Background Owing to the coronavirus disease 2019, medical learning burnout has attracted increasing attention in educational research. It has a serious negative impact on medical students and their service quality. This could impair the professional development of medical students; weaken their personal and professional quality; and lead to problems such as increased medical errors and reduced patient care quality and satisfaction. This study aimed to examine the effects of perceived stress, social support, and the Big Five personality traits on learning burnout among medical students. Methods In November 2021, a cross-sectional survey was conducted at three medical universities in China. A self-administered questionnaire was distributed to 616 third- year students. Learning burnout, perceived stress, social support, and the Big Five personality traits (neuroticism, extroversion, openness, agreeableness, and conscientiousness) were anonymously measured. A total of 583 students were included in the final sample. Hierarchical linear regression was performed to explore the effects of perceived stress, social support, and Big Five personality traits on medical students’ learning burnout. Results Perceived stress was positively associated with learning burnout (emotional exhaustion: ß = 0.577, p < 0.001; cynicism: ß = 0.543, p < 0.001; low professional efficacy: ß = 0.455, p < 0.001) whereas social support was negatively related with it (low professional efficacy: ß = -0.319, p < 0.001). Neuroticism had a positive effect on emotional burnout (ß = 0.152, p = 0.009). Extraversion (ß = -0.116, p = 0.006) and conscientiousness (ß = -0.363, p < 0.001) had a negative effect on low professional efficacy. Agreeableness negatively affected emotional exhaustion (ß = -0.181, p < 0.001) and cynicism (ß = -0.245, p < 0.001) and positively affected low professional efficacy (ß = 0.098, p = 0.008). The associated factors together accounted for an additional variance of learning burnout (emotional exhaustion: 39.0%; cynicism: 36.8%; low professional efficacy: 48.7%). Conclusions Social support is a positive resource for fighting medical students’ burnout. Perceived stress was the strongest indicator of learning burnout. In addition to reducing perceived stress, developing extraversion, agreeableness, and conscientiousness should be included in burnout prevention and treatment strategies, particularly for medical students.
Abstract. The collagen, type IX, alpha 1 (COL9A1) gene was previously identified as a candidate gene for idiopathic congenital talipes equinovarus (ICTEV), a congenital lower limb deformity in humans. In the present study, increased expression levels of COL9A1 were identified in the abductor hallucis muscle of ICTEV patients compared with those in control samples. The COL9A1 gene is regulated by SRY (sex-determining region Y)-box 9 (SOX9). Immunofluorescence analysis of SOX9 and COL9A1 proteins identified colocalization to the sarcolemma, endomysium and muscle membrane in muscle samples of ICTEV. No mutations in the exons and promoters of SOX9 were detected in blood samples of 84 ICTEV patients by denaturing gradient gel electrophoresis. mRNA and protein expression levels of SOX9 were detected by real-time polymerase chain reaction and western blot analysis, respectively and were found to be significantly higher in ICTEV muscle samples compared with those in control samples. Based on present observations, we hypothesize that overexpression of the SOX9 gene may play a role in the genetic etiology of ICTEV.
Parkinson’s disease (PD) is characterized by the presence of Lewy bodies caused by α-synuclein. The imbalance of zinc homeostasis is a major cause of PD, promoting α-synuclein accumulation. ATP13A2, a transporter found in acidic vesicles, plays an important role in Zn2+ homeostasis and is highly expressed in Lewy bodies in PD-surviving neurons. ATP13A2 is involved in the transport of zinc ions in lysosomes and exosomes and inhibits the aggregation of α-synuclein. However, the potential mechanism underlying the regulation of zinc homeostasis and α-synuclein accumulation by ATP13A2 remains unexplored. We used α-synuclein-GFP transgenic mice and HEK293 α-synuclein-DsRed cell line as models. The spatial exploration behavior of mice was significantly reduced, and phosphorylation levels of α-synuclein increased upon high Zn2+ treatment. High Zn2+ also inhibited the autophagy pathway by reducing LAMP2a levels and changing the expression of LC3 and P62, by reducing mitochondrial membrane potential and increasing the expression of cytochrom C, and by activating the ERK/P38 apoptosis signaling pathway, ultimately leading to increased caspase 3 levels. These protein changes were reversed after ATP13A2 overexpression, whereas ATP13A2 knockout exacerbated α-synuclein phosphorylation levels. These results suggest that ATP13A2 may have a protective effect on Zn2+-induced abnormal aggregation of α-synuclein, lysosomal dysfunction, and apoptosis.
Fluorosis can induce neurotoxicity. Sodium butyrate (SB), a histone deacetylase inhibitor, has important research potential in correcting glucose metabolism disorders and is widely used in a variety of neurological diseases and metabolic diseases, but it is not yet known whether it plays a role in combating uoride-induced neurotoxicity. This study aims to evaluate the effect of SB on uoride neurotoxicity and the possible associated mechanisms. The results of HE staining and Morris water maze showed that in mice exposed to 100 mg/L uoride for three months, the hippocampal cells arranged in loosely with large cell gaps and diminished in number. In addition, 1000 mg/kg/day SB treatment improved uorideinduced neuronal cell damage and spatial learning memory impairment. Western blotting showed that the abundance of malate dehydrogenase 2 (MDH2) and pyruvate dehydrogenase (PDH) in the hippocampus of mice increased after uorosis, while the abundance of pyruvate kinase M (PKM), lactate dehydrogenase (LDH) and hexokinase (HK) decreased. SB treatment reversed the decreased glycolysis in the hippocampus of uorosis mice. We suspected that the PI3K/AKT/HIF-1α pathway may be involved in mediating the protective effects of SB against uorosis invasion in the hippocampus. These results suggested that SB could ameliorate uorosis-induced neurotoxicity, which might be linked with its function in regulating glycolysis as well as inhibition of the PI3K/AKT/HIF-1α pathway.
Fluorosis can induce neurotoxicity. Sodium butyrate (SB), a histone deacetylase inhibitor, has important research potential in correcting glucose metabolism disorders and is widely used in a variety of neurological diseases and metabolic diseases, but it is not yet known whether it plays a role in combating fluoride-induced neurotoxicity. This study aims to evaluate the effect of SB on fluoride neurotoxicity and the possible associated mechanisms. The results of HE staining and Morris water maze showed that in mice exposed to 100 mg/L fluoride for three months, the hippocampal cells arranged in loosely with large cell gaps and diminished in number. In addition, 1000 mg/kg/day SB treatment improved fluoride-induced neuronal cell damage and spatial learning memory impairment. Western blotting showed that the abundance of malate dehydrogenase 2 (MDH2) and pyruvate dehydrogenase (PDH) in the hippocampus of mice increased after fluorosis, while the abundance of pyruvate kinase M (PKM), lactate dehydrogenase (LDH) and hexokinase (HK) decreased. SB treatment reversed the decreased glycolysis in the hippocampus of fluorosis mice. We suspected that the PI3K/AKT/HIF-1α pathway may be involved in mediating the protective effects of SB against fluorosis invasion in the hippocampus. These results suggested that SB could ameliorate fluorosis-induced neurotoxicity, which might be linked with its function in regulating glycolysis as well as inhibition of the PI3K/AKT/HIF-1α pathway.
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