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Medical students' motivation and study strategies are crucial in determining academic performance. This study aimed to assess the motivation and learning strategies of medical students as well as their association with performance in anatomy examinations. The Motivated Strategies for Learning Questionnaire, two focus group discussions, and students' current anatomy cumulative grade point average (cGPA) were used. Generally, the medical students strongly felt that anatomy is fundamental to the practice of medicine and surgery. This result was consistent with high task value scores of 5.99 ± 1.25. They were also driven by extrinsic goal orientation (5.59 ± 1.42) and intrinsic goal orientation (5.08 ± 1.26). Most medical students typically relied on elaboration (5.35 ± 1.25) ahead of other cognitive strategies namely rehearsal (5.30 ± 1.11), organization (5.15 ± 1.34), and lowest-rated critical thinking (4.77 ± 1.19). The students also relied on resource management strategies, effort regulation (5.15 ± 1.20) and time and study environment regulation (5.03 ± 1.03) more than the moderately scored peer learning (4.95 ± 1.50) and help-seeking (4.95 ± 1.09). In the focus group discussions, students reported that they often narrate or explain to each other what they would have read and understood from anatomy lectures, tutorials, and textbooks. They also bemoaned the lack of institutional support for stress burdens. The motivation and learning strategies subscales were not correlated with anatomy cGPA. Males were driven by extrinsic goals and experienced significantly higher levels of test anxiety than females (P

Anatomy is a challenging preclinical subject owing to the vast amount of information that students need to master. The adoption of relevant study approaches is key to the development of a long-lasting understanding of anatomical subject matter. Phenomenographic educational research describes the medical students as using a variable mix of deep, strategic, and surface approaches to study. Continually assessing students' learning preferences and approaches is crucial for achieving the desired learning outcomes. The approaches to studying anatomy in two groups of first-year Zimbabwean medical students from two newly established medical schools were collected using the Approaches and Study Skills Inventory for Students (ASSIST) instrument and than analyzed. At least 90% of the students believed that anatomy involved reproducing knowledge or personal understanding and development. Overall, the majority of the students adopted deep and strategic approaches, while a distant minority used the surface approach. There was no significant correlation between either the students' sex or age and their preference for a specific approach to studying. The mean anatomy grades for students using a strategic approach were significantly higher than those using deep or surface approaches. The number of strategic learners was double that of deep learners among the high achievers subgroup. The strategic approach positively correlated with performance in examinations. Generally, the students shared a common understanding of the concept of anatomy learning. Studies such as this can assist with the identification of students at risk of failure and empower lecturers to recommend the adoption of more beneficial strategic and deep learner traits.

The imbalance between excess reactive oxygen species (ROS) generation and insufficient antioxidant defenses contribute to a range of neurodegenerative diseases. High ROS levels damage cellular macromolecules such as DNA, proteins and lipids, leading to neuron vulnerability and eventual death. However, the underlying molecular mechanism of the ROS regulation is not fully elucidated. Recently, an increasing number of studies suggest that microRNAs (miRNAs) emerge as the targets in regulating oxidative stress. We recently reported the neuroprotective effect of miR-137-3p for brachial plexus avulsion-induced motoneuron death. The present study is sought to investigate whether miR-137-3p also could protect PC12 cells against hydrogen peroxide (H2O2) induced neurotoxicity. By using cell viability assay, ROS assay, gene and protein expression assay, we found that PC-12 cells exposed to H2O2 exhibited decreased cell viability, increased expression levels of calpain-2 and neuronal nitric oxide synthase (nNOS), whereas a decreased miR-137-3p expression. Importantly, restoring the miR-137-3p levels in H2O2 exposure robustly inhibited the elevated nNOS, calpain-2 and ROS expression levels, which subsequently improved the cell viability. Furthermore, the suppressive effect of miR-137-3p on the elevated ROS level under oxidative stress was considerably blunted when we mutated the binding site of calpain-2 targted by miR-137-3p, suggesting the critical role of calpain-2 involving the neuroprotective effect of miR-137-3p. Collectively, these findings highlight the neuroprotective role of miR-137-3p through down-regulating calpain and NOS activity, suggesting its potential role for combating oxidative stress insults in the neurodegenerative diseases.

Background: Chronic neuropathic pain often occurs with unclear mechanisms after brachial plexus root avulsion (BPRA) injuries. Emerging evidence suggests that the maladaptation of spinal glial glutamate transporter GLT-1 causes extracellular glutamate accumulation, contributing to central sensitization of chronic pain. Dexmedetomidine (DMET), an α2-adrenergic receptor (α2AR) agonist, widely used in the clinic as a sedative and analgesic drug, has been shown to inhibit glial activation. This study assessed DMET effects on BPRA induced pain and the possible involvement of GLT-1 regulation. Methods: The right C8 and T1 roots were avulsed to establish a lower trunk BPRA injury rat model and LPS-induced activation of rat primary cultured astrocytes. Then we used the molecular and behavioral assay combined with pharmacological manipulation to test the hypothesis that DMET attenuates the pain and neuroinflammation through restoring the GLT-1 function via PKA signaling.Results: The mechanical allodynia and thermal hyperalgesia appeared and reached the peak at 1-day post-injury (dpi) and persisted for at least 28 dpi. Notably, BPRA enhanced phosphorylated PKA levels, reduced GLT-1 expression, and caused an imbalance between anti- and proinflammatory cytokines in the affected spinal segments. Acute systemic or local DMET administration, at the un-sedative doses, demonstrated an analgesic effect. Moreover, a 3-days intrathecal DMET treatment ameliorated hyperalgesia and allodynia of BPRA injured rats by attenuating PKA phosphorylation, IL-1β, and IL-6, while restoring the levels of GLT-1, IL-4, and IL-10 in the spinal cord. Significantly, intrathecal administration of the selective PKA inhibitor H89 mimicked, but the PKA activator 8-Br-cAMP blocked DMET’s effects. Conclusion: Overall, these results suggest that PKA inactivation mediates DMET's analgesic effect for the pain induced by BPRA injury through the recovery of GLT-1 function.

Background Endothelin-1 (ET-1) is synthesized and upregulated in astrocytes under stroke. We previously demonstrated that transgenic mice over-expressing astrocytic ET-1 (GET-1) displayed more severe neurological deficits characterized by a larger infarct after transient middle cerebral artery occlusion (tMCAO). ET-1 is a known vasoconstrictor, mitogenic, and a survival factor. However, it is unclear whether the observed severe brain damage in GET-1 mice post stroke is due to ET-1 dysregulation of neurogenesis by altering the stem cell niche. Methods Non-transgenic (Ntg) and GET-1 mice were subjected to tMCAO with 1 h occlusion followed by long-term reperfusion (from day 1 to day 28). Neurological function was assessed using a four-point scale method. Infarct area and volume were determined by 2,3,5-triphenyltetra-zolium chloride staining. Neural stem cell (NSC) proliferation and migration in subventricular zone (SVZ) were evaluated by immunofluorescence double labeling of bromodeoxyuridine (BrdU), Ki67 and Sox2, Nestin, and Doublecortin (DCX). NSC differentiation in SVZ was evaluated using the following immunofluorescence double immunostaining: BrdU and neuron-specific nuclear protein (NeuN), BrdU and glial fibrillary acidic protein (GFAP). Phospho-Stat3 (p-Stat3) expression detected by Western-blot and immunofluorescence staining. Results GET-1 mice displayed a more severe neurological deficit and larger infarct area after tMCAO injury. There was a significant increase of BrdU-labeled progenitor cell proliferation, which co-expressed with GFAP, at SVZ in the ipsilateral side of the GET-1 brain at 28 days after tMCAO. p-Stat3 expression was increased in both Ntg and GET-1 mice in the ischemia brain at 7 days after tMCAO. p-Stat3 expression was significantly upregulated in the ipsilateral side in the GET-1 brain than that in the Ntg brain at 7 days after tMCAO. Furthermore, GET-1 mice treated with AG490 (a JAK2/Stat3 inhibitor) sh owed a significant reduction in neurological deficit along with reduced infarct area and dwarfed astrocytic differentiation in the ipsilateral brain after tMCAO. Conclusions The data indicate that astrocytic endothelin-1 overexpression promotes progenitor stem cell proliferation and astr ocytic differentiation via the Jak2/Stat3 pathway.

Background: The aim of the study was to probe the morphological features of the proximal segment (V1) of vertebral artery (VA) in a sample of Chinese cadavers. Materials and methods: The origin, course and outer diameter at origin of the pre-vertebral part of the VAs were evaluated in 119 adult cadavers. Results: It was found that 94.12% of the VAs originated from the subclavian arteries, bilaterally. The variant origins were present in 5.88% of the cadavers and all originated directly from the arch of the aorta. All the variations were observed on the left side of male cadavers. The average outer diameters at origin of the normal and variation groups were 4.35 ± 1.00 mm and 4.82 ± ± 1.42 mm, respectively, p = 0.035. In the normal group, but not in the variation group, the average diameter in the males was significantly larger than that in the females (4.50 ± 0.99 mm, 3.92 ± 0.92 mm, respectively, p = 0.000). In addition, only 5 cadavers in the normal group had hypoplastic VAs (4.20%, 4 males, 3 right-sided). Vertebral artery dominance (VAD) was present in 91 (69 males) out of 112 cadavers and more common on the left (n = 48). In addition, 3 cadavers satisfied conditions for coexistence of VAD and vertebral artery hypoplasia. All 7 cadavers in the variation group exhibited VAD, which was more common on the right side (n = 5). Conclusions: The morphologic variations and frequencies described above have implications for the early prevention, abnormal anatomy detection, accurate diagnosis, safe surgery and endovascular treatment of cardiovascular and neurological disease.

Scutellarin, a bioactive flavone isolated from Scutellaria baicalensis, has anti-inflammatory, anti-neurotoxic, anti-apoptotic and anti-oxidative effects and has been used to treat cardiovascular and cerebrovascular diseases in China. However, the mechanisms by which scutellarin mediates neuroprotection in cerebral ischemia remain unclear. The interaction between scutellarin and nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2) was assessed by molecular docking study, which showed that scutellarin selectively binds to NOX2 with high affinity. Cultures of primary astrocytes isolated from the cerebral cortex of neonatal Sprague-Dawley rats were pretreated with 2, 10 or 50 μM scutellarin for 30 minutes. The astrocytes were then subjected to oxygen/glucose deprivation by incubation for 2 hours in glucose-free Dulbecco's modified Eagle's medium in a 95% N2/5% CO2 incubator, followed by simulated reperfusion for 22 hours. Cell viability was assessed by cell counting kit-8 assay. Expression levels of NOX2, connexin 43 and caspase-3 were assessed by western blot assay. Reactive oxygen species were measured spectrophotometrically. Pretreatment with 10 or 50 μM scutellarin substantially increased viability, reduced the expression of NOX2 and caspase-3, increased the expression of connexin 43, and diminished the levels of reactive oxygen species in astrocytes subjected to ischemia-reperfusion. We also assessed the effects of scutellarin in vivo in the rat transient middle cerebral artery occlusion model of cerebral ischemia-reperfusion injury. Rats were given intraperitoneal injection of 100 mg/kg scutellarin 2 hours before surgery. The Bederson scale was used to assess neurological deficit, and 2,3,5-triphenyltetrazolium chloride staining was used to measure infarct size. Western blot assay was used to assess expression of NOX2 and connexin 43 in brain tissue. Enzyme-linked immunosorbent assay was used to detect 8-hydroxydeoxyguanosine (8-OHdG), 4-hydroxy-2-nonenal (4-HNE) and 3-nitrotyrosin (3-NT) in brain tissue. Immunofluorescence double staining was used to determine the co-expression of caspase-3 and NeuN. Pretreatment with scutellarin improved the neurological function of rats with focal cerebral ischemia, reduced infarct size, diminished the expression of NOX2, reduced levels of 8-OHdG, 4-HNE and 3-NT, and reduced the number of cells co-expressing caspase-3 and NeuN in the injured brain tissue. Furthermore, we examined the effect of the NOX2 inhibitor apocynin. Apocynin substantially increased connexin 43 expression in vivo and in vitro. Collectively, our findings suggest that scutellarin protects against ischemic injury in vitro and in vivo by downregulating NOX2, upregulating connexin 43, decreasing oxidative damage, and reducing apoptotic cell death.

Objectives The aim of this study is to determine the incidence and explore the types of aortic arch branch variations found in our cadavers. Methods The types and incidence of aortic branch variations in 120 cadavers were analysed after careful dissection. Results One hundred and six of 120 cadavers had normal aortic arch branches and gave rise to usual branches, namely the brachiocephalic trunk, the left common carotid artery and the left subclavian artery. The remaining 14 cadavers had 2 basic types of branch variations, thus accounting for an incidence of 11.67%. A total of 9 aortic arches emitted 4 branches; the brachiocephalic trunk, the left common carotid artery, the left vertebral artery and the left subclavian artery (incidence 7.5%). The second subgroup of 5 cadavers also emitted 4 aortic branches: the right common carotid artery, the left common carotid artery, the left subclavian artery and the right subclavian artery (incidence 4.16%). In this group, the right subclavian artery sprung as a distal branch of the aortic arch (descending), thus making a vascular ring that takes a superoposterior course round the back of the trachea and the oesophagus to reach the right side. There was a single cadaver, different from the other 4 aortic branches of the second group which had a common origin for the common carotid arteries, while the left subclavian artery and distally placed right subclavian artery were present. We did not observe any Kommerell's aortic diverticula. Conclusions The variations of aortic arch branching are complex and diverse due to varied possible alterations in the embryological processes. There is an imperative need for further research on these variations to elucidate the possible relationships with clinical diagnostic or surgical events.