Adolescent ; Child ; Child, Preschool ; Echocardiography, Three-Dimensional ; Female ; Heart Septal Defects, Atrial ; diagnostic imaging ; therapy ; Humans ; Male

Objective To screen the genes related with signal transducers and activators of transcription 3 (STAT3) regulating pancreatic cancer invasion and metastasis by gene chips.Methods Human pancreatic cancer cell line SW1990 stably expressing low level of Stat3 was established by lentivirus transfection,while cells transfected with mock plasmid and cells without transfection served as control groups.The differences of invasion and metastasis related genes expression among the three groups were screened by gene chips.STAT3 mRNA and protein expression was measured by real-time PCR and Western blot.Three differentially expressed genes (MMP-7,IL-1β and IgTα7) were verified.ResultsThe expression level of STAT3 mRNA was 0.391 ± 0.037 after pancreatic cancer SW1990 cell trarsfected with STAT3 targeted lentivirus,which was significantly lower than those in mock plasmid group (1.002 ± 0.015) and nontransfected group ( 1.206 ± 0.042,P ＜ 0.05 ) ; the expression level of STAT3 protein was 182.38 ± 65.32,which was significantly lower than those in mock plasmid group (223.40 ±58.40) and non-transfected group (212.33 ±53.69).Eight invasion and metastasis related genes of SW1990 lowly expressing Stat3 were upregulated,while 3 genes were down-regulated.By verification,the mRNA level of MMP-7 and IL-1β were lower than in control group transfected with mook plassmid(0.287 ± 0.115 vs 1.010 ± 0.124,t =19.45,P =0.000;0.490 ± 0.10 vs 1.002 ± 0.002,t =13.83,P =0.000),but the mRNA level of IgTα7 was not decreased (1.173 ±0.280 vs 0.998 ±0.003,t =4.236,P =0.094).Meanwhile,the protein level of MMP-7 was significantly down-regulated when Stat3 was knocked down.ConclusionsStat3 causes changes of expressions of many invasion and metastasis-related genes of SW1990,and MMP-7 may be the main target gene regulated by Stat3.

OBJECTIVETo explore treatment effect of the locking plate percutaneous external fixation to tibial fractures.

METHODSFrom July 2010 to February 2013, 8 cases with pediatric tibial fractures were treated by using unilateral locking plate percutaneous external fixation,including 6 males and 2 females with an average age of 7 years old ranging from 4 to 10. Among them, 5 cases were open fractures involving 1 case of Gustilo-Anderson type II, 3 cases of type III A, 1 case of type III B; and the other 3 cases were closed fractures involving 2 cases of AO type A3, 1 cases of type B2. The postoperative bone healing and gait impact were observed and the function was evaluated by Johner-Wruhs scores.

RESULTSAll fractures healed successfully without infection. The fracture healing time was from 3 to 6 months with an average of 3.9 months. The locking plate removal time was from 4 to 7 months with an average of 4.3 months. Among them, 7 cases were visually normal after walking with stand, 1 case of anterior tibial tendon defect affected gait. The results of Johner-Wruhs assessment were excellent in 7 cases, good in 1 case. No rub contralateral medial calf skin wounds occurenced.

CONCLUSIONThe method is simple, stable and reliable. The fixation strength is suitable for children using locking plate percutaneous external fixation. The postoperative functional recovery was excellent and the walking gait was less affected. But the point of LCP pedicle screw should be carefully selected before installation with good skin coverage.

Bone Plates ; Child ; Child, Preschool ; External Fixators ; Female ; Fracture Fixation ; methods ; Fracture Healing ; Humans ; Male ; Tibial Fractures ; physiopathology ; surgery

Abstract: Objective　To explore the early diagnostic value of peripheral blood peroxisome proliferator-activated receptor γ (PPARγ) combined with γ-interferon (IFN-γ) release assay (IGRA) in the diagnosis of pulmonary tuberculosis in patients with end-stage renal disease (ESRD), and to provide reference for clinical diagnosis and treatment. Methods　From January 2019 to December 2021, 70 ESRD patients with suspicious symptoms of pulmonary tuberculosis were treated at Hebei Chest Hospital were selected as the research objects. According to the examination results, they were divided into ESRD group (40 cases) and ESRD complicated by pulmonary tuberculosis (40 cases, comorbidity group). In addition, 40 cases with pulmonary tuberculosis were used as the PTB group. All three groups of patients underwent IGRA test, and the peripheral blood PPARγ level was detected by enzyme-linked immunosorbent assay, and the diagnostic value of PPARγ combined with IGRA test for ESRD patients with pulmonary tuberculosis was explored. Results The expression level of PPARγ and IFN-γ content in the PTB group and the comorbidity group were obviously higher than those in the ESRD group (P<0.05), while the differences in PPARγ expression level and IFN-γ content between the PTB and comorbidity groups were not statistically significant (P>0.05). The ROC curve showed that the areas under the curve (AUC) of PPARγ and IGRA in the diagnosis of end-stage renal disease combined with tuberculosis were 0.823 (95%CI: 0.722-0.925) and 0.773 (95%CI: 0.662-0.883), respectively, and the AUC of combined detection was 0.928 (95%CI: 0.871-0.984), which was better than that of PPARγ and IGRA alone (Z/P=2.057/0.039, 2.843/0.005). The Kappa values of serum PPARγ and IGRA test compared with the clinical gold standard results in the diagnosis of ESRD complicated with pulmonary tuberculosis were 0.557 and 0.444 (P<0.05). The combined screening of ESRD with pulmonary tuberculosis was consistent with the clinical gold standard (Kappa=0.661, P<0.05). Among the 30 ESRD patients complicated with pulmonary tuberculosis, the sensitivity of PPARγ combined with IGRA test in diagnosis of ESRD complicated with pulmonary tuberculosis was 93.33% (28/30), which was higher than 70.00% (21/30) of PPARγ and 66.67% (20/30) of IGRA test alone (P<0.05). Conclusions Peripheral blood PPARγ and IGRA tests have certain diagnostic value for ESRD complicated with tuberculosis, and the combined detection of the two can improve the sensitivity and reduce the rate of missed diagnosis, which is worthy of clinical promotion.

Objective To investigate the correlation between the expression of STAT3 and MMP-2 in human pancreatic cancer,and to probe the mechanism by which STAT3 signal pathway regulates the expression of MMP-2 in pancreatic cancer cells.Methods Immunohistochemistry was used to detect the expression of STAT3,phosphorylated STAT3(p-STAT3)and MMP-2 in pancreatic cancer tissues of 34 cases and normal pancreatic tissues of 10 cases.Correlation between the expression of STAT3、p-STAT3 and MMP- 2 were statistically analyzed.Human pancreatic cancer cell lines SW1990 was cultured.AG490,an inhibitor of the upstream Janus kinase(JAK)of STAT3 was added into the culture medium.Electrophoretic mobility shift assay(EMSA)was used to detect STAT3 DNA-binding activity in SW1990 cells.Western blot was used to detect the expression of STAT3,p-STAT3 in SW1990 cells.In addition,the protein and mRNA expression of MMP-2 in SW1990 cells were determined by Western blot and RT-PCR,respectively. Results Immunohistochemistry revealed that the expression rate of STAT3,p-STAT3 were both higher in pancreatic cancer tissues than in normal pancreas tissues(P

Objective: In order to investigate the effects of activating and blocking Stat3 signaling pathway on invasion ability of human pancreatic cancer cells and explore its action mechanism.Methods:Human pancreatic cancer Capan-2 cells were treated with IL-6. SW1990 human pancreatic cancer cells were treated with AG490. Cell proliferation was measured by MTT assay. Western blotting and immunocytochemistry were performed to detect expression of phosphorylated Stat3 (p-Stat3) protein. Real-time fluorogentic quantitative PCR (RFQ-PCR) and Western blotting were used to detect the mRNA and protein expression of VEGF and MMP-2 mRNA, respectively. The invasion abilities of SW1990 and Capan-2 cells were determined by cell invasion assay in vitro. Results:IL-6 stimulated the proliferation of Capan-2 cells (P<0.05), elevated the expression of p-Stat3, increased the mRNA and protein expressions of vascular endothelial growth factor (VEGF) and matrix metalloproteinase 2 (MMP-2) (P<0.05), and enhanced the invasion ability of Capan-2 cells. AG490 inhibited the proliferation of SW1990 cells (P<0.05), down-regulated the expression of p-Stat3, markedly decreased the mRNA and protein expression of VEGF and MMP-2 (P<0.05), and weakened the invasion ability of SW1990 cells. Conclusion:Stat 3 signaling pathway plays an important role in the invasion and metastasis of pancreatic cancer. Stat 3 signaling transduction pathway may provide a novel therapeutic target for the treatment of pancreatic cancer.

Objective To investigate the effect and mechanism of RNAi-mediated STAT3 gene silence on human pancreatic cancer cells growth in vivo. Methods STAT3 shRNA expression vector was stably transfected to SW1990 cells. STAT3 and p-STAT3 protein was examined using Western blot. The growth ability of SW1990 cells in vivo was determined in a subcutaneous tumor model of nude mice. Western blot was performed to detect the protein expression of Bcl-xL and cyclin D1. Results The protein expression of STAT3 and p-STAT3 decreased by 90% and 92% by stable transfection of STAT3 shRNA expressing vectors(P ＜0. 05). Inhibition of STAT3 with RNAi significantly inhibited the growth ability of SW1990 cells in vivo( P ＜ 0. 05 ). The tumor weight significantly decreased( P ＜ 0. 05 ). Moreover, the relative Bcl-xL and cyclinD1 protein expression in SW1990-RNAi cells reduced by 56% and 50% compared with that of the parental SW1990 cells, respectively (P ＜ 0. 05). Conclusions Inhibition of STAT3 with RNAi significantly inhibits the growth ability of pancreatic cancer cells through down-regulating Bcl-xL and cyclin D1.

Objective To investigate the effect of interleukin 6 (IL-6) on the growth and proliferation of human pancreatic cancer cell line Capan-2 and the signal transduction pathway. Methods MTr method was used to detect the effect of IL-6 of different concentrations on the growth and proliferation of Capan - 2 cells; cell apoptosis was detected by flow cytometry; the intracellular localization of phosphorylated STAT3 (P-STAT3) was determined by immunocytochemistry and western blot were used to detect P-STAT3, bcl-xl and Cyclin D1 in Capan-2 cells stimulated by IL-6. Results IL-6 (100 ng/ml) could remarkably promote the growth of Capan-2 cells from 1 to 4. 965 ± 0. 18 (P < 0. 05) ; the percentage of apoptosis decreased significantly from (3.21 ±0.23)% to (1.98 ±0.67)% (P <0.05) ; the expressions of P-STAT3, bcl-xl, Cyelin D1 increased significantly (P < 0.05), and the expressions of bcl-xl was positively correlated with that of P-STAT3 (r =0.985, P =0.015) ; the expressions of Cyclin DI was also positively correlated with that of P-STAT3(r=0.914,P=0.036),Conclusions IL-6 activate JAK/STAT signal transduction pathway,which played an important role in the growth and proliferation of Capan-2 cells in the presence of IL-6.

Objective To investigate the effect of RNAi-mediated sTAT3 gene silencing on the invasiveness of human pancreatic cancer cells. Methods STAT3 shRNA expression vector was stably transfected to SW1990 cells.STAT3 mRNA and protein expression were examined using reverse transcription polymerase chain reaction(RT-PCR)and Western blot,respectively.The invasion ability of SW1990 cells was determined by cell invasion assay in vitro.RT-PCR and Westem blot were performed to detect the mRNA and protein expression of the MMP-2 and VEGF,respectively. Results mRNA and protein expression of STAT3 were inhibited significantly by stable transfection of STAT3 shRNA expressing vectors.STAT3 silence with RNAi significantly inhibited the invasion ability of SW1990 cells decreasing protein and mRNA expression of MMP-2 and VEGF in SWl990 cells. Conciusion STAT3 silence with RNAi significantly inhibits the invasion ability of pancreatic cancer cells through down-regulating MMP-2 and VEGF.

OBJECTIVETo evaluate incidence of postoperative delirium after hip surgery in elderly patients by meta-analysis.

METHODSFrom January 1, 2014 to December 31, 2013, clinical literatures about postoperative delirium after hip surgery in elderly patients,were searched from the Pubmed. Literature extract table were formed according to inclusion and exclusion criteria. Stata-12.0 was applied for Meta-analysis. P was used to test heterogeneity of study, random-effect model was performed when I2 > 50%. Subgroup analysis was used according to stage of age, assessment scale of delirium and statistical area of literature. Begg test was used to test publication bias.

RESULTSTwenty-one literatures were included. Incidence of postoperative delirium after hip surgery in elderly patients by weighted and combination was 17% [95% CI (16%, 18%)]. Incidence of postoperative delirium after optional hip surgery was decreased more than emergency operation in included 5 literatures [OR = 0.32, 95% CI (0.22, 0.45)]. Incidence of postoperative delirium in patients less than 80 years old was 21% [95% CI (19%, 23%)], while 21% [95% CI (19%, 24%)] in patients more than 80 years old. Incidence of postoperative delirium in CAM evaluation scale was 23% [95% CI (21%, 26%)], while 19% [95% CI (17%, 21%)] in other evaluation scales. Incidence of postoperative delirium in Asian area was 17% [95% CI (15%, 20%)], while 23% [95% CI (21%, 25%)] in European and American area. There was no publication bias tested by Begg test (P < 0.05).

CONCLUSIONIncidence of postoperative delirium after hip surgery in elderly patients increases higher, especially in emergency operation. A standardizing research method is benefit for evaluate incidence of postoperative delirium after hip surgery in elderly patients, decreasing heterogeneity and publication bias.

Aged ; Delirium ; epidemiology ; Hip Fractures ; surgery ; Humans ; Incidence ; Postoperative Complications ; epidemiology ; Publication Bias