Objective To explore the epidemic factors for dental fluorosis of residents living around an aluminum smelter plant. Methods The contents of fluoride in 1 575 urine samples, some drinking water samples collected from the centralized water supply systems, springs and wells water, wheat, Chinese cabbage, soil and air samples were determined. The epidemic situation of dental fluorosis in 1766 residents was investigated according to the unique national standard. Results The concentration of urine fluoride [(1.913?1.413) mg/L] of 1 575 residents living around an aluminum smelter plant was higher than that (about 0.5 mg/L) in non-endemic area, the prevalence rate of dental fluorosis was 90.09%. The contents of fluoride in wheat, Chinese cabbage and soil did not exceed the related limits or background values. The concentration of fluoride in air samples exceeded the Grade II limit of Environment Air Quality Standard by 0.04-2.73 times. Conclusion Air fluoride pollution and drinking tea water containing higher concentration of fluoride are considered as the one of the factors that may cause dental fluorosis of the residents living around this aluminum smelter plant.

Objective To explore the prevalence of dental fluorosis among children in an industrial area of aluminum electrolysis. Methods 2 156 8-12-year old children were selected in a certain industrial area of aluminum electrolysis for investigation of their prevalence of dental fluorosis and the contents of fluoride in urine. At the same time, the contents of fluoride in the environmental media were investigated also. Results The prevalence of dental fluorosis was 51.11% for children, the content of fluoride in urine samples of children was (1.44

Objective: To investigate the effects of taraxerol and taraxeryl acetate on cell cycle and apoptosis of human gastric epithelial cell line AGS cells. Methods: The inhibitory effects of taraxerol and taraxeryl acetate at different concentrations on AGS cell growth were measured by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) method and the concentrations of taraxerol and taraxeryl acetate to be used in following experiments were decided. Then, cell cycle analysis was performed by FACScan flow cytometry after culture with taraxerol or taraxeryl acetate. Annexin V-fluorescein isothiocyanate/propidium iodide staining was used to measure cell apoptosis. Results: Taraxerol significantly inhibited AGS cell proliferation in a dose- and time-dependent manner. Taraxerol arrested the AGS cells at G(2)/M stage. 110 μmol/L taraxerol elevated the population of AGS cells arrested in G(2)/M phase compared with solvent (P<0.05). Taraxerol also promoted early cell apoptosis in AGS cells. 110 μmol/L taraxerol increased the early cell apoptosis rate from 4.45% to 10.29%, which was 1.31 times higher than that of the untreated cells. However, taraxeryl acetate had a lower inhibitory effect than taraxerol, and it showed a tendency of G(2)/M arrest and apoptosis promotion but with no statistical significance (P>0.05). Conclusion: Taraxerol has inhibitory effects on AGS cell growth through inducing G(2)/M arrest and promotion of cell apoptosis. Taraxeryl acetate has less effect on cell cycle arrest and apoptosis of AGS cells than taraxerol.

Objective To analyze the occurrence and prognosis of congenital heart disease interventional therapy related arrhythmias, and to discuss the prevention and treatment. Methods We retrospectively analyzed the occurrence and prognosis of congenital heart disease interventional therapy related arrhythmias among a total of 223 cases admitted for in terventional therapy between February 2014 to January 2015. Resu1ts 8 cases developed different degree and nature of arrhythmias after the interventional therapy. Among these cases, 3 of them had arrhythmias after ASD occlusion, including one was frequent atrial contraction, one was paroxysmal atrial tachycardia, and one was sinus bradycardia with accelerated junctional rhythm. All of them converted back to sinus rhythmm spontaneously from 2-3 hours to maximum 1 week after operation. 4 cases had arrhythmias after VSD occlusion, including one case of ventricular tachycardia, one case of Ⅰ° degree atrioventricular block who recovered spontaneously after surgery, one case of Ⅲ° degree atrioventricular block and one case of intermittent complete left bundle branch block who retruned to sinus rhythmn after 1 week of symptomatic treatment. One case had ventricular fibrillation after pulmonary valve balloon dilatation and was treated by defibrillation and temperany pacing to convent to sinus. Conc1usions Arrhythmias is a common complication of congenital heart disease after interventional therapy, and most of them are temporary and transient changes. However, once serious arrhythmias happened, the success rate of surgery and postoperative curative effect can be directly effected, or may even lead to mortality.

Objective: The main ingredients and the inhibitory effects of essential oil of a compound Chinese herbal medicine Weiqi Decoction (WQD) on AGS cell proliferation were to be investigated. Methods: Chemical compounds of WQD essential oil were detected by gas chromatography and mass spectrometry analysis. Cell viability was measured by methyl thiazolyl tetrazolium method. Cell cycle distribution was detected by flow cytometry. Apoptosis and necrosis of AGS cells were determined by Hoechst 33342/propidium iodine staining. Results: Chemical analysis showed that the main ingredients of WQD essential oil were bornylene and 3-n-butylphthalide. Ligustilide, which is the effective compound of Danggui (Radix Angelicae Sinensis), was not detected in WQD essential oil. The essential oil inhibited cell proliferation in a dose- and time-dependent manner, and blocked cell cycle progression at G(2)/M stage. At the concentrations that resulted in significant inhibition of cell proliferation and cell cycle arrest, essential oil induced both apoptosis and necrosis. Conclusion: The results suggest that WQD essential oil contains some effective ingredients for treating chronic atrophic gastritis and functional dyspepsia, and also has an antiproliferative effect on AGS cells through cell cycle arrest and apoptosis promotion in vitro. Therefore, essential oil should be retained as much as possible during stewing this decoction.

OBJECTIVETo investigate the effects of Coptis chinensis and Evodia rutaecarpa water extract on precancerous lesion of colon induced by DMH and proliferation and apoptosis changes of colon mucosa crypts.

METHODPrecancerous lesion of colon was induced by DMH. The changes of proliferation and apoptosis of colon mucosa crypts were detected by morphological analysis. The numbers of aberrant crypt foci (ACF) were measured by feulgen staining.

RESULTC. chinensis and E. rutaecarpa water extract could significantly inhibit the formation of ACF in model animals. The proliferative crypts were increased obviously in middle and distal colon, and decreased by C. chinensis and E. rutaecarpa water extract. The apoptosis crypts were increased in distal colon but not middle colon. C. chinensis and E. rutaecarpa water extract could promote apoptosis of both middle and distal colon.

CONCLUSIONC. chinensis and E. rutaecarpa water extract could significantly inhibit the formation of ACF in model animals. These results indicated that C. chinensis and E. rutaecarpa water extract maybe have an inhibitory and clinically therapeutic effect on colon cancer, which were partly resulted from inhibiting proliferation and promoting apoptosis of crypts in middle and distal colon.

Animals ; Apoptosis ; drug effects ; Cell Proliferation ; drug effects ; Colonic Neoplasms ; chemically induced ; drug therapy ; pathology ; physiopathology ; Coptis ; chemistry ; Dimethylhydrazines ; adverse effects ; Disease Models, Animal ; Evodia ; chemistry ; Humans ; Male ; Plant Extracts ; administration & dosage ; Random Allocation ; Rats ; Rats, Wistar

Objective To identify the protein interacting with hepatitis E virus(HEV) recombi-nant capsomeric particles(P239). Methods Protein interacting with HEV was analyzed by the pull-down, MALDI-TOF-MS, co-immunoprecipitation (Co-IP) and CONFOCAL. Results A protein interacting with HEV recombinant particle (P239) was identified as HSP90 by MALDI-TOF-MS. The interaction between HSP90 and P239 was further confirmed by Co-IP. The protein level and localization of HSP90 and P239 in HepG2 were detected. The total quantity of HSP90 didn't change, and the movement of HSP90 from plasma membrane to perinuclei region with P239 was observed. Conclusion HSP90 may play an important role in the trafficking of P239. It suggests that HSP90 participate in the transportation of HEV after infection, which may contribute to the prevention and control of the disease.

OBJECTIVETo study the effects and mechanisms of sinensetin on proliferation and apoptosis of human AGS gastric cancer cells.

METHODMTT assay was used to detect the growth inhibition rates of human AGS gastric cancer cells treated with sinsesectin in different concentrations and times. The cell cycle distribution was measured by flow cytometry. The apoptosis was examined by Annexin-FITC/PI staining and DNA fragment analysis. The apoptosis morphology was observed by inverted fluorescence microscope after Hoechst 33342 staining. The protein expressions of p21 and p53 were detected by western blot.

RESULTMTT assay showed that sinensetin inhibited the growth of AGS gastric cancer cells in a dose- and time-dependent manner. Sinensetin blocked AGS cells in G2/ M and increased the apoptosis rates of AGS cells in a dose-dependent manner. DNA ladder was observed in cells treated with 60 micromol x L(-1) sinensetin for 48 h. The typical apoptotic morphological changes including cell nucleus shrinkage, chromatin condensation and apoptotic bodies were observed when treated with different dose of sinensetin. Western blot showed that sinensetin increased expressions of p53 and p21 in a dose-dependent manner.

CONCLUSIONSinensetin could inhibit human AGS gastric cancer cells proliferation and induce cell cycle block in G2/M phase and apoptosis. The up regulation of p53 and p21 protein might be one of the mechanisms.

Apoptosis ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Cyclin-Dependent Kinase Inhibitor p21 ; analysis ; Dose-Response Relationship, Drug ; Flavonoids ; pharmacology ; Humans ; Stomach Neoplasms ; drug therapy ; pathology ; Tumor Suppressor Protein p53 ; analysis