Objective The aim of this study was to determine the effective concentration of epidural ropivacaine for analgesia in 50% of parturients (EC50) in the first stage of labor. Methods Thirty-three ASA Ⅰ -　Ⅱ nulliparous women with 2-3 cm cervical dilatation who requested epidural analgesia were enrolled in the study. Epidural catheter was placed at L3-4 and advanced for 3-4 cm in the epidural space in a cephalad direction. 20 ml of ropivacaine solution of which the EC50 was being tested was given through the catheter into epidural space. The EC50 was determined by up-and-down sequential experiment. The initial concentration of the epidural ropivacaine being tested was decided to be 0.15% . If effective the next parturient received ropivacaine of a lower concentration; if ineffective the concentration of ropivacaine was increased in the next parturient. Each time the concentration of epidural ropivacaine increased/decreased by 0.01% . Analgesia was assessed by VAS score (1-10) . If VAS score was less than 3 within 30 min of ropivacaine administration, analgesia was defined as effective.Results Among the 33 parturients enrolled, three were excluded from the study because of uncertain analgesic efficacy. The results showed that the EC50 of epidural ropivacaine for analgesia in the first stage of labor was 0.063% [95% confidence interval (CI) was 0.05972%-0.06688%] .Conclusion The EC50 epidural ropivacaine for analgesia in the first stage of labor is 0.063 % determined by sequential experiment method.

ObjectiveTo observe the synergistic action of lower He-sea and Front-mu points in treating functional dyspepsia by adopting electroacupuncture at the lower He-sea and Frong-mu points of stomach.MethodSixty patients with functional dyspepsia were randomized into a lower He-sea group, a Front-mu group, and a combining group of lower He-sea and Front-mu points, to receive treatment once daily, 5 sessions a week, totally for 4 weeks. Nepean Dyspepsia Index (NDI) was tested before and after intervention, and the general therapeutic efficacy was evaluated.ResultThe total effective rate was 100.0% in the combining group, versus 90.0% in the Front-mu group and 90.0% in the lower He-sea group, and the differences were statistically significant (P<0.05). The follow-up study showed that the total effective rate was 100.0% in the combining group, versus 90.0% in the Front-mu group and 85.0% in the lower He-sea group, and the differences were statistically significant (P<0.05). Before treatment, therewere no significant inter-group differences in comparing Nepean Dyspepsia Symptom Index (NDSI) and Nepean Dyspepsia Life Quality Index (NDLQI)(P>0.05), while there were significant differences in comparing NDSI and NDLQI after treatment (P<0.05). ConclusionIt can improve the functional dyspepsia symptoms by using the lower He-sea point and Front-mu point together or using them separately, while the combining use can produce a more significant efficacy.

Objective To introduce the general international method for estimation of lifetime risk of developed cancer,and to estimate the lifetime risk baseline values of several kinds of cancers related to radiation exposures in China.Methods The risk estimation was based on the data from Chinese Cancer Registry Annual Report (2010) and China Population & Employment Statistics Yearbook (2009),and made according to the method previously published by National Cancer Institute (NCI) in USA.Results The lifetime risk of all cancer in China in 2007 was estimated to be 27.77％,that of lung cancer 5.96％,that of breast cancer for female 3.34％,that of all leukemia 0.14％,that of thyroid cancer 0.37％.The lifetime risks of all cancer were estimated to be 32.74％ for males and 24.73％ for females,and that was 36.47％ for urban residents and 26.79％ for rural people.Conclusions The lifetime risk of all cancer for males in 2007 was about 1.25 times as much as that for females.The value of all cancer for urban residents was about 1.35 times as much as that for rural residents.The lifetime risk of developed cancers in 2007 in China is lower than that in the developed countries,such as Japan.

OBJECTIVE:To study the immunosuppressive chemical constituents from the n-butanol extract of the debark root of Tripterygium wilfordii hook.f.METHODS:Several compounds were isolated from the n-butanol extract by columns of silica gels and Sephadex LH-20,their structures were identified by NMR,MS spectral analysis and comparing with standard substances on TLC,and the immunosuppressive activity was determined.RESULTS:One of the compounds was identified as emodin,an anthraquinone,it had marked immunosuppressive effect on animal.CONCLUSION:Emodin is obtained from the plants of Tripterygium wilfordii hook.f.for the first time.

The clinical laboratory equipment on hospital ship was introduced, whose status and common faults were analyzed during Philippines humanitarian medical rescue mission and 3 times of Mission of Harmony. The experience was summarized for the maintenance of the clinical laboratory equipment. The problems and countermeasures were proposed for the clinical laboratory equipment.

Objective To investigate the effect of propofol on the high-voltage-activated calcium currents [ICa(HVA)] in rat hippocampal neurons. Methods Hippocampal neurons were prepared from Wistar rats and cultured. ICa(HVA) was recorded using whole-cell patch clamp technique. Different concentrations of propofol were added to the culture. The effect of propofol on ICa(HVA) Was evaluated. Results ICa(HVA) was inhibited by propofol in 300 μmol/L reduced peak ICa(HVA) by (24±6)%, (33 ±5) %, (36±7)% and(38±3)% respectively with a mean IC50 of 3.8 μmol/L and Hill coefficient of 0.35. Vmax was shifted from (4.0± 2.0) mV to (3.8 ± 1.6) mV. The V1/2 of inactivation curve was shifted from (- 32 ± 5) mV to (- 35 ± 4) mV and the slope factor was 31 ± 5 and 35 ± 6 before and after administration respectively. Conclusion Propofol produces significant inhibition of calcium currents in the central neurons which may partly explain the action of propofol on central nervous system.

Objective To determine whether nitric oxide may result in different effects on cardiac function at the different time points during the course of myocardial ischhemia and reperfusien of rats in viwo, and if so, to investigate the mechanisms involved.Methods Male adult rats were subjected to 30 minutes of myocardial ischemia followed by 5 hours of reperfusien. L-arginine was administrated at a bolus at both 10 minutes before and 50 minutes after reperfusion in early treatment group. The L-arginine was administrated at a bolus at both 3 and 4 hours after reperfusion in late treatment group. The following variables were measured: cardiac hemodynamic parameters, myocardial easpase 3 activity, iNOS and total NO content. Results Compared with vehicle group, administration of L-arginine at early reperfusion markedly reduced myocardial caspase 3 activity, and improved cardiac function. In strict contrast, administration of L-arginine at late reperfusion resulted in a significant increase in myocardial NOx content, myocardial apoptosis, and depressed the cadiac function. Conclusion Timely administration of L-arginine might inhibit apoptosis while late administration of L-arginine might enhance apoptosis.

Objective To develop a model of type 2 diabetes with early renal injury on spontaneously hypertensive rats (SHR). Methods The 6-week old SHR were fed with the diets enriched with sucrose (20%, W/W), lard (10%, W/W), cholesterol (2.5%, W/W) and chleolate (1%, W/W) to induce insulin resistance. Hyperglycemia was developed by intraperitoneal injection of streptozotocin (STZ, 35 mg/kg). Wistar-Kyoto rats (WKY) were used as normal controls. Rats with plasma glucose (PGL) ≥ 16.7 mmol/L were diagnosed as diabetes. Eight weeks after the induction of diabetes, plasma triglyceride (TG), cholesterol (CHO), glucose, systolic pressure(SP), 24-h urine protein excretion (Upro) were examined in all the rats, and the homeostasis model assessment of insulin resistance (HOMA-IR) was analyzed. Renal pathological changes were studied by immunohistochemical staining and electron microscope. Results After 2 weeks on the high sucrose and fat diets, the model rats exhibited significant increase in basal PGL, TG and CHO levels as compared to control rats (P<0.05, respectively). The insulin resistance was developed in model rats demonstrated by the higher HOMA-IR (5.03±0.38 vs 2.61±0.34, P<0.05). At the end of the experiment, model rats were associated with hypertension. Upro level was significantly increased in model rats compared with that in controls [(57.58±16.54) mg/24 h vs (5.35±1.90) mg/24 h, P<0.01]. The kidney hypertrophy index (KWI) was significantly increased in the model rats compared to controls (P <0.05). Moreover, the diabetic model rats showed glomerular hypertrophy, foot process effacement, micro villous transformation, glomerular basement membrane (GBM) thickening. Conclusion A rat model is successfully established, which presents typical features of human type 2 diabetes and can be served as an ideal model to study the diabetic nephropathy.

Objective To investigate whether low density lipoprotein receptor (LDLr) pathway involves in the progression of vascular calcification (VC) in hemodialysis patients under microinflammation.Methods Twenty-eight hemodialysis patients were divided into control and inflammation group according to plasma C-reactive protein level.Surgically removed tissues from radial artery of patients receiving arteriovenostomy were used in experiments.Foam cell formation and calcification deposition were observed by hematoxylin-eosin (HE) and alizarin red S staining respectively.VC-related protein expression,such as bone morphogenetic proteins-2 (BMP-2),collagen Ⅰ,alkaline phosphatase (ALP),and LDLr and its related nuclear factor of transcriptional regulation,such as sterol regulatory element binding protein-2 (SREBP-2) and SREBP cleavage-activating protein (SCAP),were detected by immunohistochemistry and immunofluorescence staining.Results HE and alizarin red S staining showed that there were parallel increased foam cell formation and calcium deposit in continuous cross-sections of radial arteries in inflammation group compared to control group,which were closely correlated with increased protein expressions of LDLr,SREBP-2,BMP-2,and collagen Ⅰ as shown by immunohistochemical and immunofluorescent staining.Confocal microscopy confirmed that inflammation enhanced the translocation of SCAP/SREBP-2 complex from endoplasmic reticulum to Golgi,thereby activating LDLr gene transcription.Inflammation increased protein expression of ALP and reduced protein expression of alpha-smooth muscle actin,contributing to the phenotype conversion of vascular smooth muscle cells in calcified vessels from the fibroblastic to the osteogenic,which were the main cell components in VC.Further analysis showed that the disruption of LDLr pathway induced by inflammation was positively correlated with the enhanced expression of BMP-2 and collagen Ⅰ (r=0.782,P＜0.01; r=0.644,P＜0.05).Conclusion Inflammation accelerates the progression of VC in hemodialysis patients through the disruption of LDLr feedback regulation.

Objective To investigate the effects of monocytes on phenotypic changes of human proximal tubular HK-2 cells and the mechanism.Methods Monocytes were co-cultured with HK-2 cells.Morphological changes of HK-2 cells were detected by inverted phase contrast microscope.Expressions of E-cadherin,α-SMA and fibronectin were assessed by RT-PCR,Western blotting and immunocytochemical staining.Flow cytometry techniques was applied to evaluate intercellular cell adhesion molecule-1 (ICAM-1) expression on HK-2 cells.The intracellular signal was investigated by gene microarr ay.Results The typical epithelial cell morphology of HK-2 cells disappeared after co-culture with monocytes,accompanied by decreased E-cadherin expression and increased α-SMA and fibronectin expression (all P＜0.05).The expression of ICAM-1 on HK-2 cells was increased by monocytes stimulation.Interestingly,administration of CD18 antibody directly inhibited the phenotypic change of HK-2 cells.Furthermore,NF-κB signaling might be critical in mediating this process,and blockade of this signaling pathway could inhibit 1CAM-1 expression and epithelial mesenchymal transition (EMT) formation.Conclusion Monocytes can directly induce EMT of HK-2 cells via up-regulating ICAM-1 through NF-κB signaling pathway.