Objective To discuss the three-dimensional reconstruction of lateral flaps of legs by Amira 4.1 based on an operational platform of personal computer,and to establish their digitized visible models.Methods A fresh adult cadaver specimen was perfused with the mixture of lead oxide-gelatine.The eikonic data were imputed into personal computer.Radiographs of CT scanning of the lower legs were digitally analyzed by Amira 4.1 software.The segmented areas for skin,arteries and flap structures were displayed in different colors using tools of Brush,Lasso and Magic wand.By several steps,according to particularities of anatomy structures and traits of images,stereo images of the flap and its blood vessel structure were performed by several algorithms.The 3D reconstruction via the Amira 4.1 software consisted of tracing the contours of the anatomical structures to be reconstructed;adjusting the contours of stacked points by geometrical alignment;modeling the surfaces by meshing the framework of the points transformed into polygons and smoothing the contours of the object reconstructed from points.Three dimensional computerized reconstructions of lateral flaps of legs were conducted from these data using Amira 4.1 by computer-assisted imaging processing.Results The 3D images of the flap and its blood vessel structure by Amira were clearly displayed,and the surface and volume information could be obtained.The 3D images could display perfectly the main structures of flap and other adjacent structures by means of personal computer and software Amira 4.1.Correlation of cross-sectional images from CT-scanning to 3D models was a more effective way for understanding the flap anatomy.Conclusion Three-dimensional computerized reconstruction for lateral flaps of legs may provide great value for clinical experiments,basic research and surgical planning,and the Amira 4.11 software is of vital for three-dimensional reconstruction.

Restriction endonucleases are important molecular biology tools for DNA recombination.Because of the cleavage of DNA,their recombinant expression is difficult with low yields and complicated purification processes.In commercial productions,the technology that uses specific methylases to protect host DNA from digestion of the expressed restriction enzymes was cumbersome and practically limited.For solving this problem the expression of restriction enzyme Not Ⅰ was performed by using the DNA methylase M.Sss Ⅰ derived from Spiroplasma sp.MQ1 which specifically kept CpG sequence methylated.The methylated DNA was protected from the cutting of Not Ⅰ whose recognition sequence contained CpG.The gene of methylase M.Sss Ⅰ was introduced into Escherichia coli ER2566 and constitutively expressed,resulting in the CpG methylation pattern of the host DNA.Restriction enzyme Not Ⅰ was successfully expressed in this E.coli strain.Furthermore,by adding a purification tag to one terminus of the enzyme,recombinant Not Ⅰ was prepared as a highly purified and active product through two simple Ni-affinity and anion exchange chromatography steps.This expression system can be applied for the preparation of a series of restriction enzymes with CpG in their recognition sequences.

Diagnosis, Differential ; Humans ; Immunohistochemistry ; Keratins ; analysis ; Male ; Prostatic Hyperplasia ; diagnosis ; Prostatic Intraepithelial Neoplasia ; diagnosis ; Prostatic Neoplasms ; diagnosis ; Racemases and Epimerases ; analysis ; Staining and Labeling ; methods

Adult ; Antigens, CD20 ; metabolism ; Diagnosis, Differential ; Female ; Humans ; Ki-1 Antigen ; metabolism ; Leukocyte Common Antigens ; metabolism ; Lymph Nodes ; metabolism ; pathology ; Lymphoma, B-Cell ; pathology ; Pseudolymphoma ; metabolism ; pathology

Acinetobacter Infections ; microbiology ; Acinetobacter baumannii ; drug effects ; isolation & purification ; Anthracosis ; microbiology ; Anti-Bacterial Agents ; pharmacology ; Drug Resistance, Bacterial ; Fosfomycin ; pharmacology ; Humans ; Imipenem ; pharmacology ; Pneumonia, Bacterial ; microbiology

This article describes a method totransfer physiological data through carrier-current communication.The microcontroller measures the data of heartrate and body temperature and sends them through the serial port tothe carrier-current module implementing carrier-current communication.This method can be used totransfer physiological data through short distance less than200meters.

Objective To evaluate the efficacy and toxicity of weekly docetaxel and cisplatin in previously untreated patients with advanced non-small-cell lung carcinoma. Methods Between January 2002 and December 2003 ,34 patients with pathologically comfirmed advanced non-small-cell lung carcinoma who had not received treatment were enrolled. The mean age was under 66 years. The patients received intravenous infusions of docetaxel(25 mg/m2,dayl ,8,15) with dexamethasone premedication and cisplatin(25 mg/m2,dayl ,8,15) ,followed by a week of rest. The remedies which were less than 6 regimens lasted to disease progression or severe toxicity. Therapeutic effect was evaluated by CT scan every two courses . The patients were followed up for 24 months. Descriptive statistics and SPSSIO. 0 software were used to analyse the results. Results 34 patients finished 90 courses. The mean was 2. 6 courses. All patients were followed up. Two patients achieved complete responses, ten patients achieved partial responses, ten patients achieved stable disease. An objective response rate of 35. 29% (95% confidence interval 19. 25%-51. 33% )was obtained. Patients life quality was significantly improved. The median time to progression was 4. 1 months, and median overall survival was 11 months. The 1-year survival rate was 47. 06% , the 2-year survival rate was 11.76% . Toxicities were mild. Grade 3 to 4 neutropenia (11.76%), anemia (5.88%), hyponatremia (5.88%), alopecie (17.64%) and nausea/vomiting (5. 88% ) were observed. Conclusion Weekly Cisplatin plus docetaxel is an effective and well-tolerated regimen in chemo-naive patients with advanced NSCLC. Well-designed clinical trials should be conducted.

Objective To observe the effect of cigarette smoking on cutaneous wound healing in rats.Methods Healthy adult SD rats,weight 200-250 g,were randomly divided into 4 groups:control group (group C),low tar content group (group L),middle tar content group (group M) and high tar content group (group H),ten rats each group.4 full thickness dermal excision wound models with the diameter of 2.0 cm were established on the back of 40 healthy male or female SD rats.The wound spacing was greater than 2 cm.Group C did not do any intervention treatment,Groups L,M and H rats were put,respectively,into homemade smoke box in 0.1,0.5,and 0.8 mg different-grade tar content of cigarettes and smoked,and the time of wound healing was observed.The wound granulation tissue was taken in 3 and 7 days after surgery.The expression of CD68+ macrophages was detected by immunohistochemical method.The wound healing rate was observed on the days 7 and 16.Results Compared with group C,wound healing time in groups L,M and H was extended (P＜ 0.05).Immunohistochemical results showed that macrophage numbers in groups L,M and H wound were significantly less than that of group C.The wound healing rates 7 days and 16 days after surgery in the three group smoked were significantly lower than that of group C.Conclusions Cigarette smoking leads to wound healing delay,and wound healing rate is reduced at fixed time point,with the decrease in the number of macrophages.

Objective To explore the effects of BSA on hypoxia inducible factor/hypoxia response element (HIF/HRE) transcription activity in rat tubular epithelial cells (NRK-52E) with HRE-Luc reporter plasmid.Methods Luciferin activity of NRK-52E cells incubated by a medium contained BSA in varying concentration (0,5,10,20 mg/ml) and stimulus duration (24,48,72 h) was detected by dual luciferase detecting system based on HRE-Luc reporter plasmid and HIF-1 α expression was detected by Western blotting.Results HIF/HRE transcription activity of NRK-52E cells was increased in BSA incubation group (10 mg/ml,48 h) compared with blank control (BSA 0 mg/ml,48 h) [(2.59±0.35)vs (1.03±0.09),P=0.000].HIF-1α expression of NRK-52E cells was increased in BSA incubation group (20 mg/ml,48 h) compared with blank control (BSA 0 mg/ml,24 h) [(0.052±0.010) vs (0.014±0.003),P=0.000].Conclusion Albumin can increase HIF/HRE transcription activity of TEC.

Objective To explore the expression of EphB4 and VEGF in esophageal cancer tissues and their relationship with microvessel density (MVD ) ,and analysis the curative effect of postoperative esophageal cancer radical under thoracoscope . Methods Theexpression of EphB4 and VEGF was detected by immunohistochemistry in tumor specimens from 76 cases of esopha-geal squamous cell carcinoma and paratumor normal specimens ,used CD34 as marker to count MVD .According to the situation of expression of EphB4 and VEGF ,we analysis their relationship with lymph node metastasis rate ,recurrence and 5-year survival rate . Results The positive expression rate of EphB4 and VEGF in cancerous tissue (57 .89% and 61 .84% ) ,were significantly higher than that in tissue adjacent to carcinoma(0 and 7 .89% )(P<0 .05) .The positive expression rate ofEphB4 and VEGF in high MVD values of patients (67 .44% and 76 .19% ) ,were significantly higher than thatin low MVD values of patients (45 .45% and 44 .11% )(P<0 .05) .The positive expression rate ofEphB4 and VEGF in the patientswith lymph node metastasis group and associ-ated with recurrence ,were significantly higher than that of group without lymph node metastasis and group without recurrence (P<0 .05) .The positive expression rate of EphB4 and VEGF in patients of greater than or equal to 5 years of survival rate(45 .00% and 45 .45% ) ,were significantly lower than in patientsof Less than 5 years of survival rate (80 .36% and 85 .19% )(P<0 .05) .Conclu-sion EphB4 and VEGF are highly expressed in esophageal cancer tissue ,which may be closely associated withmicrovessel density , and lymph node metastasis ,recurrence and 5 years survival rate ;the curative effect of positive expression rate of EphB 4 and VEGF is poor .