Objective To investigate the effect of enteral nutrition tolerance assessment form on the early enteral nutrition tolerance in patients with gastric cancer after operation. Methods According to the admission sequence, 108 patients with gastric cancer were divided into the control group and the experiment group with 54 cases in each group. Enteral nutrition was used in the control group, while enteral nutrition tolerance assessment form was used to evaulate and care patients in experiment group. Finally, the two groups were compared in the anal exhaust time and the rate of complications. Result Anal exhaust in the experiment group was significantly earlier than that in the control group and the rate of complications was significantly smaller than that of the control group (P < 0.05). Conclusions The enteral nutrition tolerance assessment form for systemic evaluation and intervention is effective in improvement of the patients′tolerance to enteral nutrition in early postoperative enteral nutrition support to patients with gastric cancer. It can promote the recovery of patients.

Little is reported about the role of PTEN gene in the progression and prognosis of GISTs. This study examined the clinical implications of the tumor suppressor gene PTEN as a prognostic factor in the GISTs. Immunohistological staining and immunoblotting were employed to examine the PTEN protein expression, and its association with clinical measures. Clinicopathological features were reviewed by a retrospective examination of medical records. Reduced PTEN expression was significantly associated with tumor diameter, mitotic figure count, metastasis and pathological stage of tumor (P<0.05), and was not correlated with age, gender and tumor location (P>0.05). The 3-year survival rate of the patients with reduced PTEN expression was significantly lower than those with high PTEN expression (P<0.01). These results suggest that the expression of PTEN gene was significantly linked with the progression and metastasis of GISTs and it is an independent prognostic factor.

Objective To investigate the expression of phosphatase and tensin homolog gene (PTEN) and 1-phosphatidylinositol 3-kinase (PI3K) in rectal cancer and its correlation with clinical pathology.Methods MaxVisionTM immunohistochemical method was used to detect the expressions of PTEN and PI3K in 60 rectal cancer tissues,30 adenoma tissues and 10 normal rectal tissues,and the correlation between the expression levels and its clinicopathologic characteristics was discussed.Results The positive expression rate of PTEN in rectal cancer tissue was significantly lower than that in normal rectal tissue and adenoma tissue [43.3％ (26/60) vs.100.0％ (10/10),93.3％ (28/30),P ＜ 0.05].The positive expression rate of PI3K in rectal cancer tissue was significantly higher than that in normal rectal tissue and adenoma tissue [75.0％ (45/60) vs.30.0％ (3/10),33.3％ (10/30),P ＜ 0.05].The positive expression of PTEN and PI3K were correlated with carcinoembryonic antigen,degree of cell differentiation,TNM stage,lymph node metastasis and distant metastasis(P＜ 0.01 or ＜ 0.05 ),but had no correlation with age,gender,neoplasm location,neoplasm appearance (P ＞ 0.05).The correlated analysis showed that the positive expression of PTEN had negative correlation with PI3K (r =-0.269,P =0.023 ).Conclusions The high expression of PI3K and down regulation of PTEN in rectal cancer are closely related to its invasion and metastasis.There are some values to monitor PTEN and PI3K expression for determining biological behavior of rectal cancer.

Objective To investigate the effects of huaier granules on invasion and metastasis of colorectal cancer SW480 cells in vitro, and explore the basic mechanism. Methods The appropriate concentration and duration of huaier granules promoting SW480 cell apoptosis were determined by SubG1 method. Wound healing assay and transwell assay were used to observe the effect of huaier granules on SW480 cell invasion and metastasis. The changes of E-cadherin, twist, snail and vimentin at protein and mRNA levels were examined by Western blotting and Real-Time PCR. Results After treatment with huaier granules at 3. 0 g·L-1 for 36 h, apoptosis of SW480 cells was most significant, and wound healing assay revealed that relative mobility was (31. 36±2. 39)%, compared with (61. 11±1. 09)% in control group (P<0. 01). Number of invaded cells per field of view was (129±12) in treatment group and (354±20) in control group (P<0. 01). After treatment with huaier granules at 3. 0 g·L-1 for 36 h, protein and mRNA levels of E-cadherin were increased, while those of twist, snail and vimentin were decreased. Conclusion Huaier granules can inhibit invasion and metastasis of colorectal cancer SW480 cells in vitro through effectively depressing epithelial-mesenchymal transition.

Objective To study the mechanism of unscheduled Cyclin B1 expression at G_1 phase which is usually at G_2/M phase.Methods Human peripheral blood lymphocytes(PBL) from healthy volunteers were firstly activated by PHA and then went into cell cycle.The cells were collected at 0,36,48 and 60 h after activation and divided into two parts:one for Cyclins/DNA muhiparameter assay,and another for Post-sorting Western blot.Results After activation by PHA,Cyclin B1 and CDK1 of lymphocytes were expressed at G_1 phase.Conclusion Unscheduled Cyclin B1/CDKl probably contributes to lymphocytes in vivo into cell cycle.

Objective To observe the effects of eluting stents coated with arsenic trioxide(As2O3)and suspended in poly-L-lactic acid(PLLA)on expression of monocyte chemoattractant protein-1 (MCP-1)and interleukin-6(IL-6)and to assess the effects of As2O3 eluting stents on local inflammatory reaction in injured coronary arteries in pigs. Methods Bare metal stents,rapamycin eluting stents and As2O3-eluting stents were randomly and double-blindly implanted into the anterior descending branches,circumflex branches and right coronary arteries in eight pigs.Animals were sacrificed and coronary arteries were isolated 7 days after stents implantation.The expression levels of protein and mRNA of MCP-1 and IL-6 were determined by Western blot analysis and reverse transcription polymerase chain reaction(RT-PCR),and the inflammatory cell infiltration was observed by HE staining and immunohistochemistry. Results Compared to bare metal stents,As2O3-eluting stents and rapamycin-eluting stents identically and markedly inhibited the protein expression level of MCP-1(0.421±0.055 and 0.406±0.042 vs.0.857±0.053,P＜0.01)and IL-6(0.151±0.032 and 0.146±0.051 vs.0.551±0.032,P＜0.01)and correspondingly lowered the mRNA expression level of MCP-1(0.338±0.047 and 0.327±0.051 vs.0.724±0.027,P＜0.01)and IL-6(0.531±0.052 and 0.523±0.061 vs.1.015±0.041,P＜0.01),and significantly reduced the inflammatory cell infiltration of injured coronary arteries in pigs. Conclusions As2O3-eluting stents can effectively inhibit the expressions of MCp-1 and IL-6 and reduce the inflammatory cell infiltration of injured coronary arteries in pigs.

DNA damage response (DDR) in different cell cycle status of human peripheral blood lymphocytes (PBLs) and the role of H2AX in DDR were investigated. The PBLs were stimulated into cell cycle with phytohemagglutinin (PHA). The apoptotic ratio and the phosphorylation H2AX (S139) were flow cytometrically measured in resting and proliferating PBLs after treatment with camptothecin (CPT) or X-ray. The expressions of γH2AX, Bcl-2, caspase-3 and caspase-9 were detected by Western blotting. DDR in 293T cells was detected after H2AX was silenced by RNAi method. Our results showed that DNA double strand breaks (DSBs) were both induced in quiescent and proliferating PBLs after CPT or X-ray treatment. The phosphorylation of H2AX and apoptosis were more sensitive in proliferating PBLs compared with quiescent lymphocytes (P<0.05). The expression levels of anti-apoptotic proteins Bcl-2 were reduced and cleaved caspase-3 and caspase-9 were increased. No significant changes were observed in CPT-induced apoptosis in 293T cells between H2AX knocking down group and controls. It was concluded that proliferating PBLs were more vulnerable to DNA damage compared to non-stimulated lymphocytes and had higher apoptosis rates. γH2AX may only serve as a marker of DNA damage but exert no effect on apoptosis regulation.

Objective:To investigate the effect of retinoid-interferon-induced mortality (GRIM-19) gene on the apoptosis of colon cancer. Methods: A GRIM-19 eukaryotic expression vector (pCMV-Flag-GRIM-19) was constructed and transfected into SW480 cells. Expressions of GRIM-19 and apoptosis-related proteins were detected by Western blotting analysis. Apoptosis of SW480 cells was measured by Annexin-V/PI assay and mitochondrial membrane potential JC-1 staining. Results: The GRIM-19 eukaryotic expression vector pCMV-Flag-GRIM-19 was successfully constructed. Expression of GRIM-19 in SW480 cells was up-regulated and that of apoptosis-related protein Bcl-xl was down-regulated after transfection with pCMV-Flag-GRIM-19. Apoptosis rate was (7.7±1.39)% in SW480 cells transfected with pCMV-Flag empty vector and (15.0 ± 2.52)% in pCMV-Flag-GRIM-19 transfected cells (P<0.05). Mitochondrial membrane potential was decreased in (7.5±2.09)% of pCMV-Flag transfected cells and (17.5±3.07)% of pCMV-Flag-GRIM-19 transfected cells (P<0.05). Conclusion: In vitro GRIM-19 transfection can effectively induce apoptosis of colon cancer SW480 cells.

In this study, CD133+ subpopulations were isolated from 41 primary colorectal cancer tissues, the proliferation and cell cycle distribution of the cells were examined without in vitro expansion, and then compared to those of cell lines. The detection of CD133 in colorectal cancer tissues, isolation of CD133+ and CD133- epithelial subpopulations, Ki-67/DNA multiparameter assay and cell volume analysis were flow cytometrically conducted. The results showed that Ki-67 expression was correlated with CD133 level in primary cancer tissues, while cell cycle G2/M phase distribution or clinicopathological characteristics was not. In addition, the CD133+ cells showed larger cell volume and higher Ki-67 expression as compared with CD133- cells. But there was no statistically significant difference in G(2)/M phase distribution between the two subpopulations. Our results demonstrated that the CD133+ subpopulation in colorectal cancer tissue contained more actively cycling and proliferating cells, which was not correlated to clinicopathological factors but might contribute to tumor progression and poor clinical outcome.

This study examined the role of regulated upon activation normal T cell expressed and secreted (RANTES) and its receptor C-C chemokine receptor type 5 (CCR5) in gastric cancer metastasis and the associated mechanism. The expression of RANTES and CCR5 was detected by using immunohistochemical staining and Western blotting in the gastric cancer tissues obtained from 60 gastric cancer patients with or without lymph node metastasis (n=30 in each). The results showed that the expression levels of RANTES and CCR5 were higher in gastric cancer with lymph node metastasis than in that without metastasis (P<0.05). The expression levels of RANTES in 30 lymph nodes with cancerous invasion were higher than in 30 normal lymph nodes (P<0.05). Chemotactic test revealed that the number of migrating gastric cancer cells (n=295.0±54.6) induced by the protein of cancer-invading lymph nodes was greater than that by the protein mixture from cancer-invading lymph nodes and RANTES antibody (n=42.5±11.6) (P<0.05). RT-PCR showed that the expression levels of the main Th1 cytokines (IL-2, Γ-IFN) were lower in gastric cancer with lymph node metastasis (2.22±0.90, 3.26±1.15 respectively) than in that without metastasis (3.07±1.67, 4.77±1.52 respectively) (P<0.05), but the expression level of the main Th 2 cytokine (IL-10) was higher in gastric cancer with lymph nodes metastasis (6.06±2.04) than in that without metastasis (4.88±1.87) (P<0.05). It was concluded that RANTES and its receptor CCR5 may contribute to gastric cancer metastasis through influencing the balance of Th1/Th2. RANTES and CCR5 may become a marker of gastric cancer metastasis.