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Background When a phosphoric acid is used, before applying an adhesive system, it is known that obtaining an effective adhesion to the root canal walls is a challenge. The aim of the present study was to evaluate the influence of phosphoric acid viscosity and application mode on the push-out bond strength (BS) values of fiberglass post to root dentin. The conditioning pattern on the root dentin was also evaluated. Materials and Methods The roots of 44 endodontically&nbsp;treated premolars were divided into 4 groups, of eleven teeth each, according to the combination of the main factors phosphoric acid viscosity (liquid or gel) and application mode (passive or sonic). [https://www.selleckchem.com/products/gdc-1971.html click here] After application of the two-step etch-and-rinse adhesive system, the fiberglass posts were cemented with a dual-cure resin-cement. Roots were sectioned transversely into six 1-mm slices for push-out BS test at 0.5 mm/min. Some roots of each group were selected for evaluation of the conditioning pattern by scanning electron microscopy. BS results (three-way ANOVA and Tukey's test) and the conditioning pattern (Kruskal-Wallis test and Mann-Whitney test) were statistically evaluated (α= 0.05). Results The highest BS value was observed with a liquid phosphoric acid under sonic application mode (p less then 0.05), being all other groups similar to one another (p less then 0.05). Also, the highest BS value was observed in the cervical third, followed by the medium and the apical thirds (p less then 0.05). The sonic application produced better smear layer removal and opening of dentinal tubules for both viscosities (p = 0.015). Conclusion A better bonding of fiberglass posts to root canals can be achieved when the post spaces are conditioned with a liquid phosphoric acid under sonic application. © 2020 Costa Scholz et al.Purpose Due to complex medical profiles, adults with neurodevelopmental disabilities (NDDs) may have a heightened risk for early development of chronic kidney disease (CKD) and accelerated CKD progression to advanced stages and kidney failure. The purpose of this study was to estimate the incidence rate of advanced CKD for adults with NDDs and compare the incidence rate to adults without NDDs. Patients and Methods Data were used from the Optum Clinformatics® Data Mart to conduct this retrospective cohort study. The calendar year 2013 was used to identify eligible participants individuals ≥18 years of age and without advanced CKD. Participants were followed from 01/01/2014 to advanced CKD, loss to follow-up, death, or end of the study period (12/31/2017), whichever came first. Diagnostic, procedure, and diagnosis-related group codes identified NDDs (intellectual disabilities, cerebral palsy, autism spectrum disorders), incident cases of advanced CKD (CKD stages 4+), diabetes, cardiovascular diseases, and hyperes used in our analysis. © 2020 Whitney et al.Purpose Although increasing lines of evidence showed associations between serum uric acid (UA) levels and schizophrenia, the causality and the direction of the associations remain uncertain. Thus, we aimed to assess whether the relationships between serum UA levels and schizophrenia are causal and to determine the direction of the association. Patients and Methods Two-sample bidirectional Mendelian randomization (MR) analyses and various sensitivity analyses were performed utilizing the summary data from genome-wide association studies within the Global Urate Genetics Consortium and the Psychiatric Genomics Consortium. Secondary MR analyses in both directions were conducted within summary data using genetic risk scores (GRSs) as instrumental variables. Results Three MR methods provided no causal relationship between serum UA and schizophrenia. Furthermore, GRS approach showed similar results in the three MR methods after adjustment for heterogeneity. By contrast, inverse variance weighted method, weighted median and GRS approach suggested a causal effect of schizophrenia risk on serum UA after adjustment for heterogeneity (per 10-symmetric percentage increase in schizophrenia risk, beta -0.039, standard error (SE) 0.013, P = 0.003; beta -0.036, SE 0.018, P = 0.043; beta -0.039, SE 0.013, P = 0.002; respectively). Moreover, in both directions' analyses, the heterogeneity and sensitivity tests suggested no strong evidence of bias due to pleiotropy. Conclusion Schizophrenia may causally affect serum UA levels, whereas the causal role of serum UA concentrations in schizophrenia was not supported by our MR analyses. These findings suggest that UA may be a useful potential biomarker for monitoring treatment or diagnosis of schizophrenia rather than a therapeutic target for schizophrenia. © 2020 Luo et al.Purpose This study was aimed to explore the anti-tumor effect of curcumin on breast cancer (BC) and the underlying mechanism involving Tafazzin (TAZ)/Yes-associated protein (YAP) axis. Methods Different concentrations of curcumin (0, 10, 20 and 30 μM) were used to treat BC cells (MCF-7 and MDA-MB-231 cells). The viability, colony formation, apoptosis, migration, and invasion of BC cells were detected by MTT, colony formation, flow cytometry, wound-healing and transwell assay, respectively. The protein expression of TAZ and YAP (effectors of Hippo signaling pathway) was detected by Western blot. MDA-MB-231 cells were injected into mice to verify the anti-tumor effect of curcumin in vivo. Results Curcumin (20 and 30 μM) inhibited the proliferation, migration and invasion, and promoted the apoptosis of MCF-7 and MDA-MB-231 cells. Curcumin decreased the protein expression of TAZ and YAP in MCF-7 and MDA-MB-231 cells. Overexpression of YAP reversed the anti-tumor effect of curcumin on MDA-MB-231 cells. In addition, curcumin (100, 200 and 300 mg/kg/d) inhibited the growth of tumor xenografts in mice, and down-regulated the protein expression of TAZ and YAP in tumor xenografts. However, curcumin at a concentration of 300 mg/kg/d slowed the increasing of body weight in mice. Conclusion Curcumin inhibited the tumorigenesis of BC by blocking TAZ/YAP axis. © 2020 Shen et al.Background Pancreatic cancer (PC) is a highly invasive tumor with a poor prognosis, short overall survival rate and few chemotherapeutic choices. Despite the importance of finding ways to treat pancreatic cancer, the mechanisms of tumor progression have not been fully elucidated. microRNA-455-3p (miR-455-3p) has been reported to play an important role in several cancers, but its function in pancreatic cancer remains unclear. Methods To investigate the biological functions, miRNAs mimics or inhibitors were transfected into pancreatic cancer cells. Flow cytometry was used to detect cell apoptosis. Wound healing and Transwell assays were employed to observe cell invasion and migration abilities. The expression of Bcl-2, Bax, caspase-3, E-cadherin, N-cadherin, Snail, β-Catenin, c-Myc and Cyclin D1 were evaluated by qPCR and Western blot. Results We confirmed that inhibition of miR-455-3p decreases cell apoptosis and increases cell migration, invasion and EMT of pancreatic cancer, whereas forced overexpression of miR-455-3p has the opposite effect.