Objective To study the safety and efficacy of damage control using percutaneous transhepatic biliary drainage (PTBD) in acute cholangitis of severe type (ACST) secondary to intrahepatic choledocholithiasis.Methods The clinical data of 8 patients who received PTBD after hospital admission followed by conventional surgery for ACST when their general condition improved were retrospectively studied.Results All patients received PTBD successfully and the amount of bile drained was 100-400 ml in the first day.The general condition of these 8 patients became better after 24 h and the total bilirubin decreased for about 25-100 mmol/L after 48 h.Three patients with a platelet count of less than 20 × 109/L showed an improved count to more than 50 × 109/L 72 h after PTBD.All patients were operated at different times after the PTBD:2 received T-tube drainage,3 T-tube drainage combined with left hepatectomy,and 3 choledochojejunostomy.Seven patients recovered uneventfully,but 1 developed hepatic failure with the total billurubin rose to more than 200 μmol/L.He was discharged home with the PTBD tube.During the waiting time of 7 days to 3 months before surgery,the tubes were kept patent and no mortality or morbidity such as bleeding,bile leakage,and peritonitis occurred.Conclusions PTBD was a safe and efficacious procedure for patients who were in a serious condition with ACST secondary to intrahepatic choledocholithiasis.It was more likely to be successful as it is minimally invasive and therefore well-tolerented.It reduced the biliary pressure,relieved the ongoing sepsis,and was a good preparatory procedure before any conventional surgery.

Objective Toinvestigatetheeffectsofpyrrolidinedithiocarbamate(PDTC)onexpressionofNF-κB,MMP-2andleft ventricular collagen remodeling following acute myocardial infarction in rats .Methods The myocardial infarction model in rat was induced by ligation of left anterior descending coronary artery .12 adult Sprague-Dawley rats survived 24 for h after acute myocardial infarction were randomly divided into the myocardial infarction (MI) group and the PDTC-treated(PD) group .Six rats were desig-nated as sham-operated group(SH group) .The PD group was intraperitoneally injected with PDTC (80 mg · kg -1 · d-1 ) for 28 d , the MI group and SH group were given normal saline as control .On 28 d ,the cardiac function of left ventricle was measured by ech-ocardiography .The infarct size was evaluated .The total collgen ,typeⅠcollgen ,typeⅢcollgen ,and Ⅰ /Ⅲ collgen ratio were quanti-fied histomorphometry .The mRNA and protein levels of NF-kappaBp65 and MMP-2 were determined by reverse transcription-poly-merase chain reaction(RT-PCR) and by Western blot ,respectively .Results Compared with the SH group ,the values of the total collgen ,typeⅠcollgen ,typeⅢcollgen ,and Ⅰ /Ⅲ collgen ratio in the MI group and the PD group were significantly increased ,the differen had statistical significance (P<0 .01) .The values of the total collgen ,typeⅠcollgen ,typeⅢcollgen ,and Ⅰ /Ⅲ collgen ratio in the PD group were notably decreased than those in the MI group(P<0 .01) .Moreover ,the mRNA and protein levels of NF-kap-paBp65 and MMP-2 in the PD group were lower than those in the MI group ,the difference had statistical significance(P<0 .01) . Conclusion Left ventricular collagen remodeling following acute myocardial infarction could be improved by PDTC to some extent , which mechanism could be related with inhibiting NF-kappaB activation and down -regulating the expression of MMP-2 in rats .

Objective:To measure the safe range from the foramen rotundum to the siphon of internal carotid artery using three-dimensional reconstruction technique, and to provide guidance for operation through pterygopalatine fossa.Methods:The skulls of 121 volunteers were scanned to get the final results with thin-section computed tomographic images.The position of the siphon of internal carotid artery (point A)and foramen rotundum (pointB)were ascertained.Three-dimensional reconstruction technique was used to build a coordinate system paralleled to the frankfort horizontal plane and the nasal septum plane.The coordinate system took point A as the coordinate origin.Point C and point D were the projections of point A in two planes parallel with frankfort horizontal plane and nasal septum plane which included point B.The distances of AC,AB,and BC were measured. The angles of the line went through A and B to the three planes were also measured.Results:The distance of AC was measured as 13.22 (3.79)mm (range,8.33 - 105.67 mm;95%CI:8.55 - 21.39 mm).The angle to the sagittal plane was measured as 33.54 (9.23)° (range,5.38- 66.58°;95%CI:30.88 - 34.20°). The angle to the coronal plane was measured as 53.17 (10.48)°(range,5.60-75.02°;95%CI:51.29-55.06°).The angle to the horizontal plane was measured as 9.43 (12.91 ) mm (range,- 28.44 - 82.22;95% CI:7.11 - 11.76 ). Conclusion:The safety distance from foramen rotundum to the siphon of internal carotid artery in the operation through pterygopalatine fossa (PPF) under nasoendoscope is obtained by thin-section computed tomographic images.

OBJECTIVE: To investigate the effect of orthodontic traction on the microstructure of dental enamel. METHODS: Forty-eight isolated premolars were randomly divided into 6 groups (=8), including Group A (blank control group), in which the teeth were bonded with the orthodontic brackets without any loading force; Groups B1, B2, and B3 where the teeth were bonded with the orthodontic brackets using clinical adhesives and loaded with 50 g force for 6 months, 200 g force for 6 months, and 200 g force for 1 month, respectively; and Groups C1 and C2, where the teeth were bonded with straight wire brackets using light curing bonding and chemical curing bonding techniques, respectively. All the teeth were embedded with non-decalcified epoxy resin. Scanning electron microscope (SEM), atomic force microscope (AFM), and energy spectrometer (EDS) were used to analyze interface morphology and elemental composition of the teeth sliced with a hard tissue microtome. RESULTS: Compared with those in Group A, the teeth in the other 5 groups showed increased adhesive residue index with microcracks and void structures on the enamel surface under SEM; AFM revealed microcracks on the enamel surface with angles to the grinding direction. A larger loading force on the bracket resulted in more microcracks on the enamel interface. The interface roughness differed significantly between Groups A and C2, and the peak-to-valley distance differed significantly between Groups A, C, and C2. CONCLUSIONS Orthodontic traction can cause changes in the microstructure of normal dental enamel.
Dental Enamel ; Materials Testing ; Orthodontic Brackets ; Resin Cements ; Surface Properties ; Traction

Objective: To investigate the aggravation of pancreatic tissue injury in rats with acute hypertriglyceridemic pancreatitis and the possible role of NADPH oxidase (NOX). Methods: Thirty SPF rats were randomly (random number)divided into five groups: N group, H group, NLAP group, HLAP group and HAPO group. AMY, TG, TC and FFA levels were detected. The pathological changes of pancreas were observed under light microscope and the ultrastructural changes of pancreatic acinar cells were observed by TEM. Serum levels of MDA, SOD, IL-1β, TNF-α and LDH were detected. The expression of NOX4, p-Akt and p-GSK3β in pancreas was detected by immunofluorescence, and the expression of NF-κB and TNF-α in pancreas was detected by immunohistochemistry. Results: Intraperitoneal injection of P-407 could significantly increase the levels of serum TG, TC and FFA in rats. After acute pancreatitis induced by L-Arg, the levels of serum AMY in the NLAP and HLAP groups were significantly increased, while Apocynin could significantly decrease the level of serum AMY. Compared with the NLAP group, the pathological injury of pancreatic tissue in the HLAP group was more serious, the level of inflammatory mediators was significantly increased, and the cell necrosis was more serious. After inhibiting NOX, the activation of Akt/GSK3β pathway was regulated and the pancreatic injury was improved. Conclusion In HTGP, NOX aggravates pancreatic injury by regulating the activation of Akt/GSK3 β pathway. Inhibition of NOX expression can play a protective role in pancreas injury of HTGP..