Effect of airborne particle abrasion on microtensile bond strength of total-etch adhesives to human dentin

Aim of this study was to investigate a specific airborne particle abrasion pretreatment on dentin and its effects on microtensile bond strengths of four commercial total-etch adhesives. Midcoronal occlusal dentin of extracted human molars was used. Teeth were randomly assigned to 4 groups according to the adhesive system used: OptiBond FL (FL), OptiBond Solo Plus (SO), Prime & Bond (PB), and Riva Bond LC (RB). Specimens from each group were further divided into two subgroups: control specimens were treated with adhesive procedures; abraded specimens were pretreated with airborne particle abrasion using 50 mu m Al2O3 before adhesion. After bonding procedures, composite crowns were incrementally built up. Specimens were sectioned perpendicular to adhesive interface to producemultiple beams, which were tested under tension until failure. Data were statistically analysed. Failure mode analysis was performed. Overall comparison showed significant increase in bond strength (p < 0.001) between abraded and no-abraded specimens, independently of brand. Intrabrand comparison showed statistical increase when abraded specimens were tested compared to no-abraded ones, with the exception of PB that did not show such difference. Distribution of failure mode was relatively uniform among all subgroups. Surface treatment by airborne particle abrasion with Al2O3 particles can increase the bond strength of total-etch adhesive

Ocorrência de incontinência urinária em cadelas castradas no Hospital Veterinário da Universidade Anhembi-Morumbi, São Paulo, Brasil

Incontinência urinária (IU) pode ocorrer após castração de cadelas, quando há diminuição nos níveis circulantes de hormônios esteroides e aumento nos de gonadotrofinas, além de alteração funcional no esfíncter uretral. Para determinar a ocorrência da IU em cadelas castradas no Hospital Veterinário da Universidade Anhembi-Morumbi, os prontuários de cadelas esterilizadas no período 2002-2009 foram analisados de agosto de 2010 a março de 2011. Foi feito contato telefônico com os proprietários para investigar um possível desenvolvimento de IU após a castração. Nesse período, foram contatados osproprietários de 227 cadelas. Destas, 73 (32,2%) vieram a óbito sem sintoma de IU pós-castração, 146 (64,3%) não apresentaram IU e oito (3,5%) desenvolveram IU no período de 3,8 ± 1,6 anos após castração

Genome sequence of Enterococcus mundtii EM01, isolated from Bombyx mori midgut and responsible for flacherie disease in silkworms reared on an artificial diet

The whole genome sequence of Enterococcus mundtii strain EM01 is reported here. The isolate proved to be the cause of flacherie in Bombyx mori. To date, the genomes of 11 other E. mundtii strains have been sequenced. EM01 is the only strain that displayed active pathological effects on its associated animal species

A "de novo" mutation of the LDL-receptor gene as the cause of familial hypercholesterolemia

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On the Mechanism of Gating Charge Movement of the Chloride/Proton Antiporter CLC-5

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On the Mechanism of Gating Charge Movement of ClC-5, a Human Cl−/H+ Antiporter

AbstractClC-5 is a Cl−/H+ antiporter that functions in endosomes and is important for endocytosis in the proximal tubule. The mechanism of transport coupling and voltage dependence in ClC-5 is unclear. Recently, a transport-deficient ClC-5 mutant (E268A) was shown to exhibit transient capacitive currents. Here, we studied the external and internal Cl− and pH dependence of the currents of E268A. Transient currents were almost completely independent of the intracellular pH. Even though the transient currents are modulated by extracellular pH, we could exclude that they are generated by proton-binding/unbinding reactions. In contrast, the charge movement showed a nontrivial dependence on external chloride, strongly supporting a model in which the movement of an intrinsic gating charge is followed by the voltage-dependent low-affinity binding of extracellular chloride ions. Mutation of the external Glu-211 (a residue implicated in the coupling of Cl− and proton transport) to aspartate abolished steady-state transport, but revealed transient currents that were shifted by ∼150 mV to negative voltages compared to E268A. This identifies Gluext as a major component of the gating charge underlying the transient currents of the electrogenic ClC-5 transporter. The molecular events underlying the transient currents of ClC-5 emerging from these results can be explained by an inward movement of the side chain of Gluext, followed by the binding of extracellular Cl− ions

"Open Sesame" to the complexity of pattern recognition receptors of myeloid-derived suppressor cells in cancer

Pattern recognition receptors are primitive sensors that arouse a preconfigured immune response to broad stimuli, including nonself pathogen-associated and autologous damage-associated molecular pattern molecules. These receptors are mainly expressed by innate myeloid cells, including granulocytes, monocytes, macrophages, and dendritic cells. Recent investigations have revealed new insights into these receptors as key players not only in triggering inflammation processes against pathogen invasion but also in mediating immune suppression in specific pathological states, including cancer. Myeloid-derived suppressor cells are preferentially expanded in many pathological conditions. This heterogeneous cell population includes immunosuppressive myeloid cells that are thought to be associated with poor prognosis and impaired response to immune therapies in various cancers. Identification of pattern recognition receptors and their ligands increases the understanding of immune-activating and immune-suppressive myeloid cell functions and sheds light on myeloid-derived suppressor cell differences from cognate granulocytes and monocytes in healthy conditions. This review summarizes the different expression, ligand recognition, signaling pathways, and cancer relations and identifies Toll-like receptors as potential new targets on myeloid-derived suppressor cells in cancer, which might help us to decipher the instruction codes for reverting suppressive myeloid cells toward an antitumor phenotype