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 effect of reserpine,an efflux pumps inhibitor,on the activities of fluoroquinolones (FQNs) against Enterococci,and the distribution of efflux pump genes emeA and its correlation with the resistance of Enterococci.To elucidate the relationship between FQN resistance in Enterococci and active efflux.Methods One hundred isolates of enterococci were identified by VITEK microbe automatic system.The antibacterial agent susceptibility tests were performed by the disc diffusion method (K-B) in accordance with the CLSI standards.The minimum inhibitory concentration (MIC) of each FQN was tested by the agar dilution method,and the MIC changes were detected after adding reserpine.The distribution of emeA in 100 isolates of Enterococci was determined by PCR.Thex2 test was used to compare the differences of statistical results.Results After reserpine was used,three-FQN resistance in Enterococci was reduced.Ciprofloxacin,gatifloxacin and levofloxacin resistance was reduced from 42％ (42/100) to 28％ (28/100),from 30％ (30/100) to 17％ (17/100),and from 33％ (33/100) to 23％ (23/100),respectively.The positive rate of emeA gene in 100 strains of Enterococci was 55％ (55/100).There were 45 positive strains(72.6％) in 62 E.faecalis and 10 positive strains (26.4％) in 38 E.faecium.The positive rate of emeA gene in the resistant strains against ciprofloxacin,gatifloxacin and levofloxacin was 73.8％ (31/42),76.7％ (23/30),75.8％ (25/33),respectively,and the positive rate of emeA gene in the susceptible strains against above 3 antibacterials were 41.4％ (24/58),45.7％ (32/70),44.8％ (30/67).Efflux pump genes emeA in resistant strains is higher than the sensitive strains,with the statistically significant difference(x2 =13.02,8.13 and 8.57,P ＜ 0.005).Conclusions Reserpine could inhibit the active efflux of in FON Enterococci and reduce the MIC for drug-resistant strains in vitro.Multidrug-resistant efflux pump gene emeA was relevant to antimicrobial drug resistance in Enterococci.

Biomarkers ; blood ; Biopsy, Needle ; utilization ; Hepatitis C ; complications ; Humans ; Liver ; pathology ; Liver Cirrhosis ; diagnosis ; pathology

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 study the pharmacokinetic characteristics of triflusal capsule in healthy volunteers. METHODS:In ran-domized test,36 healthy volunteers were randomly divided into 3 groups. They were given low-dose,medium-dose and high-dose of Triflusal capsule(300 mg,600 mg and 900 mg),qd,for one day,and then pharmacokinetic study of single dose of Triflusal capsule was conducted;Triflusal capsule medium-dose group was continuously given medicine for 13 days,and then pharmacokinetic study of multiple dose of Triflusal capsule was conducted. The plasma concentration of triflusal was determined by LC-MS/MS,and Zorbax SB-C18 column was used with methanol-0.2% formic acid (80:20,V/V) at the flow rate of 0.2 ml/min. ESI was adopted in MRM mode,negative ion detection was carried out,quantitative analysis m/z 247.1→161.1(triflusal),m/z 294.0→250.0(internal standard, diclofenac sodium). Pharmacokinetic parameters were calculated by using WinNonlin 6.2 software,and the difference of them were compared. RESULTS:The linear range of triflusal were 0.05-20 μg/ml. The main pharmacokinetic parameters of triflusal capsules high-dose,medium-dose and low-dose groups were as follows:t1/2 were (0.45 ± 0.20),(0.47 ± 0.10),(0.43 ± 0.20) h;tmax were (0.56±0.20),(0.60±0.20),(0.47±0.40)h;cmax were(3.30±0.98),(10.65±3.26),(13.96±4.88)μg/ml;AUC0-8 h were(3.99±0.93), (13.29±1.72),(19.62±6.78)μg·h/ml;within dose of 300-900 mg,linear relationship was found between cmax,AUC0-8 h and dose(R2=0.954,0.986). When reaching stable state of multiple dose,average blood concentration was(0.71±0.20)μg/ml;main pharmacokinetic parameters were as follows:AUCs(17.10±4.82)μg·h/ml,t1/2(0.49±0.10)h,tmax(0.85±0.62)h,cmax(11.58±3.99)μg/ml,AUC0-8 h (16.99±4.84)μg·h/ml,AUC0-∞(17.08±4.81)μg·h/ml;accumulation factor(1.28±0.40). tmax and t1/2 of single dose were similar to those of multiple dose. CONCLUSIONS:LC-MS/MS can determine the content of triflusal in human plasma rapidly and accurately, and accumulation phenomena exist in healthy Chinese volunteers,which shows linear pharmacokinetic characteristics.

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.

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.

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.