Objective To compare the dissolution behavior between domestic trepibutone tablets and original reference product, and provide a basis for evaluating the quality consistency of generic drugs. Methods Four dissolution media recommended by Japanese Orange Book and a domestic standard dissolution media were selected to determined the dissolution profile,and f2 factor was calculated to investigate the consistency of stripping curves. Results In water,pH 4.0 and pH 1.2,the f2 of domestic formulation and reference formulation was under 50,and the dissolution profile was inconsistent.Dissolution behavior of domestic preparations of different manufacturers was dissimilar.In water,the f2 of domestic preparations of different batches of the same manufacturer was over 99.9,and the dissolution behavior was similar. Conclusion The dissolution method of existing domestic standard can not distinguish the dissolution behavior of different products,and it should be revised and completed.There is still great difference in quality between the domestic preparations and reference preparations.

Objective To investigate the radiosensitivity of stem cells in pancreatic adenocarcinoma PANC‐1 cell line and the possible mechanism of its radiation resistance .Methods Using flow cytometry ,the cells were isolated and sorted into CD44+CD24+ ,CD44-CD24+ ,CD44+CD24- ,and CD44-CD24- .Multi‐target click model was used to fit cell survival curves and deter‐mine the sensitizer enhancement ratio .The apoptosis and cycle distribution of the four cell subsets were determined using flow cy‐tometry ,and the level of ROS was determined by DCFH‐DA probe .Results The ratio of CD44+ and CD24+ in the sorted PANC‐1 cell line was 92 .0% and 4 .7% respectively .Before radiation ,there was no statistically significant difference between four groups (P>0 .05);After treated with 6MV‐X ray ,The ratio of apoptosis was the lowest in CD44+CD24+ (P<0 .01);The percentage G0/G1 cell was the highest in CD44+CD24+ (P<0 .01) ,the sensitizer enhancement ratio of CD44+ CD24- ,CD44-CD24+ and CD44-CD24- were 1 .61 ,1 .81 ,1 .94 ,respectively .The level of ROS in CD44+CD24+ was lower (P<0 .01) .Conclusion Tumor stem cells of pancreatic adenocarcinoma have properties of a lower level of ROS and relative stationary that maybe the reasons of radio resist‐ance .

Objective To investigate the effect of signal transducer and activator of transcription-3(STAT-3)-mediated non-dependent vascular endothelial growth factor receptor-2(VEGFR-2) pathway on the radiosensitivity of non-small cell lung cancer (NSCLC) cells and its possible mechanism.Methods NSCLC cells were divided into control group, apatinib (VEGFR-2 inhibitor) group, apatinib+S3I-201(STAT-3 inhibitor) group, radiation (RT) group, RT+apatinib group, and RT+apatinib+S3I-201 group.Q-PCR and Western blot were used to measure the mRNA and protein expression of VEGFR-2, STAT-3, other proteins involved in the signaling pathway, hypoxia-inducible factor 1α(HIF-1α), and cyclin D1.The cellular radiosensitivity was determined by colony-forming assay and cell apoptosis and cell cycle distribution were evaluated by flow cytometry.Results For Calu-1 cells, there was no significant difference in the expression of VEGFR-2 mRNA and STAT-3 mRNA between the apatinib group and the control group (P>0.05);the apatinib group had significantly lower expression of HIF-1α mRNA and cyclin D1 mRNA than the control group (P<0.05);the apatinib+S3I-201 group had significantly lower mRNA and phosphorylated protein expression of VEGFR-2, STAT-3, and related downstream target proteins than the control group (F=304.54, P<0.01;F=118.99, P<0.01, F=144.34, P<0.01;F=529.66, P<0.01);compared with the control group, the apatinib+S3I-201 group and the apatinib group showed increases in apoptosis rate and proportion of cells in G2+M phase, and the apatinib+S3I-201 group had significantly greater increases than the apatinib group (F=72.37, P<0.01).Compared with Calu-1 cells, the radiosensitizing effect of apatinib on A549 cells was limited (SER[sensitizer enhancement ratio]=1.39).The radiosensitizing effect of apatinib+S3I-201 on A549 cells was significantly higher than that of apatinib (SER:1.72 vs.1.39, P=0.000).Conclusions The inhibition of STAT-3 can enhance the radiosensitivity of NSCLC cells.When VEGFR-2 is inhibited by apatinib, activated STAT-3 regulates the expression of cyclin D1 directly or indirectly to affect the radiosensitivity of NSCLC cells.The inhibition of VEGFR-2 and STAT-3 has a good radiosensitizing effect on NSCLC cells.

Objective To determine the effects of endostatin on the expression of vascular endothelial growth factor receptor?2 ( VEGFR?2 ) in non?small cell lung cancer cells ( human A549 lung adenocarcinoma cells and human Calu?1 lung carcinoma cells) , and to investigate the possible mechanisms underlying its radiosensitizing effect. Methods The CCK8 method was used to determine the inhibitory effect of endostatin on cell proliferation and calculate the drug concentration that caused a 20% reduction in cell proliferation within 24 h ( IC20 ) . RT?PCR and Western blot assays were used to assess the mRNA and protein expression of VEGFR?2, proteins within its related signaling pathways, and HIF?1α, respectively. The radiosensitivity of cells in each group was determined by colony formation assay;cell apoptosis and cell cycle distribution were determined by flow cytometry. Comparison of mean values between multiple samples was made by one?way analysis of variance, and comparison of mean values between two samples was made by t test. Results Endostatin significantly inhibited the proliferation of Calu?1 cells ( F=50?36,P<0?01) with an IC20 of 296?5 μg/ml;the mRNA and protein expression of VEGFR?2 and HIF?1α was also significantly inhibited in endostatin?treated Calu?1 cells ( F=25?43,10?44, all P<0?05) . Moreover, the phosphorylation of Akt, ERK 1/2, and p38 was significantly reduced in endostatin?treated Calu?1 cells ( F=2?89,0?24, 1?09, all P<0?05) . The radiosensitivity enhancement ratios for Calu?1 cells and A549 cells were 1?38 and 1?09, respectively. Endostatin significantly induced apoptosis ( F=44?15, P<0?01) and G2/M blockage ( F= 104?24, P< 0?01 ) in Calu?1 cells. Conclusions Endostatin induces apoptosis and enhances radiosensitivity in Calu?1 cells with high expression of VEGFR?2, but it has a limited impact on A549 cells with low expression of VEGFR?2.

Objective To investigate the effects of vascular endothelial growth factor receptor?2 ( VEGFR?2) on proliferation, migration, invasion, and apoptosis after radiotherapy in lung cancer cell line Calu?1, and to explore the probable mechanisms. Methods Small interference RNA ( siRNA )?mediated silencing of VEGFR?2 gene was performed on Calu?1 cells, and the mRNA and protein expression of VEGFR?2 was determined by quantitative real?time PCR and Western blot, respectively. The cells were divided into control group, vascular endothelial growth factor ( VEGF ) group, VEGFR?2 specific siRNA (siKDR) group, and siKDR+VEGF group. The changes in proliferation, migration, and invasion were evaluated by the CCK8 assay, cell scratch wound?healing assay, and transwell migration assay, respectively. The protein expression of VEGFR?2 and proteins in the related downstream signaling pathway was measured by Western blot. Apoptosis in each group was determined after radiotherapy. Results After RNA interference?mediated silencing of VEGFR?2, the mRNA and protein expression of VEGFR?2 was significantly reduced ( P=0. 001,P=0. 000);the proliferation, migration, and invasion of Calu?1 cells were also significantly reduced ( P=0. 000,P=0. 000,P=0. 000);the phosphorylation levels of AKT, ERK 1/2, and p38 were significantly reduced in Calu?1 cells ( P=0. 336,P=0. 986,P=0. 553);the apoptosis in Calu?1 cells was significantly elevated ( P=0. 0012);the protein expression of HIF?1α was significantly inhibited ( P= 0. 016 ) . Conclusions The VEGFR?2 gene silencing significantly inhibits several physiological functions of Calu?1 cells and elevates the apoptosis rate after radiotherapy.

Objective:To explore the factors affecting bone mineral density (BMD) in adult males with low-to-moderate fluoride exposure in Henan Province.Methods:Adult male villagers from low-to-moderate fluoride exposure areas in Tongxu County, Kaifeng City, Henan Province were recruited from April to May 2017 based on cluster random sampling. Questionnaire survey, physical measurements and urinary samples collection were conducted respectively. Urinary fluoride (UF) was determined by fluoride ion-selective electrode. Ultrasound bone densitometer was used to measure BMD (T-score). Partial correlation analysis and multiple linear regression were used to analyze the influence factors of BMD.Results:A total of 439 adult males were included in this study. Age, body mass index (BMI), UF content, and T-score of the participants were (47.99 ± 8.49) years, (25.77 ± 3.23) kg/m 2, (1.34 ± 0.74) mg/L, and-1.79 ± 0.79, respectively. Partial correlation analysis showed a significantly positive correlation between BMI and T-score after age adjustment ( r = 0.194, P < 0.05). Multiple linear regression showed that T-score decreased by 0.015 (95% CI:-0.024 -- 0.005, P < 0.05) for each 1-year increase in age and T-score increased by 0.034 (95% CI: 0.009-0.059, P < 0.05) for each 1.0 kg/m 2 increase in BMI. Interaction analysis showed that T-score was closely related to the interaction between overweight (≥24.0 kg/m 2), non-smoking, tea drinking and UF [ β (95% CI): 0.134 (0.001-0.269), 0.163 (- 0.015-0.337), 0.215 (- 0.006-0.436), P < 0.10]. Conclusions:Our findings reveal a negative correlation between age and BMD, and a positive correlation between BMI and BMD in adult males with low-to-moderate fluoride exposure in Henan Province. In addition, low-to-moderate fluoride exposure is more likely to damage the BMD of smokers.

A temporary demand pacemaker with electrocardiosignal display is introduced in this paper. Double way low-noise electrocardiosignal preamplifier, amplitude limiter, high and low pass filter, 50 Hz notch filter, TTL level generator and stimulating pulse formation circuit are components of the hardware electrocircuit. The demand pacing and the electrocardiosignal display are separately controlled by the software in which the double microcontrollers communications technique is used. In this study, liquid crystal display is firstly used in body surface electrocardiosignal display or intracardial electrophysiologic signal display when the temporary demand pacemaker is installed and put into use. The machine has proven clinically useful and can be of wide appliation.
Electrocardiography ; Humans ; Pacemaker, Artificial

Objective To identify the electrophysiological charateristics and cause of ridge gap related reentry after MI ablation in atrial ifbrillation patients. Methods Activation and entrainment mapping was performed in 82 redo cases for OAT recurrence in whom MI was ablated during the index produre. Once ridge gap related reentry was conifrmed, detailed mapping was performed in MI and ridge region. In addition, in 36 cases undergoing MI ablation and fulfilling criterion for bidirectional block, differential pacing was repeated at the ridge to identify a ridge gap. Results Out of 82 redo cases for OAT recurrence in whom MI was ablated during the index produre, 7 (8.5%) was found to be ridge gap related reentry. TCL was (247.9±19.2) ms, and the left atrial endocardial activation time was (145.4±17.7) ms, accounting for (58.5±3.2)%of TCL. However, wide double potential was recorded along the previous ablated MI line where PPI was (34.3±6.6) ms longer than TCL, while PPI was signiifcantly shorter at the ridge[PPI-TCL (11.4±3.9) ms, P<0.001]. Tachycardia was terminated at the ridge in 6 cases and at the corresponding site in coronary sinus in 1 case. No recurrence was found during follow-up for (11.1±4.5) months. In addition, in 36 patients undergoing MI ablation in whom criterion of bi-directional block was fuliflled, conduction gap located at the ridge was found in 5 (13.9%) cases. Conclusions MI ridge gap related reentry is a distinctive OAT, in which the ridge was used as the critical isthmus, whereas the previous ablated MI line is not part of the reentry. MI pseudo-block due to the ridge gap may lead to this type of recurrent tachycardia.

Objective To observe the management and outcome of the cardiac tamponade patients during the ablation procedure using two different anticoagulation strategies. Methods All the patients developed tamponade during the ablation procedure were enrolled from January 2007 to December 2013 in our center. In group 1, warfarin was discontinued 3 to 5 days before the procedure and low molecular weight heparin (LMWH) was administered subcutaneously until ablation procedure day. In group 2, warfarin was not discontinued and the international normalized ratio INR was to maintained between 2 and 3. Results There were 27 patients (0.6%) developed cardiac tamponade out of a total 4487 patients received ablation in our center. The baseline clinical characteristics including age, left atrium, the heparin dose and ACT during the procedure had no signiifcant difference between the groups, except that the INR was higher in the group 2 (0.9±0.1 vs. 2.3±0.5, P<0.001). There was no signiifcant difference in the amount of pericardiac drainage between the two groups (365±222 ml vs. 506±300 ml, P=0.137). Two patients in group 1 patient (11.1%) and 1 in group 2 (11.1%) needed emergency surgical repair (P>0.999). The median hospital day was similar in the 2 groups [(9.6±3.3) d vs. (12.1±4.5) d, P=0.167]. There were no other serious complications and no hospital death. Conclusions Non-discontinuation of warfarin during peri-procedural catheter ablation of AF is not signiifcantly different to bridging with LMWH in the management and outcome of acute cardiac tamponade.

Objective Identify the mechanism of induced atrial arrhythmias after pulmonary vein isolation (PVI) in patients with paroxysmal atrial ifbrillation(PAF), and investigate its long-term prognosis. Methods All patients with PAF undergoing PVI and induction test afterwards between Feburary 2010 and October 2010 were included. The induction protocol was rapid pacing initiated at cycle length of 250 ms with progressive shortening in a decrement of 10 ms down to 180 ms or refractoriness. Isoproterenol of 2-4μg/min was administrated as well. Inducibility was deifned as induction of atrial arrhythmia lasting >1 min. The mechanism of induced tachycardia was identiifed by activation mapping and entrainment mapping under the guidance of CARTO system. All patients were followed up by 36 months. Results Forty-nine atrial tachycardia were induced in 39 (19.7%) patients, including 35 organized atrial tachycardia (OAT) and 14 atrial ifbrillation (AF). The LA diameter was signiifcantly larger in inducible group than non-inducible group (39.5±6.6 mm vs. 36.7±5.2 mm, P=0.004). Macroreentry was the most common mechanism in induced OATs (28, 80.0%), and mitral isthmus was the most common critical site (20, 40.8%), followed by cavo-tricuspid isthmus (12, 24.5%), PV (6, 12.2%), LA septum (4, 8.2%), superior vena cava (3, 6.1%) and LA roof (1, 2.0%). Conclusions The most common mechanism of induced tachycardia by IV isoproterenol and rapid pacing is MI and CTI dependent after PVI in PAF patients, which can be succssefully eliminated by liner ablation, not increasing long-term recurrence rate.