Objective To investigate the significance and expression of E-cadherin(E-CD),focal adhesion kinase(FAK)and FAK py397 in rectal cancer.Methods Thirty paraffin specimens of rectal cancer and adjacent tissues collected from 2001 to 2002 and 35 fresh specimens of rectal cancer and adjacent tissues resected from 2006 to 2007 at People's Hospital of Wuhan University were adopted in this study.The expression of E-CD,FAK and FAK py397 was detected by immunohistochemistry and Western blot.All data were analyzed using chi-square test.Results E-CD was positively expressed in the membranes of epithelial cells in normal rectal mucosa,while no E-CD expression was found in the membranes of epithelial cells in rectal cancer tissues.There was a significant correlation between the expression of E-CD,FAK,FAK py397 and tumor difierentiation,depth of invasion and lymph node metastasis(χ~2=7.099,18.358,25.612;12.316,28.823,23.168;8.927,18.122,22.620,P＜0.05),while no relationship between the expression of E-CD,FAK,FAK py397 and age,sex was detected(χ~2=0.439,1.899,3.676;0.541,4.051,1.135,P＞0.05).The expression levels of FAK and FAK py397 were 83% (54/65)and 68% (44/65)in rectal cancer tissues,and were 31%(20/65)and 26% (17/65)in adjacent tissues,with significant difference(χ~2=33.707,34.163,20.897,P＜0.05).Conclusion Lost expression of E.CD in the membrane of rectal cancer tissue and elevated expression of FAK and FAK py397 in the rectal cancer tissue might be related to the invasion and metastasis of rectal cancer,which may predict the biological behavior of rectal cancer.

Objective To examine the sensitivity of human colorectal carcinoma cells to 5-fluorouracil treatment by stable transfection of extrinsic Fas-associated death domain protein(FADD) gene，both in vitro and in vivo，so as to investigate the feasibility of combination therapy of FADD gene and 5-fluorouracil in human colorectal carcinoma.Methods①RT-PCR and Western blotting were used to detect the expressions of both mRNA and protein of FADD gene in SW480／FADD (stably transfected with FADD)，SW480／neo and SW480 cells.②After treatment with 5-fluorouracil as an apoptotic inducer，in vitro cell growth activities were investigated by MTT assay.Cell apoptosis and its rates were determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL)assay and flow cytometry of annexin V-FITC／PI staining.The expressions of caspase-8 and caspase-3 were examined by Western blotting.③To examine the inhibitory effect of FADD gene combined with 5-fluorouracil, tumor xenograft model was prepared for in vivo study.Results ① Compared with SW480 and SW480/neo cells, FADD mRNA and protein levels of SW480/FADD cells were higher (P<0.05). ② Inhibitory rate of SW480/FADD cells was remarkably higher than SW480 and SW480/neo cells (P＜0.05 ). ③ Forty-eight hours after treatment with 5-fluorouracil (10 mg/L), the apoptotic rate of SW480/FADD cells was (33.3 ± 4.5)%, which was higher than SW480 [(13. 9 ± 3. 2)%3 and SW480/neo [(14. 1 ± 3. 4)%], with significant difference (P< 0.05).④ Forty-eight hours after treatment with 5-fluorouracil (10 mg/L),procaspase-8 and procaspase-3 expressions of SW480 and SW480/neo cells were higher than SW480/FADD cells, whereas their cleaved caspase-8 and cleaved caspase-3 expressions were lower than SW480/FADD cells (P＜0. 05).⑤ In in vivo study, SW480/FADD cells increased the efficacy of fluorouracil-induced inhibition of tumor growth in nude mice. ConclusionsStable overexpression of FADD increases sensitivity of the cells to 5-fluorouracil and combination of FADD with 5-fluorouracil will he a promising alternative in colorectal cancer treatment.

The clinicopathological data of 173 cases of inflammatory myofibroblastic tumor (IMT)were retrospectively analyzed.Among them 125 were males and 48 females with a mean age of 47.9 y (5-78 y).The lesions of 117 cases were located in lungs,41 cases in eyes,8 in ileocecum,2 in liver,2 in spleen,1 in abdominal wall,1 in maxillary sinus and 1 in face.The average diameter of lesions were 3.5 cm,ranging from 1.0 cm to 7.0 cm.The clinical manifestations were not specific,depending on the locations of tumor.The imaging examinations were helpful for diagnosis.The prcsence of slender-spindled myofibroblasts and proliferation of fibroblast cells,with infiltration of chronic inflammatory cells were the basic histopathological features of the disease.Combined with the histological characteristics and immunohistochemical staining IMT can be differentiated from other spindle cell tumors.Appropriate surgical resection is the main treatment for IMT.

ObjectiveTo investigate the effects of niacin on the lipid metabolism in rat model of non-alcoholic fatty liver disease (NAFLD). MethodsForty Sprague-Dawley rats were randomly divided into control group, model group, intervention group 1 (0.5% niacin), and intervention group 2 (1% niacin). Rats were fed with high-fat diet for 8 weeks to induce an NAFLD model. The serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase, levels of total cholesterol (TC), triglyceride, and free fatty acid in serum and liver tissue, and level of malondialdehyde (MDA) in liver tissue were measured using assay kits. The morphological and histopathological changes in the liver were observed under a microscope. Comparison of data between groups was made by univariate analysis of variance using SPSS software; moreover, least significant difference test (equal variance assumed) and Tamhane's T2 test (equal variance not assumed) were used for pairwise comparison. ResultsCompared with the model group, every intervention group had significantly lower levels of ALT, TC, AST, TG, and FFA (all P＜0.05) in serum and level of MDA in liver tissue (P＜0.05), and had significantly increased expression of PPARα mRNA (P＜0.05), DGAT2 mRNA (P＜0.05), and SREBP1c mRNA (P＜0.05). Intervention group 2 had significantly reduced expression of DGAT2 mRNA and SREBP1c mRNA compared with intervention group 1 (P＜0.05). Compared with the model group, the intervention groups had relieved fatty degeneration of hepatocytes and alleviated inflammatory cell infiltration in the centrilobular portion of the liver. ConclusionNiacin regulates lipid metabolism in NAFLD animal models, reduces lipid oxidative stress, and significantly reduces liver steatosis and fibrosis by regulating the expression of PPARα mRNA, DGAT2 mRNA, and SREBP1c mRNA, so as to realize the protective effect against NAFLD.

ObjectiveTo investigate the effect of human umbilical cord mesenchymal stem cells （hUCMSCs） in the treatment of mice with liver fibrosis and its mechanism. MethodsA total of 18 specific pathogen-free C57BL/6 mice， aged 6 weeks， were selected and divided into control group （n=6）， carbon tetrachloride （CCl₄） model group （CCl₄ group， n=6）， and hUCMSCs treatment group （MSC group， n=6） using a random number table. The mice in the CCl₄ group and the MSC group were given intraperitoneal injection of CCl₄ solution to establish a mouse model of liver fibrosis， while those in the control group were injected with the same dose of corn oil， and the mice in the MSC group were injected with hUCMSCs via the caudal vein during the injection of CCl₄. At the end of week 8， mouse serum was collected， and the mice were sacrificed to collect and fix the liver. Enzyme-linked immunosorbent assay was used to measure the levels of inflammatory factors； an automatic biochemical detector was used to measure liver function parameters； HE staining， Masson staining， Sirius Red staining， and α-SMA immunofluorescence assay were used to evaluate liver fibrosis. Hepatic stellate cells （HSCs） stimulated by TGF-β were co-cultured with hUCMSCs in the medium with or without chitinase-3 like-protein-1 （CHI3L1）， and Western blot was used to measure the expression levels of proteins. A one-way analysis of variance was used for comparison of continuous data between multiple groups， and the Dunnett’s t-test was used for further comparison between two groups. ResultsMasson staining and Sirius Red staining showed that the CCl₄ group had a significantly higher degree of fibrosis than the control group （both P<0.05）， and the MSC group had significant alleviation of fibrosis compared with the CCl₄ group （both P<0.05）. Compared with the control group， the CCl₄ group had significant increases in the levels of interleukin-1β， interleukin-6 （IL-6）， aspartate aminotransferase （AST）， alanine aminotransferase （ALT）， and alkaline phosphatase （ALP） （all P<0.05）， and compared with the CCl₄ group， the MSC group had significant reductions in the levels of IL-6， AST， ALT， and ALP （all P<0.05）. The CCl₄ group had significantly higher expression levels of CHI3L1 and α-SMA than the control group and the MSC group （all P<0.05）. The cell culture experiment showed that the MSC+HSC group had a significantly higher expression level of Bax than the HSC group and the MSC+CHI3L1 group （both P<0.05）， suggesting that CHI3L1 reversed the pro-apoptotic effect of MSC on activated HSCs. ConclusionThis study shows that hUCMSCs can improve liver fibrosis in mice， possibly by inhibiting CHI3L1 to promote the apoptosis of HSCs.