Analysis of surface characteristics of (Y, Nb)-TZP after finishing and polishing

PURPOSE@#. This in vitro study aimed to evaluate the surface characteristics of a full veneer crown fabricated chairside (CS) from a (Y, Nb)-TZP zirconia block in response to conventional zirconia grinding and polishing. @*MATERIALS AND METHODS@#. Zirconia crowns (n = 40) were first prepared and divided into two groups of materials: Labside (LS) and CS, after which each specimen went through a five-step grinding and polishing procedure. Following each surface treatment, surface characteristics were analyzed using confocal laser microscopy (CLSM), average surface roughness (Ra) values were processed from the profile data through Gaussian filtering, and X-ray diffraction pattern analysis was performed to evaluate the monoclinic (M) phase content. Then, a representative specimen was selected for field-emission scanning electron microscopy (FE-SEM), followed by a final analysis of the roughness and X-ray diffraction of the specimens using the independent t-test and repeated measures analysis of variance (RM-ANOVA). @*RESULTS@#. In every group, polishing significantly reduced the Ra values (P < .001).There was no significant difference in Ra between the polished state CS and LS.Furthermore, CLSM and FE-SEM investigations revealed that even though grain exposure was visible in CS specimens throughout the as-delivered and ground states, the exposure was reduced after polishing. Moreover, while no phase transformation was visible in the LS, phase transformation was visible in CS after every surface treatment, with the M phase content of the CS group showing a significant reduction after polishing (P < .001). CONCLUSION. Within the limits of this study, clinically acceptable level of surface finishing of (Y, Nb)-TZP can be achieved after conventional zirconia polishing sequence.

Recent Improvements in Genomic and Transcriptomic Understanding of Anaplastic and Poorly Differentiated Thyroid Cancers

Anaplastic thyroid cancer (ATC) is a lethal human cancer with a 5-year survival rate of less than 10%. Recently, its genomic and transcriptomic characteristics have been extensively elucidated over 5 years owing to advance in high throughput sequencing. These efforts have extended molecular understandings into the progression mechanisms and therapeutic vulnerabilities of aggressive thyroid cancers. In this review, we provide an overview of genomic and transcriptomic alterations in ATC and poorly-differentiated thyroid cancer, which are distinguished from differentiated thyroid cancers. Clinically relevant genomic alterations and deregulated signaling pathways will be able to shed light on more effective prevention and stratified therapeutic interventions for affected patients.

Transcriptome analyses of chronic traumatic encephalopathy show alterations in protein phosphatase expression associated with tauopathy

Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disorder that is associated with repetitive head injury and has distinctive neuropathological features that differentiate this disease from other neurodegenerative diseases. Intraneuronal tau aggregates, although they occur in different patterns, are diagnostic neuropathological features of CTE, but the precise mechanism of tauopathy is not known in CTE. We performed whole RNA sequencing analysis of post-mortem brain tissue from patients with CTE and compared the results to normal controls to determine the transcriptome signature changes associated with CTE. The results showed that the genes related to the MAP kinase and calcium-signaling pathways were significantly downregulated in CTE. The altered expression of protein phosphatases (PPs) in these networks further suggested that the tauopathy observed in CTE involves common pathological mechanisms similar to Alzheimer's disease (AD). Using cell lines and animal models, we also showed that reduced PPP3CA/PP2B phosphatase activity is directly associated with increases in phosphorylated (p)-tau proteins. These findings provide important insights into PP-dependent neurodegeneration and may lead to novel therapeutic approaches to reduce the tauopathy associated with CTE.

Hepatic STAMP2 decreases hepatitis B virus X protein-associated metabolic deregulation

Six transmembrane protein of prostate 2 (STAMP2) plays a key role in linking inflammatory and diet-derived signals to systemic metabolism. STAMP2 is induced by nutrients/feeding as well as by cytokines such as TNFalpha, IL-1beta, and IL-6. Here, we demonstrated that STAMP2 protein physically interacts with and decreases the stability of hepatitis B virus X protein (HBx), thereby counteracting HBx-induced hepatic lipid accumulation and insulin resistance. STAMP2 suppressed the HBx-mediated transcription of lipogenic and adipogenic genes. Furthermore, STAMP2 prevented HBx-induced degradation of IRS1 protein, which mediates hepatic insulin signaling, as well as restored insulin-mediated inhibition of gluconeogenic enzyme expression, which are gluconeogenic genes. We also demonstrated reciprocal expression of HBx and STAMP2 in HBx transgenic mice. These results suggest that hepatic STAMP2 antagonizes HBx-mediated hepatocyte dysfunction, thereby protecting hepatocytes from HBV gene expression.