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1.
Chinese Journal of School Health ; (12): 597-601, 2021.
Artículo en Chino | WPRIM (Pacífico Occidental) | ID: wpr-876410

RESUMEN

Objective@#To understand and compare the differences in help-seeking behavior among junior high school students and senior high school students and their association with non-suicidal self-injury to provide a basis for the prevention and control of non-suicidal self-injury among middle school students.@*Methods@#Three middle schools in Nanchang were selected,and the survey were conducted among 4 434 students through the General Situation Questionnaire, the Ottawa Self-injury Judgment Entry, and the Middle School Students Help Seeking Behavior Questionnaire, and SPSS 22.0 was used for statistical analysis.@*Results@#The NSSI detection rate among middle school students was 33.3% , and junior high school students detection rate(36.0%) were higher than high school students(29.6%) (χ 2=19.41,P<0.01). Differences in willingness to ask for help, asking for help from family and teachers, and talking face-to-face for help were statistically significant (all P<0.01) among NSSI participants and non-NSSI participants, for both junior high school and high school students. Females (OR=1.45), class cadres (OR=1.26), urban household registration (OR=1.45), frequent scolding by elders (OR=1.98) and a high academic burden (OR=1.39) all possible increased the risk of NSSI in junior high school students, while assistance to family members (OR=0.95) or teachers (OR=0.95) possible reduced the risk of NSSI in junior high school students. Females (OR=1.50), class cadres (OR=1.34), only children (OR=1.45), fathers with college education and above (compared to junior high school and below) (OR=1.56), frequent scolding by elders (OR=2.08), frequent corporal punishment from elders (OR=4.12) and high academic burden (OR=1.38) possibly increased the risk of NSSI among high school students, while willingness to ask for help (OR=0.82), asking for help from family (OR=0.95) and teachers (OR=0.96) possible reduced the risk of NSSI among high school students.@*Conclusion@#There are some differences in help-seeking behavior between junior and high school students, and school and parents should actively focus on middle school students help-seeking behavior and encourage them to seek help.

2.
J Cell Biochem ; 119(7): 5437-5448, 2018 07.
Artículo en Inglés | MEDLINE | ID: mdl-29369410

RESUMEN

This study aims to explore the effect of miR-330 targeting VAV1 on amyloid ß-protein (Aß) production, oxidative stress (OS), and mitochondrial dysfunction in Alzheimer's disease (AD) mice through the MAPK signaling pathway. Putative targeted gene of miR-330 was performed by a miRNA target prediction website and dual-luciferase reporter gene assay. AD mouse model was successfully established. Fourteen C57 mice were randomized into AD and control groups. The positive protein expression rate of VAV1 was measured by immunohistochemistry. Neuron cells were assigned into control, blank, negative control (NC), miR-330 mimics, miR-330 inhibitors, siRNA-VAV1, and miR-330 inhibitors + siRNA-VAV1 groups. Expression of miR-330, VAV1, ERK1, JNK1, P38MAPK, Aß, COX, and lipoprotein receptor-related protein-1 (LRP-1) were determined using RT-qPCR and Western blotting. Colorimetry was applied to measure the levels of OS parameters of superoxide dismutase (SOD) and malondialdehyde (MDA). Aß production in brain tissue was detected using ELISA, while that in neuron cell was measured by radioimmunoassay. MiR-330 was down-regulated in neuron cells of AD mice and VAV1 was negatively regulated by miR-330. Compared with the control group, the positive protein expression rate of VAV1 was significantly elevated in the AD group. Overexpression of miR-330 decreased the expression of VAV1, ERK1, JNK1, P38MAPK, and Aß, but increased the expression of COX and LRP-1. AD mice revealed elevated Aß production and MDA with decreased SOD level. The result indicates that overexpressed miR-330 targeting VAV1 through the MAPK signaling pathway reduces Aß production and alleviates OS and mitochondrial dysfunction in AD.


Asunto(s)
Enfermedad de Alzheimer/prevención & control , Péptidos beta-Amiloides/metabolismo , Sistema de Señalización de MAP Quinasas , MicroARNs/farmacología , Mitocondrias/genética , Estrés Oxidativo/genética , Sustancias Protectoras/farmacología , Proteínas Proto-Oncogénicas c-vav/antagonistas & inhibidores , Enfermedad de Alzheimer/genética , Enfermedad de Alzheimer/metabolismo , Animales , Modelos Animales de Enfermedad , Ratones , Ratones Endogámicos C57BL , MicroARNs/genética , Mitocondrias/metabolismo , Neuronas/efectos de los fármacos , Neuronas/metabolismo , Neuronas/patología , Proteínas Proto-Oncogénicas c-vav/genética , Proteínas Proto-Oncogénicas c-vav/metabolismo , Transducción de Señal
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