Objective:To explore the effects of double circumferential fibrotomy(CF)in the improvement of periodontal attachment of the teeth with periodontal disease.Methods:22 migrated incisors of 4 adults were randomly assigned to one-time CF group (T1 )and double CF group(T2)by center line.Periapical intraoral radiographic examination was performed using paralleling technique at pre-and post-leveling-alignment stage of the teeth.Root length,crown-root ratio and the distance of CEJ-AC were measured.The periodontal in-dicators were also recorded during the orthodontic treatment.Data were statistically analysed by comparative t-test.Results:CEJ-AC and crown root ratio reduction was greater in T2 group than those in T1 group(P <0.01 ),but the periodontal indices did not show sig-nificant difference between the 2 groups(P >0.05).Conclusion:Double circumferential fibrotomy can improve periodontal attachment, reasonable orthodontic force does not lead to remarkable root resorption of the periodontitis inflicted teeth.

Objective:To evaluate the application value of three-dimensional shear wave elastography(3D-SWE) with quantitative parameters and qualitative analysis of stiff rim sign in differentiating benign and malignant breast masses.Methods:One hundred and seventeen female patients (121 breast masses) admitted to the First Affiliated Hospital of Soochow University from January 2020 to February 2021 were examined by conventional ultrasound, two-dimensional shear wave elastography (2D-SWE) and 3D-SWE. Surgical or puncture pathology were used as the gold standard, the ROC curves of 2D-SWE and 3D-SWE were drawn to obtain the optimal qualitative and quantitative indicators. Afterwards, BI-RADS category was adjusted according to the optimal indicators, which could be used to evaluate the diagnostic value in differentiating benign and malignant breast masses.Results:The area under ROC curve (AUC) of BI-RADS category was 0.846, the sensitivity and specificity were 89.6% and 79.6%, respectively. The AUC value of mass-to-fat elasticity ratio(Eratio) of coronal plane was 0.869, which was the highest among all quantitative parameters and was significantly higher than that of 2D-SWE ( P<0.05). In addition, the AUC value of stiff rim sign of coronal plane was significantly higher than those of 2D-SWE, sagittal plane and transverse plane (All P<0.05). The AUC of combination of stiff rim sign of coronal plane and conventional US was 0.901, which was significantly higher than that using conventional ultrasound alone( P<0.05). Conclusions:Compared with 2D-SWE, Eratio and stiff rim sign of coronal plane of 3D-SWE yield better diagnostic efficiency.Adjusting stiff rim sign coronal plane to BI-RADS category can effectively improve the diagnostic efficiency.

Background and purpose:Silent information regulator proteins(sirtuins,SIRT)are a class Ⅲ histone deacetylases with nicotinamide adenine dinucleotide(NAD+)as coenzyme.YME1 like 1 ATPase(YME1L1)is essential for the maintenance of mitochondrial morphology,function and plasticity.Optic atrophy 1(OPA1)mainly mediates mitochondrial fusion.The aim of this study was to explore the expression of SIRT3 in the endocrine resistance of breast cancer,the relationship between SIRT3 and YME1L1 and OPA1,and the mechanism of SIRT3 in the endocrine resistance of breast cancer.Methods:4-hydroxytamoxifen was used to induce tamoxifen-resistant MCF-7/TAM cells.cell counting kit-8(CCK-8)was used to detect cell proliferation and verify drug resistance.The mitochondrial morphology was observed by transmission electron microscopy(TEM)and immunofluorescence staining.The expressions of SIRT3 and OPA1 were detected by real-time fluorescent quantitative polymerase chain reaction(RTFQ-PCR)and Western blot.JC-1 staining was used to detect mitochondrial membrane potential,and dihydroethidium(DHE)staining was used to detect reactive oxygen species(ROS)to verify mitochondrial function.SIRT3 was knocked down in drug-resistant cells by RNA interference,and SIRT3 and YME1L1 wild type(WT),simulated acetylation state mutant(MUT K237Q),and simulated deacetylation state mutant(MUT K237R)were overexpressed in parental cells by overexpression plasmid.Immunoprecipitation assay(IP)and immunofluorescence(IF)were used to verify the interaction between SIRT3 and YME1L1.Results:RTFQ-PCR and Western blot results showed that SIRT3 gene expression and protein level was significantly higher in drug-resistant cells than in parental cells.Overexpression of SIRT3 in parental cells decreased the sensitivity of breast cancer cells to tamoxifen.Knockdown of SIRT3 in drug-resistant cells enhanced the sensitivity of drug-resistant cells to tamoxifen.DHE staining showed that the ROS level was lower in tamoxifen resistant cells than in parental cells at the same concentration.Transmission electron microscopy and fluorescence staining showed that the mitochondria of the drug-resistant cells were elongated compared with the parental cells.Western blot results showed that the expression level of L-OPA1 protein was higher in drug-resistant cells than in parental cells.Overexpression of SIRT3 in the parental cells resulted in enhanced mitochondrial function and longer mitochondrial morphology compared with the control cells.Western blot showed that the expression of L-OPA1 was upregulated.When SIRT3 was knocked down in drug-resistant cells,the opposite result was obtained.We further verified how SIRT3 regulated OPA1 protein,affected the morphology and function of mitochondria,and promoted drug resistance of breast cancer.Overexpression of YME1L1(wild-type and mutant plasmids)in parental cells showed that overexpression of YME1L1 in the simulated deacetylation state resulted in similar results as overexpression of SIRT3,and overexpression of YME1L1 in the acetylated state resulted in similar results as knockdown of SIRT3.IP assay confirmed the interaction between SIRT3 and YME1L1 in breast cancer cells.The acetylation level of YME1L1 was different at different SIRT3 expression levels.IF assay showed that YME1L1 was co-localized with SIRT3 in MCF-7 cells.Conclusion:SIRT3 is highly expressed in tamoxifen-resistant breast cancer cells.SIRT3 upregulates L-OPA1 expression by deacetylating YME1L1,thereby promoting mitochondrial fusion and enhancing mitochondrial function,and promotes tamoxifen resistance in breast cancer.