Effect of fluoride-containing desensitizing agents on the bond strength of resin-based cements to dentin

OBJECTIVE: The objective of this study was to evaluate the effect of desensitizing agents containing different amounts of fluoride on the shear bond strength of a dual polymerized resin cement and a resin-modified glass ionomer cement (RMGIC) to dentin. MATERIAL AND METHODS: One hundred human molars were mounted in acrylic resin blocks and prepared until the dentin surface was exposed. The specimens were treated with one of four desensitizing agents: Bifluorid 12, Fluoridin, Thermoline and PrepEze. The remaining 20 specimens served as untreated controls. All groups were further divided into 2 subgroups in which a dual polymerized resin cement (Bifix QM) or a resin-modified glass ionomer cement (AVANTO) was used. The shear bond strength (MPa) was measured using a universal testing machine at a 0.5 mm/min crosshead speed. The data were analyzed statistically with a 2-way ANOVA, Tukey HSD test and regression analysis (α=0.05). The effect of the desensitizing agents on the dentin surface was examined by scanning electron microscopy. RESULTS: The fluoride-containing desensitizing agents affected the bond strength of the resin-based cements to dentin (

Temperature dependent negative capacitance behavior in (Ni/Au)/AlGaN/AIN/GaN heterostructures

Cataloged from PDF version of article.The temperature dependent capacitance voltage (C-V) and conductance voltage (G/omega-V) characteristics of (Ni/Au)/Al(0.22)Ga(0.78)N/AlN/GaN heterostructures were investigated by considering the series resistance (R(s)) effect in the temperature range of 80-390 K. The experimental results show that the values of C and G/omega are strongly functioning of temperature and bias voltage. The values of C cross at a certain forward bias voltage point (similar to 2.8 V) and then change to negative values for each temperature, which is known as negative capacitance (NC) behavior. In order to explain the NC behavior, we drawn the C vs I and G/omega vs I plots for various temperatures at the same bias voltage. The negativity of the C decreases with increasing temperature at the forward bias voltage, and this decrement in the NC corresponds to the increment of the conductance. When the temperature was increased, the value of C decreased and the intersection point shifted towards the zero bias direction. This behavior of the C and G/omega values can be attributed to an increase in the polarization and the introduction of more carriers in the structure. R(s) values increase with increasing temperature. Such temperature dependence is in obvious disagreement with the negative temperature coefficient of R or G reported in the literature. The intersection behavior of C-V curves and the increase in R(s) with temperature can be explained by the lack of free charge carriers, especially at low temperatures. (C) 2010 Elsevier B.V. All rights reserve

Frequency and temperature dependence of the dielectric and AC electrical conductivity in (Ni/Au)/AlGaN/AIN/GaN heterostructures

Cataloged from PDF version of article.The dielectric properties and AC electrical conductivity (sigma(ac))of the (Ni/Au)/Al(0.22)Ga(0.78)N/AlN/GaN heterostructures, with and without the SiN(x) passivation, have been investigated by capacitance-voltage and conductance-voltage measurements in the wide frequency (5kHz-5 MHz) and temperature (80-400 K) range. The experimental values of the dielectric constant (epsilon'), dielectric loss (epsilon ''), loss tangent (tan delta), sigma(ac) and the real and imaginary part of the electric modulus (M' and M '') were found to be a strong function of frequency and temperature. A decrease in the values of epsilon' and epsilon '' was observed, in which they both showed an increase in frequency and temperature. The values of M' and M '' increase with increasing frequency and temperature. The sigma(ac) increases with increasing frequency, while it decreases with increasing temperature. It can be concluded, therefore, that the interfacial polarization can occur more easily at low frequencies and temperatures with the number of interface states density located at the metal/semiconductor interface. It contributes to the epsilon' and sigma(ac). (C) 2009 Elsevier B.V. All rights reserved

Hypoxia induces dilated cardiomyopathy in the chick embryo: mechanism, intervention, and long-term consequences

Background: Intrauterine growth restriction is associated with an increased future risk for developing cardiovascular diseases. Hypoxia in utero is a common clinical cause of fetal growth restriction. We have previously shown that chronic hypoxia alters cardiovascular development in chick embryos. The aim of this study was to further characterize cardiac disease in hypoxic chick embryos. Methods: Chick embryos were exposed to hypoxia and cardiac structure was examined by histological methods one day prior to hatching (E20) and at adulthood. Cardiac function was assessed in vivo by echocardiography and ex vivo by contractility measurements in isolated heart muscle bundles and isolated cardiomyocytes. Chick embryos were exposed to vascular endothelial growth factor (VEGF) and its scavenger soluble VEGF receptor-1 (sFlt-1) to investigate the potential role of this hypoxia-regulated cytokine. Principal Findings: Growth restricted hypoxic chick embryos showed cardiomyopathy as evidenced by left ventricular (LV) dilatation, reduced ventricular wall mass and increased apoptosis. Hypoxic hearts displayed pump dysfunction with decreased LV ejection fractions, accompanied by signs of diastolic dysfunction. Cardiomyopathy caused by hypoxia persisted into adulthood. Hypoxic embryonic hearts showed increases in VEGF expression. Systemic administration of rhVEGF165 to normoxic chick embryos resulted in LV dilatation and a dose-dependent loss of LV wall mass. Lowering VEGF levels in hypoxic embryonic chick hearts by systemic administration of sFlt-1 yielded an almost complete normalization of the phenotype. Conclusions/Significance: Our data show that hypoxia causes a decreased cardiac performance and cardiomyopathy in chick embryos, involving a significant VEGF-mediated component. This cardiomyopathy persists into adulthood

JC Virus T-Antigen Regulates Glucose Metabolic Pathways in Brain Tumor Cells

Recent studies have reported the detection of the human neurotropic virus, JCV, in a significant population of brain tumors, including medulloblastomas. Accordingly, expression of the JCV early protein, T-antigen, which has transforming activity in cell culture and in transgenic mice, results in the development of a broad range of tumors of neural crest and glial origin. Evidently, the association of T-antigen with a range of tumor-suppressor proteins, including p53 and pRb, and signaling molecules, such as β-catenin and IRS-1, plays a role in the oncogenic function of JCV T-antigen. We demonstrate that T-antigen expression is suppressed by glucose deprivation in medulloblastoma cells and in glioblastoma xenografts that both endogenously express T-antigen. Mechanistic studies indicate that glucose deprivation-mediated suppression of T-antigen is partly influenced by 5′-activated AMP kinase (AMPK), an important sensor of the AMP/ATP ratio in cells. In addition, glucose deprivation-induced cell cycle arrest in the G1 phase is blocked with AMPK inhibition, which also prevents T-antigen downregulation. Furthermore, T-antigen prevents G1 arrest and sustains cells in the G2 phase during glucose deprivation. On a functional level, T-antigen downregulation is partially dependent on reactive oxygen species (ROS) production during glucose deprivation, and T-antigen prevents ROS induction, loss of ATP production, and cytotoxicity induced by glucose deprivation. Additionally, we have found that T-antigen is downregulated by the glycolytic inhibitor, 2-deoxy-D-glucose (2-DG), and the pentose phosphate inhibitors, 6-aminonicotinamide and oxythiamine, and that T-antigen modulates expression of the glycolytic enzyme, hexokinase 2 (HK2), and the pentose phosphate enzyme, transaldolase-1 (TALDO1), indicating a potential link between T-antigen and metabolic regulation. These studies point to the possible involvement of JCV T-antigen in medulloblastoma proliferation and the metabolic phenotype and may enhance our understanding of the role of viral proteins in glycolytic tumor metabolism, thus providing useful targets for the treatment of virus-induced tumors

BKV Agnoprotein Interacts with α-Soluble N-Ethylmaleimide-Sensitive Fusion Attachment Protein, and Negatively Influences Transport of VSVG-EGFP

Background: The human polyomavirus BK (BKV) infects humans worldwide and establishes a persistent infection in the kidney. The BK virus genome encodes three regulatory proteins, large and small tumor-antigen and the agnoprotein, as well as the capsid proteins VP1 to VP3. Agnoprotein is conserved among BKV, JC virus (JCV) and SV40, and agnoprotein-deficient mutants reveal reduced viral propagation. Studies with JCV and SV40 indicate that their agnoproteins may be involved in transcription, replication and/or nuclear and cellular release of the virus. However, the exact function(s) of agnoprotein of BK virus remains elusive. Principal Findings: As a strategy of exploring the functions of BKV agnoprotein, we decided to look for cellular interaction partners for the viral protein. Several partners were identified by yeast two-hybrid assay, among them a-SNAP which is involved in disassembly of vesicles during secretion. BKV agnoprotein and a-SNAP were found to partially co-localize in cells, and a complex consisting of agnoprotein and a-SNAP could be co-immunoprecipitated from cells ectopically expressing the proteins as well as from BKV-transfected cells. The N-terminal part of the agnoprotein was sufficient for the interaction with a-SNAP. Finally, we could show that BKV agnoprotein negatively interferes with secretion of VSVG-EGFP reporter suggesting that agnoprotein may modulate exocytosis. Conclusions: We have identified the first cellular interaction partner for BKV agnoprotein. The most N-terminal part of BKV agnoprotein is involved in the interaction with a-SNAP. Presence of BKV agnoprotein negatively interferes with secretion of VSVG-EGFP reporter