The relationship between self-consciousness and depression in college students: the chain mediating effect of meaning life and self-efficacy, with the moderating effect of social support.

BACKGROUND: This study aimed to investigate the impact of self-consciousness on depression of college students, and mainly focus on confirming the mediator role of life meaningful and self-efficacy, as well as the moderator role of social support. METHODS: In the present study, convenient sampling method was adopted, 583 college students were recruited from Harbin city and Wenzhou city in China. All students were assessed using self-assessment scales, including self-consciousness scale, life meaningful scale, self-efficacy scale, social support scale, and self-rating depression scale. Descriptive statistical analysis and correlation analysis, structural equation model analysis were conducted by SPSS 25.0 and M-plus. RESULTS: Results showed that self-consciousness was negatively related to depression, life meaningful and self-efficacy partially mediated the relation between self-consciousness and depression. Moderated mediation analysis further indicated that the relation between self-efficacy and depression were moderated bu social support. Compare with college students who had high social support, depression in those with low social support was more susceptible to the effect of self-efficacy. CONCLUSION: These findings imply that college students with low levels of self-consciousness are more easy to be depressive, enhancing their sense of life meaning and self-efficacy can effectively alleviate depression, and college student with high social support can benefit more from self-efficacy. Therefore we should pay more attention to the mental health problems of low levels self-consciousness college students in university.

Altered Jagged1-Notch1 Signaling in Enhanced Dysfunctional Neovascularization and Delayed Angiogenesis After Ischemic Stroke in HFD/STZ Induced Type 2 Diabetes Rats.

Diabetes exacerbates brain damage in cerebral ischemic stroke. Our previous study has demonstrated that after cerebral ischemia, type 2 diabetes rats displayed worse neurological outcomes, larger cerebral infarction and severer blood-brain barrier disruption. However, our knowledge of the mechanisms of how diabetes impacts the cerebrovascular repair process is limited. This study was aimed to characterize structural alterations and potential mechanisms in brain microvessels before and after ischemic stroke in type 2 diabetic rats treated with high-fat diet and streptozotocin (HFD/STZ). Furtherly, we tested our hypothesis that dysregulated intercellular Jagged1-Notch1 signaling was involved in the dysfunctional cerebral neovascularization both before and after ischemic stroke in HFD/STZ rats. In our study, we found increased yet dysfunctional neovascularization with activated Jagged1-Notch1 signaling in the cerebrovasculature before cerebral ischemia in HFD/STZ rats compared with non-diabetic rats. Furthermore, we observed delayed angiogenesis as well as suppressed Jagged1-Notch1 signaling after ischemic stroke. Our results elucidate the potential mechanisms underlying diabetes-related cerebral microvasculature dysfunction after ischemic stroke.

Mild hypothermia alleviates diabetes aggravated cerebral ischemic injury via activating autophagy and inhibiting pyroptosis.

Diabetic patients manifest with more severe neurological deficits than non-diabetes after ischemic stroke. It has been shown that hypothermia has neuroprotective effects on cerebral ischemia, but whether it is effective for cerebral ischemia in diabetic patients remains unknown. The aim of this study was to investigate whether hypothermia can alleviate cerebral ischemic injury in diabetic rats and the regulation of autophagy and pyroptosis of the treatment. We introduced permanent middle cerebral artery occlusion (pMCAO) in a model of type 2 diabetic rats prepared by high-fat diet combined with intraperitoneal injection of STZ in vivo and mimicked cerebral ischemia with diabetes by employing high glucose stimulation and oxygen-glucose deprivation/reoxygenation (OGD/R) in vitro. Moreover, 3-methyladenine and bafilomycin A1 were used to evaluate the association between autophagy and pyroptosis in vitro. Our results showed that diabetes aggravated neurological deficits, increased the volume of cerebral infarction and brain edema as well as the blood brain barrier permeability after cerebral ischemia, which were alleviated by mild hypothermia. Compared with the pMCAO model in non-diabetic rats and OGD/R model without high glucose stimulation in vitro, the expression of P62, NOD-like receptor protein 3 (NLRP3), cleaved caspase-1 and Gasdermin-N increased and the ratio of microtubule-associated protein 1 light chain 3B (LC3B) Ⅱ/Ⅰ decreased in the pMCAO model in diabetic rats and OGD/R model with high glucose stimulation, which could be reversed by mild hypothermia. In conclusion, mild hypothermia alleviated diabetes aggravated cerebral ischemic injury via activating autophagy and inhibiting pyroptosis.

Clinical significance of joint detection of CD44v6 and CD62P in nasopharyngeal carcinoma.

AIM: The aim of this study was to investigate the expression and clinical prognostic significance of adhesion molecules in nasopharyngeal carcinoma (NPC) tissues and peripheral blood. MATERIALS AND METHODS: Flow cytometry assays for the expression levels of CD44v6 and CD62P protein in peripheral blood and tissues from controls and NPC patients were performed. Clinical and pathological features were reported and analyzed, and a survival study was carried out. RESULTS: The expression of CD44v6 and CD62P in NPC tissues and peripheral blood was higher than that of the control group (p < 0.05). Expression levels in peripheral blood of stage III/IV NPC patients was markedly higher than that of patients in stage I/II (p < 0.05), while it had no statistically significant difference in tissues (p > 0.05). The expression levels of CD44v6 and CD62P in the lymph gland metastasis and distant metastasis group were higher than groups without such metastasis (p < 0.05), and there was no statistical difference in NPC tissues (p > 0.05). The survival rates of NPC groups with low expression in the peripheral blood were higher than those of high-expression groups (p < 0.05). CONCLUSION: Joint detection of CD44v6 and CD62P in the peripheral blood or tissues of NPC patients has diagnostic and prognostic value as a marker of poor clinical outcome.

[Detection and clinical significance of vascular endothelium growth factor and microvessel density in patients with nasopharyngeal carcinoma].

OBJECTIVE: To investigate the role of VEGF in angiogenesis of nasopharyngeal carcinoma tissue. METHOD: Serum and tissue VEGF were detected by the quantitative enzyme-linked immunosorbent assay (ELISA) method both in 62 nasopharyngeal carcinoma without therapy and 20 nasopharyngitis. The expression of microvessel density in tissue of nasopharyngeal carcinoma and nasopharyngitis were detected by immunohistochemical method. RESULT: (1) There was no significant relationship compared VEGF and MVD in nasopharyngeal carcinoma patient, gender and ages (P>0.05), while the expression of VEGF and MVD in later stage (III+IV) were significant higher than that in earlier stage (I+I) (P<0.01), and in positive lymph node group or metastasis group were higher than in negative group (P<0.01); (2) The expression of VEGF and MVD in nasopharyngeal carcinoma serum and tissue were higher than in nasopharyngitis (P<0.05); (3) There was positive correlation between VEGF and MVD in nasopharyngeal carcinoma tissue (r=0.865, P<0.01), but negative correlation in their serum (r=0.328, P>0.05). CONCLUSION: VEGF could induce angiogenesis in nasopharyngeal carcinoma tissue, and play an important role in progression in nasopharyngeal carcinoma, VEGF could be an important marker for monitoring prognosis of disease.