Objective To explore the risk factors of liver metastasis from colorectal cancer. Methods The clinic data of 1341 patients with colorectal cancer who had been admitted to our department from January 1989 to December 2004 were analyzed retrospectively. Results The incidence of the liver metastasis from colorectal cancer was 11.56% (155/1341). Univariate analysis showed that sex, location and size of the primary tumor site, regional lymph node metastasis, infiltration depth of the bowel wall, involvement of the adjacent viscera, complications and peritoneal implantation were relevant to liver metastasis (X2=6.517, 10.208, 11.173, 42.160, 80.731,6.593, 3.887, 14.352, P < 0.05). Logistic regression analysis showed that sex, regional lymph node metastasis, infiltration depth of the bowel wall, complications and primary tumor site were correlated with liver metastasis ( b = 0.655, -0.488, 1.355, -0.752, 0.273, P <0.05). Conclusions Male patients, patients with regional lymph node metastasis or with involvement of tissues out of the serosa have higher chance of liver metastasis from coloreetal cancer. Patients with colon cancer are apt to develop liver metastasis than those with rectal cancer. The incidence of liver metastasis in colorectal cancer patients complicated with other diseases is low.

To reveal the innate immunity of mast cells against recombinant VP1-VP4 protein of foot-and-mouth disease virus (FMDV), mouse peritoneal mast cells (PMCs) were pulsed with recombinant VP1-VP4 protein. The supernatants harvested from PMCs cultures were applied to the high throughput ELISA array. Our results show that the expression levels of CCL19, L-selectin, CCL17, and TNF alpha released from PMCs pulsed with recombinant VP1-VP4 were significantly down-regulated compared with PMCs alone (P<0.001). Surprisingly, in comparison with PMCs alone, the expression levels of CCL19, IL-15, IL-9, G-CSF, and Galectin-1 in PMCs with the mannose receptor (MR) inhibitor were significantly up-regulated (Plt;0.01), and the expression level of IL-10 was also remarkably up-regulated (Plt;0.05). Importantly, the protein expression levels in PMCs treated with MR inhibitor were higher than PMCs pulsed with VP1-VP4, including IL-10, IL-17, CCL20, IL-15, IL-9, L-selectin, CCL17, TNF alpha, and CCL19 (Plt;0.01) as well as CCL21, and G-CSF (Plt;0.05). Differential expression analysis in bioinformatics shows that both L-selectin and CCL17 were recognized as differentially expressed protein molecules (Log2(ratio)≤-1) when compared with PMCs alone. Furthermore, the up-regulation of the expression levels of CCL20, CCL19, L-selectin, and IL-15 in PMCs treated with MR inhibitor was defined as differential expression (Log2(ratio)≥1). These data indicate that PMCs are capable of secreting CCL19, L-selectin, CCL17, and TNF alpha spontaneously and the recombinant VP1-VP4 has an inhibitive potential to PMCs during their performance of innate immune response. Given the protein expression levels from PMCs pre-treated with MR inhibitor were significantly increased, it can be deduced that immunosuppression of FMDV is presumably initiated by the VP1 recognition of MR on mast cells.
Animals ; Capsid Proteins ; immunology ; Cells, Cultured ; Cytokines ; immunology ; Enzyme-Linked Immunosorbent Assay ; Foot-and-Mouth Disease ; Foot-and-Mouth Disease Virus ; Interleukins ; immunology ; Mast Cells ; immunology ; Mice ; Proteome ; immunology ; Recombinant Proteins ; immunology ; Viral Structural Proteins ; immunology

Objective: Positron emission tomography-computed tomography (PET-CT) has been used to quantify inflammatory response in the body. The aim of the present study was to explore the possibility of using this method to evaluate the stability of atherosclerotic plaques and the efficacy of atorvastatin in stabilizing atherosclerotic plaques. Methods: Twenty New Zealand male white rabbits were included and divided into the atorvastatin intervention group and the control group, with 10 rabbits in each group. Rabbits in both groups were fed with a high fat diet for 20 weeks, and treated with thoracoabdominal aortic balloon-pulling to establish atherosclerosis model at the end of the 2nd week. Rabbits in atorvastatin intervention group was given atorvastatin intragastrically once a day. At the 8th week, thoracoabdominal aortic ultrasound was used to detect plaques in all rabbits. Blood was drawn at the 3rd and the 20th week, respectively, to measure blood lipids, high-sensitive C-reactive protein (hs-CRP) and matrix metalloproteinase-9 (MMP-9). At the end of experiment, survival animals were scanned by ¹⁸F-FDG PET-CT, and the average and maximum standard uptake values (SUVmean, SUVmax) of aortic segments were measured. Thereafter, the animals were sacrificed and aortic specimens of rabbits were taken and examined by immunohistochemistry. The pathological indexes were measured and compared. Results: At the end of experiment, the total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), hs-CRP [ (4.58±0.51) ng/ml vs.(5.87±0.66) ng/ml, P<0.01], MMP-9[ (43.93±2.16) ng/ml vs. (50.77±2.32) ng/ml, P<0.01], SUVmean (0.59±0.15 vs. 0.68±0.20, P<0.05) , SUVmax (0.68±0.20 vs. 0.81±0.27, P<0.05) , plaque area [ (0.36±0.24) mm² vs. (0.50±0.34) mm², P<0.05) ] and density of macrophage[ (4.34±1.54) % vs. (5.65±1.89) %, P<0.01] in the atorvastatin intervention group were significantly lower than those in the control group. In contrast, fiber cap thickness of the plaque[ (4.12±0.66) μm vs. (2.96±0.37) μm, P<0.01] in the atorvastatin intervention group was higher than that of the control group, and the difference was statistically significant. The arterial plaque areas were positively correlated with SUVmean (r=0.27, P<0.05) and SUVmax (r=0.43, P<0.01) . Fiber cap thickness was negatively correlated with SUVmean (r=-0.38, P<0.05) and SUVmax (r=-0.47, P<0.01) . The density of macrophage were positively correlated with SUVmean (r=0.52, P<0.01) and SUVmax (r=0.51, P<0.01) . Conclusion ¹⁸F-FDG PET/CT can be used to evaluate the efficacy of atorvastatin by the stability of atherosclerotic plaques.