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ObjectivesTo evaluate student academic performance and perception towards blended learning and flipped classrooms in comparison to traditional teaching. MethodsThis study was conducted during the hematology block on year three students. Five lectures were delivered online only. Asynchronous discussion boards were created where students could interact with colleagues and instructors. A flipped classroom was introduced with application exercises. Summative assessment results were compared with previous year results as a historical control for statistical significance. Student feedback regarding their blended learning experience was collected. ResultsA total of 127 responses were obtained. Approximately 22.8% students felt all lectures should be delivered through didactic lecturing, while almost 35% felt that 20% of total lectures should be given online. Students expressed satisfaction with blended learning as a new and effective learning approach. The majority of students reported blended learning was helpful for exam preparation and concept clarification. However, a comparison of grades did not show a statistically significant increase in the academic performance of students taught via the blended learning method. ConclusionsLearning experiences can be enriched by adopting a blended method of instruction at various stages of undergraduate and postgraduate education. Our results suggest that blended learning, a relatively new concept in Saudi Arabia, shows promising results with higher student satisfaction. Flipped classrooms replace passive lecturing with active student-centered learning that enhances critical thinking and application, including information retention.

During ischaemia neurons depolarize and release the neurotransmitter L-glutamate, which accumulates extracellularly and binds to postsynaptic receptors. This initiates a sequence of events thought to culminate in immediate and delayed neuronal death. However, there is growing evidence that during ischaemia the development of spreading depression (SD) can be an important determinant of the degree and extent of ischaemic damage. In contrast, SD without metabolic compromise (as occurs in migraine aura) causes no discernible damage to brain tissue. SD is a profound depolarization of neurons and glia that propagates like a wave across brain tissue. Brain cell swelling, an early event of both the excitotoxic process and of SD, can be assessed by imaging associated intrinsic optical signals (IOSs). We demonstrate here that IOS imaging clearly demarcates the ignition site and migration of SD across the submerged hippocampal slice of the rat. If SD is induced by elevating [K+]O, the tissue fully recovers, but in slices that are metabolically compromised at 37.5 degrees C by oxygen/glucose deprivation (OGD) or by ouabain exposure, cellular damage develops only where SD has propagated. Specifically, the evoked CA1 field potential is permanently lost, the cell bodies of involved neurons swell and their dendritic regions increase in opacity. In contrast to OGD, bath application of L-glutamate (6-10 mM) at 37.5 degrees C evokes a non-propagating LT increase in CA1 that reverses without obvious cellular damage. Moreover, application of 2-20 mM glutamate or various glutamate agonists fail to evoke SD in the submerged hippocampal slice. We propose that SD and OGD together (but not alone) constitute a 'one-two punch', causing acute neuronal death in the slice that is not replicated by elevated glutamate. These findings support the proposal that SD generation during stroke promotes and extends acute ischaemic damage.

BackgroundTo assess the prevalence of burnout symptoms among preclinical and clinical medical students studying at AlFaisal University in Riyadh, Saudi Arabia.MethodsA cross-sectional study was conducted using Maslach Burnout Inventory questionnaire on 276 medical students from Alfaisal University, Riyadh, Saudi Arabia. The study was approved by Alfaisal University research ethics committee. Chi-square test was used to identify statistically significant differences, and binary logistic regression was used to identify predictors of burnout.Results276 entered into final data analysis with a mean age 20.62 ± 1.58, of whom 54% were males, and 46% were females. The overall burnout prevalence was 13.4%, of which PA was the most prevalent domain of burnout with 64.9%. Female gender was a significant predictor of EE and DP [OR = 4.34; 95% Cl 1.86–10.13; P-value 0.001] and [OR = 2.01; 95% Cl 1.07–3.79; P-value 0.030] respectively as per multivariate analysis for demographic characteristics. Regarding the total level of burnout, females (75.7%) had significantly higher levels of burnout compared to males (41.4%); (P-value < 0.001).ConclusionBurnout is prevalent among medical student. Gender was found to exhibits effect on the burnout. Mutual proactive strategies and reactive coping mechanisms between the students and the universities are encouraged to prevent and reduce burnout among medical students.

This study argues that, in contrast to accepted excitotoxicity theory, O2/glucose deprivation damages neurons acutely by eliciting ischemic spreading depression (SD), a process not blocked by glutamate antagonists. In live rat hippocampal slices, the initiation, propagation, and resolution of SD can be imaged by monitoring wide-band changes in light transmittance (i.e., intrinsic optical signals). Oxygen/glucose deprivation for 10 minutes at 37.5 degrees C evokes a propagating wave of elevated light transmittance across the slice, representing the SD front. Within minutes, CA1 neurons in regions undergoing SD display irreversible damage in the form of field potential inactivation, swollen cell bodies, and extensively beaded dendrites, the latter revealed by single-cell injection of lucifer yellow. Importantly, glutamate receptor antagonists do not block SD induced by O2/glucose deprivation, nor do they prevent the resultant dendritic beading of CA1 neurons. However, CA1 neurons are spared if SD is suppressed by reducing the temperature to 35 degrees C during O2/glucose deprivation. This supports previous electrophysiologic evidence in vivo that SD during ischemia promotes acute neuronal damage and that glutamate antagonists are not protective of the metabolically stressed tissue. The authors propose that the inhibition of ischemic SD should be targeted as an important therapeutic strategy against stroke damage.