Purpose:Constructing a high-flux tissue microarray/tissue chip and detecting IGF-Ⅱprotein expression of cases by it, and to determine the correlation between IGF-Ⅱprotein expression and lung cancer. Methods:A series of tissue chips were prepared by using tissue arrayer with samples from lung cancers of different histological classifications. Specimens from 54 cases of lung cancer and 10 cases of normal lung tissues were detected immunohistochemically on a tissue chip for IGF-Ⅱprotein expression and its correlation to clinic-pathological parameters was analyzed statistically. Results:Positive rate of IGF-Ⅱprotein in lung cancer was 42.6%(23/54), which was higher than that of normal lung(0.0%, 0/10, P0.05). Conclusions:IGF-Ⅱprotein might be related to the malignant behaviors of lung cancer. Detecting the expression of IGF-Ⅱ protein probably can predict the prognosis of lung cancer. It is feasible to utilize tissue chip for screening of clinical tissue specimens on a large scale.

Objective To investigate the role of KAI1, intergrin ?5?1 and FAK proteins in occurrence and development and invasion and metastasis of lung cancer and their value in predicting the prognosis of lung cancer by analyzing the expression levels of KAI1, intergrin ?5?1 and FAK proteins in lung cancer and the relationship between them and clinicopathological parameters.Methods Lung cancer and normal lung tissue and metastasis cancer were detected and analyzed for their KAI1, and FAK protein level using immunobiochemical method. Results The positive rate of KAI1 in normal tissue, primary cancer and metastasis cancer was respectively 100.0, 24.7 and 0.0. The positive rate of intergrin?5?1 was respectively 0.0, 49.4 and 83.3. The positive rate of FAK was respectively 10.0,48.3 and 83.3. The difference of above three marker among three groups was significant (P

Objective To find out the incidence tendency and characteristics of bladder tumors during the past 28 yesrs in our institution. Methods The data from 1980 to 2007 were divided into three stages:1980-1989,1990-1999和2000-2007.Microsoft excel and SPSSl3.O were used to analyze the sex,age and histological types. Results There were 2350 cases of bladder tumors in 28 years.There were 92(66 males,26 females)cases of benign tumors and 2258(1788 males,470 females)malignant tumors,the incidence in male was 3.8 times higher than that in female.The cases of bladder malignant tumors increased,and the female increased faster than male.The peak age of incidence changed from 50-69 in 1980-1989 to 60-79 in 2000-2007.The average age of squamous cell carcinomas was 68 years,which was the oldest;and the average of paraganglioma was 35,which was the youngest.The age of urinary bladder carcinoma in 1980-1989,1990-1999 and 2000-2007 were significantly different(male:57.5±11. 7,62.6±12.3,65.9±11.3;female:58.7±13.6,60.75±12.1,65.85±12.0,respectively,P<0.05).In male,the age of squamous cell carcinomas was significantly different from the age of urothelial cell carcinomas and adenocarnomas(68.0±9.7 vs 59.85±14.1 and 63.4±9.9,respectively,P<0.05).Inverted papillomas were the most common bladder benign tumors;urothelial cell carcinomas were the most common bladder malignant tumors,and adenocarcinomas were the second,squamous cell carcinomas were the third. Conclusion The incidence of bladder malignant carcinomas in our institution increased and the female increased more quickly than male.

Identifying the importance of improving pricing control in military hospitals based on a review of the status quo of such management.In addition to an analysis of difficulties in pricing control in these hospitals,proposing to build an efficient pricing control system with a better understanding of the significance of pricing control.Establishing rules and regulations on medical charges to regulate pricing;making use of computer networks in the management for medical charges transparency;enhancing charges securitization to rule out excessive charges;improving general competence of pricing workers to regulate pricing control,All these five measures will help enhance pricing control in military hospitals.

At present, the development of hospital in transition period the doctor-patient contradiction, mutu-al trust foundation weak such outstanding contradictions and problems, based on the analysis of facing the outpatient service charge first overall service consciousness; Contradiction link concentration; Hospital information system support does not reach the designated position; Charge personnel are not familiar with services such as business management status, on the basis of train first service consciousness concrete measures are put forward. Namely:strengthen the psychological counseling, advocate humanistic care;carry out training assessment, improve human-istic quality;strengthen the construction of standardization, the standard outpatient service charging process;develop information platform, optimize charging way;strengthen the department cooperation, build a system integration work.

Objective To sum up the experience of nursing patients with spinal tuberculosis combined with open pulmonary tuberculosis? Methods Preoperative nursing was done to 16 patients with spinal tuberculosis combined with open pulmonary tuberculosis to enhance their medical appliance? The careful postoperative observations of conditions and incisions were done to prevent pulmonary infections? Results Of the 16 patients,15 were well cured and 1 was discharged with antituberculotics for home treatment due to refusing to transfer to other hospitals for financial reason? Conclusion The enhanced perioperative health education and nursing is significant for the success of the operations and rehabilitation of the disease?

Objective To investigate the growth inhibition and apoptosis induction effect of vitamin E succinate on MCF-7 human breast cancer cells and to analyze the modulation of Fas expression in this process. (Methods) Estrogen receptor positive MCF-7 human breast cancer cells were treated with VES for 12h, 24h and 48h. The concentrations of VES were 5?g/mL, 10?g/mL and 20?g/mL. The inhibitory effect was measured with MTT method and the cell cycle and cell surface Fas expression were analyzed with flow (cytometry). Fas protein level was detected by Western blotting assay. Results VES had significant inhibitory effect on the growth of MCF-7 human breast cancer cells and the effect was dependently related to time and dosage. The apoptotic rate rose from 1.2% to 11.2%,16.4%, 41.2%,after treated with VES for 48h at the concentrations of 5?g/mL,10?g/mL,20?g/mL respectively. Fas protein level and cell (surface) Fas expression in cancer cells increased after the administration of VES. Conclusions VES had (significant) growth inhibition and apoptosis induction effect on MCF-7 estrogen receptor positive breast cancer cells. The mechanism was related to Fas upregulation on the surface of cancer cells.

Objective: To investigate the growth inhibition and apoptosis induction effect of vitamin E succinate (VES) on human colon cancer cells and to analyze the modulation of apoptosis-mediator Fas expression in this process. Methods: Human colon cancer cell line LS174T was treated with VES for 12 h, 24 h and 48 h at the concentrations of 5 mg/L, 10 mg/L and 20mg/L. 1-(4,5-dimethylthiazo-2-yl)-3,5-diphenylformazan (MTT) assay was employed to detect the inhibitory effect of VES on the growth of colon cancer cells. Flow cytometry was then used to analyze the cell cycle of the colon cancer cells after being treated with VES and the apoptotic rate was calculated at the same time. To find out whether the Fas protein expression was modulated in this process, Western blotting assay and flow cytometry were used to detect the Fas protein level in whole cell lystates and on cell surface. Results: VES exhibited a significant inhibitory effect on the growth of human colon cancer cells in a doseand time-dependent manner. After being treated with VES at 5 mg/L, 10 mg/L and 20 mg/L for 48 h, the apoptotic rate of LS174T cells rose from 0.90% to 15.9%, 46.7% and 64.5%, respectively. Fas neutralizing antibody can significantly block VES-induced apoptosis. After the administration of VES, total Fas protein in whole-cell extracts increased in a dose-dependent manner. The flow cytometry showed that the mean fluorescence intensity rose from 5.43 to 9.88, 13.21 and 18.0 after being treated with VES. Conclusion: VES can induce significant growth inhibition and apoptosis in human colon cancer cells. The modulation of Fas expression is one of the mechanisms involved in this process and may be related to the upregulation of Fas molecule on the cancer cell surface.

BACKGROUNDKAI1 is a new identified metastasis-suppressor gene whose expression in many types of tumors has been reported. The aim of study is to investigate the role of KAI1 protein in development of lung cancer and its values in predicting the prognosis of lung cancer.

METHODSThe expressions of KAI1 protein were detected in benign pulmonary disease tissue, precancerous disease tissue, lung cancer tissue and metastatic lung cancer tissue in local lymph node using tissue microarray and immunohistochemical method. The relationship between expression of KAI1 protein and clinicopathological parameters of patients with lung cancer was analyzed by Chi-Square test and Fisher exact test.

RESULTSThe positive rate of KAI1 expression was 100.0% in 10 cases of benign pulmonary diseases, 66.7% in 12 cases of precancerous diseases, 24.7% in 89 cases of primary lung cancer and 0 in metastatic lung cancer tissue in local lymph node respectively. The KAI1 protein expression in primary lung cancer tissues had no remarkable relationship with age and gender of the patients and the location of cancer, but had significant relationship with the histological type and differentiated degree of tumor, P-TNM stages and lymph node metastatic status.

CONCLUSIONSThe abnormal expression of KAI1 protein may participate in malignant progression of lung cancer. Its downregulation may promote the invasion and metastasis of tumor cell. Detection of the expression of KAI1 protein may be helpful to predict the prognosis of lung cancer.

BACKGROUNDFragile histidine triad (FHIT) is a candidate tumor suppressor gene. Aberrant expression of FHIT has been observed in multiple carcinomas induced by environmental carcinogens, especially in lung cancer. In this study, the expression of FHIT protein in lung cancer progression tissue microarray was detected and their roles in oncogenesis and progression of lung cancer were discussed.

METHODSThe expression of FHIT protein in tissue microarray with 270 cores was detected by SP immunohistochemistry method, in which there were 89 cases of primary lung cancer, 12 cases of lymph node metastasis of lung cancer, 12 cases of precancerous lesion and 10 cases of normal lung tissue, and the clinicopathological features of lung cancer were analyzed.

RESULTSThe expression of FHIT was localized in the cytoplasm. Loss of FHIT expression in primary cancers, precancerous lesion and lymph node metastasis of lung cancer was 46.1%, 41.7% and 50.0% respectively, while 0 in 10 cases of normal tissues. A significant difference of FHIT expression was observed among four groups (P < 0.05). Loss of FHIT expression in precancerous lesion, primary lung cancer and lymph node metastasis of lung cancer was significantly higher than that in normal lung tissue (P < 0.05). The difference among precancerous lesion, primary lung cancer and lymph node metastasis of lung cancer groups was not statistically significant (P > 0.05). Loss of FHIT expression was related to tumor histologicol types, degree of cell differentiation and the smoking history of patients (P < 0.05), but not to sex, age, gross appearance types, TNM stages, or lymph node metastasis (P > 0.05).

CONCLUSIONSThe protein expression level of FHIT is reduced in primary cancers and precancerous tissues, especially in most squamous cell carcinomas, poorly differentiated group and the patients with a smoking history. These results indicate that loss of FHIT expression might correlate with carcinogenesis, development of lung cancer and the carcinogenesis induced by smoking.