Objective To investigate the expression of a novel oncogene Stat3 in colorectal cancer. Methods Western blot analysis was performed on cancerous and normal colonic tissue of 45 patients with colorectal carcinoma. ResultsStat3 protein level increased in colorectal cancer compared with adjacent normal mucosa ( P

Adolescent ; Adult ; Aged ; Child ; Female ; Follow-Up Studies ; Gastrointestinal Hemorrhage ; complications ; surgery ; Humans ; Hypertension, Portal ; mortality ; surgery ; Male ; Middle Aged ; Renal Veins ; surgery ; Splenic Vein ; surgery ; Time Factors

Objective To clarify the role of a cell cycle regulator, cyclin D1 and CDK6 in patients with gastric carcinoma. Method Tissue samples from 48 patients with gastric carcinoma were included in the current study. Expression levels of cyclin Dl and CDK6 in samples of normal mucosa and tumor tissue were analyzed by Western blot. Result Overexpression of cyclin Dl and CDK6 protein were demonstrated in 58% and 69% of gastric cancer tissues, respectively. Several clinicopathologic parameters, including depth of tumor invasion, pathologic lymph node status and tumor stage ( P

AIM: The purpose of the study was to examine colon cancer cell lines to determine whether Stat5b/Survivin plays an important role in the process of apoptosis in colon cancer cells. METHODS: Protein lysates were extracted from colon cancer cells. Human colon cancer cell line HT29 was transfected with Stat5b antisense oligonucleotide mediated by liposome. MTT assay was used to measure the proliferation. Flow cytometry was applied to analyze the cell cycle and apoptosis. EMSA was used to detect the activity of Stat5. Western blotting was applied to measure the expression of Stat5, p-Stat5, cyclin D1, Survivin, Bcl-2 and Bcl-xL. RESULTS: Targeting of Stat5 using antisense oligonucleotide against the translation site resulted in apoptosis and downregulaed the expressions of Stat5, p-Stat5, cyclin D1 and Survivin, but not Bcl-2 and Bcl-xL. CONCLUSION: Constitutive activation of Stat5 is associated with the carcinogenesis of colon cancer cells. Blocking of Stat5 signaling inhibits the expression of Survivin and induces apoptosis in colon cancer cells.

Objective: To explore the effect of ultrasound on dentin smear layer's surface and bonding strength of the universal resin adhesive under self-etching mode. Methods: Forty mandibular third molars without caries were randomly divided into two groups; one was polished with silicon carbide sandpaper; the other was polished with silicon carbide sandpaper followed by ultrasonic treatment. Scanning electron microscope (SEM) was used to observe surface of the dentin. Treated teeth were bonded with two universal resin adhesives, Clearfil Universal Bond (pH=2.3) and All-Bond Universal (pH=3.1), and the penetration of the bonding interface was observed with a confocal laser scanning microscope (CLSM) after Rhodamine B staining. Finally, the micro tensile bond strength test was conducted to test the adhesion. Results: The SEM showed that after polishing with silicon carbide sandpaper, the smear layer of the dentin surface was scratched, and dentin tubules were almost completely blocked, with no obvious dentin tubules exposed. After ultrasonic treatment, the scratches were reduced, and a large number of dentin tubules were exposed. CLSM showed that both adhesives could penetrate the dentin along the dentin tubules more deeply after ultrasound treatment. Micro tensile bond strength tests showed that ultrasonic treatment could enhance the bonding strength of two universal resin adhesives. However, there was no statistical difference in bonding strength between these two universal resin adhesives under the same treatment. . Conclusion Ultrasound can partially remove the smear layer on dentin's surface, expose dentin tubules, and increase universal resin adhesives' penetration depth and bonding strength under self-etching mode

Objective To explore the reconstructive methods of benign bone tumor defects in proximal joint. Methods Operative treatment was performed in 11 cases with benign bone tumor defects in proximal joint, a-mong whom 4 cases were treated by curettage,cauterization of wall and bone grafting,3 cases were treated by filling branch through segment fibula transplantation with vascular,2 cases were treated by fibula head transplantation with vascular to reconstruct the glenohumeral joint and rediocarpal joint, and 2 cases were treated by artificial joint re-placement. Results The follow-up ranged from 1.5 to 6 years. All of cases got excellent bone unioned without re-lapse and 2 cases of them developed with little limitation in joint function. Conclusion The importance and recon-structive achievement of fibula transplantation in treating the benign bone tumor defects in proximal joint should be thought fully. The indication of artificial tumor prosthesis replacement should be strictly mastered.

Different materials for skull repair possess varying properties and clinical effects. Metal materials are the first to be applied, but most of them induce corrosion and heat conduction; Non-metal bone substitutes, such as organic glass, have ever been commonly used, but the poor biocompatibility and high infection rate of subcutaneous exudation limit their application; Bone cement shows good histocompatibility, but the repair scale is not complete; Medical silica gel is cheap and effective, but the appearance is not satisfactory resulting from local infections and material exposures; Titanium possesses good biocompatibility and well junctures with the skull, thus it is a promising materials although the shortages still remain. With the development of bioengineering research, the skull repair materials will open up concerning the study of bone tissue engineering, cartilage tissue engineering and cornea tissue engineering. This paper is aimed to search a well-biocompatible and clinically effective material for the skull repair by the comparison on the property and clinical application of varying materials.

Objective To explore the mechanism of HPV infection in carcinogenesis and progression of colon cancer. Methods Human colon cancer cells, HCT116 (with wild-type p53) and SW480 (with mutant-type p53), were transfected by HPV16 E6E7 oncogenes using a recombinant adeno-associated virus vector system. The transfection efficiency was determined by flow cytometry. The expression of HPV16 E6 genes was determined by Western blot. The cell proliferation and cell cycle was studied by MTT method and flow cytometry. Results Western blot confirmed the expression of E6 gene in colon cells that were infected by rAAV-E6E7. The population doubling time of HCT116 cell, which was more than 48 hours at control group, decreased to 33 hours. HPV16 E6E7 increased cell percentage of S phase and decreased cell percentage of G0/G1. The population doubling time of SW480 cell was 77.06% decreased and the OD540 was 47.18% increased with interference of HPV16 E6E7 gene. Conclusion HPV16 E6E7 oncogene precipitates the proliferation and positively controls cell cycle of HCT116 and SW480 human colon cancer cells. HPV infection may closely relate to the carcinogenesis and progression of colon cancer.

Objective To investigate the relationship between HPV infection and human colorectal carcinogenesis. Methods Colorectal carcinoma specimens from 72 Chinese patients were studied. DNA extracted from colorectal tissue was screened for HPV L1 by polymerase chain reaction (PCR), HPV subtype 6,11, 16, and 18 were detected by PCR using specific primers and in situ hybridization using specific probe. Results Twenty-four specimens out of 72 (33%) colorectal cancer were HPV L1 positive. The normal colorectal mucosa was HPV L1 negative. The location, infiltration and metastasis of colorectal carcinoma were all significantly related with HPV infection. The predominant HPV subtype was HPV 16,which was found in 58% of all HPV-positive colorectal carcinoma. Conclusion The presence of HPV DNA suggests that HPV may be involved in the carcinogenesis of colorectal carcinoma. HPV infection is closely related with the malignant potential of colorectal cancer.

Objective To explore the effect of EBV infection on proliferation and invasiveness of gastric cancer cell. Method BGC823, an EBV-negative human gastric cancer cell line, was infected by EBV. The cell proliferation and ability of invasion were studied by MTT method and in vitro invasive assay, respectively. Cell cycle was investigated by flow cytometry. RT-PCR was used to detect the EBNAs, LMP1 and EBER1 in the infected cell. Result The A ratio of EBV-infected cells increased by 34. 34% and the population of invasive cells increased by 28.72%. The cell percentage of S phase, which was 36. 7% at control group cell, was increased to 41. 9% while the cell percentage of G0/G1 was decreased. EBNA1 and EBER1 were detected in EBV infected gastric cancer cells while EBNA2 and LMP1 were both negative. Conclusion Epstein-Barr virus infection promoted proliferation and upregulated invasion of human gastric cancer cell. EBV infection may play an important role in the carcinogenesis and progression of human gastric cancer.