IHC-65 was found to be a potent inhibitor of platelet function . It inhibited platelet aggregation induced by threshold concentration of ADP, arachidonic acid and collagen with dose-dependent manner in vitro, and at 96?mol/L, AIR ( aggregation inhibition rate,) were 71.56, 66.93 and 68.47% respectively. IHC-65 inhibited platelet serotonin release induced by collagen,and at 96 ?mol/L, release inhibition rate was 82.97%. IHC-65 did not influence cAMP level in platelet significantly. It is concluded that IHC-65 inhibited platelet aggregation and its action mechanism may be related to inhibition of serotonin release and to antagonizing Ca ++ .

Objective This study is to explore the expression of CIP2A mRNA in hepatocellular carcinoma (HCC), and its correlations with clinicopathologic features and prognosis of HCC patients.Methods CIP2A mRNA expression was analyzed in four liver cancer cell lines (Hep-G2, MHCC97,SMMC-7721 and BEI-7402), one immortalized liver cell line L-O2, neoplastic tissues and adjacent matched non-neoplastic liver tissues in 120 HCC patients and normal liver tissues of 20 cases using semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). The correlations between CIP2A mRNA and clinicopathologic features and prognosis of HCC were analyzed. Results CIP2A mRNA was detected in Hep-G2, MHCC-97H, SMMC-7721 and BEL-7402, but not in L-O2.The positive rate of CIP2A mRNA expression was significantly increased in HCC tissues (78.3%)than in adjacent matched non-neoplastic liver tissues (28.3%) and normal liver tissues (5.0%,P＜0. 01). CIP2A mRNA expression was correlated with tumor size, differentiation and TNM stage (P＜0.05). Patients with positive expression of CIP2A mRNA had lower overall survival and diseasefree survival rates. Conclusions CIP2A mRNA, which is highly expressed in liver cancer cell lines and HCC tissues, may be involved in hepatocarcinogenesis. CIP2A mRNA may be a valuable biomarker for assessing the prognosis of HCC.

Purpose: Four and a half LIM protein 1 (FHL1) is involved in breast cancer (BC) development, but the regulatory mechanism involved remain unclear. In the present study, we examined the role of FHL1 in BC development. Methods: The expression of FHL1, miR-183-5p, and miR-96-5p in BC tissues was analyzed using StarBase analysis. FHL1 expression in BC tissues, a normal human breast epithelial cell line, and BC cell lines was detected using quantitative reverse transcription polymerase chain reaction (qRT-PCR). The relationship between FHL1 and miR-183-5p/miR-96-5p was analyzed via Pearson's rank correlation, TargetScan, and a dual-luciferase reporter assay. BT549 and MDA-MB-231 cells were transfected with either FHL1 and miR-183-5p mimics, or siFHL1 and a miR-183-5p inhibitor, respectively. The viability, colony number, migration, invasion, and tube length of BT549 and MDA-MB-231 cells were examined using cell counting kit-8, colony formation, wound-healing, Transwell, and tube formation assays, respectively. The levels of FHL1, vascular endothelial growth factor (VEGF), p53, E-cadherin, N-cadherin, and vimentin were quantified using western blotting and qRT-PCR. Results: FHL1 expression was downregulated in BC tissues and cells, whereas miR-183-5p and miR-96-5p were upregulated in BC tissues (negative correlation with FHL1 expression).FHL1 overexpression inhibited the viability, colony number, migration, and invasion of BC cells and the expression of VEGF, N-cadherin, and vimentin, and increased the expression of FHL1, p53, and E-cadherin in BT549 cells. Furthermore, a miR-183-5p mimic reversed these effects of FHL1 overexpression, whereas FHL1 silencing caused opposite results to those observed in MDA-MB-231 cells; however, this was reversed by a miR-183-5p inhibitor. Conclusion Our study suggests that miR-183-5p promotes cell proliferation, metastasis, and angiogenesis by negatively regulating FHL1 in BC.

Objective To investigate the value of preoperative platelet count (Plt) in predicting prognosis of patients with hepatocellular carcinoma (HCC) after hepatectomy. Methods Clinical data of 399 patients who underwent hepatic resection for HCC in Department of Hepatobiliary Oncology, Sun Yat-sen University Cancer Center from January 1987 to December 1994 were analyzed retrospectively. The informed consents of all patients were obtained and the ethics committee approval was received. Of the 399 patients, 356 cases were male, and 43 cases were female with age ranging from 21 to 78 years old and a median age of 48 years old. The relations between preoperative Plt and patients' gender, age, gamma-glutamyl transpeptidase (GGT), hepatitis B surface antigen (HBsAg), alpha fetal protein (AFP), cirrhosis, tumor encapsulation, tumor diameter, tumor number, vascular invasion and histological differentiation were observed. Patients were divided into 3 groups according to the level of preoperative Plt:group 1 (<100×109/L, n=41), group 2 (100×109/L-300×109/L, n=321), group 3 (>300×109/L, n=37). Survival analysis of patients in 3 groups was conducted. The relations between preoperative Plt and clinicopathological parameters were compared using t test. Survival analysis was conducted using Kaplan-Meier method and Log-rank test. Survival prognosis was analyzed using Cox's proportional hazard model. Results Preoperative Plt was associated with HBsAg, AFP, and tumor diameter (t=2.069, 2.222,-3.911;P<0.05). The 5-, 10-, 15-year cumulative survival rates were 41.2%, 25.2%, 11.8%in group 1, 33.7%, 23.0%, 18.1%in group 2, and 11.4%, 8.6%, 5.7%in group 3 respectively. The survival rate in group 3 was signiifcantly lower than those in group 1 and group 2 (χ2=5.706, 11.361;P<0.05). Increasing preoperative Plt was an independent risk factor for postoperative prognosis. The prognosis in group 3 was poorer than those in group 1 and group 2 (HR=1.761, 1.845;P<0.05). Conclusions Increasing preoperative Plt is an independent risk factor for postoperative prognosis of patients with HCC after hepatectomy. Patients with increasing preoperative Plt have poor prognosis.

Objective To investigate the influence of portal hypertension (PHT) on the postoperative complications after hepatectomy for patients with hepatocellular carcinoma (HCC). Methods Clinical data of 152 HCC patients undergoing hepatectomy in Sun Yat-sen University Cancer Center from March 2003 to October 2005 were retrospectively analyzed. The patients were divided into the PHT and non-PHT groups. There were 76 patients in the PHT group including 62 males and 14 females, with a mean age of (49±11) years. There were 76 patients in the non-PHT group including 66 males and 10 females, with a mean age of (49±12) years. The informed consents of all patients were obtained and the local ethical committee approval had been received. After hospitalization, all patients received routine examination. The incidence of postoperative complications in two groups was observed and the independent risk factors for postoperative complications were evaluated. Normally distributed data were compared using t test. Non-normally distributed data were compared using Z test. The comparison of rate was conducted using Chi-square test. Independent risk factors for the incidence of postoperative complications were analyzed by Logistic multivariate regression test. Results The incidence of postoperative complications was 42%(32/76) and the liver function-related complications was 36% (27/76) in the PHT group, and were 20% (15/76), 16% (12/76) respectively in the non-PHT group, significant difference was observed between two groups (χ2=8.901, 7.760;P<0.05). No signiifcant difference was observed in the percentage of patients with grade I-II complications between PHT group [75%(24/32)] and non-PHT group [73%(11/15)] (χ2=0.015, P>0.05). No significant difference was observed in the 90-day mortality between PHT group [7%(5/76)] and non-PHT group [3%(2/76)] (χ2=0.599, P>0.05). Logistic regression analysis revealed that PHT complication (OR=3.376, 95%CI:1.564-7.287, P<0.05) and number of tumors>2 (OR=1.984, 95%CI:1.248-3.154, P<0.05) were the independent risk factors for postoperative complications. PHT complication (OR=3.231, 95%CI:1.431-7.298, P<0.05), number of tumors>2 (OR=1.832, 95%CI:1.137-2.952, P<0.05) and intraoperative transfusion > 400 ml (OR=2.776, 95%CI: 1.123-6.864, P<0.05) were the independent risk factors for liver function-related complications. Conclusions PHT can increase the incidences of postoperative complications and liver function-related complications after hepatectomy in HCC patients and is the independent risk factor for both complications. However, PHT will not increase the severity of postoperative complications or postoperative mortality.