitously expressed in eukaryotes. Emerging studies have indicated that dysregulation of circRNAs was related to neurological diseases. However, the biogenesis, regulation, function, and mechanism of circRNAs in Parkinson's disease (PD) remain largely unclear. In this study, thirty-three differentially expressed circRNAs (DECs) were detected by RNA-sequencing between the MPTP-induced PD mice model and the wild-type mice. Quantitative real-time PCR was used to determine the RNA level of DECs in the striatum (STR), substantia nigra pars compacta (SNpc), and serum exosomes, and it was found that circSV2b was downregulated in PD mice. Then, functional experiments in vivo were employed to explore the effect of circSV2b in PD. For the mechanism study, dual-luciferase reporter, fluorescence in situ hybridization (FISH), RNA immunoprecipitation (RIP), RNA pull-down, gene editing, and CUT & Tag were performed in vitro to confirm that circSV2b directly sponged miR-5107-5p and alleviated the suppression of the expression of the target gene Foxk1, and then positively regulated Akt1 transcription. In vivo, the mechanistic analysis demonstrated that circSV2b overexpression resisted oxidative stress damage through the ceRNA-Akt1 axis in PD models. Taken together, these findings suggested that the miR-5107-5p-Foxk1-Akt1 axis might serve as a key target of circSV2b overexpression in PD treatment, and highlighted the significant change of circSV2b in serum exosomes. Therefore, circSV2b might be a novel biomarker for the diagnosis and treatment of PD.

Inducible nitric oxide synthase (iNOS) is a key enzyme in regulating nitric oxide (NO) synthesis under stress, and NO has varying ability to regulate apoptosis. The aim of this study was to investigate the effects and possible mechanism of action of iNOS on neuronal apoptosis in a rat model of cerebral focal ischemia and reperfusion injury in rats treated with S‐methylisothiourea sulfate (SMT), a high‐selective inhibitor of iNOS. Seventy‐two male Sprague‐Dawley (SD) rats were randomly divided into three groups: the sham, middle cerebral artery occlusion (MCAO) + vehicle, and MCAO + SMT groups. Neurobehavioral deficits, infarct zone size, and cortical neuron morphology were evaluated through the modified Garcia scores, 2,3,5‐triphenyltetrazolium chloride (TTC), and Nissl staining, respectively. Brain tissues and serum samples were collected at 72 hr post‐reperfusion for immunohistochemical analysis, Western blotting, Terminal deoxynucleotidyl transferase‐mediated dUTP‐biotin Nick End Labeling assay (TUNEL) staining, and enzyme assays. The study found that inhibition of iNOS significantly attenuated the severity of the pathological changes observed as a result of ischemia‐reperfusion injury: SMT reduced NO content as well as total nitric oxide synthase (tNOS) and iNOS activities in both ischemic cerebral hemisphere and serum, improved neurobehavioral scores, reduced mortality, reduced the infarct volume ratio, attenuated morphological changes in cortical neurons, decreased the rate of apoptosis (TUNEL and caspase‐3‐positive), and increased phospho (p)‐AKT expression in ischemic penumbra. These results suggested that inhibition of iNOS might reduce the severity of ischemia‐reperfusion injury by inhibiting neuronal apoptosis via maintaining p‐AKT activity. Anat Rec, 299:246–255, 2016.

Dihydromyricetin ameliorates chronic liver injury by reducing pyroptosis

High altitude (HA) has become one of the most challenging environments featuring hypobaric hypoxia, which seriously threatens public health, hence its gradual attraction of public attention over the past decade. The purpose of this study is to investigate the effect of HA hypoxia on iron levels, redox state, inflammation, and ferroptosis in adipose tissue. Here, 40 mice were randomly divided into two groups: the sea-level group and HA hypoxia group (altitude of 5000 m, treatment for 4 weeks). Total iron contents, ferrous iron contents, ROS generation, lipid peroxidation, the oxidative enzyme system, proinflammatory factor secretion, and ferroptosis-related biomarkers were examined, respectively. According to the results, HA exposure increases total iron and ferrous iron levels in both WAT and BAT. Meanwhile, ROS release, MDA, 4-HNE elevation, GSH depletion, as well as the decrease in SOD, CAT, and GSH-Px activities further evidenced a phenotype of redox imbalance in adipose tissue during HA exposure. Additionally, the secretion of inflammatory factors was also significantly enhanced in HA mice. Moreover, the remarkably changed expression of ferroptosis-related markers suggested that HA exposure increased ferroptosis sensitivity in adipose tissue. Overall, this study reveals that HA exposure is capable of inducing adipose tissue redox imbalance, inflammatory response, and ferroptosis, driven in part by changes in iron overload, which is expected to provide novel preventive targets for HA-related illness.