目的:观察社会支持与自我效能对颅脑创伤伴面部组织挫伤患者术后瘢痕修复意愿及心理状态的影响。方法:选取笔者医院2015年2月-2020年9月收治的80例颅脑创伤伴面部组织挫伤患者,调查其社会支持量表(Social support rating scale,SSRS)评...目的:观察社会支持与自我效能对颅脑创伤伴面部组织挫伤患者术后瘢痕修复意愿及心理状态的影响。方法:选取笔者医院2015年2月-2020年9月收治的80例颅脑创伤伴面部组织挫伤患者,调查其社会支持量表(Social support rating scale,SSRS)评分、自我效能量表(General self-efficacy scale,GSES)评分、术后瘢痕修复意愿与心理痛苦温度计(Distress thermometer,DT)评分,并进行Logistic回归分析与Pearson相关性分析。结果:相关性分析显示,SSRS评分、GSES评分与DT评分均呈显著负相关(P<0.05)。80例患者中,48例有术后瘢痕修复意愿,32例无瘢痕修复意愿;两组性别、年龄和颅脑创伤原因比较差异无统计学意义(P>0.05);愿意组SSRS评分、GSES评分明显高于不愿意组,DT评分明显低于不愿意组,差异有统计学意义(P<0.05)。Logistic回归分析显示,SSRS评分、GSES评分及DT评分与患者术后瘢痕修复意愿有关(P<0.05)。结论:社会支持、自我效能与颅脑创伤伴面部组织挫伤患者术后瘢痕修复意愿及心理痛苦关系密切,社会支持水平与自我效能高者,其心理痛苦程度较轻,且更愿意接受术后瘢痕修复治疗。展开更多
BAF45Dis a member of BAF complex,which may play a crucial role in neural development.PAX6 determines neuroectoderm formation,which is highly level sensitive.BAF45D is required for retinoic acid(RA)induced PAX6 express...BAF45Dis a member of BAF complex,which may play a crucial role in neural development.PAX6 determines neuroectoderm formation,which is highly level sensitive.BAF45D is required for retinoic acid(RA)induced PAX6 expression.PAX6 expression is also regulated by TGF-beta/SMAD signaling.However,mechanism of such regulation remains elusive.We therefore sought to explore whether BAF45D regulates PAX6 expression through cooperating with TGF-beta/SMAD signaling.Here we identified BAF45D is required for expression of phosphorylated SMAD3 and PAX6 induced by RA.Genome-wide analysis revealed that during RA-induced early neural differentiation,BAF 45D knockdown failed to activate TGF-beta/SMAD signaling and induce expression of STAT3 and SMAD7,two negative regulators of TGF-beta/SMAD signaling.Moreover,in RA treated P19 and H9 cells,BAF45D interacts with BRG1 and phosphorylated SMAD3.展开更多
文摘BAF45Dis a member of BAF complex,which may play a crucial role in neural development.PAX6 determines neuroectoderm formation,which is highly level sensitive.BAF45D is required for retinoic acid(RA)induced PAX6 expression.PAX6 expression is also regulated by TGF-beta/SMAD signaling.However,mechanism of such regulation remains elusive.We therefore sought to explore whether BAF45D regulates PAX6 expression through cooperating with TGF-beta/SMAD signaling.Here we identified BAF45D is required for expression of phosphorylated SMAD3 and PAX6 induced by RA.Genome-wide analysis revealed that during RA-induced early neural differentiation,BAF 45D knockdown failed to activate TGF-beta/SMAD signaling and induce expression of STAT3 and SMAD7,two negative regulators of TGF-beta/SMAD signaling.Moreover,in RA treated P19 and H9 cells,BAF45D interacts with BRG1 and phosphorylated SMAD3.