Dental Research ; Humans ; Tooth Bleaching

Objective: To measure the color of dental CAD/CAM alumina-glass-composites(AGC). Methods: Dental CAD/CAM alumina block were infiltrated at 1 120 ℃ by laboratory made AG1,AG2,AG3 and AG4 color serials of infiltration glass powder and Vita In-Ceram Alumina AL1,AL2,AL3 and AL4 infiltration glass respectively. Specimens were made with the area of 10 mm?10 mm,thickness of 0.5,1 and 1.5 mm respectively. Color parameters were measured by Minolta CM-2600d spectrophotometer. Results:The specimen with the thickness of 1 mm was used as the standard for color measurement.After infiltration with AL1-AL4 glass powder,the color parameters of Vita alumina core ceramic were L*: 69.39-78.41,a*:1.82- 4.02,b*:18.35-24.42,when infiltrated with AG1-AG4 glass powder, the color parameters of CAD/CAM AGC were L*:68.80-78.44,a*:1.32- 4.75,b*:16.85- 21.86. b*value and chroma of the AG3 core ceramic were lower than that of AL3 core ceramic,while a* value was higher.b* value and chroma of the AG1 and AG2 core ceramic were lower than that of AL1 and AL2 core ceramic. The reflectance curve of CAD/CAM AGC infiltrated by AG1-AG4 glass powder demonstrated the similar trend as that of the core ceramic infiltrated by Vita In-Ceram glass powder. Conclusion: The color range and surface reflection rate of laboratory made AG1-AG4 AGC are similar with those of Vita AL1-AL4 In-Ceram Alumina core and may meet the need of color match with veneer ceramics.

objective: To investigate the effects of cerium oxide content on the color of alumina glass composite. Methods: Infiltration glass powder with different content of cerium oxide (1%～4%) were fabricated. Alumina glass composite was prepared by infiltrating molten glass into presintered alumina block at 1 250 ℃ for 2 h, and the color of the alumina glass composite were measured with Minolta chromatic instrument(CR 321) . For comparison, the color of VITA In Ceram alumina technical shade guide was recorded too. Results: After infiltration, the b * range of the alumina glass composite was in accord with that of the shade guide. With the increasing content of the cerium oxide, a *, b * and chroma increased, L * decreased, the hue of the alumina glass composite shifted from yellow green to yellow red. Conclusion: Cerium oxide may effectively enhance b * of the alumina glass composite, but its ability of reducing L * and enhancing a * is weak.

Adult ; Churg-Strauss Syndrome ; complications ; Humans ; Male ; Myocardial Infarction ; complications

Cochlear Implantation ; Cochlear Implants ; Humans ; Tinnitus

Aim To investigate the role of chemokine-like factor 1 ( CKLF1 ) in SH-SY5 Y cell migration and its molecular regulatory mechanism. Methods SH-SY5Y cells were stimulated with CKLF1 for 0. 5 h, 2 h, 8 h and 24 h, respectively. The migration distance and the percentage of migration cells were recorded by CELLocate analysis. The phosphorylation of focal ad-hesion kinase ( FAK) at Tyr-397 site was detected by Western blot analysis. By chemotaxis assays, we con-firmed the chemotaxis of CKLF1. Furthermore, FAK inhibitor PF-573228 and PLCγ inhibitor U73122 were used for the research of molecular regulatory mecha-nisms involved. Results CKLF1 promoted cell migra-tion and induced a strong increase in the phosphoryla-tion level of FAK-pY397 , which were significantly at-tenuated by the presence of U73122 ( a specific inhibi-tor for PLCγ) . In addition, the chemotaxis of CKLF1 was obviously blocked by the FAK inhibitor PF-573228 . Conclusion CKLF1 induces SH-SY5 Y cell migration via PLCγ/FAK signaling pathway.

Objective To investigate the destructive effect of cadmium (Cd)and the protective effect of astragaloside ( Asd) on TM3 cells.Methods The best protective concentration of Asd on TM 3 cells after Cd treatment was selected by MTT cell viability experiment .The apoptosis rate of TM3 cells was measured by flow cytometry .The expression of connexin 43(Cx43) was detected by immunohistochemistry .The morphological changes of TM3 cells were observed by electron mi-croscopy .Results The viability of TM3 cells in both control and Asd-treated group was not significantly different after 24 h or 48 h,but it was significantly decreased in Cd group .However , the viability of TM3 cells in Cd +As group was higher than that in Cd group .Flow cytometry showed that there was no significant difference in the apoptosis rate of TM 3 cells be-tween the control and Asd-treated group after 24 h,but it was obviously increased with the Cd concentration .The apoptosis rate of Cd+Asd group was lower than that in Cd group (P<0.01).Immunohistochemistry demonstrated that the average optical density (AOD) of the positive product of Cx43 in Cd-treated TM3 cells was obviously decreased (P<0.01), but the average gray value (AGV) was significantly increased when compared with the control group (P<0.01).The ultra-structural changes in TM3 cells were obvious after Cd treatment ,but those in Cd+Asd group were improved when compared with Cd group.Conclusion Cd reduces the expression of Cx 43 and damages the morphology of TM 3 cells.Asd has protec-tive effect on Cd-induced TM3 cell injury.

Objective To investigate the clinical characteristic and the predicting value of plasma Apelin in elderly patients with sepsis.Methods A retrospective analysis was conducted in 26 sepsis patients aged (72.9±9.7) years in average and 30 healthy controls.Serum Apelin level was measured by ELISA.Body mass index (BMI) and C-reaction protein (CRP) were detected.Patients were divided into survival group (n=18) and death group (n 8).According to acute physiology and chronic health evaluation (APACHE) Ⅱ,patients were divided into subgroup A (n=14,APACHE Ⅱ score≤20) and subgroup B (n=12,APACHE Ⅱ score＞20).Results The Apelin concentration was higher in sepsis patients than in healthy controls [(0.38±0.15)ng/L vs.(0.19±0.12)ng/L,t=2.011,P＜0.05].The Apelin concentration was lower in survival group than in death group[(0.21 ± 0.29)ng/L vs.(0.49 ± 0.32) ng/L,t =2.094,P＜0.05].The Apelin level was increased with APACHE Ⅱ scores increment in sepsis patients (P＜0.05).Multivariable logistic analysis showed that when taking survival/death as the dependent variable and Apelin as the independent variable,the ()R value was 4.162 with 95％ CI:1.115-15.535(P＜0.05).Conclusions Increased serum Apelin level reflects the severity of illness in patients with sepsis,which is a risk factor for death in prognosis of sepsis.

Objective To evaluate the incidence,severity,risk tactors and impact to prognosis of acute kidney injury (AKI) in patients with severe traumatic brain injury (sTBI) by using acute kidney injury network (AKIN) classification system.Methods A retrospective analysis was carried out in 136 patients with sTBI hospitalized between January 2007 and May 2011.Demographic data,admission evaluation (whether with hernia or not on admission,systolic pressure and mean arterial blood pressure,serum creatinine and urea nitrogen,and blood glucose),outcome at 6 months post-injury and mortality were collected.Renal function was assessed using AKIN criteria.The patients were divided into two groups based on the presence or absence of AKI (non-AKI group and AKI group).According to the severity of AKI,AKI group was further classified as AKI grade 1 group,AKI grade 2 group and AKI grade 3 group.The differences among groups were analyzed.Results According to AKIN classification system,31 (23％) out of the 136 patients were diagnosed as being with AKI,including 21 cases (68％) in AKI grade 1 group and 10 cases (32％) in AKI grade 2 and 3 groups.The patients at older age and with lower Glasgow coma scale (GCS) on admission,higher levels of serum creatinine and blood urea nitrogen on admission were prone to AKI.As compared with TBI patients with normal renal function,TBI patients associated with AKI had higher mortality and worse outcome.Conclusions AKI is a common complication of patients with sTBI.AKIN classification system can early diagnose AKI in sTBI patients and may contribute to improvement of the outcome.

Objective To observe the effect of astragaloside IV (A) and SB203580 antagonize cadmium (Cd) toxicity on expression of associated protein and blood-testis barrier(BTB) in rats and to study the protective mechanism of A on it.Methods Totally 21 SD male rats were randomly divided into 7 groups, 3 rats per group:Cd [ intraperitoneally injected with 0.1%CdCl2,1mg/(kg?d)],Cd+A [at the above dose of CdCl2,at the same time with A,10mg/(kg?d)], and Cd +SB203580 [at the above dose of CdCl2,at the same time with SB203580,100μg/(kg?d)], each of the above groups was further divided into continuous five and ten days treatment groups .The control group was intraperitoneally injected with equal dosage of normal saline .The testes were studied by light , electron microscopy , immunohistochemistry and Western blotting .Results In the control group ,irregular and lightly stained nuclei of Sertoli cell ( Sc) in seminiferous tubules were observed by HE staining .A continuous electron density line of tight junction ( TJ) and normal ultrastructure of BTB were observed .After Cd treatment ,the vesicular formation in the Sc was observed .The ultrastructural damage of Sc and TJ was observed .Compared with the corresponding time point of Cd group ,these were weakened in morphology of testis and ultrastructure of TJ after Cd +A or Cd +SB203580 treatment .The positive products of zonula occludens-1 ( ZO-1 ) and claudin-11 were localized mainly in the base of the seminiferous tubule .After Cd treatment , the average absorbance (AA) of ZO-1 and Claudin-11 was decreased significantly compared with that of the control group (P<0.05).After Cd +A or Cd +SB203580 treatment,AA of ZO-1 and Claudin-11 were increased significantly compared with that of the Cd group(P<0.05),though lower than that of the control group .The result of Western blotting showed that phosphorylation-p38MAPK in Cd group was increased significantly compared with that of the control group (P<0.05).After Cd +A or Cd+SB203580 treatment, it was decreased significantly compared with that of the Cd group (P<0.05).Conclusion Cd decreases ZO-1 and Claudin-11 expression and damages ultrastructure of TJ in BTB , asⅣhas protective effect on it , and is related to inhibiting activation of p 38 MAPK pathway .