Effect of Different Thicknesses of Pressable Ceramic Veneers on Polymerization of Light-cured and Dual-cured Resin Cements

Aim: This study evaluated the effects of ceramic veneer thicknesses on the polymerization of two different resin cements. Materials and methods: A total of 80 ceramic veneer disks were fabricated by using a pressable ceramic material (e.max Press; Ivoclar Vivadent) from a Low Translucency (LT) ingot (A1 shade). These disks were divided into light-cured (LC; NX3 Nexus LC; Kerr) and dual-cured (DC; NX3 Nexus DC; Kerr) and each group was further divided into four subgroups, based on ceramic disk thickness (0.3, 0.6, 0.9, and 1.2 mm). The values of Vickers microhardness (MH) and degree of conversion (DOC) were obtained for each specimen after a 24-hour storage period. Association between ceramic thickness, resin cement type, and light intensity readings (mW/cm2) with respect to microhardness and degree of conversion was statistically evaluated by using analysis of variance (ANOVA). Results: For the DOC values, there was no significant difference observed among the LC resin cement subgroups, except in the 1.2 mm subgroup; only the DOC value (14.0 ± 7.4%) of 1.2 mm DC resin cement had significantly difference from that value (28.9 ± 7.5%) of 1.2 mm LC resin cement (p \u3c 0.05). For the MH values between LC and DC resin cement groups, there was statistically significant difference (p \u3c 0.05); overall, the MH values of LC resin cement groups demonstrated higher values than DC resin cement groups. On the other hands, among the DC resin cement subgroups, the MH values of 1.2 mm DC subgroup was significantly lower than the 0.3 mm and 0.6 mm subgroups (p \u3c 0.05). However, among the LC subgroups, there was no statistically significant difference among them (p \u3e 0.05). Conclusion: The degree of conversion and hardness of the resin cement was unaffected with veneering thicknesses between 0.3 and 0.9 mm. However, the DC resin cement group resulted in a significantly lower DOC and MH values for the 1.2 mm subgroup. Clinical Significance: While clinically adequate polymerization of LC resin cement can be achieved with a maximum 1.2 mm of porcelain veneer restoration, the increase of curing time or light intensity is clinically needed for DC resin cements at the thickness of more than 0.9 mm

Die Spacer Thickness Reproduction for Central Incisor Crown Fabrication with Combined Computer-aided Design and 3D Printing Technology: An in vitro Study

Statement of problem The inability to control die spacer thickness has been reported. However, little information is available on the congruency between the computer-aided design parameters for die spacer thickness and the actual printout. Purpose The purpose of this study was to evaluate the accuracy and precision of the die spacer thickness achieved by combining computer-aided design and 3-dimensional printing technology. Material and Methods An ivorine maxillary central incisor was prepared for a ceramic crown. The prepared tooth was duplicated by using polyvinyl siloxane duplicating silicone, and 80 die-stone models were produced from Type IV dental stone. The dies were randomly divided into 5 groups with assigned die spacer thicknesses of 25 μm, 45 μm, 65 μm, 85 μm, and 105 μm (n=16). The printed resin copings, obtained from a printer (ProJet DP 3000; 3D Systems), were cemented onto their respective die-stone models with self-adhesive resin cement and stored at room temperature until sectioning into halves in a buccolingual direction. The internal gap was measured at 5 defined locations per side of the sectioned die. Images of the printed resin coping/die-stone model internal gap dimensions were obtained with an inverted bright field metallurgical microscope at ×100 magnification. The acquired digital image was calibrated, and measurements were made using image analysis software. Mixed models (α=.05) were used to evaluate accuracy. A false discovery rate at 5% was used to adjust for multiple testing. Coefficient of variation was used to determine the precision for each group and was evaluated statistically with the Wald test (α=.05). Results The accuracy, expressed in terms of the mean differences between the prescribed die spacer thickness and the measured internal gap (standard deviation), was 50 μm (11) for the 25 μm group simulated die spacer thickness, 30 μm (10) for the 45 μm group, 15 μm (14) for the 65 μm group, 3 μm (23) for the 85 μm group, and -10 μm (32) for the 105 μm group. The precision mean of the measurements, expressed as a coefficient of variation, ranged between 14% and 33% for the 5 groups. Conclusions For the accuracy evaluation, statistically significant differences were found for all the groups, except the group of 85 μm. For the precision assessment, the coefficient of variation was above 10% for all groups, showing the printer’s inability to reproduce the uniform internal gap within the same group

Γ-Tocotrienol Inhibits Nuclear Factor-κB Signaling Pathway Through Inhibition of Receptor-Interacting Protein and TAK1 Leading to Suppression of Antiapoptotic Gene Products and Potentiation of Apoptosis

Unlike the tocopherols, the tocotrienols, also members of the vitamin E family, have an unsaturated isoprenoid side chain. In contrast to extensive studies on tocopherol, very little is known about tocotrienol. Because the nuclear factor-κB (NF-κB) pathway has a central role in tumorigenesis, we investigated the effect of γ-tocotrienol on the NF-κB pathway. Although γ-tocotrienol completely abolished tumor necrosis factor α (TNF)-induced NF-κB activation, a similar dose of γ-tocopherol had no effect. Besides TNF, γ-tocotrienol also abolished NF-κB activation induced by phorbol myristate acetate, okadaic acid, lipopolysaccharide, cigarette smoke, interleukin-1β, and epidermal growth factor. Constitutive NF-κB activation expressed by certain tumor cells was also abrogated by γ-tocotrienol. Reducing agent had no effect on the γ-tocotrienol-induced down-regulation of NF-κB. Mevalonate reversed the NF-κB inhibitory effect of γ-tocotrienol, indicating the role of hydroxymethylglutaryl-CoA reductase. γ-Tocotrienol blocked TNF-induced phosphorylation and degradation of IκBα through the inhibition of IκBα kinase activation, thus leading to the suppression of the phosphorylation and nuclear translocation of p65. γ-Tocotrienol also suppressed NF-κB-dependent reporter gene transcription induced by TNF, TNFR1, TRADD, TRAF2, TAK1, receptor-interacting protein, NIK, and IκBαkinase but not that activated by p65. Additionally, the expressions of NF-κB-regulated gene products associated with antiapoptosis (IAP1, IAP2, Bcl-xL, Bcl-2, cFLIP, XIAP, Bfl-1/A1, TRAF1, and Survivin), proliferation (cyclin D1, COX2, and c-Myc), invasion (MMP-9 and ICAM-1), and angiogenesis (vascular endothelial growth factor) were down-regulated by γ-tocotrienol. This correlated with potentiation of apoptosis induced by TNF, paclitaxel, and doxorubicin. Overall, our results demonstrate that γ-tocotrienol inhibited the NF-κB activation pathway, leading to down-regulation of various gene products and potentiation of apoptosis

Down-regulation of phosphoglucomutase 3 mediates sulforaphane-induced cell death in LNCaP prostate cancer cells

<p>Abstract</p> <p>Background</p> <p>Sulforaphane (SFN) is an isothiocyanate found in cruciferous vegetables that exerts anti-oxidant, anti-inflammatory, anti-cancer and radio-sensitizing activities. Nonetheless, the mechanism responsible for SFN-induced cell death is not fully understood. In the present study, anti-cancer mechanism of SFN was elucidated in LNCaP prostate cancer cells.</p> <p>Results</p> <p>SFN exerted cytotoxicity and increased TUNEL positive cells in a concentration-dependent manner in LNCaP cells. Proteomics study revealed that levels of nine proteins including tubulin β-2, phosphoglucomutase-3 (PGM3), melanoma-derived leucine zipper containing extra-nuclear factor, activin A type I receptor precursor, smoothelin-A, KIA0073, hypothetical protein LOC57691 and two unnamed proteins were changed over 8 folds in SFN treated LNCaP cells compared to untreated control. We have further confirmed that SFN reduced PGM3 expression with western blotting and showed that PGM3 siRNA enhanced cytotoxicity demonstrated by cell morphology and TUNEL assays in LNCaP cells.</p> <p>Conclusion</p> <p>Taken together, these findings suggest that PGM3 plays a role in mediating SFN-induced cell death in LNCaP cells, and is a potential molecular therapeutic target for prostate cancer.</p

Capnography for Assessing Nocturnal Hypoventilation and Predicting Compliance with Subsequent Noninvasive Ventilation in Patients with ALS

BACKGROUND: Patients with amyotrophic lateral sclerosis (ALS) suffer from hypoventilation, which can easily worsen during sleep. This study evaluated the efficacy of capnography monitoring in patients with ALS for assessing nocturnal hypoventilation and predicting good compliance with subsequent noninvasive ventilation (NIV) treatment. METHODS: Nocturnal monitoring and brief wake screening by capnography/pulse oximetry, functional scores, and other respiratory signs were assessed in 26 patients with ALS. Twenty-one of these patients were treated with NIV and had their treatment compliance evaluated. RESULTS: Nocturnal capnography values were reliable and strongly correlated with the patients' respiratory symptoms (R(2) = 0.211-0.305, p = 0.004-0.021). The duration of nocturnal hypercapnea obtained by capnography exhibited a significant predictive power for good compliance with subsequent NIV treatment, with an area-under-the-curve value of 0.846 (p = 0.018). In contrast, no significant predictive values for nocturnal pulse oximetry or functional scores for nocturnal hypoventilation were found. Brief waking supine capnography was also useful as a screening tool before routine nocturnal capnography monitoring. CONCLUSION: Capnography is an efficient tool for assessing nocturnal hypoventilation and predicting good compliance with subsequent NIV treatment of ALS patients, and may prove useful as an adjunctive tool for assessing the need for NIV treatment in these patients

Suppression of STAT3 and HIF-1 Alpha Mediates Anti-Angiogenic Activity of Betulinic Acid in Hypoxic PC-3 Prostate Cancer Cells

Background: Signal transducer and activator of transcription 3 (STAT3) is a transcription factor that regulates various cellular processes such as cell survival, angiogenesis and proliferation. In the present study, we examined that betulinic acid (BA), a triterpene from the bark of white birch, had the inhibitory effects on hypoxia-mediated activation of STAT3 in androgen independent human prostate cancer PC-3 cells. Methodology/Principal Findings: BA inhibited the protein expression and the transcriptional activities of hypoxia-inducible factor-1a (HIF-1a) under hypoxic condition. Consistently, BA blocked hypoxia-induced phosphorylation, DNA binding activity and nuclear accumulation of STAT3. In addition, BA significantly reduced cellular and secreted levels of vascular endothelial growth factor (VEGF), a critical angiogenic factor and a target gene of STAT3 induced under hypoxia. Furthermore, BA prevented in vitro capillary tube formation in human umbilical vein endothelial cells (HUVECs) maintained in conditioned medium of hypoxic PC-3 cells, implying anti-angiogenic activity of BA under hypoxic condition. Of note, chromatin immunoprecipitation (ChiP) assay revealed that BA inhibited binding of HIF-1a and STAT3 to VEGF promoter. Furthermore, silencing STAT3 using siRNA transfection effectively enhanced the reduced VEGF production induced by BA treatment under hypoxia. Conclusions/Significance: Taken together, our results suggest that BA has anti-angiogenic activity by disturbing th

Hexane Fractions of Bupleurum falcatum L.

Bupleurum falcatum L. has been used traditionally as a medicinal herb in Korean medicine. The hexane fraction of BF (HFBF), which was profiled with Direct Analysis in Real Time-Mass Spectrometry (DART-MS), activates the secretion of glucagon-like peptide-1 (GLP-1) in NCI-H716 cells significantly. We performed a microarray analysis and GLP-1 ELISA assay, as well as calcium imaging experiments with inhibitors, to investigate the mechanism of action of the HFBF. Through the microarray analysis, it was found that the ITPR2 gene that encodes the inositol 1,4,5-trisphosphate (IP3) receptor is up-regulated and the HFBF induces cell depolarization by inhibiting the voltage-gated channel expression in NCI-H716 cells. In addition, we found that the intracellular calcium in NCI-H716 cells, with Gallein, U73122, and 2APB as inhibitors, was decreased. These results suggest that the HFBF activates the GLP-1 secretion through the Gβγ pathways in the enteroendocrine L cells after treatment with the HFBF

Chlorophyll and Total Suspended Materials Concentrations and Remote Sensing Reflectance Data measured at the Red Tide Area of Jinhae, Geoje, and East Sea during August from 1998 to 2003 and August 2013

The chlorophyll and total suspended materials concentrations and remote sensing reflectance data were observed for red tides occurring every summer in waters around the Korean Peninsula. In observation area and date, the field survey were performed (1) in the Jinhae and Geoje coasts during August 1998, August 1999, August 2001, and August 2003, (2) in East Sea coast during August 2013. The remote sensing reflectance data were obtained from portable spectroradiometer. The chlorophyll concentration data were obtained from spectrophotometric method and the total suspended materials concentration data were obtained from filter-weight difference method. The remote sensing reflectance data were validated using Moon et al.(2012). The chlorophyll concentration data were validated using baseline correction and subtraction of 750 nm value, and the total suspended materials concentration data were validated using variation of humidity