Meta-Analysis of the Development of Teacher Education in University in the Educational Research of China

This research is based on 67 articles related with the meta-analysis of the teacher education in the university, which was published on CNKI from 2001 to 2014. The study found that: Articles about this field were mainly published in 2011, presenting a falling and curving trend as a whole. The main 6 authors of these articles include Zhu Xudong, Zhou Jun, Shen Qibiao, He Xi, Zhang Guoqiang and Zhao Binghui while the main Research institutes involve Beijing Normal University, Fujian Normal University and Southwest University. However, little inter-academic cooperation has been conducted among authors and universities. These articles are mainly in the fields of comparative education and higher education, which focus on the formation path, the institutional environment, teacher education models and evaluation in universities.

Analysis of the Division of Arts and Science Subjects in Ordinary High School in Late Qing Dynasty (1909-1911)

The division of Arts and Science in China originated from late Qing dynasty, when the Education Department submitted a memorial to the throne Proposal of Dividing the School Curriculum into Arts and Science in 1909. Then the two disciplines went through combinations and separations repeatedly over the past 100 years. This paper will investigate the separated education system’s evolution history in late Qing dynasty and its resulting drawbacks ever since from a historical perspective. We can not only draw some lessons from the investigation, but also acquire a clearer understanding of the division of Arts and Science subjects when facing the same or contradicting problems nowadays

Roles of LonP1 in Oral-Maxillofacial Developmental Defects and Tumors: A Novel Insight

Recent studies have indicated a central role for LonP1 in mitochondrial function. Its physiological functions include proteolysis, acting as a molecular chaperone, binding mitochondrial DNA, and being involved in cellular respiration, cellular metabolism, and oxidative stress. Given its vital role in energy metabolism, LonP1 has been suggested to be associated with multi-system neoplasms and developmental disorders. In this study, we investigated the roles, possible mechanisms of action, and therapeutic roles of LonP1 in oral and maxillofacial tumor development. LonP1 was highly expressed in oral-maxillofacial cancers and regulated their development through a sig-naling network. LonP1 may therefore be a promising anticancer therapy target. Mutations in LONP1 have been found to be involved in the etiology of cerebral, ocular, dental, auricular, and skeletal syndrome (CODAS). Only patients carrying specific LONP1 mutations have certain dental abnormalities (delayed eruption and abnormal morphology). LonP1 is therefore a novel factor in the development of oral and maxillofacial tumors. Greater research should therefore be conducted on the diagnosis and therapy of LonP1-related diseases to further define LonP1-associated oral phenotypes and their underlying molecular mechanisms

PER2 regulates odontoblastic differentiation of dental papilla cells in vitro via intracellular ATP content and reactive oxygen species levels

Background Dental papilla cells (DPCs) are one of the key stem cells for tooth development, eventually forming dentin and pulp. Previous studies have reported that PER2 is expressed in a 24-hour oscillatory pattern in DPCs in vitro. In vivo, PER2 is highly expressed in odontoblasts (which are differentiated from DPCs). However, whether PER2 modulates the odontogenic differentiation of DPCs is uncertain. This research was to identify the function of PER2 in the odontogenic differentiation of DPCs and preliminarily explore its mechanisms. Methods We monitored the expression of PER2 in DPCs differentiated in vivo. We used PER2 overexpression and knockdown studies to assess the role of PER2 in DPC differentiation and performed intracellular ATP content and reactive oxygen species (ROS) assays to further investigate the mechanism. Results PER2 expression was considerably elevated throughout the odontoblastic differentiation of DPCs in vivo. Overexpressing Per2 boosted levels of odontogenic differentiation markers, such as dentin sialophosphoprotein (Dspp), dentin matrix protein 1 (Dmp1), and alkaline phosphatase (Alp), and enhanced mineralized nodule formation in DPCs. Conversely, the downregulation of Per2 inhibited the differentiation of DPCs. Additionally, downregulating Per2 further affected intracellular ATP content and ROS levels during DPC differentiation. Conclusion Overall, we demonstrated that PER2 positively regulates the odontogenic differentiation of DPCs, and the mechanism may be related to mitochondrial function as shown by intracellular ATP content and ROS levels

3β-Hydroxysteroid-Δ24 Reductase (DHCR24) Protects Pancreatic β Cells from Endoplasmic Reticulum Stress-Induced Apoptosis by Scavenging Excessive Intracellular Reactive Oxygen Species

There is accumulating evidence showing that apoptosis induced by endoplasmic reticulum (ER) stress plays a key role in pancreatic β cell dysfunction and insulin resistance. 3β-Hydroxysteroid-Δ24 Reductase (DHCR24) is a multifunctional enzyme located in the endoplasmic reticulum (ER), which has been previously shown to protect neuronal cells from ER stress-induced apoptosis. However, the role of DHCR24 in type 2 diabetes is only incompletely understood so far. In the present study, we induced ER stress by tunicamycin (TM) treatment and showed that infection of MIN6 cells with Ad-DHCR24-myc rendered these cells resistant to caspase-3-mediated apoptosis induced by TM, while cells transfected with siRNAs targeting DHCR24 were more sensitive to TM. Western blot analysis showed that TM treatment induced upregulation of Bip protein levels in both cells infected with Ad-LacZ (the control group) and Ad-DHCR24-myc, indicating substantial ER stress. Cells infected with Ad-LacZ exhibited a rapid and strong activation of ATF6 and p38, peaking at 3 h after TM exposure. Conversely, cells infected with Ad-DHCR24-myc showed a higher and more sustained activation of ATF6 and Bip than control cells. DHCR24 overexpression also inhibited the generation of intracellular reactive oxygen species (ROS) induced by ER stress and protected cells from apoptosis caused by treatment with both cholesterol and hydrogen peroxide. In summary, these data demonstrate, for the first time, that DHCR24 protects pancreatic β cells from apoptosis induced by ER stress

Identification and analysis of key hypoxia- and immune-related genes in hypertrophic cardiomyopathy

Abstract Background Hypertrophic cardiomyopathy (HCM), an autosomal dominant genetic disease, is the main cause of sudden death in adolescents and athletes globally. Hypoxia and immune factors have been revealed to be related to the pathology of HCM. There is growing evidence of a role for hypoxia and inflammation as triggers and enhancers in the pathology in HCM. However, the role of hypoxia- and immune-related genes in HCM have not been reported. Methods Firstly, we obtained four HCM-related datasets from the Gene Expression Omnibus (GEO) database for differential expression analysis. Immune cells significantly expressed in normal samples and HCM were then screened by a microenvironmental cell population counter (MCP-counter) algorithm. Next, hypoxia- and immune-related genes were screened by the LASSO + support vector machine recursive feature elimination (SVM-RFE) and weighted gene co-expression network analysis (WGCNA). Single-gene enrichment analysis and expression validation of key genes were then performed. Finally, we constructed a competing endogenous RNA (ceRNA) network of key genes. Results In this study, 35 differentially expressed hypoxia genes were found. By using LASSO + SVM-RFE analysis, 10 more targets with differentially expressed hypoxia genes were identified. The MCP-count algorithm yielded five differentially expressed immune cells, and after assessing them for WGCNA characteristics, 612 immune genes were discovered. When hypoxia and immune genes were combined for cross-tabulation analysis, three hypoxia- and immune-related genes (ATP2A2, DDAH1, and OMA1) were identified. Conclusion Based on hypoxia characteristic genes, three key genes were identified. These were also significantly related to immune activation, which proves a theoretical basis and reference value for studying the relationship between HCM and hypoxia and immunity. Graphical Abstrac

Effects of Transition Metals on the Electrical Conductivity of M‑Doped MnCo₂O₄ (M = Cu, Ni, Zn) as Contact Layer on Precoated SUS441 in Solid Oxide Cells

Spinels have been widely employed as contact layers (CLs) on metallic interconnects for solid oxide cells (SOCs) with the required electrical conductivity and Cr block ability. In this work, MnCo2O4 spinels doped with different transition metals (Cu, Ni, and Zn) were deposited on precoated SUS441 stainless steel as CLs. A positive doping effect of Cu and Ni on increasing the concentration of Mn4+/Mn3+ and Co3+/Co2+ hopping pairs was observed, whereas a negative doping effect of Zn on electrical conductivity was confirmed, which was reflected in the data of X-ray photoelectron spectroscopy (XPS) and X-ray absorption spectra (XAS). The Cu-doped Mn1Co1.7Cu0.3O4 spinel exhibited the best electrical conductivity with a low area specific resistance (ASR) value of 4.5 mΩ·cm2 at 850 °C. A relative degradation test demonstrated that Mn1Co1.7Cu0.3O4 maintained significant performance during a 200 h isothermal process. Cross-sectional observations revealed that the thickness of the Cr oxide scale formed during the degradation test was much reduced by the Mn1Co1.7Cu0.3O4 CL, which was attributed to the improved resistance to Cr oxidation. The present work shed light on the design of highly conductive CLs in SOCs

Selective and Scalable CO₂ Electrolysis Enabled by Conductive Zinc Ion-Implanted Zeolite-Supported Cadmium Oxide Nanoclusters

Catalyst supports play an essential role in catalytic reactions, hinting at pronounced metal–support effects. Zeolites are a propitious support in heterogeneous catalysts, while their use in the electrocatalytic CO2 reduction reaction has been limited as yet because of their electrically insulating nature and serious competing hydrogen evolution reaction (HER). Enlightened by theoretical prediction, herein, we implant zinc ions into the structural skeleton of a zeolite Y to strategically tailor a favorable electrocatalytic platform with remarkably enhanced electronic conduction and strong HER inhibition capability, which incorporates ultrafine cadmium oxide nanoclusters as guest species into the supercages of the tailored 12-ring window framework. The metal d-bandwidth tuning of cadmium by skeletal zinc steers the extent of substrate–molecule orbital mixing, enhancing the stabilization of the key intermediate *COOH while weakening the CO poisoning effect. Furthermore, the strong cadmium–zinc interplay causes a considerable thermodynamic barrier for water dissociation in the conversion of H+ to *H, potently suppressing the competing HER. Therefore, we achieve an industrial-level partial current density of 335 mA cm–2 and remarkable Faradaic efficiency of 97.1% for CO production and stably maintain Faradaic efficiency above 90% at the industrially relevant current density for over 120 h. This work provides a proof of concept of tailored conductive zeolite as a favorable electrocatalytic support for industrial-level CO2 electrolysis and will significantly enhance the adaptability of conductive zeolite-based electrocatalysts in a variety of electrocatalysis and energy conversion applications