Dose-Response Relationship, Radiation ; Humans ; Radiation, Ionizing ; Radiation, Nonionizing ; adverse effects

The effects of positive end-expiratory pressure (PEEP) on pulmonary shunt were studied during gen- eral anesthesia and postoperative period.Twenty cholecystectomy patients were randomly divided into experiment group (group P) and control group (group Z). PEEP and ZEEP were used separately after induction. Artery blood and mixed blood from the right ventricle were taken for blood gas analysis and determine the amount of pulmonary shunting before anesthesia. half and hour, one and half an hour and two and half an hour after anesthesia and one hour after the operation.The results showed that shunt in group P decreased gradually during general anesthesia and returned to the level of preoperation at an hour after operation. Shunt in group Z was increased continually and the level was significantly higher than preoperation an hour after operation. Shunt between two groups was significant difference (P

The purpose of this study was to investigate the cytotoxicity of the nickel ion and provide with basic data for the biological evaluation of those medical devices containing nickel. Seven cell lines were chosen. They were L929, h9c2(2-1), 293[HEK-293], hFOB1.19, THLE-3, H9 and IM-9 respectively. According to the principle of biological evaluation of medical devices, MTT method was chosen to test the cytotoxicity in different concentrations of nickel ion. For each cell line, the relative growth rate (RGR) was obtained and the cytotoxic grade was classified. Besides, IC50 values were calculated. As a result, it was found that the sensitivity was different among all cell lines. H9 was the most sensitive one, while the L929 was the most tolerant one. The concentration which is not above 1.25 mg/L was safe for all seven cell lines, because the cytotoxicity for all cells exposed in this concentration were not higher than grade 1. According to the criteria for medical devices, the concentrations not above 5 mg/L were safe for L929 cells. This result helps us to roughly assess the cytotoxicity and systematic toxicity caused by nickel contained in medical devices.
Cell Line ; Equipment and Supplies ; HEK293 Cells ; Humans ; Ions ; toxicity ; Nickel ; toxicity

Objective To investigate the effects of chrysin(ChR) on the induction of differentiation and apoptosis-promoting of HepG 2 human primary hepatocacinoma cells. Methods The HepG 2 cells were cultured in vitro, and then treated with ChR and all-trans retinotic Acid (RA), respectively, the alterations of nucleocytoplasm and tubulin arrangement after Gimsa staining and Coomassie brilliant blue staining were observed. The survival rate and the inhibitory rates of HepG 2 cells were determine by trypan blue counting method and MTT assay. The Alpha-fetoprotein(AFP) secretory amounts of the cells were detected by radioimmunoassay(RIA). The activities of alkaline phosphatase(ALP) andγ-glutamyltranspeptidase(γ-GT) were assayed by enzymatic reaction kit. The synthesis of tyrosine-α-ketoglutaric acid transaminase(TAT) in cells were investigated by Diamondstone spectrophotometry. Results After treatment with ChR or RA at 1.0~100μmol/L for 48 h, the proliferation of HepG 2 cells were inhibited significantly, compared with vehicle group (P<0.05 or P<0.01), the inhibitory potency of both ChR and RA on HepG 2 cells was equivalent and indicated in dose-dependent manner. After treatment with 10μmol/L ChR or RA for 48 h, HepG 2 cells disaggregated and grew to spindle-shape, their nuclei became smaller and the number of nucleolus were fewer. Furthermore, tubulin arrangement of cells tended to be more ordered and the tubulin synthesis increased significantly. At 24~96 hours treated with 10μmol/L ChR, the activities of TAT and ALP in cells were all increased distinctly (P<0.05, P<0.01), and the secretory amounts of AFP and the specific activities ofγ-GT were decreased significantly (P<0.05, P<0.01). Conclusion Chrysin can inhibit the proliferation of HepG 2 cells and induce them to differentiate to mature cells.

Objective To investigate the methylation status of Foxp3 gene and its roles in immunological pathogenesis of Kawasaki disease(KD). Methods Thirty children with KD and eighteen agematched healthy children consented to participate in this study. Quantitative methylation specific polymerase chain reaction(MSQP) was used to assess the methylation status of Foxp3 promoter and regulatory T cells specific demethylated region(TSDR) in CD4+ T cells. The proportion of CD4+ CD25 + Foxp3 + regulatory T (Tr) cells was analyzed by flow cytometry. Transcriptional levels of CD4+ CD25 + Foxp3 + Tr associating genes (Foxp3, CTLA4, GITR, LAG3 and CCR8 ) and Foxp3-dependent molecules (UBD and LGAIS3)were measured by real-time PCR. Results ( 1 ) Demethylation level of Foxp3 promoter in CD4 + T cells from patients with KD was lower significantly than that of health subjects( P ＜ 0.01 ), and increased significantly after treated with intravenous gamma globulin therapy(IVIG) (P ＜ 0.01 ). No difference of demethylation level of TSDR region was observed among all groups ( P ＞ 0. 05 ). ( 2 ) The proportion of CD4 + CD25 + Foxp3 + Tr in peripheral blood from patients with KD , as well as mRNA levels of Foxp3 gene in CD4+ T cells, was significantly lower than those of health subjects ( P ＜0. 01 ), and increases significantly after IVIG therapy (P ＜0.01 ). Significant positive correlations between demethylation level of Foxp3 promoter and the proportion of CD4 + CD25 + Foxp3 + Tr , or expression levels of Foxp3 in CD4 + T cells, were observed during acute phase of KD (CD4+CD25+ Foxp3+ Tr: r=0.76, P＜0. 01; Foxp3: r=0.89, P＜0. 01). (3)Transcription level of CD4+ CD25+ Foxp3+ Tr associating factors, such as CTLA4, GITR, LAG3 and CCR8, was significantly down-regulated in acute phase of KD(P＜0. 01 ), and up-regulated to some extent after treated with IVIG(P ＜0. 01 ). Expression levels of Foxp3-dependent molecules UBD and LGALS3 in CD4 + T cells decreased significantly during acute phase of KD (P ＜ 0.01 ), and basically recovered to the levels of health subjects( P ＜ 0.01 ). Conclusion Decrease of demethylation level of Fopx3 promoter is correlated with immune dysfunction in Kawasaki disease.

Objective To discuss the diagnosis and treatment of renal tuberculosis.Methods A retrospective study was made on 96 cases.Results Frequency (51.8%), urgency (37.2%),odynuria (33.4%),lumbodynia (41.0%),and hematuria(48.1%)were the most common symptoms. The diagnostic accuracy of IVU, B-type ultrasonography, CT and biopsy of mucous membrane of urinary bladder were 69.1%,12.5 %,37.5% and 33.3% respectively. 96 cases were given medicine (INH+RFP+PZA or PIA for 6-8 months).38 cases(39.6%)have been cured, while symptoms of 43 cases (44.8%) have been improved. Operation was performed on 15 cases that were ineffective treated by chemical therapy. Conclusions Urine routine, IVP, cystoscopy+biopsy of mucous membrane of urinary bladder provide important information for the diagnosis of renal tuberculosis. INH, REP and EMB or PIA combination therapy yields satisfactory outcome for early cases.

Objective To explore the inhibiting effects of arsenic trioxide and cisplatin on MG-63 cells. Methods Using MTT assay,flowcytometry,phase contrast microscopy and electron microscopy methods,the therapeutic effect of arsenic trioxide was studied for the osteosarcoma in the cultured MG-63 cells in vitro,and compared these effects with cisplatin. The inhibitory rotes of cell growth and the effect of apoptosis and cell cycle were compared between arsenic trioxide and cisplatin on MG-63 cells. Results The contrast phase microscope revealed the adhesion ability of normal groups was good and cellular morphology showed epithelium cells. But the celhdar morphology showed irregular arrangement in arsenic trioxide groups and cytoplasmic vacuoles in cisplatin group. Electron microscope revealed the globular plasmalemma ecphymas in cell surface of control groups,the enlarged crista mitochondriales and the double-deck membrane structure appeared clearly. But electron microscope revealed globular plasmalemma processes in cell surface of arsenic trioxide groups,thinned crista mitochondriales and clearly seen karyopycnosis and nuclear membrane of apoptotic cells. The globular plasmalemma processes in cell surface of cisplatin groups were separated,nuclear membrane thickened and chromatin were in sandy shape. Both arsenic trioxide and cisplatin inhibited effectively MG-63 cells growth. There was a significant difference in different groups of inhibition ratios to the growth of cells(all P < 0.05). In 2,4,8,16,32,64,128 hours,the inhibition ratios(%) of arsenic trioxide(56.31±0.03,70.00±0.06,79.84±0.03,87.31±0.13,84.70±0.09,90.68±0.06,91.18±0.05) and cisplatin groups(7.55±0.15,15.70±0.17,30.72±0.07,49.80±0.05,45.11± 0.13,61.62±0.08,93.80±0.12) were obviously increased as compared with those in the control group(2.03± 0.07,2.78±0.08,3.11±0.01,5.67±0.04,12.23±0.04,18.65±0.04,24.45±0.04,all P < 0.05). Moreover the inhibition ratio of arsenic trioxide group in 2 to 32 hour was significantly higher than that of cisplatin group and the effect was more faster(all P < 0.05). Both arsenic trioxide and cisplatin could induce apoptosis MG-63 cells. There was a significant difference in different groups of the inhibition ratio to the growth of cells(F = 13.317,P < 0.05). The inhibition ratios(%) of arsenic trioxide on 24,36,48 hour(20.50±3.78,45.76±9.90,25.16±15.41),and cisplatin groups on 24,36,48 hour(12.55±1.51,18.85±3.40,12.37±5.43),were obviously increased as compared with those in the control group at the same time(6.57±1.48,8.03±2.08,6.54±1.30,P< 0.05 or<0.01). Both arsenic trioxide and cisplatin inhibited MG-63 cells cycle. There was a significant difference in different groups of the inhibition ratio to the growth of cells(F = 54.579,43.429,21.795,P < 0.05 or < 0.01). And the total inhibition ratios(%) in G1 cycle of arsenic trioxide(78.26±5.24) and cisplatin groups(80.48±2.81) were obviously increased as compared with those in the control group(57.49±6.65,all P < 0.05 or < 0.01). Conclusions Arsenic trioxide and cisplatin can effectively inhibit the proliferation of MG-63 cell line and induce the apoptosis of MG-63 cell line. And the effects induced by arsenic trioxide group were faster than that of cisplatin groups. Moreover arsenic trioxide can arrest the cell cycle of MG-63 cell line at G1 phase.

Objective To study the correlations between bone fracture types and healing time in patients with osteofluorosis. Methods Thirty-seven patients with osteefluorosis and long tubular bone fracture were diagnosed in accordance with radiogram retrospectively. The fractures were divided into two groups: sclerotic and osteoporotic. Twenty four fractured patients with non osteofluorosis were included in the study as controls. All of the patients had operation(open reduction and nickelclad internal fixation). Fracture healing in patients with sclerotic and osteoporotic groups was compared with the control group after operation. Results There were notable differenees(F=4.30,P< 0.05) in term of fracture healing time among the three groups [sclerotic group:(18.4±5.3)weeks; osteoporotic group: (24.5±5.1)weeks; control group: (17.6±3.8)weeks]. Notably, there were significant differences between the osteoporotic and control groups(q=2.34,P<0.05), and between sclerotic and osteoporotic gronps(q=2.51, P<0.05). The healing time of the osteoporotic group was longer than that of sclerotic group. The constituent ratios of fracture healing in sclerotic, osteoporotic and control groups were 73.1% (19/26) ,54.5% (6/11),75.0% (18/24) respectively, and the differences among the three groups were statistically significant(X2=3.67,P<0.05). The healing rate of the osteoporotic group was lower than that of sclerotic and control groups(X2=3.12, 3.36, all P< 0.05). The constituent ratios of healing in the sclerotic, osteoporotic and control groups were 26.9% (7/26),45.5% (5/11),25.0%(6/24), respectively, and there differences among the three groups were statistically significant (X2=4.07 ,P<0.05). The delayed healing rate of the osteoperotic group was higher than those of the sclerotic and control groups(X2= 3.87,3.95, all P<0.05). Conclusions Fracture healing time of osteoporotic osteofluorosis after fracture is longer than normal, and the cause might be the loss of bone mass.

This paper presents a probability segmentation algorithm for lung nodules based on three-dimensional features. Firstly, we computed intensity and texture features in region of interest (ROI) pixel by pixel to get their feature vector, and then classified all the pixels based on their feature vector. At last, we carried region growing on the classified result, and got the final segmentation result. Using the public Lung Imaging Database Consortium (LIDC) lung nodule datasets, we verified the performance of proposed method by comparing the probability map within LIDC datasets, which was drawn by four radiology doctors separately. The experimental results showed that the segmentation algorithm using three-dimensional intensity and texture features would be effective.
Algorithms ; Databases, Factual ; Humans ; Imaging, Three-Dimensional ; Lung ; pathology ; Probability

Objective To provide the service for scientific innovation and competition in biomedical industry of Hunan Province and the reference for working out biomedical patent strategies.Methods The data of biomedical patents in Hunan Province were collected using the patentEX and processed by metrics.Results The application number of patents increased from year to year with a high expiry rate.The technology of biomedical patents has entered into its mature period and the application of patents was focused on several important IPC classifications.Conclusion Tra-ditional technologies play a main role in biomedical industry of Hunan Province, but Hunan Province is relatively backward in modern biological technologies.The application number of invented biomedical patents is rather large, but their overall academic level is rather low.The majority of biomedical industry enterprises lack of competition awareness.It is thus necessary to strengthen the development of modern biological technologies, improve the aca-demic level of biomedical patents, increase the competition awareness of biomedical industry enterprises, lay stress on cooperative development of biomedical patents and on support of biomedical industry enterprises.