Objective To investigate the relationship between the changes of portal pressure gradient after selective devascularization with postoperative complications and recurrent bleeding of gastroesophageal varix in patients of portal hypertension. Methods The clinical data of 135 cases of portal hypertension undergoing selective devascularization was collected. Portal pressure gradient was measured before splenectomy and after selective devascularization, and was analyzed against postoperative complications and recurrent bleeding. Results In this study, 135 patients of portal hypertension underwent selective devascularization, two cases died during perioperative period ( 1.5% ). Postoperatively patients were divided into three groups based on PPG ＜ 12 mm Hg after selective devascularization (62 cases), HVPG ≥ 12 mm Hg but a more than 20% of decrease off the pre-splenectomy baseline (41 cases) and HVPG ≥12 mm Hg with less than 20% of decrease from the baseline (32 cases). The postoperative complications between the three groups were of no significant difference ( P ＞ 0. 05 ). The 1,2,3 year cumulative rate of no variceal rebleeding of the three groups were 100% vs. 100% vs. 95%; 100%vs. 97% vs. 90%; and 100% vs. 93% vs. 87% (x2 =6. 859, P = 0. 032). COX regression analysis indicated portal vein pressure gradient was an independent prognostic factor of variceal bleeding recurrence (P=0.002). 1,2,3 year cumulative survival rates of the three groups were 100% vs. 100% vs. 94%; 98% vs. 95% vs. 92%; 97% vs. 93% vs. 88%, there were no significant difference among the three groups ( x2 = 2. 917, P = 0. 233 ). Conclusions The decrease in the PPG after selective devascularization is a predictor for the risk of rebleeding but not for survival after selective devascularization.

Objective To explore the correlation between coagulation and coagulation suppresion system disorders of portal vein thrombosis in patients of portal hypertension undergoing splenectomy.Methods Clinical data of 33 patients with postoperative portal vein thrombosis were enrolled.The clotting and coagulation inhibitor in portal vein blood and peripheral blood was detected and analyzed.Results The Hb,APTT,FIB,factor Ⅶ,protein C,AT-Ⅲ,CD62P of portal vein blood and peripheral blood before the surgery and on postoperative day 1,day 7,day 14 were no significant difference (P ＞ 0.05).The WBC,PLT,PT,D-Dimer of in portal vein blood before surgery were (2.9 ± 1.4) × 109/L,(37.5 ± 20.7) × 109/L,(16.1 ± 2.9) seconds,(0.7 ± 0.3) μg/ml,which were significantly different from those on postop day 1 (13.7 ±4.4) × 109/L,(86.3 ±34.6) × 109/L,(6.9 ±5.7) seconds,(16.1 ±2.9) μg/ml; day 7 (10.7 ±4.3) × 109/L,(312.4 ±137.2) × 109/L,(14.4 ±2.9) seconds,(7.6 ±4.4) μg/ml and day 14 (7.7 ± 3.3) × 109/L,(486.3 ± 216.7) × 109/L,(14.4 ± 2.9) seconds,(5.5 ± 4.4) μg/ml (P ＜ 0.05).WBC,PLT,PT,D-Dimer in preop peripheral blood were (2.4 ±0.8) × 109/L,(44.4 ± 25.8) × 109/L,(16.3 ± 3.0) seconds,(0.6 ± 0.4) μg/ml,which were significantly different from those on postop day 1 (13.7 ± 5.7) × 109/L,(75.1 ± 29.3) × 109/L,(13.7 ± 2.6) seconds,(6.8 ± 5.3) μg/ml; day 7 (10.6 ± 4.8) × 109/L,(337.9 ± 141.3) × 109/L,(14.0 ± 2.1) seconds,(7.6 ± 5.5) μg/ml and day 14 (7.8 ±3.9) × 109/L,(504.9 ±237.4) × 109/L,(14.0 ±2.1) seconds,(5.4 ±4.9) μg/ml postoperative (P ＜ 0.05).Conclusions The cause of postsplenectomy portal vein thrombosis is multifactorial.The dysfunction of coagulation-coagulation suppression system was just one of the conditions conducive to portal vein thrombosis after splenectomy.

Objective To compare the recmrence and survival rate between small hepatocellular carcinoma (HCC)patients with and without folfox4 adjuvant chemotherapy after radical resection.Methods From April 2006 to October 2012 46 HCC eases after curative resection received folfox4 adjuvant chemotherapy, 51 cases served as control.Results The clinical and pathological data of the two groups were not significantly different.The 1, 2, 3, 4, 5-year disease-free survival of the group with folfox4 adjuvant chemotherapy was 89％ , 70％ , 59％ , 48％ , 35％ ,and that was 78％ , 65％ , 53％ , 37％ , 27％in control group, the difference was not statistically significant (P =0.459).The 1, 2, 3,4, 5-year overall survival rate of the group with folfox4 adjuvant chemotherapy was 96％ , 76％ , 63％ , 57％ , 52％ , that in control group was 96％ , 73％ , 59％ , 51％ , 47％ , the difference was not statistically significant (P =0.459).COX-hazards regression showed folfox4 adjuvant chemotherapy was not independent factors of recurrence and prognosis (P =0.467, P =0.834).Conclusions For patients with hepatocellular carcinoma smaller than 5 cm in diameter,folfox4 adjuvant chemotherapy after radical resection did not reduce the recurrence rate and did not improve survival.

In order to investigate the chemical constituents of glycosides in Piper sintenense Hatusima, column chromatographic techniques such as silica gel, ODS, MCI GEL CHP20P, Sephadex LH-20, and semi-preparative high performance liquid chromatography were used to afford nine glycosides from the n-butanol part of the 95% ethanol extract of Piper sintenense Hatusima. Based on the physicochemical properties and NMR data, the above compounds were identified as (2S)-2-hydroxy-1-(4-hydroxy-3-methoxyphenyl)-1-propanone-2-O-β-D-glucopyranoside (1), 2-phenylethyl β-D-glucopyranoside (2), benzyl α-L-arabinopyranosyl-(1''→6')-β-D-glucopyranoside (3), benzyl β-D-xylopyanosyl-(1''→6')-β-D-glucopyranoside (4), phenethyl β-D-apiofuranosyl-(1''→ 2')-β-D-glucopyranoside(5), salidroside (6), phenethanol β-D-xylopyanosyl-(1''→6')-β-D-glucopyranoside (7), (Z)-hexenyl-O-α-L-arabinopyranosyl-(1''→6')-O-β-D-glucopyranoside (8), (Z)-hexenyl-O-β-D-xylopyanosyl-(1''→6')-O-β-D-glucopyranoside (9). Compound 1 was identified as a new compound, and compounds 3-9 were isolated from the genus Piper for the first time.

Tryptophan 2,3-dioxygnease 2 (TDO2) is specific for metabolizing tryptophan to kynurenine (KYN), which plays a critical role in mediating immune escape of cancer. Although accumulating evidence demonstrates that TDO2 overexpression is implicated in the development and progression of multiple cancers, its tumor-promoting role in esophageal squamous cell carcinoma (ESCC) remains unclear. Here, we observed that TDO2 was overexpressed in ESCC tissues and correlated significantly with lymph node metastasis, advanced clinical stage, and unfavorable prognosis. Functional experiments showed that TDO2 promoted tumor cell proliferation, migration, and colony formation, which could be prevented by inhibition of TDO2 and aryl hydrocarbon receptor (AHR). Further experimentation demonstrated that TDO2 could promote the tumor growth of KYSE150 tumor-bearing model, tumor burden of C57BL/6 mice with ESCC induced by 4-NQO, enhance the expression of phosphorylated AKT, with subsequent phosphorylation of GSK3