PURPOSE: The aim of this study was to test the modulus of elasticity (E) across the interfaces of yttria stabilized zirconia (YTZP) / veneer multilayers using nanoindentation. MATERIALS AND METHODS: YTZP core material (KaVo-Everest, Germany) specimens were either coated with a liner (IPS e.max ZirLiner, Ivoclar-Vivadent) (Type-1) or left as-sintered (Type-2) and subsequently veneered with a pressable glass-ceramic (IPS e.max ZirPress, Ivoclar-Vivadent). A 5 µm (nominal tip diameter) spherical indenter was used with a UMIS CSIRO 2000 (ASI, Canberra, Australia) nanoindenter system to test E across the exposed and polished interfaces of both specimen types. The multiple point load – partial unload method was used for E determination. All materials used were characterized using Scanning Electron Microscopy (SEM) and X – ray powder diffraction (XRD). E mappings of the areas tested were produced from the nanoindentation data. RESULTS: A significantly (P<.05) lower E value between Type-1 and Type-2 specimens at a distance of 40 µm in the veneer material was associated with the liner. XRD and SEM characterization of the zirconia sample showed a fine grained bulk tetragonal phase. IPS e-max ZirPress and IPS e-max ZirLiner materials were characterized as amorphous. CONCLUSION: The liner between the YTZP core and the heat pressed veneer may act as a weak link in this dental multilayer due to its significantly (P<.05) lower E. The present study has shown nanoindentation using spherical indentation and the multiple point load - partial unload method to be reliable predictors of E and useful evaluation tools for layered dental ceramic interfaces.
Ceramics* ; Elastic Modulus ; Hot Temperature ; Methods ; Microscopy, Electron, Scanning ; Powder Diffraction

Tumor necrosis factor-α (TNF) is well known to be involved in the immune system and ovarian inflammation. Ovarian cancer is an inflammation-related malignancy that lacks early screening strategies, resulting in late diagnosis followed by high mortality. Based on our previous data, TNF induced abundant serum amyloid A (SAA), an acute phase protein linked to inflammation, in ovarian granulosal cells. To date, the regulation and expression of SAA in ovarian cancer is not fully elucidated. Here, we investigated the relationship between TNF and SAA by comparing human normal ovarian tissues and serous ovarian tumors. We found that SAA1/2 was significantly expressed in tumor tissues, but no or trace expression levels in normal tissues. TNF was also significantly upregulated in ovarian tumor tissues compared to normal tissues. Moreover, TNF significantly increased SAA1/2 levels in human ovarian cancer cell lines, OVCAR-3 and SKOV-3, in a time-dependent manner. Since the SAA1 promoter contains two nuclear factor (NF)-κB sites, we examined whether TNF regulates SAA1 promoter activity. Deletion analysis revealed that the proximal NF-κB site (−95/−85) played a critical role in regulating TNF-induced SAA1 promoter activity. Within 2 h after intraperitoneal injection of lipopolysaccharide, a product known to stimulate release of TNF, SAA preferably localized to ovarian epithelial cells and the thecal-interstitial layers compared to granulosal cell layers. Based on Gene Expression Omnibus (GEO) database, SAA1/2 and TNF were dominantly expressed in advanced grade ovarian cancer. Taken together, the accumulation of SAA1/2 in ovarian cancer could be mediated by TNF-induced NF-κB activation.
Acute-Phase Proteins ; Amyloid* ; Cell Line ; Delayed Diagnosis ; Epithelial Cells ; Gene Expression ; Humans* ; Immune System ; Inflammation ; Injections, Intraperitoneal ; Mass Screening ; Mortality ; Necrosis ; Ovarian Neoplasms ; Serum Amyloid A Protein ; Tumor Necrosis Factor-alpha

One-fifth of cancer deaths are associated with obesity. Because the molecular mechanisms by which obesity affects the progression of ovarian cancer (OC) are poorly understood, we investigated if obesity could promote the progression of OC cells using the postmenopausal ob/ob mouse model and peritoneal dissemination of mouse ID8 OC cells. Compared to lean mice, obese mice had earlier OC occurrence, greater metastasis throughout the peritoneal cavity, a trend toward shorter survival, and higher circulating glucose and proinflammatory chemokine CXCL1 levels. Ascites in obese mice had higher levels of macrophages (Mφ) and chemokines including CCL2, CXCL12, CXCL13, G-CSF and M-CSF. Omental tumor tissues in obese mice had more adipocytes than lean mice. Our data suggest that obesity may accelerate the peritoneal dissemination of OC through higher production of pro-inflammatory chemokines and Mφ recruitment.
Adipocytes ; Animals ; Ascites* ; Chemokine CXCL1 ; Chemokines ; Glucose ; Granulocyte Colony-Stimulating Factor ; Macrophage Colony-Stimulating Factor ; Macrophages* ; Mice ; Mice, Obese ; Neoplasm Metastasis ; Obesity ; Ovarian Neoplasms* ; Peritoneal Cavity

Ovarian cancer (OC) has the highest mortality rate among gynecological malignancies. Because chemokine network is involved in OC progression, we evaluated associations between chemokine expression and survival in tumor suppressor protein p53 (TP53) wild-type (TP53WT) and mutant (TP53m) OC datasets. TP53 was highly mutated in OC compared to other cancer types. Among OC subtypes, CXCL14 was predominantly expressed in clear cell OC, and CCL15 and CCL20 in mucinous OC. TP53WT endometrioid OC highly expressed CXCL14 compared to TP53m, showing better progression-free survival but no difference in overall survival (OS). TP53m serous OC highly expressed CCL8, CCL20, CXCL10 and CXCL11 compared to TP53WT. CXCL12 and CCL21 were associated with poor OS in TP53WT serous OC. CXCR2 was associated with poor OS in TP53m serous OC, while CXCL9, CCL5, CXCR4, CXCL11, and CXCL13 were associated with better OS. Taken together, specific chemokine signatures may differentially influence OS in TP53WT and TP53m OC.
Chemokines ; Dataset ; Disease-Free Survival ; Mortality ; Mucins ; Ovarian Neoplasms* ; Tumor Suppressor Protein p53