Purpose To establish a golden hamster model of intrahepatic cholangiocarcinoma (ICC) using BOP [N-nitrosobis (2-oxo-propyl) amine] and to explore the protein expression of Wisp-1,β-catenin, TGF-β1 and Smad4 in ICC and their relationship with the tumorigenesis. Methods 57 female golden hamsters aged 8 to 9 weeks (39 in experimental group, 18 in control group), the experi-mental animals were subjected to subcutaneous injection of BOP, the control group was injected with saline. The liver was removed and paraffin sections were prepared for histopathological observation. The protein expression of Wisp-1,β-catenin, TGF-β1 and Smad4 was detected by immunohistochemistry (IHC) in these blocks. Results Most of the animals in the experimental group (29/39) developed ICC, part of the animal (8/39) developed bile duct dysplasia, 1 developed focal bile duct hyperplasia, and 1 was not found bile duct hyperplasia. The positive expression rates of four protein markers in ICC, bile duct dysplasia and normal intrahepatic bile duct tissues were Wisp-1,79. 3%, 87. 5% and 5. 0%,β-catenin, 96. 6%, 100. 0% and 15. 0%, Smad4, 96. 6%, 100. 0% and 25. 0%, TGF-β1, 62. 1%, 12. 5% and 5. 0%, respectively. The positive expression rates of Wisp-1, beta-catenin and Smad4 protein in both the ICC and the tissue of bile duct dysplasia were higher than that of normal intrahepatic bile duct tissue ( P<0. 001 ) , The positive ex-pression of TGF-β1 in the ICC tissue was higher than that of normal intrahepatic bile duct tissue and bile duct dysplasia (P<0. 001). Conclusions The study showed that BOP can induce a golden hamster model of ICC and provides a reliable animal model for the study of ICC. The high expression of Wisp-1,β-catenin, TGF-β1 and Smad4 in BOP-induced intrahepatic cholangiocarcinoma is closely re-lated to occurrence, development and infiltration of ICC.

Objective To investigate the clinicopathologic and immunohistochemicalcharacteristics of primary squamous cell carcinoma of the breast(PSCCB). Methods Sixteen patients with primary squamous cell carcinoma of the breast were retrospectively reviewed. Twelve cases with a follow-up information were evaluated for ER, PR, C-erbB-2, HCK, Ki-67 expression. Results PSCCB is a very rare neoplasm,constituting 0.8 % of all breast carcinoma over 28 years(1981-2008) in our hospital. The patients age varied from 25 to 72, median age is 49 years old. All patients received operative treatment. Seven patients had metastatic disease in axillary lymph nodes. Three patients died from metastases and tumour recurrence.Tumors were usually ER-negative, but most cases showed high molecular cytokeratin (HCK) expression.Conclusion In terms of the clinical feature, there were no differences between the PSCCB and the other breast cancer. PSCCB could be confirmed by pathology. The prognosis is in controversial. Standard therapy should be studied and recommended in future.

Objective To evaluate the effect of glucose-insulin-potassium (GIK) on intestinal injury in endotoxemic rats.Methods Sixty male Sprague-Dawley rats, weighing 200-250 g, were equally and randonly divided into endotoxemia group (lipopolysaccharide [LPS] group) and GIK group.LPS 8 mg/kg was injected intraperitoneally once a day for 3 times in total to establish the model of endotoxemia-caused intestinal injury.Starting from 2 h after the initial injection of LPS, normal saline was continuously infused at 4 ml · kg 1 · h-t in group LPS, and GIK 4 ml · kg 1 · h 1was infused intravenously in group GIK.Before establishment of the model, and at 3 and 5 days after establishment of the model, 10 rats in each group were sacrificed, and blood samples were collected from the abdominal aorta for determination of tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10) and diamine oxidase (DAO) concentrations in plasma by enzyme-linked immunosorbent assay.TNF-α/IL-10 ratio was calculated.A segment of ileum of 2 cm in length, 20 cm from the ileocecal junction, was removed for microscopic examination.The degree of damage to the intestinal mucous membrane was scored according to Chiu.Results Compared with the values before establishment of the model, the plasma TNF-α/IL-10 ratio, DAO concentration, and Chiu's scores were significantly increased at 3 days after establishment of the model in the two groups, the plasma TNF-α/IL-10 ratio, DAO concentration, and Chiu's scores were increased at 5 days after establishment of the model in group LPS, and the plasma DAO concentration, and Chiu's scores were increased at 5 days after establishment of the model in group GIK (P＜0.05).Compared with the values at 3 days after establishment of the model, the TNF-α/IL-10 ratio and plasma DAO concentration were significantly increased in group LPS, and the TNF-α/IL-10 ratio and plasma DAO concentration were decreased in group GIK at 5 days after establishment of the model in group GIK (P＜0.05).Compared with group LPS, the TNF-α/IL-10 ratio, plasma DAO concentration, and Chiu's scores were significantly decreased at 3 and 5 days after establishment of the model in group G1K (P＜0.05).Conclusion GIK can reduce intestinal injury in endotoxemic rats.

Objective To explore the biological effect of transcription factor B1,mitochondrial(TFB1M)on hepatocellular carcinoma(HCC)cells,and to explore the molecular mechanism of its regulation on malignant metastasis of HCC.Methods The expression level of TFB1M in liver cancer and its relationship with clinical characteristics of patients with HCC was analyzed based on TCGA-LIHC and GEO databases.Based on the median expression level of TFB1M,the TCGA-LIHC samples were divided into low expression group of TFB1 M(n=170)and high expression group of TFB1M(n=170),and GSEA was used for gene set enrichment analysis.The overexpressed TFB1M plasmid was constructed to transfect HepG2 and Huh7 cells.Cell migration and invasion were assessed by scratch healing and Transwell chamber assays.Results The expression of TFB1M was significantly decreased in HCC,and the expression of TFB1M was related with gender in HCC.The results of GSEA analysis indicated that the low expression of TFB1M might be related to liver cancer subclass proliferation up gene set,stem cell hepatocellular carcinoma gene set,and extracellular matrix assembly gene set in HCC.Overexpression of TFB1M remarkably attenuated the migration and invasion activity of HCC cells.Conclusions The expression of TFB1M was significantly decreased in HCC,and overexpression of TFB1M could attenuated the migration and invasion activity of HCC cells.