Characteristics of staff–child interaction in 1–3-year-olds’ risky play in early childhood education and care

Despite increased interest in children’s risk-taking in play, little is known of this aspect considering children under three years. Therefore, this study aimed to investigate the concept of scaffolding to potentially describe patterns in staff–child interaction in 1–3-year-olds’ risky play. Empirical data were taken from an exploratory study, executed as a focused ethnography with multiple data collecting techniques, resulting in a sample of 198 instances of risky play. Findings indicate that scaffolding is a pertinent theoretical foundation for describing high-quality staff–child interaction in risky play, leading to increased opportunities for developmentally appropriate stimulation. Of the 171 instances where staff were present, staff did not interact at all in 70 of the instances (41%). Staff–child interaction, directly related to children’s risky play, occurred in the remaining 101 instances. Of these 101 instances, ‘Scaffolding’- and ‘Non-scaffolding’-interaction were observed in 78% and 22% of the instances, respectively. Implications are discussed.     

肠道菌群与中药相互作用的研究进展

肠道菌群作为人体内庞大的微生态系统,与人体健康状况有着密切的关联。其特点是数量大、种类多,一旦失调,将会引发各种疾病。中药对肠道菌群的稳态具有调节作用,同时肠道菌群对中药成分具有代谢转化作用,中药与肠道菌群的相互作用研究对实现中药现代化具有重要意义。对近年来关于肠道菌群与中药相互作用的研究成果进行整理归纳,为后续进一步深入研究中药与肠道菌群的关系提供参考。     

基于蛋白互作网络分析祛风湿药川乌的抗炎机制

炎症是风湿性疾病的重要危险因素之一。川乌是临床常用祛风湿药,具有显著抗炎作用,然其分子层面作用机制尚不清楚。为深入探索祛风湿药川乌抗炎作用的分子层面机制,该研究以川乌抗炎活性成分乌头碱、次乌头碱和新乌头碱为代表,通过数据库检索获得化合物的作用靶点及其蛋白质相互作用信息,构建川乌的蛋白互作网络。在此基础上,利用分子复合物检测算法(MCODE),对网络进行模块分析及功能注释,结果显示川乌抗炎作用机制主要与前列腺素代谢过程,趋化因子介导的白细胞趋化作用有关。该研究从分子网络水平系统探讨了川乌的抗炎机制,为川乌治疗风湿性疾病的研究提供科学依据。     

基于网络药理学的生脉散作用机制分析

目的:探讨生脉散的作用机制。方法:本研究选取生脉散中3味中药人参、麦冬、五味子含有的33个活性成分,通过Pharm Mapper服务器预测其活性成分的潜在靶点,进而构建化合物-靶点网络、构建蛋白互作(protein-protein interaction,PPI)网络、进行基因本体(gene ontology,GO)富集分析、进行基于京都基因与基因组百科全书(Kyoto encyclopedia of genes and genomes,KEGG)的生物通路富集分析,研究生脉散作用机制。结果:化合物-靶点网络包含249个节点,关键靶点涉及转甲状腺素蛋白(TTR)等。PPI网络包含155个节点,关键靶点涉及酪氨酸蛋白激酶Src(SRC),蛋白激酶Bα(Akt1)等。GO条目95个,其中生物过程相关的条目67个,分子功能相关的条目22个,细胞组成相关的条目6个。KEGG通路8条,涉及肿瘤信号通路(pathways in cancer),前列腺癌(prostate cancer),胰岛素信号通路(insulin signaling pathway)等。结论:本研究结果初步验证了生脉散的基本药理作用及其机制,并为进一步深入揭示其作用机制奠定了良好基础。     

建构主义理念下的《医古文》趣味互动教学设计

《医古文》课程的传统教学模式存在较大问题,难以达到良好的教学效果。为了改进教学方法,提升教学质量,现以建构主义和形成性教学评价为理论基础,举例采用两种趣味互动教学方式,培养学生对传统文化的兴趣,夯实学生的基础知识,提高学生的古文应用能力。证明趣味互动教学法符合当今学生的认知规律,具有独到的优势,并值得推广。     

Effect of Myd88 deficiency on gene expression profiling in salivary glands of female non-obese diabetic (NOD) mice

ObjectivesSjögren's syndrome (SS) is a chronic autoimmune disease characterized by inflammatory lesions in the salivary and lacrimal glands, which are caused by distinct lymphocytic infiltrates. Female non-obese diabetic (NOD) mice spontaneously develop inflammatory lesions of the salivary glands with SS-like pathological features. Previous studies have shown that MyD88, a crucial adaptor protein that activates innate immune signaling, affects lymphocytic infiltration, but its detailed role remains unclear. In this study, we investigated the role of MyD88 through gene expression profiling in the early phase of pathogenesis in the salivary glands of female NOD mice.MethodsSubmandibular glands collected from 10-week-old female wild-type and Myd88-deficient NOD mice were used for RNA preparation, followed by microarray analysis. The microarray dataset was analyzed to identify Myd88-dependent differentially expressed genes (DEGs). Data generated were used for GO enrichment, KEGG pathway, STRING database, and INTERFEROME database analyses.ResultsMyd88 deficiency was found to affect 230 DEGs, including SS-associated genes, such as Cxcl9 and Bpifa2. Most of the DEGs were identified as being involved in immunological processes. KEGG pathway analysis indicated that the DEGs were putatively involved in autoimmune diseases, such as systemic lupus erythematosus and rheumatoid arthritis. Furthermore, the DEGs included 149 interferon (IFN)-regulated genes.ConclusionsMyD88 is involved in the expression of specific genes associated with IFN-associated immunopathological processes in the salivary glands of NOD mice. Our findings are important for understanding the role of MyD88-dependent innate immune signaling in SS manifestation.     

程序性细胞坏死参与急慢性损伤脑内神经元死亡的研究进展

 程序性细胞坏死是一种新发现的细胞死亡形式。这类死亡细胞形态类似坏死,而其死亡过程受胞内主动机制的调节,由此改变了坏死细胞不受内在机制调控的经典概念。当细胞膜上死亡受体与其配体结合,细胞内凋亡因子caspase-8被抑制时,激活受体相互作用蛋白（receptor interaction protein,RIPK1/RIPK3）激酶及关键底物——混合谱系激酶结构域样蛋白（mixed lineage kinase domain-like protein,MLKL）的信号通路,从而触发细胞发生程序性细胞坏死。后者参与多种疾病的病理过程,如肿瘤、免疫炎症、神经退行性疾病、脑缺血损伤等。本文就程序性细胞坏死的信号通路、重要调控分子及在神经损伤相关疾病致病机制进行综述,并对研究方法和分析工具药物进行了归纳总结。     

寨卡病毒感染的辅助性宿主因子研究进展

 寨卡病毒(Zika virus,ZIKV)感染可造成宿主神经系统损伤,与胎儿头小畸形和格林-巴利综合征的发生相关。有许多针对包括ZIKV在内的黄病毒疫苗与抗病毒药物正处于研发阶段。本文总结了辅助ZIKV感染的宿主因子研究现状,有助于揭示ZIKV的感染机制。