Objective To investigate the intra-splenic blood cell count of posthepatitic cirrhotic portal hypertension,and compare it with patients' peripheral blood cell count to explore the role the spleen plays in peripheral cytopenia often seen in posthepatitic cirrhotic portal hypertension.Methods A prospective study was made on 15 cases with post hepatitis B cirrhotic portal hypertension undergoing splenectomy.Intrasplenic blood was sampled from upper pole,hilus (central pole),and lower pole of the spleen respectively for blood cell count.Results were compared with that of preoperative peripheral blood.Results There were significant statistical differences in the WBC count between splenic blood and peripheral blood,(11.20 ± 4.73) × 109/L vs.(4.06 ± 1.75) × 109/L,t =5.05,P ＜ 0.05),and in PLT count,(182.45±66.57) × 109/L vs.(63.54 ±28.40) × 109/L,t =7.285,P ＜0.05.There was no differences in the RBC count,(3.55 ± 0.94) × 1012/L vs.(3.01 ± 0.62) × 1012/L,t =1.874,P ＞ 0.05.Positive correlations were found between splenic PLT count and peripheral PLT count (r =0.610,P ＜0.05).Conclusions In posthepatitic B cirrhotic portal hypertension patients the intra-megalosplenic PLT and WBC count are significantly higher than that in peripheral blood.Megalosplenic PLT count correlates positively with peripheral PLT count.

Objective To investigate the causes of bile duct dilatation. Methods Clinical data of 1 430 patients with bile duct dilatation who were admitted to People's Hospital of Hainan Province between January 2000 and December 2014 were retrospectively analyzed. Among them, 876 were males and 554 were females, aged 13-85 years old with a median age of 56 years old. The informed consents of all patients were obtained and the local ethical committee approval was received. The causes and severity of bile duct dilatation were observed. The relationship between the degree of secondary bile duct dilatation and serum total bilirubin (TB) level was analyzed by Kruskal-Wallis rank-sum test. Results Congenital cystic dilatation of common bile duct accounted for 6.3% (90/1 430). And secondary bile duct dilatation accounted for 93.7%(1 340/1 430), including 28.4% (380/1 340) of mild dilatation, 35.8% (479/1 340) of moderate, 25.4%(341/1 340) of severe and 10.4%(140/1 340) of extremely severe. Common causes of secondary bile duct dilatation were common bile duct stone, pancreatic head carcinoma, periampullary carcinoma, extrahepatic cholangiocarcinoma and chronic pancreatitis, in the order. The degree of secondary bile duct dilatation induced by common bile duct stone, pancreatic head carcinoma, periampullary carcinoma and chronic pancreatitis was correlated with the serum TB level (H=29.401, 9.483, 9.722, 11.907; P<0.05). Conclusions Bile duct dilatation is mainly secondary. The common causes are common bile duct stone, pancreatic head carcinoma, periampullary carcinoma, extrahepatic cholangiocarcinoma and chronic pancreatitis, in the order. The degree of secondary bile duct dilatation induced by common bile duct stone, pancreatic head carcinoma, periampullary carcinoma and chronic pancreatitis is correlated with serum TB level.

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.