ObjectiveTo observe the effect of forced expansion of occlusion on radiation ankylosis of tempormandibular joint of patients with nasopharynx cancer after radiotherapy.Methods166 patients with ankylosis of tempormandibular joint were randomly divided into the treatment group (83 cases, treated with forced expansion of occlusion) and control group (83 cases, with other treatment).ResultsThe absoluteness value of degree of mouth opening in the treatment group was significantly higher than that in the control group( P<0.01), and the course of ankylosis of tempormandibular joint in the treatment group was obviously delayed compared with the control group ( P<0.01).ConclusionThe forced expansion of occlusion can delay the course of ankylosis of tempormandibular joint, expand the degree of mouth opening, recover or partially recover the occlusion and chaw function.

OBJECTIVETo evaluate the reliability and validity of the Chinese version of addiction severity index (ASI)-5th version (ASI-C-5), in illegal drug users receiving methadone maintenance treatment (MMT) in China.

METHODSOne hundred and eighty-six heroin addicts (144 men and 42 women) receiving MMT at three clinics in Guizhou province, southwest China, were recruited. They were all interviewed with a questionnaire of ASI-C-5 and 35 were re-interviewed at an interval of seven days to assess its test-retest reliability.

RESULTSCronbach's alpha for internal consistency of CSs varied from 0.60 to 0.81 in all domains. Test-retest reliability of composite scores (CSs) of ASI-C-5 were satisfactory (r=0.38-0.97). Based on item analysis and expert's suggestions, five items were deleted and one item was modified in ASI-C-5. Criterion validity of ASI-C-5 was found acceptable, as compared to addicts' self-rating anxiety scale (SAS) and self-rating depression scale (SDS) (r=0.59 and 0.45) except for social support rating scale (SSRS).

CONCLUSIONSASI-C-5 can be used for heroin addicts receiving MMT with acceptable reliability and validity.

Adult ; China ; Female ; Heroin Dependence ; drug therapy ; physiopathology ; Humans ; Male ; Methadone ; therapeutic use ; Reproducibility of Results ; Severity of Illness Index ; Surveys and Questionnaires

Objective To understand the situation of client-retention to methadone maintenance treatment(MMT)program and related factors.Methods A Cohon study was adopted.In toml,1003 heroin addicts who were treated at 8 local MMT clinics with less than one month period.were recruited under nominal informed consent from Guizhou province.southwest part of China.during June to October 2006.Face-to-face interview and questionnaire administered to collect relevant information from the clients who were also followed nntil June 2007 to understand the situation on retention.Data were analyzed with Kaplan-Meier method to estimate the retention rate at different time spans while factors related to retention were analyzed with Cox proportional hazard regression model.Results All the clients were followed-up for 14 months,with an average retention of ten months.The retention rates of the clients were 68.8%and 57.4%at 6th-month and 12th-month of the treatment program.estimated by Kaplan-Meier method.Results of Cox regression analysis showed that factors influencing retention rate on MMT among the clients,including their awareness on MMT,dailv dose of methadone intake,and difierent MMT clinics which they were attached to.Risk influencing the withdrawal from MMT had a 20%decrease along with the increase when the daily dose of methadone intake reached 25 mg,with a hazard ratio of 0.80(P＜0.01).If the clients were aware that methadone was a life-time treatment when they began the MMT program.the risk for withdrawal would be lower than those who were not and the hazard ratio became 0.66(P＜0.05).Conclusion Our data showed that about half of the clients who were at the MMT program would still stick to it after 12-months.suggesting that the retention rate was not satisfactory and need to be improved.Factors as the MMT clinics themselves that the clients visited,(Laily methadone dosage they took,and the awareness on MMT etc.were important predictors to the rate of retention on MMT program.

Cardiac Tamponade/etiology* ; Female ; Humans ; Pericardial Effusion/etiology*

Captopril can have nephrotoxic effects, which are largely attributed to accumulated renin and "escaped" angiotensin II (Ang II). Here we test whether angiotensin converting enzyme-1 (ACE1) inhibition damages kidneys via alteration of renal afferent arteriolar responses to Ang II and inflammatory signaling. C57Bl/6 mice were given vehicle or captopril (60 mg/kg per day) for four weeks. Hypertension was obtained by minipump supplying Ang II (400 ng/kg per min) during the second 2 weeks. We assessed kidney histology by periodic acid-Schiff (PAS) and Masson staining, glomerular filtration rate (GFR) by FITC-labeled inulin clearance, and responses to Ang II assessed in afferent arterioles in vitro. Moreover, arteriolar H₂O₂ and catalase, plasma renin were assayed by commercial kits, and mRNAs of renin receptor, transforming growth factor-β (TGF-β) and cyclooxygenase-2 (COX-2) in the renal cortex, mRNAs of angiotensin receptor-1 (AT₁R) and AT₂R in the preglomerular arterioles were detected by RT-qPCR. The results showed that, compared to vehicle, mice given captopril showed lowered blood pressure, reduced GFR, increased plasma renin, renal interstitial fibrosis and tubular epithelial vacuolar degeneration, increased expression of mRNAs of renal TGF-β and COX-2, decreased production of H₂O₂ and increased catalase activity in preglomerular arterioles and enhanced afferent arteriolar Ang II contractions. The latter were blunted by incubation with H₂O₂. The mRNAs of renal microvascular AT₁R and AT₂R remained unaffected by captopril. Ang II-infused mice showed increased blood pressure and reduced afferent arteriolar Ang II responses. Administration of captopril to the Ang II-infused mice normalized blood pressure, but not arteriolar Ang II responses. We conclude that inhibition of ACE1 enhances renal microvascular reactivity to Ang II and may enhance important inflammatory pathways.
Angiotensin II/pharmacology* ; Animals ; Arterioles/metabolism* ; Captopril/pharmacology* ; Hydrogen Peroxide/pharmacology* ; Kidney ; Mice