Objective To investigate the signal pathway of platelet activation in acute respiratory distress syndrome (ARDS). Methods Thirty healthy Sprague-Dawley (SD) rats were randomly divided into control group (n = 6) and model group (n = 24). The model of ARDS was reproduced by intravenous injection of oleic acid (0.25 mL/kg), and the rats in control group were injected with the same amount of normal saline. The blood of abdominal aorta was collected at 2, 6, 24, and 72 hours after model reproduction, the platelets were separated, and c-Jun N-terminal kinase phosphorylation (pJNK) levels which was one of major protein kinases in the mitogen-activated protein kinases (MAPKs) signal pathway was determined by Western Blot. The rats were sacrificed, the lung tissues were harvested, and lung coefficient (lung weight/body weight ×100%) and lung wet/dry (W/D) ratio were calculated. Pathological changes in the lung tissue were observed with hematoxylin-eosin (HE) staining in light microscope. Results Comp ared with the control group, platelet pJNK level in ARDS model group was significantly increased at 2 hours after model reproduction (gray value: 0.72±0.09 vs. 0.22±0.01), and peaked at 6 hours (gray value: 0.91±0.03 vs. 0.22±0.01), then it was decreased gradually. It was also significantly higher than that of control group till 72 hours after model reproduction (gray value: 0.39±0.06 vs. 0.22±0.01, all P < 0.05). Lung coefficient and lung W/D ratio in ARDS model group were significantly increased at 2 hours after model reproduction as compared with those of control group [(1.30±0.20)% vs. (0.60±0.10)%, 6.00±0.60 vs. 3.30±0.30], then they were decreased gradually. They were also significantly higher than those of control group till 72 hours after model reproduction [(0.90±0.10)% vs. (0.60±0.10)%, 4.80±0.70 vs. 3.30±0.30, all P < 0.05]. It was showed by light microscopy that lung tissue of rats in the control group had no significant pathological changes. At 2 hours after model reproduction in model group, clearly visible alveolar edema and interstitial edema, interstitial lung infiltration of inflammatory cells, small blood vessels dilation and congestion were found, and the re were a lot of protein exudates. The lesions of lung peaked at 24 hours. At 72 hours, absorption of most of fluid leaking in alveolar, alveolar space narrow, alveolar septum thickening, the reduction of inflammatory cells infiltration, fibrous tissue proliferation, and micro thrombosis formation were found. Conclusion In ARDS, in addition to pathological changes in the lung tissue, platelet activation occurs, and its activation process is related to the priming of JNK signal transduction pathways.

Objective To design a new cancer vaccine by using alpha-galactosylceramide (α-Galcer,α-GC) loaded tumor cells in combination with TLR 9 ligand and to evaluate its therapeutic effects on colon canc-er in mice.Methods MC38 cells were transfected with lentivirus (GFP-CD1d) to prepare CD1d-MC38 cells. The expression of CD1d molecules in CD1d-MC38 cells was detected by fluorescence microscopy , RT-PCR and flow cytometry.The sorted CD1d-MC38 cells were loaded with α-Galcer to prepare CD1d-MC38/α-GC complex. Flow cytometry was performed to evaluate the efficiency of combination .A mouse model of colon cancer was es-tablished to investigate the therapeutic effects of α-Galcer loaded tumor cells in combination with TLR 9 ligand ( CD1d-MC38/α-GC+CpG1826) on colon cancer in mice by analyzing tumor growth and mice survival time .Im-munohistochemical staining was used to detect CD 4+T and CD8+T infiltrating lymphocytes in tumor tissues .Re-sults The MC38 cancer cells that expressed CD 1d and GFP were successfully constructed , among which 98.10%±2.53%were positive for CD1d.Moreover, the CD1d-MC38 cells could combine with α-Galcer effec-tively in a dose and time dependent manner .Compared with PBS treated group ,α-GC treated group and TLR9 ligand treated group , the experimental vaccine strategy was sufficient to inhibit the growth of established tumors and prolong survival of tumor-bearing mice (P<0.01).Immunohistochemistry analysis revealed that levels of CD4+T cells and CD8+T cells in experiment group were significantly higher than those in groups treated with PBS,α-GC and TLR9 ligand (P<0.01).Conclusion CD1d-MC38/α-GC in combination with CpG1826 could efficiently inhibit the growth of established tumors and prolong survival of tumor-bearing mice .Immunohisto-chemistry analysis revealed that CD 4+T cells and CD8+T cells played important roles in anti-tumor immunity.

Objective:To study the relation between promyelocytic leukemia protein (PML) and gastric and colorectal cancers , and explore the relation between PML and epidermal growth factor receptor (EGFR) and vascular endothelial growth factor (VEGF) .Methods:The expression situations of PML ,EGFR ,and VEGF in gastric and colorectal cancer were detected by immunohistochemistry ,and their relations with tumor invasions ,lymph node metastases ,TNM stages and patients’ survival were analyzed .Results:PML was positively expressed in normal tissue adjacent to gastrointestinal cancer .The rate of PML deficiency was 33 .8% (54/160) in gastric cancer tissue ,while it was 38 .1% (64/168) in colorectal cancer tissue .PML deficiency in gastric cancer tissue was positively correlated with gastric wall invasion (P<0 .001) ,lymph node metastases (P=0 .018) and TNM stage (P<0 .001) ,and the survival period of patients with positive PML was longer than that of patients with negative PML (52 months vs 39 months , P<0 .001) .Age ,PML deficiency and TNM stage were the independent risk factors of gastric cancer prognosis .PML deficiency in colorectal cancer tissue was positively correlated with TNM stage (P=0 .012) ,and the survival period of patients with positive PML was longer than that of patients with negative PML (53 months vs 44 months , P= 0 .001) .The positive expression of EGFR was positively correlated with colorectal wall invasion (P<0 .001) ,lymph node metastases (P<0 .001) and TNM stage (P<0 .001) .PML deficiency ,TNM stage and EGFR expression were the independent risk factors of colorectal cancer prognosis .PML expression was negatively correlated with EGFR and VEGF expression (P<0 .05) .Conclusions:PML deficiency may promote the progression of gastric and colorectal cancer by up‐regulating the expression of EGFR and VEGF .PML deficiency is correlated with prognosis of gastric and colorectal cancer patients .