Objective To evaluate the effect of stellate ganglion block (SGB) on cerebral vasospasm in patients undergoing intracranial aneurysm surgery. Methods Forty ASA Ⅱ or Ⅲ patients aged 14-64 yr weighing 40-81 kg undergoing intracranial aneurysm clipping were randomly divided into 2 groups ( n = 20 each): group control (group C) and group SGB. Left SGB was performed with 0.25% ropivacaine 10 ml immediately after intubation. Successful block was verified by development of Homer syndrome within 15 min after block. Anesthesia was induced with midazolam, propofol, fentanyl and vecuronium and maintained with isoflurane inhalation and intermittent iv boluses of fcntanyl and vecuronium. The patients were intubated and mechanically ventilated. PETCO2 was maintained at 30-35 mm Hg. BIS was maintained at 50-60. Right internal jugular vein was cannulated and the catheter was threaded cranially until resistance was met for blood sampling. Blood samples were collected before skin incision (T1), before clipping of aneurysm (T2), at 30 min after clipping (T3 ), and at the end of surgery (T4) for determination of plasma concentrations of endothelin (ET), calcium gene-related peptide (CGRP) and S100B protein. Transcranial Doppler was used to measure the flow rate of blood in bilateral middle cerebral artery and extracranial carotid artery at 1 and 3 days after surgery. All patients were observed for incidence of brain ischemia during 1-7 days after surgery. Results Plasma ET and S100B protein concentrations were significantly decreased, while plasma CGRP concentration was significantly increased after clipping of aneurysm at T3 and T4 in group SGB as compared with group C. The incidence of cerebral vasospasm and brain ischemia was significantly lower in group SGB than in group C. Conclusion SGB performed before operation can significantly reduce the incidence of cerebral vasospasm after clipping of intracranial aneurysm by inhibiting the release of ET and promoting the release of CGRP.

Multiple cellular factors and molecular signal pathways including PI 3K/AKT pathway;MAPK pathway;growth factors and receptors like HER , VEGF/VEGFR and MET ;inflammation‐related factors like COX‐2 ,NF‐κB ,STAT and interleukins ,are involved in the occurrence and development of gastric cancer ,these factors play a key role in apoptosis inhibition ,proliferation promotion and cell cycle regulation of gastric cancer cells ,as well as invasion ,migration and angiogenesis of stomach malignancy .They are also expressed at a higher level in gastric cancer tissue compared with normal gastric mucosa and characterized as biomarkers ,whose target therapies mostly have been in clinical trials . Based on these theoretical foundations , the research on molecular diagnosis of gastric cancer has made some progress .Instruments for target detection tend to be mature .However , the research of molecular probes is still in pre‐clinical trials ,which remains to be further developed .

Objective To investigate the survival status of liver cirrhosis patients without upper gastrointestinal hemorrhage after transjugular intrahepatic portosystemic shunt (TIPS).Methods From 2004 to 2013,15 liver cirrhosis patients without upper gastrointestinal hemorrhage volunteered received TIPS treatment were followed up to find out the difficulty and the success rate of TIPS procedure,the incidence of hepatic encephalopathy,upper gastrointestinal hemorrhage and improving of hypersplenism.Results The success rate of operation was 100％.The average of operation time was 60 minutes.During follow-up,no stent angulation occurred,no gastrointestinal hemorrhage happened and no one died in all 15 patients after TIPS operation.There were four patients with hepatic encephalopathy in eight weeks after operation.The anemia of four patients improved compared with that before operation.Conclusions TIPS is a safe and effective threapy in the prevention of gastrointestinal hemorrhage in the patients with liver cirrhosis accompanied with severe gastroesophageal varices.It may become the primary prophylaxis for liver cirrhosis patients without upper gastrointestinal hemorrhage.

Objective To comfirm the anti-fibrotic effect of spironolactone and investigate the influence of spironolactone on concentration of angiotensinⅡ(AngⅡ) in rat hepatic fibrosis. Methods Ninety male Sprague-Dawly rats were randomly divided into three groups: control group (8 rats, subcutaneous injection of pure peanut oil, normal diet), model group (42 rats, subcutaneous injection of 40% CCl 4, 0.3 mL/100 g, twice a week, high cholesterol and low protein diet, 5% alcohol as the drink), and spironolactone group (40 rats, same dosage of CCl 4, high cholesterol and low protein diet, gastropufusion of spironolactone at the dose of 100 mg?kg -1?d -1). The animals were sacrificed at 2, 4, 6 and 8 weeks of administration. AngⅡ was assayed by radioimmunoassay. The liver tissues were stained, coded and examined. Results ① The general conditions of the rats of spironolactone group were better than those of the model group. The degree of fibrosis and the area of collagen in the liver of spironolactone group were less than those of the model group after the 4th week (P

Objective To evaluate the relationship between the expression of cyclooxygenase-2(Cox-2) and inducible nitric oxide synthase (iNOS) and the angiogenesis in gastric carcinoma. Methods Immunohistochemical stain was used to detect the expression of Cox-2, iNOS and MVD in 45 resected specimens of gastric carcinoma. The monoclonal antibody against CD34 was used for displaying vascular endothelial cells, and MVD was detected by counting the CD34-positive vascular endothelia cells. Paracancerous tissues were examined as the control. Results The expression rates of Cox-2, iNOS and MVD in gastric cancer were significantly increased, compared with those in the paracancerous tissues (77.78% vs. 33.33%, 68.89% vs. 17.78%, 58.13?19.99 vs. 24.02?10.28, P

Objective To investigate whether there is a correlation between the esophageal length of the adult Chinese people and their height, sitting height, sex or age. Methods The length from the upper end of esophagus to the dentate line of the cardia was measured by watching esophageal cavity with endoscope. A total of 613 cases (378 males and 235 females) were studied. Results ① The average length of esophagus was (24.8?2.1)cm for male and (22.8?1.9)cm for female. The difference between male and female was statistically significant (P

Objective To investigate the anticancer effects and detailed mechanisms of Saikosaponin D (SSD) in human hepatoma HepG2 cells. Methods Cell proliferation and apoptosis were tested by MTT assay and Annexin-V/PI assay respectively. The expressions of CCAAT enhancer binding protein β(C/EBPβ) and p53 were detected by RT-PCR and Western blotting. Results SSD inhibited cell proliferation in a dose-dependent manner and induced apoptosis at the concentration of 5.0mg/L. SSD significantly increased the mRNA and protein levels of C/EBPβ and p53 in a dose-dependent manner. Conclusion SSD exerts its anticancer effect by inhibiting cell proliferation and inducing apoptosis partly through C/EBPβ-p53 signal pathway in HepG2 cells.

ABSTRACT:Objective To observe the influence of saikosaponin-d (SSd)on the proliferation and the function of autophagy of human hepatocellular carcinoma (HCC)cell line SMMC-7721 to explore the possible mechanisms. Methods SMMC-7721 was cultured invitro and then treated with SSd of various concentrations (5.0,7.5,10.0, 12.5,15.0 and 17.5 mg/L)for 24,48 and 72 h.We used MTT to detect cell proliferation,selected the optimal concentration and time,and detected the expressions of BECN1 at mRNA and protein levels by PCR and Western blot.Results The inhibition rate of the proliferation of SMMC-7721 cell line increased with the increase of the concentration of SSd,and the highest inhibition rate (60%)appeared when the concentration reached 12.5 mg/L. The expression of BECN1 in the group with SSd was obviously higher than that in the control group (P<0.05). 3-MA decreased not only the expressions of BECN1 at mRNA and protein levels but also the expression of BECN1 when used in conjunction with SSd.Conclusion The inhibiting function of SSd on SMMC-7721 presents a dependency between drug concentration and function time,basically in line with the drug dose-effect relationship. SSd induces the occurrence of autophagic cell death through up-regulating the expression of BECN1 ,thus inhibiting the proliferation of SMMC-7 7 2 1 .

Objective:To explore the expression of polypyrimidine tract-binding protein 1 (PTBP1) in gastric cancer (GC) tissues and GC cell lines, and the role of PTBP1 in the proliferation and metastasis of GC cells.Methods:From January to June in 2019 at The First Affiliated Hospital of Xi′an Jiaotong University, the cancer tissues and corresponding para-cancer tissues of GC patients underwent surgical resection were collected. The Kaplan-Meier Plotter database was used to analyze the survival of GC patients. The expression of PTBP1 was down-regulated by transfecting small interfering RNA (siRNA) in human GC cell lines SGC7901 and AGS with relatively high expression of PTBP1. The cells were divided into blank control group, negative control group, and PTBP1 knockdown group. The expression of PTBP1 at mRNA and protein level were detected by real-time fluorescence quantification polymerase chain reaction (RT-qPCR) and Western blotting. At 24, 48, 72 and 96-hour after transfection, the effect of PTBP1 on the proliferation of GC cells was observed by 3-(4, 5 dimethylthiazol)-2, 5 diphenyltetrazolium bromide (MTT) experiment. The changes of invasion and migration of GC cells after down-regulation of PTBP1 were detected by transwell assay. The expression changes of epithelial-mesenchymal transition (EMT) markers E-cadherin, N-cadherin and vimentin after down-regulation of PTBP1 in GC cells were determined by Western blotting. Indenpendent samples t test, analysis of variance and rank sum test were used for statistical analysis. Results:The Kaplan-Meier Plotter prognostic analysis showed that the overall survival of GC patients with high PTBP1 expression was shorter than that of GC patients with low PTBP1 expression (9.2 months, 6.2 months to 17.2 months vs. 19.0 months, 14.5 months to 28.4 months), and the difference was statistically significant ( Z=5.31, P<0.05). The results of RT-qPCR showed that in GC cell lines SGC7901 and AGS, the expression of PTBP1 at mRNA level of PTBP1 knockdown group was lower than that of blank control group and negative control group (SGC7901: 0.78±0.11 vs.3.10±0.19 and 2.99±0.23; AGS: 0.80±0.09 vs. 3.55±0.24 and 3.50±0.18), and the differences were statistically significant ( tSGC7901=10.57 and 8.08, tAGS=10.91 and 13.42; all P<0.01). The results of Western blotting indicated that in GC cell lines SGC7901 and AGS, the expression of PTBP1 at protein level of PTBP1 knockdown group was lower than those of blank control group and negative control group (SGC7901: 0.38±0.04 vs. 1.42±0.05 and 1.35±0.09; AGS: 0.17±0.02 vs. 1.52±0.08 and 1.38±0.45), and the differences were statistically significant ( tSGC7901=15.94 and 10.57, tAGS=16.60 and 20.80; all P<0.01). The results of MTT showed that at 48, 72 and 96-hour after transfection the absorbance values of PTBP1 knockdown group decreased by 0.25±0.01, 0.38±0.02, and 0.84±0.04 as compared with those of negative control group, and the decrease was the most significant at 96-hour after transfection, and the differences were statistically significant ( t=10.21、14.32, both P<0.01). The results of transwell experiment demonstrated that the number of invasion and migration cells of PTBP1 knockdown group were both less than that of the blank control group and the negative control group (SGC7901: 42.00±5.91 vs. 116.40±10.23 and 114.40±10.43; 39.60±6.77 vs. 125.80±11.51 and 122.40±5.90; AGS: 40.20±7.25 vs. 115.60±14.63 and 117.40±9.12; 36.00±5.20 vs. 122.40±12.10 and 125.40±12.74), and the differences were statistically significant ( tSGC7901=14.07, 13.50, 14.43 and 20.62; tAGS=10.27, 14.75, 14.68 and 16.76; all P<0.01). The results of Western blotting showed that the expression of E-cadherin of PTBP1 knockdown group was higher than that of the blank control group and the negative control group (SGC7901: 1.42±0.05 vs. 0.53±0.05 and 0.57±0.03; AGS: 1.34±0.04 vs. 0.54±0.03 and 0.61±0.01), however the expression levels of N-cadherin and vimentin were both lower than those of the blank control group and the negative control group (SGC7901: 0.50±0.03 vs. 1.64±0.05 and 1.46±0.07; 0.32±0.07 vs. 1.42±0.07 and 1.33±0.07; AGS: 0.37±0.06 vs. 1.47±0.04 and 1.36±0.04; 0.41±0.04 vs. 1.53±0.06 and 1.37±0.04), and the differences were statistically significant ( tSGC7901=11.63, 13.19, 18.83, 11.68, 11.43 and 10.43; tAGS= 15.02, 16.23, 14.67, 12.97, 14.45 and 17.18; all P<0.01). Conclusions:The expression levels of PTBP1 increase in GC tissues and cells, which may be involved in regulating the proliferation, metastasis and EMT of GC cells.