Objective To evaluate the efficacy of ~(125)I radioactive seeds implantation and ~(125)I plaque brachytherapy for oral carcinoma. Methods Eighteen patients with oral carcinoma confirmed by cytology or histopathology were included in this study, Twelve patients with tongue cancer and six patients with gingival carcinoma, there were 20 ulcerative lesions and 10 metastatic cervical lymph nodes. The mean diameter is (2.3±0.7)cm and(2.8±1.7)cm respectively. The patients were treated with both interstitial implantation of ~(125)I seeds and ~(125)I plaque brachytherapy or with ~(125)I plaque brachytherapy only according to patient's individual conditions.The metastatic cervical lymph nodes were treated with CT-guided interstitial implantation of ~(125)I seeds.The sizes of ulcerative lesions and lymph nodes were observed at 1,3,6 months following treatment,and statistical analysis of the sizes of ulcerative lesions were evaluated by paired t-test.Results After 1,3,6 months follow-up,The mean diameters of ulcerative lesions were(2.1±0.6)cm(t=3.559,P＜0.01),(1.7±0.5)cm(t=7.609,P＜0.01),(0.7±0.6)cm(t=11.508,P＜0.01),the cervical lymph nodes showed reduced size. Furthermore, PET-CT images showed a significant decrease in the metabolic activity of treated tumor. After six months, the focus of infection were healing in 8 patients, the cervical lymph nodes of one patient relapsed after ~(125)I implantation again. Patients were followed for 7 to 28 months, all patients were still alive. Conclusion Interstitial ~(125)I radioactive seeds implantation and ~(125)I plaque brachytherapy provide an effective, safe treatment for oral cancer.

Objective To assess the toxicity risks of diphenylchlorarsine (DA) to environments, human beings and livestock. Methods Totally 120 mice were randomly divided into 6 groups and given DA by gastric gavage at the doses of 32, 30, 28, 26, 24, 22 mg/kg respectively for LD_(50) of DA in mice. The toxicity of DA in rat skin were evaluated by smearing 50 ?l DA at the concentrations of 140, 70, 35, 17.5, and 8.8 mg/ml to an area of 4 cm2, and that of eyes exposure was carried out by dropping 10 ?l DA of 140.7, 70, 7, 0.7 mg/ml in rat eyes. The counterpart skin area and eyes served as control. Results LD_(50) of DA in mice was 28.07 mg/kg, the estimated doses for no-observed-adverse-effect levels (NOELs) were 8.8 mg/ml (0.44 mg) to the skin and 0.7 mg/ml (0.014 mg) to the eyes respectively. Conclusion DA can induce the injuries on the liver, kidneys, esophagus and stomach. High concentration of DA can cause inflammation of the skin and lens opacification, even blind.

During the treatment of neurosurgical patients, the changing of intracranial pressure (ICP) monitoring is the main monitoring objects, while most of the clinical equipment are wireline. With the rapid development of transducer and wireless network, miniaturization, micromation and wireless transmission become one of the research hotspots. This paper designed a wireless ICP monitoring system based on ZigBee technology, which can continuously measure the patient's intracranial pressure and temperature, and send monitoring data of patients of different ward to nurse station through the wireless network, and save it. Then we can inquiry the intracranial pressure and temperature using the intracranial pressure monitoring and management software we designed. The wireless system can be instaled in the hospital very conveniently, which can reduce the work intensity of medical staff. The system is very useful in clinical work.

A system was designed in this paper, which can be used in clinical cerebral oxygen data acquisition and display, it is based on STM32 and NIRS(Near-infrared Spectroscopy). First of all, this paper introduced the basic principle of SaO2 detection, and system scheme. Next, it illustrated the hardware system which is composed of the modules of LED, light source driver, photoelectric detection, and the signal processing. Then, the software system based on uC/OS-Ⅲ of the system was presented. At last, the feasibility and effectiveness of the system were verified by forearm occlusion and 3-D TV experiment. This system is noninvasive, small-volume, mobile- convenient, easy to use and can storage data.

BACKGROUND: Gene promoter methylation is a major epigenetic change in cancers, which plays critical roles in carcinogenesis. As a crucial regulator in the early stages of B-cell differentiation and embryonic neurodevelopment, the paired box 5 (PAX5) gene is downregulated by methylation in several kinds of tumors and the role of this downregulation in esophageal squamous cell carcinoma (ESCC) pathogenesis remains unclear. METHODS: To elucidate the role of PAX5 in ESCC, eight ESCC cell lines, 51 primary ESCC tissue samples, and eight normal esophageal mucosa samples were studied and The Cancer Genome Atlas (TCGA) was queried. PAX5 expression was examined by reverse transcription-polymerase chain reaction and western blotting. Cell apoptosis, proliferation, and chemosensitivity were detected by flow cytometry, colony formation assays, and 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assays in ESCC cell lines with PAX5 overexpression or silencing. Tumor xenograft models were established for in vivo verification. RESULTS: PAX5 methylation was found in 37.3% (19/51) of primary ESCC samples, which was significantly associated with age (P = 0.007) and tumor-node-metastasis stage (P = 0.014). TCGA data analysis indicated that PAX5 expression was inversely correlated with promoter region methylation (r = -0.189, P = 0.011 for cg00464519 and r = -0.228, P = 0.002 for cg02538199). Restoration of PAX5 expression suppressed cell proliferation, promoted apoptosis, and inhibited tumor growth of ESCC cell lines, which was verified in xenografted mice. Ectopic PAX5 expression significantly increased p53 reporter luciferase activity and increased p53 messenger RNA and protein levels. A direct interaction of PAX5 with the p53 promoter region was confirmed by chromatin immunoprecipitation assays. Re-expression of PAX5 sensitized ESCC cell lines KYSE150 and KYSE30 to fluorouracil and docetaxel. Silencing of PAX5 induced resistance of KYSE450 cells to these drugs. CONCLUSIONS As a tumor suppressor gene regulated by promoter region methylation in human ESCC, PAX5 inhibits proliferation, promotes apoptosis, and induces activation of p53 signaling. PAX5 may serve as a chemosensitive marker of ESCC.
Animals ; Carcinoma, Squamous Cell/genetics* ; Cell Line, Tumor ; Cell Proliferation/genetics* ; Epithelial Cells/metabolism* ; Esophageal Neoplasms/genetics* ; Esophageal Squamous Cell Carcinoma/genetics* ; Gene Expression Regulation, Neoplastic ; Humans ; Mice ; PAX5 Transcription Factor/genetics* ; Tumor Suppressor Protein p53/genetics* ; Xenograft Model Antitumor Assays