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1.  Effects of cementation surface modifications on fracture resistance of zirconia 
Objectives
To examine the effects of glass infiltration (GI) and alumina coating (AC) on the indentation flexural load and four-point bending strength of monolithic zirconia.
Methods
Plate-shaped (12 mm × 12 mm × 1.0 mm or 1.5 mm or 2.0 mm) and bar-shaped (4 mm × 3 mm × 25 mm) monolithic zirconia specimens were fabricated. In addition to monolithic zirconia (group Z), zirconia monoliths were glass-infiltrated or alumina-coated on their tensile surfaces to form groups ZGI and ZAC, respectively. They were also glass-infiltrated on their upper surfaces, and glass-infiltrated or alumina-coated on their lower (tensile) surfaces to make groups ZGI2 and ZAC2, respectively. For comparison, porcelain-veneered zirconia (group PVZ) and monolithic lithium disilicate glass-ceramic (group LiDi) specimens were also fabricated. The plate-shaped specimens were cemented onto a restorative composite base for Hertzian indentation using a tungsten carbide spherical indenter with a radius of 3.2 mm. Critical loads for indentation flexural fracture at the zirconia cementation surface were measured. Strengths of bar-shaped specimens were evaluated in four-point bending.
Results
Glass infiltration on zirconia tensile surfaces increased indentation flexural loads by 32% in Hertzian contact and flexural strength by 24% in four-point bending. Alumina coating showed no significant effect on resistance to flexural damage of zirconia. Monolithic zirconia outperformed porcelain-veneered zirconia and monolithic lithium disilicate glass-ceramics in terms of both indentation flexural load and flexural strength.
Significance
While both alumina coating and glass infiltration can be used to effectively modify the cementation surface of zirconia, glass infiltration can further increase the flexural fracture resistance of zirconia.
doi:10.1016/j.dental.2015.01.013
PMCID: PMC4374004  PMID: 25687628
ceramic restorative materials; surface modification; zirconia; graded zirconia; alumina coating; indentation flexural load; flexural strength
2.  Edge chipping and flexural resistance of monolithic ceramics☆ 
Objective
Test the hypothesis that monolithic ceramics can be developed with combined esthetics and superior fracture resistance to circumvent processing and performance drawbacks of traditional all-ceramic crowns and fixed-dental-prostheses consisting of a hard and strong core with an esthetic porcelain veneer. Specifically, to demonstrate that monolithic prostheses can be produced with a much reduced susceptibility to fracture.
Methods
Protocols were applied for quantifying resistance to chipping as well as resistance to flexural failure in two classes of dental ceramic, microstructurally-modified zirconias and lithium disilicate glass–ceramics. A sharp indenter was used to induce chips near the edges of flat-layer specimens, and the results compared with predictions from a critical load equation. The critical loads required to produce cementation surface failure in monolithic specimens bonded to dentin were computed from established flexural strength relations and the predictions validated with experimental data.
Results
Monolithic zirconias have superior chipping and flexural fracture resistance relative to their veneered counterparts. While they have superior esthetics, glass–ceramics exhibit lower strength but higher chip fracture resistance relative to porcelain-veneered zirconias.
Significance
The study suggests a promising future for new and improved monolithic ceramic restorations, with combined durability and acceptable esthetics.
doi:10.1016/j.dental.2013.09.004
PMCID: PMC4000448  PMID: 24139756
Edge chipping; Flexural fracture; Monolithic restorations; Zirconia-based ceramic; Glass–ceramic; Graded glass–zirconia
3.  SNP analysis of follistatin gene associated with polycystic ovarian syndrome 
Follistatin has been reported as a candidate gene for polycystic ovarian syndrome (PCOS) based on linkage and association studies. In this study, investigation of polymorphisms in the FST gene was done to determine if genetic variation is associated with susceptibility to PCOS. The nucleotide sequence of human follistatin and the protein sequence of human follistatin were retrieved from the NCBI database using Entrez. The follistatin protein of human was retrieved from the Swiss-Prot database. There are 344 amino acids and the molecular weight is 38,007 Da. The ProtParam analysis shows that the isoelectric point is 5.53 and the aliphatic index is 61.25. The hydropathicity is −0.490. The domains in FST protein are as follows: Pfam-B 5005 domain from 1 to 92; EGF-like subdomain from 93 to 116; Kazal 1 domain, occurred in three places, namely, 118–164, 192–239, and 270–316. There are 31 single-nucleotide polymorphisms (SNPs) for this gene. Some are nonsynonymous, some occur in the intron region, and some in an untranslated region. Two nonsynonymous SNPs, namely, rs11745088 and rs1127760, were taken for analysis. In the SNP rs11745088, the change is E152Q. Likewise, in rs1127760, the change is C239S. SIFT (Sorting Intolerant from Tolerant) showed positions of amino acids and the single letter code of amino acids that can be tolerated or deleterious for each position. There were six SNP results and each result had links to it. The dbSNP id, primary database id, and the type of mutation whether silent and if occurring in coding region are given as phenotype alterations. The FASTA format of protein was given to the nsSNP Analyzer tool, and the variation E152Q and C239S were given as inputs in the SNP data field. E152Q change was neutral and C239S causes disease. Using PANTHER for evolutionary analysis of coding SNPs, the protein sequence was given as input and analyzed for the E152Q and C239S SNPs for deleterious effect on protein function. The genetic association database results showed that FST gene SNPs are linked to PCOS coming under the disease class of metabolic disorders. The list of intronic and synonymous SNPs, with their nucleotide position, amino acid change information, and dbSNP link, is provided for further analysis.
doi:10.2147/AABC.S11013
PMCID: PMC3170008  PMID: 21918632
FST; polycystic ovarian syndrome; single-nucleotide polymorphism analysis

Results 1-3 (3)