Objective:The present research aimed to explore the involvement of ERK signaling pathway in apoptosis of hepatic carcinoma induced by decitabine combined sodium valproate.Methods: HepG2 cell line was incubated with decitabine combined sodium valproate and the inhibition rate was detected by MTT method.The apoptotic related protein and ERK signal pathway proteins were assayed by Real-time PCR or Western blot.Results: The HepG2 cell line was inhibited greatly by decitabine combined sodium valproate medication with an increased expression of Caspase3,Caspase9 and Bax (P<0.05).The expression of Ras,Raf,MEK and ERK1/2 was increased dramatically after incubation with decitabine combined sodium valproate when compared with control group ( P<0.05).Conclusion:Decitabine combined sodium valproate exert a significant inhibition on the proliferation of HepG2 cell line by nor-malizing the abnormal MEK/ERK signaling pathway.

Acute appendicitis is the most common general surgical problem encountered during pregnancy, which may be associated with serious maternal and /or fetal complications such as appendiceal perforation or premature delivery.Clinical presentation and imaging remains vital in the diagnosis of appendicitis.As a general rule,the clinical suspicion of acute appendicitis during pregnancy is an indication for an urgent surgical intervention.Appendectomy is the preferred treatment.Laparoscopic appendicectomy(LA)can also be performed safely and effectively in pregnant patients without bringing additional maternal complications.

Objective:To investigate the related factors of pancreatic fistula after laparoscopic-assisted distal gastrectomy (LADG).Methods:A retrospective analysis was performed of 189 patients who underwent LADG in Beijing Friendship Hospital, Capital Medical University from June 2017 to March 2018. Twenty-seven patients with postoperative pancreatic fistula and 27 randomly selected normal patients were included in the study. The preoperative characteristics and surgical data of all patients were recorded, including body mass index, visceral fat area, past history, preoperative tumor staging, operation time and bleeding volume, etc. The related factors of postoperative pancreatic fistula were analyzed. Measurement data were expressed as mean±standard deviation ( Mean± SD), and t-test was used for comparison between groups. Chi-square test was used to compare the count data between groups. Results:The patients with high body mass index ( t=3.956, P=0.003), high visceral fat area ( t=6.161, P=0.038), long operation time ( t=2.650, P=0.024), profuse hemorrhage ( t=1.887, P=0.042), complete lymphadenectomy ( t=2.092, P=0.001) were prone to postoperative pancreatic fistula, while there was no significant difference of visceral fat area/total abdominal fat area ( χ2=1.334, P=0.324), preoperative with pulmonary diseases ( χ2=0.750, P=0.379), coronary heart disease ( χ2=0.081, P=0.500), hypertension ( χ2=0.667, P=0.239), diabetes mellitus ( χ2=2.030, P=0.127), chronic kidney disease ( χ2=0.587, P=0.352), tumor stage( χ2=1.388, P=0.500) and other factors between the two groups. Conclusions:Obesity patients and LADG patients with long operation time are more likely to have postoperative pancreatic fistula. Comprehensive preoperative assessment and prudent intraoperative operation may be one of the effective methods to avoid postoperative pancreatic fistula.

Objective To investigate the influence of Norcantharidin(NCTD)on apoptosis-related gene expression of gastric cancer cell line SGC-7901.Methods The experiment was divided into control group,5-Fu group,NCTD group and 5-Fu+NCTD group.The inhibitory rate,apoptosis rate and expression of survivin,bcl-2,and caspase-3 were detected by MTT assay,flow cytometry and SABC immunohistochemical method,respectively.Results NCTD showed that the inhibitory effect on growth of SGC-7901 cells with a dose-and time-effective dependent manner.The apoptotic rate increased from(8.30?1.49)% to(20.56? 1.32)%.The expressions of survivin decreased from(86.57?4.39)% to(26.11?2.27)% and bcl-2 from(85.35? 3.25)% to(30.26?1.83)%,while caspase-3 increased from(54.49?3.07)% to(92.78?2.47)%,5-Fu had the synergistic effects with NCTD.Conclusion NCTD can inhibit the growth of SGC-7901 cell lines.5-Fu had the synergistic effects with NCTD.The mechanism might correlate with induction of cell apoptosis via effect of the expression of apoptotic-related genes such as survivin,bcl-2 and caspase-3.

Animals ; Humans ; Hypertension, Pulmonary ; complications ; Hypothermia ; complications ; Hypoxia ; etiology ; therapy ; Respiratory Distress Syndrome, Adult ; complications ; Shock, Septic ; complications

Objective To evaluate the feasibility of 153　Sm-EDTMP for multiple bone metastasis.Methods 32 patients with multiple bone metastases were treated with 153　Sm-EDTMP injected into the veins,0.4～1.0 mci/kg,of which 7 cases received therapy for 2～3 times.Results 53.1%(17/32)was relieved completely,25.0%(8/32)was relieved partially and 9.4%(3/32)was relieved slightly.No effects were found in 12.5%(4/32).The overall effective rate was 78.1%.Side effects that were the decreasing of WBC and PLT were found in 15.6%(5/32),which rose to the preoperative levels within 6～8 weeks.Conclusion Internal radiotherapy with 153　Sm-EDTMP is safe and effective in the treatment of multiple bone metastases.

Several kinds of epidemiological methods in studies of illicit drug use were described in this article.These include case-finding,capture-recapture,privileged access interviewer,mortality multiplier method and nomination method.

Th17 cells play an important role in the pathogenesis of various immune-mediated diseases,including psoriasis,rheumatoid arthritis,multiple sclerosis,inflammatory bowel disease,asthma,and so on.The discovery of Th17 cells has offered scientists a new insight into the etiology and treatment of a broad spectrum of diseases.This article presents an overview of the differentiation,cytokine expression and trafficking of Th17 cells.

Objective To investigate the potential roles of tumor necrosis factor -related apoptosis -indu-cing ligand(TRAIL)signaling system in the pathogenesis of colorectal cancer.Methods Immunohistochemistry tech-niques were used,the TRAIL and its receptor(TRAILR3,TRAILR4)protein were analyzed in both 41 colorectal cancer samples(colorectal cancer group)and normal samples beside cancer tissue(normal group).Results The lev-els of TRAIL and TRAILR3 protein expression in the colorectal cancer group were significantly lower than those in the normal group[(0.237 ±0.036)vs.(0.289 ±0.069);(0.226 ±0.052)vs.(0.281 ±0.068),t =4.125,4.025,all P <0.01],while the positive rate of them were nonsignificant difference between the two groups(88% vs.90%;95%vs.93%,χ2 =0.125,0.213,all P >0.05).The expression levels of them in the colorectal cancer group with poorl differentiation were notably lower than those with high -moderate differentiation[(0.205 ±0.021 )vs (0.245 ± 0.034);(0.185 ±0.032)vs (0.236 ±0.051),t =4.025,2.664,P <0.01,P <0.05],but they were not strongly correlated to lymph nodes metastasis[(0.235 ±0.035 )vs (0.241 ±0.338);(0.216 ±0.048)vs (0.231 ± 0.054),t =0.448,0.862,all P >0.05].Moreover,the positive rate and expression levels of TRAILR4 protein was non -statistic significant difference between the two groups[93% vs 98%;(0.196 ±0.085)vs (0.219 ±0.061),χ2 =1.051,t =1.353,all P >0.05],and it was also non -significantly correlated with cancer cell differentiation and lymph nodes metastasis[(0.176 ±0.052)vs (0.201 ±0.091);(0.194 ±0.054)vs (0.197 ±0.100),t =0.667, 0.448,all P >0.05].Conclusion The levels of TRAIL and TRAILR3 expression are attenuated at colorectal cancer tissue.The expression of them are correlated with cancer cell differentiation grade.These findings indicate that TRAIL system may be associated with the malignant phenotype in colorectal cancer.

Objective To observe the effect of ghrelin on the expression of procollagen type Ⅰ and alpha smooth muscle actin (α-SMA) synthesis in vitro cultured human hepatic stellate cell (HSC-LX2) stimulated by Platelet-derived growth factor-BB (PDGF-BB).Besides,the effect of PI3K-AKT pathway was studied.Methods Cultured LX2 were intervented and jointing intervented according to the different ghrelin concentration by ghrelin and PDGF:control group,0.1 μmol/L Ghrelin group,10 μg/L PDGF group,0.05 μmol/L Ghrelin +10 μg/L PDGF group,0.1 μmol/L Ghrelin + 10 μg/L PDGF group,0.15 μmol/L Ghrelin + 10 μg/L PDGF group.Culture HSC-LX2 in vitro,joint intervention cells with different concentrations.Procollagen Ⅰ mRNA expression were detected by Polymerase chain reaction (PCR),besides,α-SMA and AKT expression were detected by Western blot in each groups.After treatment by PI3K specific inhibitor LY294002 in LX2,three groups were divided into PDGF,Ghrelin + PDGF and LY294002 + Ghrelin +PDGF.Procollagen Ⅰ mRNA expression were detected by PCR,and α-SMA was detected by Western blot.Results PCR results showed that procollagen Ⅰ expression in PDGF treated group was significantly higher than the control group ((6.91 ± 0.46) vs.(1.00 ± 0.08),P ＜ 0.05),so PDGF can promote the expression of procollagen type Ⅰ.Procollagen Ⅰ mRNA expression between ghrelin group(0.60±0.13) and blank control group had no significant change(P＞0.05).Procollagen Ⅰ mRNA expression between different concentrations of Ghrelin and PDGF (3.11 ± 0.28,2.03 ±0.23,0.70 ± 0.06) was significantly reduced than PDGF group.The difference was statistically significant (P ＜0.05),and with the increase of the ghrelin concentration of the inhibition,the effect was more obvious in a concentration dependent manner.Western blot showed that α-SMA expression was lower in Ghrelin +PDGF group than PDGF group.AKT expression was higher in Ghrelin +PDGF group than PDGF group,indicating that PI3K-AKT may participate in the anti-fibrosis effect of ghrelin in LX2.After treatment of PI3K specific inhibitor,procollagen Ⅰ expression in LY294002+Ghrelin +PDGF group was significantly higher than Ghrelin +PDGF group((4.13±0.21) vs.(2.34±0.25),P＜0.05).Western blot also showed that α-SMA expression was higher in LY294002 + Ghrelin + PDGF group than Ghrelin + PDGF group.It was suggested that after inhibitation of PI3K,the anti-fibrosis effect of ghrelin in LX2 was attenuated.Conclusion After stimulated by PDGF in hepatic stellate cell,ghrelin can inhibit procollagen type Ⅰ and alpha-SMA synthesis in the process of hepatic fibrosis via PI3K-AKT pathway,thus,ghrelin may become one of the new ways of prevention and treatment of liver fibrosis.