Objective:to construct and test the structural equation model of influencing factors of clinical nursing teaching quality, and analyze the influencing factors and strength of clinical nursing teaching quality.Methods:Based on the literature, 20 indexes influencing the quality of clinical nursing teaching were selected. In July 2019, clinical nursing teachers of a third class a medical institution were selected for convenient sampling survey. Through factor analysis, 20 indexes were classified into 6 dimensions, namely, teaching environment, teaching attitude, teacher quality, teacher behavior, teaching management and teaching quality.Results:The structural equation model of influencing factors of clinical nursing teaching quality was constructed. The fitting index of the model reached the standard value, and the model had a good fit.Conclusion:With the help of this model, the nursing administrators can find out the factors and intensity that affect the quality of clinical nursing teaching, which is helpful to put forward the improvement strategies of improving the quality of clinical nursing teaching, to improve the effect of clinical nursing teaching, to improve the quality of clinical nursing teaching, and to provide reference for the research of similar clinical nursing teaching quality.

The evolution of hepatocellular carcinoma (HCC) is a compound process which involves many kinds of genes and transductional pathways. The expression of the peptidyl-proplyl-isomerase PIN1 gene, the mutation in exon 3 of beta-catenin and its correspondent abnormal expression and their roles in the hepatocellular carcinogeneisis were investigated. Among 29 pair cases of HCC and non-carcinoma tissues, the expression of PIN1 gene was detected by immunochemical staining. Mutations in exon 3 of beta-catenin gene and differential expression of beta-catenin gene were investigated by the methods of PCR-SSCP, direct sequencing and immunohistochemical technique as well. The results indicated: (1) 44.8% (13/29) cases of HCC presented higher level of PIN1 gene expression than non-cancerous tissues (chi2=32.63, P<0.05), especially in cytoplasm and nucleus, while there was lower level of PIN1 expression in non-cancerous tissues; (2) 58.6% (17/29) HCC tissues showed beta-catenin protein accumulation in cytoplasm and nucleus. 46.2% (6/13) HCC tissues indicated beta-catenin protein accumulation with higher level of PIN1 expression, while 53.8% (7/13) HCC tissues indicated beta-catenin protein accumulation with lower level or trace of PIN1 expression (chi2=0.00, P>0.05); (3) 24.1% (7/29) of primary tumor lesions carried gene mutations in exon 3 of beta-catenin, and accompanied by beta-catenin protein accumulation. There was no mutation in non-cancerous tissues. All the mutation presented in tissues with low level of PIN1 expression. There was no mutation of beta-catenin gene in tissues with high PIN1 expression level (chi2=58.12, P<0.05). So it was postulated that the increase of PIN1 gene expression could promote hepatocellular carcinogenesis via a way different from beta-catenin gene mutation.

In order to construct an expression vector carrying small hairpin (sh) RNA (shRNA) for toll-like receptor 4 mRNA and a reporter gene of enhanced green fluorescence protein (EGFP) and study the inhibition of cytokine release by RAW264.7 cell induced by lipopolysaccharide (LPS) stimulation through transfection and expression of shRNA targeting TLR4 gene via the RNAi mechanism, the reporter gene plasmid pEGFP-C1 (4.7 kb) and psiRNA-hHlneo (2979 bp) were used. The H1 promotor and double Bbs I restrict endoenzyme site were cloned from plasmid psiRNA-hH1neo and reconstructed them into plasmid pEGFP-C1 in the Mlu I restrict endoenzymic site, forming plasmid pEGFP-H1/siRNA, which contained Bbs site and reporter EGFP gene. Then an oligonuclear hairpin sequence targeting TLR4 gene was designed by internet tool and inserted into the plasmid pEGFP-H1/siRNA forming plasmid pEGFP-H1/TLR4-siRNA. After transfection of pEGFP-H1/TLR4-siRNA into RAW264.7 cells, tumor necrosis factor-alpha (TNF-alpha) release by the cells after stimulation by LPS was detected. The results showed that the constructed pEGFP-H1/TLR4-siRNA carrying hairpin RNA for TLR4 gene and reporter EGFP gene were proven to be right by restriction endonuclease analysis. The expression of EGFP gene was (50.37+/-8.23) % and after transfection of the plasmid pEGFP-H1/ TLR4-siRNA the level of TNF-alpha released by RAW264.7 cell was down regulated. It was concluded that shRNA targeting TLR4 gene could inhibit the TNF-alpha release by RAW264.7 cells evoked by LPS.

Objective To explore the preventive effect of early umbilical cord mesenchymal stem cells (UC-MSCs) transplantation on MRL/lpr mice and the underly mechanisms.Methods Fourteen 10-week-old MRL/lpr mice were labeled and numbered.They were randomly divided into 2 groups by using random number table and injected with 1 ×106 UC-MSCs or PBS via tail vein respectively.Proteinuria was measured with Bradford method every 4 weeks.All mice were sacrificed at the age of 28 weeks, with the level of serum antidsDNA antibody and IL-17 detected by enzyme linked immunosorbent assay (ELISA).Splenic Th17 cells, as well as regulatory T cells (Treg) were examined by flow cytometry.Data were analyzed with t test and Pearson's correlation test.Results The onset of proteinuria was delayed for 4 weeks in UC-MSC-treated group compared with that in the control group.At the age of 28 weeks, the 24 hour proteinuria [(1.78±0.17) mg vs (4.77±0.98)mg, t=2.99, P＜0.05] and the spleen weight [(0.149±0.009) g vs (0.273±0.052) g, t=2.33, P＜0.05] in UC-MSCtreated group were significantly lower than those in the control group.There was also a trend of the decline of serum anti-dsDNA antibody and IL-17 level after UC-MSCs transplantation.Compared with those in the control group, both the percentage and the absolute number of Th17 cells were significantly decreased in UC-MSC-treated group [(0.90±0.19)％ vs (2.81±0.50)％, t=3.54, P＜0.01 and (3.7±0.8)×105 vs (19.3±3.7)×105, t=4.12,P＜0.01].Meanwhile, the percentage of Treg elevated after UC-MSCs treatment.The ratio of Th17/Treg was significantly lower in UC-MSC-treated group than that in the control group (0.11±0.03 vs 0.50±0.09, t=4.23,P＜0.01).Both the ratio of Th17/Treg (r=0.73, P＜0.01;r=0.59, P＜0.05) and serum IL-17 level (r=0.78, P＜0.01;r=0.56, P＜0.05) was positively correlated with the level of 24 hour proteinuria and anti-dsDNA antibody respectively in MRL/lpr mice.Conclusion Early UC-MSCs transplantation helps to delay disease onset and ameliorate disease progression in MRL/lpr mice, which may act through the modulation of Th17/Treg balance.

Objective Whether the bone marrow cells (BMC) derived from systemic lupus erythematosus (SLE) could transmit autoimmune disease was studied for the purpose of clarifying the role of BMC in SLE pathogenesis.The effects of bone marrow mesenchymal stem cells (MSC) from SLE and control mice on the SLE BMC-induced symptoms were compared to elucidate the role of MSC in SLE.Methods Six-week-old B6.MRL-Fas mice were randomly divided into 3 groups.One group was transplanted with BMC from the 30-week-old B6.MRL-Faslg mice.One group was co-transplanted with BMC from the 30-week-old B6.MRL-Fasr mice and bone marrow MSC from the age-matched B6.MRL-Faslpr mice.One group was co-transplanted with BMC from the 30-week-old B6.MRL-Faslg mice and bone marrow MSC from the age-matched C57BL/6 mice.Before transplantation,the recipient mice received irradiation by an X-ray source.The levels of serum antinuclear antibody (ANA) and proteinuria were measured with enzyme linked immunosorbent assay (ELISA) and Bradford method every 4 weeks,respectively.The survival rate was recorded.All mice were sacrificed 18 weeks later.Splenic plasma cells,Th1,Th2 and Th17 cells were measured by flow cytometry.Statistical analyses were performed using the independent t test and ANOVA.Results Eight weeks after transplantation,ANA was positive in all the recipient mice.However,there was no significant difference between the three groups (P＞0.05).No proteinuria was observed in all the recipient mice.The mice received BMC from the 30-week-old B6.MRL-Fasr mice and bone marrow MSC from the age-matched B6.MRL-Fasr mice showed an elevated trend of the percentages of splenic plasma cells,Th1,Th2 and Th17 cells compared with the other two groups,plasma cells [(1.05±0.16)％,(0.58±0.11)％,t=2.53,P＞0.05;(1.05±0.16)％,(0.71±0.18)％,t=1.45,P＞0.05],Th1 cells [(6.6±2.2)％,(5.7±1.0)％,t=0.38,P＞0.05;(6.6±2.2)％,(4.0±1.7)％,t=0.96,P＞0.05],Th2 cells [(3.3±0.4)％,(2.1±0.6)％,t=1.76,P＞0.05;(3.3±0.4)％,(2.2±0.6)％,t=1.51,P＞0.05],Th17 cells [(2.30±0.71)％,(1.31±0.31)％,t=1.27,P＞0.05;(2.30±0.71)％,(1.12±0.27)％,t=1.67,P＞0.05].However,there was no significant difference between the groups.The survival rate of the three groups was 43％,43％ and 80％ respectively.And the survival rate of the mice received BMC from the 30-week-old B6.MRL-Fasr mice and bone marrow MSC from the age-matched C57BL/6 mice was significantly higher than those of the other groups.Conclusion Our results indicate that BMC from SLE can transmit autoimmune disease.The bone marrow MSC can not prevent lupus-like presentations induced by BMC from SLE.Transplantation of bone marrow MSC from C57BL/6 mice can significantly elevate the survival rate.

Objective The purpose of this study is to observe the changes of immune cell subsets in lupus mice after umbilical cord mesenchymal stem cells (UC-MSCs) transplantation. Methods B6.MRL-Faslpr lupus mice were randomly divided into the following three groups: the UC-MSCs treated group, the fibroblast like synoviocytes (FLS) treated group and the untreated group. MSC (1×106) or FLS (1×106) were injected into the tail vein of lupus mice respectively. Four weeks after treatment, the spleen index was calculated. The pathological changes of kidney were assessed by HE staining. The frequencies of immune cell subsets in spleen and macrophage in kidney as well as abdominal cavity were analyzed by flow cytometry. Data were analyzed with t test. Results The spleen index of UC-MSCs treated lupus mice [(79 ±9) mg/10 g] and IgG level [(7.5±1.5) mg/ml] were significantly decreased when compared with FLS treated group [(147±23) mg/10 g, t=2.78, P<0.01] [(17.0 ±2.8) mg/ml, t=3.00, P<0.01] and the untreated group [(156 ±16) mg/10 g, t=4.29, P<0.01] [(16.7 ±1.6) mg/ml,t=4.01, P<0.01]. HE staining also showed that the pathological changes of kidney were alleviated after MSCs transplantation. In addition, the frequency of plasma cells in the untreated group [(2.61 2± 0.318)% vs (0.306±0.017)%, t=7.22, P<0.01] and the FLS treated group [(2.412±0.297)% vs (0.306±0.017)%, t=7.07, P<0.01] were markedly higher than MSCs treatment [(0.306 ±0.017)%]. Moreover, the frequency of CD25+Foxp3+/CD4+Treg in the MSCs treated group [(15.08±0.81)%] was significantly increased compared with the untreated group [(8.02 ±0.47)%, t=7.45, P<0.01] and FLS treated group [(8.80 ±0.23)%, t=7.39, P<0.01]. MSCs treatment resulted in a decrease in CXCR5+PD1+/CD4+Tfh and IFNγ+/CD4+Th1 subset, compared with the untreated group [(14.3±1.5)%vs (31.5±3.3)%, t=5.25, P<0.01] [(1.78±0.27)% vs (5.93±1.56)%, t=2.60, P<0.05] and the FLS treated group [(14.3±1.5)%vs (28.8±2.2)%, t=5.49, P<0.01] [(1.78±0.27)%vs (4.88±0.81)%, t=3.61, P<0.01]. The frequency of macrophage in kidney of the MSCs treated group [(3.52 ±0.37)%] was markedly increased compared with the untreated group[(1.58±0.29)%, t=3.25, P<0.01], while neither the IL4+/CD4+Th2 subset nor the IL17+/CD4+Th17subset and the frequency of macrophage in abdominal cavity showed significant changes in the three groups. Conclusion These findings suggest that the therapeutic effects of MSCs on lupus mice may mediate through increasing the frequency of spleen Treg and renal macrophage and decreasing the frequency of Tfh, Th1 and plasma cells.

Objective:To explore the application effect of medical science competition in nursing interns whocontribute to "healthy China" , and to improve their health education awareness, ability, method and self-confidence.Methods:A total of 205 nursing interns who worked in Union Hospital of Tongji Medical College of Huazhong University of Science and Technology from 2019 to 2020 were selected as the research objects. They were divided into the control group (105 cases) and the experimental group (100 cases) according to whether they participated in the medical science competition. The control group learned the form and method of health education in clinical rotation according to the traditional practice teaching plan. The experimental group volunteered to participate in the medical science competition, which required the dissemination of health knowledge through various forms. Before and after the competition, the health education ability assessment scale was used for comparison.Results:Before the medical science competition, there was no significant difference in the total score of assessment, planning, implementation, evaluation and health education between the control group and the experimental group ( t values were 0.765 - 1.749, all P>0.05). After the medical science competition, the total scores of assessment, planning, implementation, evaluation and health education ability of nursing interns in the experimental group were (24.38 ± 4.72), (17.98 ± 3.98), (25.16 ± 5.36), (12.57 ± 2.96) and (80.09 ± 15.65) respectively, while those in the control group were (22.45 ± 6.29), (16.61 ± 4.77), (23.04 ± 6.55), (11.31 ± 3.46) and (73.41 ± 19.69).The differences between the two groups were statistically significant ( t values were 2.226 - 2.795, all P<0.05). Conclusions:The medical science competition can improve the health education ability of assessment, planning, implementation, evaluation of nursing interns and contribute to "healthy China" .

The evolution of hepatocellular carcinoma (HCC) is a compound process which involves many kinds of genes and transductional pathways. The expression of the peptidyl-proplyl- isomerase PIN1 gene, the mutation in exon 3 of β-catenin and its correspondent abnormal expression and their roles in the hepatocellular carcinogeneisis were investigated. Among 29 pair cases of HCC and non-carcinoma tissues, the expression of PIN1 gene was detected by immunochemical staining. Mutations in exon 3 of β-catenin gene and differential expression of β-catenin gene were investigated by the methods of PCR-SSCP, direct sequencing and immunohistochemical technique as well. The results indicated: (1) 44.8% (13/29) cases of HCC presented higher level of PIN1 gene expression than non-cancerous tissues (x2 =32.63, P＜0.05), especially in cytoplasm and nucleus, while there was lower level of PIN1 expression in non-cancerous tissues; (2) 58.6% (17/29) HCC tissues showed β-catenin protein accumulation in cytoplasm and nucleus. 46.2% (6/13) HCC tissues indicated β-catenin protein accumulation with higher level of PIN1 expression, while 53.8% (7/13) HCC tissues indicated β-catenin protein accumulation with lower level or trace of PIN1 expression (x2 =0.00, P＞0.05); (3) 24.1% (7/29) of primary tumor lesions carried gene mutations in exon 3 of β-catenin, and accompanied by β-catenin protein accumulation. There was no mutation in non-cancerous tissues. All the mutation presented in tissues with low level of PIN1 expression. There was no mutation of β-catenin gene in tissues with high PIN1 expression level (x2=58.12, P＜0.05). So it was postulated that the increase of PIN1 gene expression could promote hepatocellular carcinogenesis via a way different from β- catenin gene mutation.

The corpus callosum is the largest white matter structure in encephalic structure , which mainly provides communication between the hemispheres .Clinical manifestations of its infarction are complex and diverse ,including symptoms such as corpus callosum disconnection syndrome and speech disorders .Due to the lack of exact localization signs ,clinical imaging techniques are often used to improve diagnosis rate .Therefore ,the present article reviews clinical and imaging features of patients with corpus callosum infarction in order to improve the understanding and diagnosis of corpus callosum infarction .

In order to construct an expression vector carrying small hairpin (sh) RNA (shRNA) for toll-like receptor 4 mRNA and a reporter gene of enhanced green fluorescence protein (EGFP) and study the inhibition of cytokine release by RAW264.7 cell induced by lipopolysaccharide (LPS)stimulation through transfection and expression of shRNA targeting TLR4 gene via the RNAi mechanism, the reporter gene plasmid pEGFP-C1 (4.7 kb) and psiRNA-hHlneo (2979 bp) were used. The H1 promotor and double Bbs Ⅰ restrict endoenzyme site were cloned from plasmid psiRNA-hHlneo and reconstructed them into plasmid pEGFP-C1 in the Mlu Ⅰ restrict endoenzymic site, forming plasmid pEGFP-H1/siRNA, which contained Bbs site and reporter EGFP gene. Then an oligonuclear hairpin sequence targeting TLR4 gene was designed by internet tool and inserted into the plasmid pEGFP-H 1/siRNA forming plasmid pEGFP-H 1/TLR4-siRNA. After transfection of pEGFP-H1/TLR4-siRNA into RAW264.7 cells, tumor necrosis factor-alpha (TNF-α) release by the cells after stimulation by LPS was detected. The results showed that the constructed pEGFP-H1/TLR4-siRNA carrying hairpin RNA for TLR4 gene and reporter EGFP gene were proven to be right by restriction endonuclease analysis. The expression of EGFP gene was (50.37±8.23) %and after transfection of the plasmid pEGFP-H1/ TLR4-siRNA the level of TNF-α released by RAW264.7 cell was down regulated. It was concluded that shRNA targeting TLR4 gene could inhibit the TNF-α release by RAW264.7 cells evoked by LPS.