Objective:To test the validity and reliability of the Chinese Version Scale of Social Skill for Nursing(C-SSSN).Methods:The Japanese version SSSN was translated into Chinese according to Beaton's Translation Model.Totally 547 clinical nurses who met the criterion in a tertiary hospital in Yinchuan were selected for analyzing the items and investigating content validity,structure validity and internal consistency reliability.After 2 weeks,30 nurses were randomly selected for reassessment.Results:The content validity index (S-CVI) of C-SSSN was 0.87,the items content validities (I-CVI) varied from 0.86-1.00.Exploratory factor analysis was employed for extracting the 7 common factors and conformed 6 dimensions.The loads of items in the common factors were 0.43-0.88 correspondingly.The cumulative contribution rate was 60.38％.The Cronbach alpha coefficient of the scale was 0.89,the alpha coefficients of the 6 dimensions arranged 0.76-0.93.The retest reliabilities (r) were 0.83 for the total scale and 0.77-0.83 for the six dimensions.Conclusion:The Chinese Version Scale of Social Skill for Nursing has been proved to be reliable and valid which could be used to evaluate clinical nurses' social skill.

Objective:To investigate the maternal pre-pregnancy body mass index (BMI) and gestational weight gain (GWG) during pregnancy at advanced maternal age for their second child at advanced maternal age, and to explore the relationship with neonatal outcomes.Methods:This study involved 1 965 women of advanced maternal age who delivered the second child in the Northwest Women's and Children's Hospital from July 1 to December 31, 2017. Clinical data of these women and their newborns were collected through the electronic medical record information system. According to pre-pregnancy BMI, all subjects were divided into four groups: underweight group (<18.5 kg/m 2, n=139), normal weight group (18.5-23.9 kg/m 2, n=1 342), overweight group (24.0-27.9 kg/m 2, n=404) and obese group (≥28.0 kg/m 2, n=80). According to the GWG standard recommended by the American Institute of Medicine (IOM) in 2009, they were also divided into three groups: inadequate GWG group ( n=478), normal GWG group ( n=884) and excessive GWG group ( n=603). Mann-Whitey U test, Chi-square test or Fisher's exact test were used as statistical methods. Effects of pre-pregnancy BMI and GWG on gestational age and birth weight of the newborns were analyzed by binary and multi-class logistic regression models. Results:The median pre-pregnancy BMI of the 1 965 women was 22.1 (20.3-23.9) kg/m 2 and patients with abnormal pre-pregnancy BMI accounted for 31.7% (623/1 965). Their median GWG was 13.0 (10.0-16.0) kg and 55.0% (1 081/1 965) of them were abnormal. Compared with normal pre-pregnant weight women, overweight and obesity subjects were associated with increased risks of preterm birth ( OR=2.100, 95% CI: 1.398-3.156), low birth weight infants (LBWI) ( OR=3.187, 95% CI: 1.892-5.367) and macrosomia ( OR=1.758, 95% CI: 1.182-2.614); pre-pregnancy underweight reduced the incidence of large for gestational age (LGA) infants ( OR=0.476, 95% CI: 0.236-0.960). Compared with the normal GWG group, the inadequate GWG group had increased risks of preterm birth ( OR=2.316, 95% CI: 1.530-3.505) and LBWI ( OR=1.850, 95% CI: 1.103-3.104), while the excessive GWG group showed increased risks of macrosomia ( OR=1.828, 95% CI: 1.225-2.726) and LGA infants ( OR=1.955, 95% CI: 1.448-2.640), but a reduced risk of LBWI ( OR=0.359, 95% CI: 0.193-0.667) and small for gestational age infants ( OR=0.452, 95% CI: 0.240-0.852). Conclusions:Both abnormal pre-pregnancy BMI (underweight, overweight and obese) and GWG (inadequate and excessive) have adverse effects on neonatal outcomes in women of advanced age in pregnancy for their second baby. Weight management should be addressed during the whole pregnancy, including both adjusting the pre-pregnancy BMI to normal range and maintaining reasonable GWG, so as to reduce potential adverse outcomes in newborns.

Objective To investigate the mechanism of rapamycin inhibiting the differentiation and proliferation of newborn porcine pancreatic adult stem cells, and to explore the therapeutic methods that may effectively reduce the side effects of rapamycin. Method Porcine NPCCs were treated with rapamycin alone or in combination with IGF-Ⅱ, and the caspase-3 and [ 3 H ]-thymidine uptake assays were performed to detect apoptosis and proliferation. The expression of insulin, PDX-1, NeuroD/Beta2, and Foxo1, a downstream transcription factor of IGF-Ⅱ, were analyzed by RT-PCR and Western blot to evaluate the differentiation ability of pancreatic adult stem cells. Results The NPCCs treated with rapamycin inhibited the proliferation ofβ-cells, increased apoptosis, reduced insulin secretion, inhibited the expression of PDX-1 and NeuroD/Beta2, and decreased the expression of IGF-Ⅱ. Foxo1 expression and induction of Foxo1 from the cytoplasm to the nucleus of the ectopic. The combined treatment of rapamycin and IGF-Ⅱcan reduce the side effects of rapamycin, inhibit the decrease ofβ-cell number and insulin content, repair the expression of insulin, PDX-1, NeuroD/Beta2, inhibit Foxo1 expression and intracellular ectopic. Conclusion Aberrant expression of IGF-Ⅱ and Foxol genes is the key inducing factor of rapamycin inhibiting the proliferation and differentiation of NPCCs, and IGF-Ⅱtreatment can effectively reduce the side effects of rapamycin on NPCCs differentiation.

Idiopathic pulmonary fibrosis (IPF) is a progressive disease with unknown etiology and limited therapeutic options. Activation of fibroblasts is a prominent feature of pulmonary fibrosis. Here we report that lncRNA DACH1 (dachshund homolog 1) is downregulated in the lungs of IPF patients and in an experimental mouse model of lung fibrosis. LncDACH1 knockout mice develop spontaneous pulmonary fibrosis, whereas overexpression of LncDACH1 attenuated TGF-β1-induced aberrant activation, collagen deposition and differentiation of mouse lung fibroblasts. Similarly, forced expression of LncDACH1 not only prevented bleomycin (BLM)-induced lung fibrosis, but also reversed established lung fibrosis in a BLM model. Mechanistically, LncDACH1 binding to the serine/arginine-rich splicing factor 1 (SRSF1) protein decreases its activity and inhibits the accumulation of Ctnnb1. Enhanced expression of SRSF1 blocked the anti-fibrotic effect of LncDACH1 in lung fibroblasts. Furthermore, loss of LncDACH1 promoted proliferation, differentiation, and extracellular matrix (ECM) deposition in mouse lung fibroblasts, whereas such effects were abolished by silencing of Ctnnb1. In addition, a conserved fragment of LncDACH1 alleviated hyperproliferation, ECM deposition and differentiation of MRC-5 cells driven by TGF-β1. Collectively, LncDACH1 inhibits lung fibrosis by interacting with SRSF1 to suppress CTNNB1 accumulation, suggesting that LncDACH1 might be a potential therapeutic target for pulmonary fibrosis.