Validity and reliability of the Chinese version of object attachment questionnaire in college students / 中华行为医学与脑科学杂志

Objective:To offer a revised Chinese version of the object attachment questionnaire(OAQ), and to examine its reliability and validity in Chinese college students.Methods:Totally 1 350 college students were tested with the Chinese version of OAQ, Chinese version of the saving inventory-revised scale(SI-R), experiences in close relationships inventory(ECR) and emotion attachment questionnaire(EAQ). A total of 100 college students from the sample were followed to complete the Chinese version of OAQ after 4 weeks.Item analysis, correlation analysis, exploratory factor analysis and reliability test were conducted by SPSS 24.0 software, while confirmatory factor nalaysis and convergent validity were conducted by AMOS 21.0.Results:The exploratory factor analysis showed that Chinese version of OAQ included two factors and twelve items.Confirmatory factor analysis showed that the two-factor model fitted well( χ2/ df=3.76, GFI=0.93, CFI=0.90, TLI=0.87, IFI=0.90, RMSEA=0.08). The OAQ positively correlated with SI-R, ECR and EAQ ( r=0.22, 0.34, 0.63, all P<0.01, CR=0.74-0.85, P<0.01.AVE=0.29-0.39, P<0.01). The OAQ had good internal reliability with Cronbach’s α coefficients from 0.78 to 0.83, retest reliability coefficients from 0.87 to 0.97 and split-half reliability coefficients from 0.60 to 0.76(all P<0.01). Conclusion:The Chinese version of OAQ has acceptable reliability and validity.

Efficient derivation of extended pluripotent stem cells from NOD-scid Il2rg mice

Recently we have established a new culture condition enabling the derivation of extended pluripotent stem (EPS) cells, which, compared to conventional pluripotent stem cells, possess superior developmental potential and germline competence. However, it remains unclear whether this condition permits derivation of EPS cells from mouse strains that are refractory or non-permissive to pluripotent cell establishment. Here, we show that EPS cells can be robustly generated from non-permissive NOD-scid Il2rg mice through de novo derivation from blastocysts. Furthermore, these cells can also be efficiently generated by chemical reprogramming from embryonic NOD-scid Il2rg fibroblasts. NOD-scid Il2rg EPS cells can be expanded for more than 20 passages with genomic stability and can be genetically modified through gene targeting. Notably, these cells contribute to both embryonic and extraembryonic lineages in vivo. More importantly, they can produce chimeras and integrate into the E13.5 genital ridge. Our study demonstrates the feasibility of generating EPS cells from refractory mouse strains, which could potentially be a general strategy for deriving mouse pluripotent cells. The generation of NOD-scid Il2rg EPS cell lines permits sophisticated genetic modification in NOD-scid Il2rg mice, which may greatly advance the optimization of humanized mouse models for biomedical applications.

Rapid generation of gene-targeted EPS-derived mouse models through tetraploid complementation

One major strategy to generate genetically modified mouse models is gene targeting in mouse embryonic stem (ES) cells, which is used to produce gene-targeted mice for wide applications in biomedicine. However, a major bottleneck in this approach is that the robustness of germline transmission of gene-targeted ES cells can be significantly reduced by their genetic and epigenetic instability after long-term culturing, which impairs the efficiency and robustness of mouse model generation. Recently, we have established a new type of pluripotent cells termed extended pluripotent stem (EPS) cells, which have superior developmental potency and robust germline competence compared to conventional mouse ES cells. In this study, we demonstrate that mouse EPS cells well maintain developmental potency and genetic stability after long-term passage. Based on gene targeting in mouse EPS cells, we established a new approach to directly and rapidly generate gene-targeted mouse models through tetraploid complementation, which could be accomplished in approximately 2 months. Importantly, using this approach, we successfully constructed mouse models in which the human interleukin 3 (IL3) or interleukin 6 (IL6) gene was knocked into its corresponding locus in the mouse genome. Our study demonstrates the feasibility of using mouse EPS cells to rapidly generate mouse models by gene targeting, which have great application potential in biomedical research.

Correction to: Efficient derivation of extended pluripotent stem cells from NOD-scid Il2rg mice

In the original publication Fig. 1D and supplementary material is incorrect. The correct figure and supplementary material is provided in this correction.

Sulforaphane ameliorates oxidative stress induced vascular calcification by regulating Nrf-2 and Sirt-1 / 中华肾脏病杂志

Objective To investigate the role and mechanism of sulforaphane (SFN) in vascular calcification induced by oxidative stress.Methods The uremic vascular calcification model was established by treating rat vascular smooth muscle cells (RASMCs) with β-glycerophosphate.RASMCs were divided into 6 groups:normal control (NC) group,1 μmol/L SFN group,5 μmol/L SFN group,calcification group,1 μmol/L SFN+calcification group,5 μmol/L SFN+calcification group,and were all cultured for 72 h.Cell viability was measured by MTT.RASMCs calcification was visualized by Von Kossa staining.Calcium content was quantified by the microplate test,and mRNA level of FGF-23 was tested by real-time PCR.The expressions of OPN,Runx-2,Nrf-2 and Sirt-1 were evaluated by Western blotting.Confocal microscope was employed to observe mitochondria damage in RASMCs and the production of ROS in RASMCs was measured by reactive oxygen species assay.Results (1) SFN did not affect cell viability of the NC group,but both low dosage and high dosage increased the cell viability of calcification group (all P ＜ 0.05).(2) Compared with calcification group,SNF treatment decreased the calcium concentration,intracellular calcium deposition and the mRNA level of FGF-23 (all P ＜ 0.05).(3) Compared with calcification group,SNF treatment decreased the fluorensence intensity,mitochondria injury and the protein expressions of OPN and Runx-2,but increased the protein expressions of Nrf-2,Sirt-1 and cleaved caspase-3 (all P ＜ 0.05).Conclusion SNF can effectively protect RASMCs against vascular calcification induced by oxidative stress,since it prevents the ROS production and mitochondria dysfunction through Nrf-2 and Sirt-1.