China ; Humans ; Periodontics ; trends

Dental Scaling ; Dentistry ; manpower ; General Practice, Dental ; manpower ; Health Education, Dental ; manpower ; Humans ; Oral Hygiene ; Outcome Assessment (Health Care) ; Periodontitis ; therapy ; Toothbrushing

Pseudomonas aeruginosa exhibits an inherently reduced susceptibility to most antibiotics compared with most other Gram-negative bacterial species because its low outer membrane permeability and the multiple ways in which P.aeruginosa can become drug-resistant.Pseudomonas aeruginosa has joined the “super bacteria”.Recent researches, using mutant library screening, microarray technology, and mutation frequency analysis have demonstrated that antibiotics themselves can induce very large groups of genes in vivo growth conditions or complex adaptation conditions ( for example, biofilm growth or swarming motility), resulting in resistance as well as new forms of adaptive resistance.

Objective To investigate the influence of different concentrations of allicin in apoptosis of A549 cells induced by porphyromonas gingivalis (P.gingivalis). Methods The minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) of allicin in inhibiting P.gingivalis were investigated by broth dilution methods. The tetrazolium salts (MTT) assay was used to detect the viability of A549 cells infected by P.gingivalis and treated with different concentrations of allicin (64 mg/L, 96 mg/L and 128 mg/L). The flow cytometry FITC/PI staining was used to detect apoptotic rates of A549 cells treated by P.gingivalis and/or allicin for 24 h. Results The values of MIC and MBC of allicin for inhibiting P.gingivalis were 64 mg/L and 128 mg/L respectively. MTT assay showed that the cell viability was significantly increased with the increased concentration of allicin in a concentration-dependent manner (P < 0.05). There was no significant difference in cell viability between allicin (128 mg/L) group and control group, which showed that allicin was no significant cytotoxicity in A549 cells. Flow cytometry assay showed that the apoptotic rates from high to low were P. gingivalis group>P. gingivalis+allicin group>allicin group>control group with significant differences (P<0.01). The apoptosis of A549 cells induced by P.gingivalis was significantly inhibited by allicin (P<0.01). Conclusion Allicin can inhibit P.gingivalis infection in lung epithelial cells. There is a good prospect in the application of allicin in the treatment of pulmonary infection in patients with periodontitis.

Objective To observe the effects of epileptiform discharge and its influence on humpwave sleep spindles after sleep deprivation(SD)in children with epilepsy.Methods Monitoring the wakefulness and sleep EEG of samples of 160 children who were diagnosed epilepsy after SD.Results The detection rate of epileptiform discharge(59.3%)in sleep EEG was higher than that in wakefulness EEG after SD(16.3%)(P

Purpose To evaluate papillary muscle function in ischemic mitral regurgitation (IMR) with two-dimensional speckle tracking imaging (2D-STI) and three-dimensional ultraphonic technology,and to investigate the primary factors influencing IMR so as to provide clinical information for the prediction of IMR.Materials and Methods Seventy-six IMR patients were enrolled as research group and other 66 healthy volunteers as control group.Two groups were both examined by transthoracic echocardiography and 2D-STI.The parameters including fractional shortening of anterior and posterior papillary muscles (AFS,PFS),length of anterior or posterior papillary muscle tips to contralateral anterior mitral annular (APM-AMA,PPM-AMA),mitral leaflet closure (MLC),inter distance papillary muscle (IPMD),the angle between the anterior papillary muscle and the anterior LV free wall (Ang Ⅰ) and the angle between the posterior papillary muscle and the anterior LV free wall (Ang Ⅱ),anterior and posterior papillary muscle longitudinal strain (ALS,PLS) and peak time (APT,PPT),delay time (DT),left ventricular end-diastolic diameter (LVIDD),left ventricular end-diastole volume (LVEDV),and left ventricular ejection fraction (LVEF) were compared.Results Compared with control group,LVIDD,LVEDV,LVEF,AFS,PFS,IPMD,MLC,ALS,PLS and DT in research group were all significantly different (all P＜0.05).ALS,PLS,AFS,and PFS had positive correlation with LVEF (P＜0.05) and negative correlation with LVEDV (P＜0.05).MLC,IPMD,DT had negative correlation with LVEF (P＜0.05).ALS,PLS,MLC,AFS,PFS,IPMD were significantly correlated with Gensini score (r=-0.65,-0.78,0.54,-0.51,-0.57,0.49,respectively,P＜0.05).The multivariant Logistic regression analysis showed that IMR was correlated with IPMD,MLC,PLS and DT (OR=1.26,1.32,1.37,1.52,respectively,P＜0.05).Conclusion 2D-STI can accurately evaluate the papillary muscle dysfunction caused by myocardial ischemia.Moreover,the risk factors of IMR include increase of IPMD and MLC,decrease of PLS,and desynchronization of papillary muscles.These findings contribute to the clinical prediction of IMR.

Objective To explore the effects of different degrees of hypoxia-ischemia(HI)on neuronal apoptosis and astrocyte proliferation in neonatal rats.Methods A total of 72 rat pups aged 7 days were randomly divided into 3 groups(n=24 each group):sham operated group,mild HI group,and severe HI group.The rats were subjected to right carotid artery occlusion and exposed to a hypoxic gas mixture (8% oxygen and 92% nitrogen)for 40 minutes at 34.5℃ in mild HI group and for 65 minutes at 35.5℃ in severe HI group.The expression of glial fibrillary acidic protein(GFAP)was detected by immunohistochemistry,and TUNEL method was performed to observe the proliferation of astrocytes and the neuronal apoptosis.Results Compared with sham operated group,the number of GFAP-positive cells signifiantly increased throughout the cortex and white matter in the ischemic hemisphere 48 hours(P＜0.01)and 1 week(P＜0.05)after mild HI,and in some areas the increase continued until week 4(P＜0.05).The number of GFAP-positive astrocytes in the cortex and white matter was signficantly higher in severe HI group than in mild HI group(P＜0.05)and sham operated group(P＜0.01)48 hours and 1 week after severe HI,but the increase was not detectable at week 4.Compared with sham operated group,the number of TUNEL-positive cells in the subcortical white matter in the ischemic hemisphere signficantly increased in mild HI group 48 hours,1 week,and 4 weeks following a mild HI insult(P＜0.05),but no signficant difference in the number of TUNEL-positive cells in the cortex was found.Following a severe HI insult,the number of TUNEL-positive cells in the cortex and white matter in the ischemic hemisphere significantly increased at 48 hours(P＜0.01),and in peri-infarct regions the number of TUNEL-positive cells increased until weeks 1 and 4(P＜0.05).Conclusion Mild HI causes neuronal apoptosis mainly in subcortical white matter and prolonged proliferation of astrocytes.Severe HI is associated with widespread neuronal apoptosis in the ischemic hemisphere,and the proliferation of astrocytes is rapid and prominent after severe HI.

Objective To investigate papillary muscle function and construction in myocardial infarction(MI) patients by two-dimensional speckles tracking imaging(2D-STI),and to analyze the influence factors of ischemic mitral regurgitation.Methods Fifty myocardial infarction with ischemic mitral regurgitation(IMR) patients were brought into case group.The patients were divided into two groups:Ant MI group and Inf-Pos-MI group.Forty-five health volunteers were involved as control group.Anterior,posterior papillary muscle longitudinal strain (ALS,PLS),delay time(DT),fractional shortening (FS),length between the posterior or anterior papillary muscle tips and the contralateral anterior mitral annualr (APM AMA,PPM AMA),mitral leaflet closure (MLC),inter distance papillary muscle (IPMD) were aquired respectively.Papillary muscle function and construction among the groups were compared,and the effective factors of IMR were evaluated.Results Between the control group and Ant-MI group,the left ventricular end-diastolic diameter(LVEDD),left ventricular end-diastolic and end-systolic volume(LVEDV,LVESV),left ventricular ejection fraction(LVEF),ALS,delay time(DT),A FS,IPMD,MLC,APM-AMA,PPM-AMA were significantly different(all P ＜0.05).Between the control group and Inf-Pos-MI group the LVEDD,LVEDV,LVESV,EF,DT,PPM-AMA,MLC,PLS,P-FS were significantly different(P ＜0.05).Between the Ant-MI group and Inf-Pos-MI group,the LVEDD,LVEDV,LVESV,EF,MLC,ALS,PPM-AMA,PLS were significantly different (all P ＜ 0.05).In the Ant-MI group,LVEDV,ALS,MLC were significantly correated with Gensini score(r =0.71,-0.65,0.56;P ＜0.05).In the Inf-Pos-MI group,PPM AMA,PLS were significantly correated with Gensini score(r =0.65,-0.76;P ＜0.05).In the Ant MI group and Inf-Pos-MI group,the ALS,PLS,PPM-AMA were significantly different (P ＜ 0.05).Its correlates in Logistic analysis of Ant-MI group included LVEDV,MLC,DT with OR 1.48,1.72,1.54(P ＜0.05),respectively.Its correlates in logistic analysis of Inf Pos-MI group included PLS,PPM-AMA,DT with OR 1.78,1.57,1.56 (P ＜0.05),respectively.Conclusions There are different extent of damage of papillary muscle function and construction in Ant-MI group and Inf-Pos-MI group.The increases of LVEDV and MLC and desynchronization of PMs are risk factors of IMR in Ant-MI group.The increases of PMP-AMA,decrease PLS and desynchronization of PMs are risk factors of IMR inInf-Pos-MI group.

Aggressive Periodontitis ; diagnosis ; therapy ; Humans

OBJECTIVE:To study the effects of arsenic trioxide(As 2 O 3 )on the encoding protein expressions of nm23and P53in gastric cancer cells and to study the anti-canecer mechanism of which in the tumor.METHODS:A control group and a test group were set up.The expressions of gene coding proteinum nm23and P53of the gastric cancer cells cultured in vitro by the action of As 2 O 3 were determined by immunohistochemistry method.RESULTS:The expression levels of nm23and P53in gastric cancer cells have been lowered compared with the control group.CONCLUSION:As 2 O 3 can exert its anti-tumor effect by decreasing the expression of gene coding proteinum of nm23and P53.