Objective To investigate the effect of psychological intervention combined with parecoxib on cognitive function in patients after liver resection of hepatocellular carcinoma. Methods From March 2015 to March 2017 in the first people's hospital of Yongkang city for diagnosis and treatment of liver cancer were 40 cases according to different nursing, drug intervention were divided into control group and observation group, the control group were treated with basic nursing + saline intervention, observation group with psychological intervention + Tenai (parecoxib sodium) intervention. The changes of cognitive function (MMSE score), inflammatory factors (TNF-α, IL-6 and S100) levels were recorded before and after intervention in the two groups, and the data obtained were analyzed and summarized. Results The psychological intervention and intervention Tenai (observation group) resection for hepatocellular carcinoma is better than the basic nursing + saline patients (control group) intervention, patients with MMSE score and TNF- α, IL-6, beta S100 levels were better than the control group, the difference was statistically significant (P<0.05). Conclusion Resection for hepatocellular carcinoma patients psychological intervention + Tenai intervention effect, it can reduce the level of inflammatory factors in patients, and has a good effect on the recovery of cognitive function after surgery.

Objective To investigate the application effect of psychological intervention combined with parecoxib in rehabilitation of patients with bile duct carcinoma after the operation. Methods According to the different intervention models from January 2015 to March 2017 in the first people's hospital of Yongkang city surgical treatment of bile duct carcinoma,40 cases of patients groups: control group with routine nursing plus saline intervention, observation group with psychological nursing + Tenai (parecoxib sodium) mode of intervention; on the psychological state of the two groups before and after intervention to improve patients the cognitive function, to improve the situation, changes in pain scores were recorded, and the related data for comparative analysis. Results The psychological nursing + Tenai (parecoxib sodium) model (observation group) intervention in the treatment of patients with bile duct cancer surgery clinical effect is better than that of routine nursing mode + normal saline (control group) the clinical effect of intervention, the psychological state of patients to improve the situation, improve cognitive function, pain score changes were better than the control group, there was statistical significant differences (P<0.05). Conclusion The surgical treatment of patients with cholangiocarcinoma patients psychological nursing + Tenai (parecoxib sodium) intervention effect significantly, can effectively improve the patients psychological status, cognitive function, and can reduce postoperative pain fully, has an excellent role in promoting the rehabilitation of patients after surgery, worthy of clinical application.

OBJECTIVE To investigate the occurrence of injuries by sharp instrument among new medical staff and their preventive consciousness and measures.METHODS Through questionaires,one hundred and fifty four interns who graduated from 2004 to 2006 were surveyed retrospectively.RESULTS Of the new interns,126(81.8%)persons were injured 585 times by sharp instrument,87.8% of whom were injured twice.During the internship,83 persons had passed sharp instrument injury prevention training,and earned priorities in its prevention.In the group of 83 persons trained,59 persons(71.1%) were injured;in another group of 71 persons untrained,67 persons(94.4%) were injured,there was significant difference at the rate of injuries between two groups.Opening ampules,and manipulating needles of syringes or infusion devices were the three major causes due which sharp injuries happened,were accounted for 35%,27% and 22%.CONCLUSIONS New medical staff have high rate of the sharp instrument injuries during internship,the occurrences of injuries are mostly due to the inadequacy in consciousness,the inpreficiency in operating,the high rate of with sharp instrument.Therefore,to reduce the sharp instrument injuries,developing good operating habit;performing operating procedure conscientiously;using medical equipment which can prevent injuries are the effective measures.

Objective To explore the relationship between quality of life and acceptance of disability of colostomy patients.Methods Using convenience sampling method to investigate 111 colostomy patients.General information questionnaire,QLQ-C30 scale,QLQ-CR38 scale and Acceptance of Disability Scale were used to investigate patients' general condition,quality of life and acceptance of disability.Data was analyzed by SPSS 17.0.Results The general health condition of colostomy patients was better than reference value and the score of ADS was at an average level.There was a relationship between general health condition,functioning dimensions,symptom dimensions and acceptance of disability.Conclusions There was a close relationship between quality of life and acceptance of disability.The acceptance of disability should be improved to help patients to obtain better quality of life.

BACKGROUNDTumor-necrosis factor related to apoptosis inducing ligand protein(TRAIL), like tumor-necrosis factor (TNF) and Fas, is a member of TNF cytokine supper family. Many researches have showed that TNF-α can reverse the resistance to some chemotherapeutic agents in cancer cell lines, and some anticancer drugs can result in up-regulations of death receptor (DR) and further lead to the enhancement of apoptosis induced by TRAIL. In order to clarify if TRAIL can reverse the resistance to cisplatin in cancer cells, the effects of recombinant human tumor-necrosis factor related to apoptosis inducing ligand protein (rhTRAIL) on apoptosis in human lung adenocarcinoma cell lines resistant to cisplatin (DDP) in vitro was explored.

METHODSHuman lung adenocarcinoma cell lines resistant to cisplatin, A549/DDP cells, were cultured in regular condition. At 24 hours after TRAIL and DDP, alone or combined, microculture tetrazolium (MTT) dye was used to evaluate the cytotoxic effects. And besides, to detect the apoptotic effects of rhTRAIL on A549/DDP cells, flow cytometry assay was used to test the apoptosis proportion, diphenylamine assay (DPA) was applied to detect the percent of DNA fragmentation and Caspase-3 chluorometric assay was performed to test the activity of Caspase-3 among these cells.

RESULTSA549/DDP cells were not sensitive to low-dose rhTRAIL alone. The rate of growth inhibition and the apoptotic indexes such as the apoptosis proportion, the percent of DNA fragmentation and the activity of Caspase-3, had all no significant changes with rhTRAIL concentration less than 25μg/L (P > 0.05). But treated with higher-dose rhTRAIL more than 50μg/L, the four values changed obviously: 68.6%, (27.13± 0.66)%, (37.4±2.0)% and 0.117±0.011, respectively (P < 0.05). With combination of different concentration of rhTRAIL and 3mg/L DDP, the cyto-toxic and apoptotic effect was comparatively more apparent. The combination of rhTRAIL and 3mg/L DDP presented synergistic effect on A549/DDP, 12.5μg/L concentration of rhTRAIL together with 3mg/L DDP could kill 30.4% of A549/DDP cells. Furthermore, the rate of cell apoptosis, percent of DNA fragmentation and activity of caspase-3 increased to (19.39±0.54)%,(17.3±4.1)% and 0.138±0.009, which were significantly different from those of rhTRAIL alone (P < 0.01).

CONCLUSIONSHigh-dose rhTRAIL can also induce the cells resistant to cisplatin to apoptosis, but the cytotoxic and apoptotic effects of rhTRAIL alone are weaker than those of combination of rhTRAIL and low-dose cisplatin which can augment the apoptotic effect induced by rhTRAIL. rhTRAIL is expected to be an efficient biologic drug for treatment of lung cancer resistant to chemotherapy.

BACKGROUNDThe excision repair cross-complementing gene 1 (ERCC1), which is important in the repair of cisplatin-DNA adducts, is reported to be related to cisplatin resistance in tumor cells. The aim of this study is to investigate the influence of low-dose cisplatin on expression of ERCC1 gene and to confirm the correlation between ERCC1 and cisplatin resistance in human lung adenocarcinoma cell lines.

METHODSA549 and A549/DDP cell lines were treated with 10 μmol/L cisplatin for 12, 24, 48 and 72 h, or treated with 5, 10, 20, 40 μmol/L cisplatin for 24 h respectively. Then the expression of ERCC1 mRNA and protein was measured by RT-PCR and immunocytohistology SABC assay respectively. The resistance of A549/DDP cells was measured by MTT assay.

RESULTSAfter treating with 10 μmol/L cisplatin for 12 h, up-regulation of ERCC1 mRNA and protein was observed in A549 cells, then reached the peak levels in 72 h group. After treating with 5 μmol/L cisplatin for 24 h, up-regulation of ERCC1 mRNA and protein was observed in A549 cells, and when treated with 20 μmol/L cisplatin for 24 h, the ERCC1 mRNA and protein reached the peak levels. Comparing with the parental cells, ERCC1 expression increased obviously in A549/DDP cells, which were established by continuous low-dose cisplatin treatment.

CONCLUSIONSUp-regulation of ERCC1 expression can be induced by low-dose cisplatin in human lung adenocarcinoma cell line A549, and ECRR1 may play roles in cisplatin resistance.

PURPOSE: Vascular endothelial growth factor (VEGF) signal transduction mainly depends on its binding to VEGF receptor 2 (VEGFR-2). VEGF downstream signaling proteins mediate several of its effects in cancer progression, including those on tumor growth, metastasis, and blood vessel formation. The activation of VEGFR-2 signaling is a hallmark of and is considered a therapeutic target for breast cancer. Here, we report a study of the regulation of the VEGFR-2 signaling pathway by a small molecule, isomangiferin. METHODS: A human breast cancer xenograft mouse model was used to investigate the efficacy of isomangiferin in vivo. The inhibitory effect of isomangiferin on breast cancer cells and the underlying mechanism were examined in vitro. RESULTS: Isomangiferin suppressed tumor growth in xenografts. In vitro, isomangiferin treatment inhibited cancer cell proliferation, migration, invasion, and adhesion. The effect of isomangiferin on breast cancer growth was well coordinated with its suppression of angiogenesis. A rat aortic ring assay revealed that isomangiferin significantly inhibited blood vessel formation during VEGF-induced microvessel sprouting. Furthermore, isomangiferin treatment inhibited VEGF-induced proliferation of human umbilical vein endothelial cells and the formation of capillary-like structures. Mechanistically, isomangiferin induced caspase-dependent apoptosis of breast cancer cells. Furthermore, VEGF-induced activation of the VEGFR-2 kinase pathway was down-regulated by isomangiferin. CONCLUSION: Our findings demonstrate that isomangiferin exerts anti-breast cancer effects via the functional inhibition of VEGFR-2. Pharmaceutically targeting VEGFR-2 by isomangiferin could be an effective therapeutic strategy for breast cancer.
Angiogenesis Inhibitors ; Animals ; Apoptosis ; Blood Vessels ; Breast Neoplasms ; Cell Proliferation ; Heterografts ; Human Umbilical Vein Endothelial Cells ; Humans ; In Vitro Techniques ; Mice ; Microvessels ; Neoplasm Metastasis ; Phosphotransferases ; Rats ; Receptors, Vascular Endothelial Growth Factor* ; Signal Transduction ; Vascular Endothelial Growth Factor A* ; Vascular Endothelial Growth Factor Receptor-2*

Objective : To investigate the effects of hederagenin (HDG) on proliferation , migration , invasion and apoptosis of glioblastoma (GBM) cells and involved mechanism. Methods : Human GBM cell lines U87 , U251 and human brain glial cell line (HEB) were selected as the study subjects , and HDG 0 μmol/L ( or 0 mg/kg) was used as the control group. MTT , EdU staining and cell plate cloning were used to detect the effect of HDG on the proliferation of GBM cells. Trypan blue staining was used to detect GBM cell death affected by HDG. The effects of HDG on migration and invasion of GBM cells were detected by cell scratch and Transwell assay. To analyze the effects of HDG on apoptosis of GBM cells , apoptosis⁃related proteins Bcl⁃2 , Bax , p53 and cleaved caspase⁃3 were detected by Western blot. Mitochondrial potential change was detected by JC⁃10 staining , and apoptotic cell count was displayed by Annexin V ⁃FITC staining. The effect of HDG on tumor bearing in GBM was analyzed by xeno transplantation in BALB/C mice. Results : Compared with the control group (HDG 0 μmol/L) , HDG significantly inhibited the proliferation , migration and invasion of U87 and U251 cells , and they were dependent on the use dose of HDG. Trypan blue staining showed that HDG obviously increased death number of GBM cells. The mitochondrial potential of GBM cells was remarkedly decreased , the number of apoptotic GBM cells obviously increased , the expressions of apoptosis⁃related proteins p53 , Bax , cleaved⁃caspase3 were up⁃regulated and Bcl⁃2 was down⁃regulated by HDG in U87 and U251 cells. HDG significantly inhibited the size of subcutaneous GBM , the Ki67 positive rate of GBM cells and caused a large number of GBM cells to die in BALB/C mice. HDG had no obvious toxic effect on human HEB cells and the liver of tumor⁃bearing mice. Conclusion HDG can significantly inhibit the proliferation , migration and invasion of GBM cells and induce the apoptosis of them. The mechanism of HDG induced apoptosis of GBM cells may be through mitochondrial damage and regulation of p53 and Bcl⁃2/Bax expression.