Objective To evaluate the effect of 3-dimensional conformal radiotherapy (3D CRT) and prognostic factors for cervical and upper-thoracic esophageal cancer. Methods Between July 1998 and July 2001, 33 patients with cervical and upper-thoracic esophageal cancer were treated with 3D CRT(2?Gy per day, 5 sessions a week to a total dose of 66-68?Gy over 6-7 weeks). Acute toxicities and survival rates were evaluated by Kaplan-Meier method and prognostic factors were analyzed by Cox proportional hazard model. Results The 1-, 2-, 3-year local control rates were 87.9%, 75.8%, 45.5% respectively. The 1-, 2-, 3-year disease-free and overall survival rates were 72.7%, 60.6%, 30.3% and 78.8%, 66.8%, 44.2% respectively. GradeⅠ-Ⅱ acute esophagitis and bronchitis were the most common radiation side effects. Multivariate analysis revealed that the depth of primary tumor invasion, regional lymph node metastasis and tumor length were independent prognostic factors (P

AIM:To investigate the effects of ox-LDL on TLR2 and TLR4 expression and production of TNF-?,IL-10,IL-12,NO and MDA in macrophages and to observe intervention effect of GW1929 in above procedure.METHODS:The mouse peritoneal macrophages were pretreated with ox-LDL(50 mg/L,100 mg/L)and GW1929(20 ?mol/L)respectively for 24 h.The concentrations of MDA,NO-2/NO-3,TNF-?,IL-10 and IL-12 in the culture fluid were detected.Flow cytometry was used to observe TLR2 and TLR4 expressions after the mouse peritoneal macrophages were pretreated with ox-LDL(50 mg/L)and GW1929(20 ?mol/L)respectively for 6 h,12 h,and 24 h.RESULTS:The concentrations of MDA,NO-2/NO-3,TNF-? and IL-10 in ox-LDL(50 mg/L,100 mg/L)group were higher than those in control and GW1929 group obviously,but the concentrations of above index in ox-LDL(50 mg/L,100 mg/L)+GW1929 group were lower than those in ox-LDL(50 mg/L,100 mg/L)group apparently.No IL-12 in every group was detected.Expressions of TLR-2 in ox-LDL+GW1929(6 h,12 h,24 h)group were lower than those in ox-LDL(6 h,12 h,24 h)group respectively.TLR-4 expressions in ox-LDL+GW1929(12 h)were lower than those in ox-LDL(12 h)apparently.CONCLUSION:ox-LDL up-regulates TLR2 and TLR4 expressions and promotes the production of ROX,NO,TNF-? and IL-10 in macrophages.GW1929 is capable of inhibiting the above ox-LDL effects.

This article systematically summarizes the theoretical framework, training content, training methods, and evaluation tools of TeamSTEPPS curriculum, and explores its application status and future research directions in nursing clinical training and college teaching, in order to provide a basis for further promoting this curriculum in nursing clinical training and college teaching in China.

Background: Interferon lambda receptor 1 (IFNLR1) is a type II cytokine receptor that clings to interleukins IL-28A, IL29B, and IL-29 referred to as type III IFNs (IFN-λs). IFN-λs act through the JAK-STAT signaling pathway to exert antiviral effects related to preventing and curing an infection. Although the immune function of IFN-λs in virus invasion has been described, the molecular mechanism of IFNLR1 in that process is unclear. Objectives: The purpose of this study was to elucidate the role of IFNLR1 in the pathogenesis and treatment of porcine reproductive and respiratory syndrome virus (PRRSV). Methods: The effects of IFNLR1 on the proliferation of porcine alveolar macrophages (PAMs) during PRRSV infection were investigated using interference and overexpression methods. Results: In this study, the expressions of the IFNLR1 gene in the liver, large intestine, small intestine, kidney, and lung tissues of Dapulian pigs were significantly higher than those in Landrace pigs. It was determined that porcine IFNLR1 overexpression suppresses PRRSV replication. The qRT-PCR results revealed that overexpression of IFNLR1 upregulated antiviral and IFN-stimulated genes. IFNLR1 overexpression inhibits the proliferation of PAMs and upregulation of p-STAT1. By contrast, knockdown of IFNLR1 expression promotes PAMs proliferation. The G0/G1 phase proportion in IFNLR1-overexpressing cells increased, and the opposite change was observed in IFNLR1-underexpressing cells. After inhibition of the JAK/STAT signaling pathway, the G2/M phase proportion in the IFNLR1-overexpressing cells showed a significant increasing trend. In conclusion, overexpression of IFNLR1 induces activation of the JAK/STAT pathway, thereby inhibiting the proliferation of PAMs infected with PRRSV. Conclusion Expression of the IFNLR1 gene has an important regulatory role in PRRSVinfected PAMs, indicating it has potential as a molecular target in developing a new strategy for the treatment of PRRSV.

Background: Interferon lambda receptor 1 (IFNLR1) is a type II cytokine receptor that clings to interleukins IL-28A, IL29B, and IL-29 referred to as type III IFNs (IFN-λs). IFN-λs act through the JAK-STAT signaling pathway to exert antiviral effects related to preventing and curing an infection. Although the immune function of IFN-λs in virus invasion has been described, the molecular mechanism of IFNLR1 in that process is unclear. Objectives: The purpose of this study was to elucidate the role of IFNLR1 in the pathogenesis and treatment of porcine reproductive and respiratory syndrome virus (PRRSV). Methods: The effects of IFNLR1 on the proliferation of porcine alveolar macrophages (PAMs) during PRRSV infection were investigated using interference and overexpression methods. Results: In this study, the expressions of the IFNLR1 gene in the liver, large intestine, small intestine, kidney, and lung tissues of Dapulian pigs were significantly higher than those in Landrace pigs. It was determined that porcine IFNLR1 overexpression suppresses PRRSV replication. The qRT-PCR results revealed that overexpression of IFNLR1 upregulated antiviral and IFN-stimulated genes. IFNLR1 overexpression inhibits the proliferation of PAMs and upregulation of p-STAT1. By contrast, knockdown of IFNLR1 expression promotes PAMs proliferation. The G0/G1 phase proportion in IFNLR1-overexpressing cells increased, and the opposite change was observed in IFNLR1-underexpressing cells. After inhibition of the JAK/STAT signaling pathway, the G2/M phase proportion in the IFNLR1-overexpressing cells showed a significant increasing trend. In conclusion, overexpression of IFNLR1 induces activation of the JAK/STAT pathway, thereby inhibiting the proliferation of PAMs infected with PRRSV. Conclusion Expression of the IFNLR1 gene has an important regulatory role in PRRSVinfected PAMs, indicating it has potential as a molecular target in developing a new strategy for the treatment of PRRSV.

To investigate the effect of miR-331-3p on the proliferation of porcine renal epithelial cells (PK15) and its mechanism, the pcDNA 3.1(+) overexpression vector of miRNA-331-3p (pcDNA 3.1(+)-miR-331-3p) was constructed. PK15 cells were divided into four groups, including experimental group, experimental control group, inhibitor group and inhibitor control group. Experimental group and experimental control group were transfected with pcDNA 3.1(+)-miR-331-3p and pcDNA 3.1(+), respectively. Inhibitor group and inhibitor control group were transfected with miR-331-3p inhibitor and miR-331-3p negative control (miR-331-3p NC), respectively. Above all, CCK-8 reagent was used to plot the cell proliferation curve and Propidium (PI) staining was used to detect the proportion of cell stages. Secondly, its expression change were detected by quantitative real-time PCR that included the growth inhibitory protein family member 5 (ING5), cyclin-dependent kinase 2 (CDK2), cyclin-dependent kinase 3 (CDK3), cyclin-dependent kinase 4 (CDK4), Cyclin B and cyclin-dependent kinase inhibitor 1A (CDKN1A). The results showed that the expression of miRNA-331-3p was significantly increased in the experimental group. The cell proliferation curve showed that the number of cells in experimental group was significantly higher than that in experimental control group or inhibitor control group at 48 h and 72 h (P<0.05). Simultaneously, Inhibitor group was significantly lower than experimental control group or inhibitor control group in the number of cells at 48 h and 72 h (P<0.05), but there was no significant difference between the experimental group and the control group. Compared with the experimental control group, the proportion of cells of experimental group in G0/G1 phase decreased, the proportion of S phase and G2/M phase increased, and the inhibitor control group showed the opposite trend. Simultaneously, the expression levels of CDK2, CDK3, CDK4 and Cyclin B genes in the experimental group were significantly increased, while ING5 and CDKN1A genes inhibiting proliferation showed a significant downward trend. These results demonstrate that the miR-331-3p overexpression vector was successfully constructed, and miR-331-3p has the ability to promote the proliferation of PK15 cells. The study lays a solid foundation for further research for its role in pig growth and development.
Animals ; Cell Line ; Cell Proliferation ; genetics ; Epithelial Cells ; cytology ; Genetic Vectors ; MicroRNAs ; genetics ; Swine