Effects of A Fluoride-Containing Casein Phosphopeptide-Amorphous Calcium Phosphate Complex on The Shear Bond Strength of Orthodontic Brackets

The purpose of this study was to investigate the effects of enamel pre-treatment with a new fluoride-containing casein phosphopeptide-amorphous calcium phosphate (CPP-ACP) complex on the shear bond strength (SBS) of brackets bonded with etch-and-rinse or self-etching adhesive systems. The material comprised 66 extracted human premolars randomly divided into six equal groups with respect to the enamel pre-treatment and adhesive system employed: 1. No pre-treatment and brackets bonded with the etch-and-rinse adhesive system (Transbond XT). 2. Pre-treatment with fluoride-containing CPP-ACP paste (MI Paste Plus) and Transbond XT. 3. Pre-treatment with non-fluoride CPP-ACP paste (MI Paste) and Transbond XT.4. No pre-treatment and brackets bonded with the self-etching adhesive system (Transbond Plus). 5 and 6. Enamel pre-treated as for groups 2 and 3, respectively, and the Transbond Plus. Bonded specimens were subjected to thermal cycling (x1000) before SBS testing. The residual adhesive on the enamel surface was evaluated after debonding with the adhesive remnant index (ARI). Data evaluation was made using one-way analysis of variance and Tukey test for SBS results, and Kruskal-Wallis test for ARI results. The results showed that enamel pre-treatment with either fluoride or non-fluoride CPP-ACP paste had no significant effect on the SBS of the self-etching adhesive system (P > 0.05). Enamel pre-treatment with non-fluoride CPP-ACP in group 3 significantly reduced the SBS of the etch-and-rinse adhesive (P 0.05). The fluoride-containing CPP-ACP did not compromise the SBS of brackets bonded with the tested etch-and-rinse and self-etching systems, but its non-fluoride version significantly decreased the SBS of the etch-and-rinse adhesive system.WoSScopu

Towards a compact, high-speed optical linkbased 3D optoacoustic imager

We demonstrate the feasibility of a compact real-time 3D optoacoustic (OA) imager employing a novel low-cost software-defined ultrasound digital acquisition platform. It supports simultaneous signal acquisition from up to 192 ultrasound channels and a direct optical link (2x 100G Ethernet) to the host-PC for high-frame-rate image acquisitions. Real-time 3D imaging experiments with light-absorbing phantoms and the wrist of a healthy volunteer are reported. These results pave the way toward a new generation of compact, affordable, and flexible hand-held OA scanners

Ultrafast four-dimensional imaging of cardiac mechanical wave propagation with sparse optoacoustic sensing

Propagation of electromechanical waves in excitable heart muscles follows complex spatiotemporal patterns holding the key to understanding life-threatening arrhythmias and other cardiac conditions. Accurate volumetric mapping of cardiac wave propagation is currently hampered by fast heart motion, particularly in small model organisms. Here we demonstrate that ultrafast four-dimensional imaging of cardiac mechanical wave propagation in entire beating murine heart can be accomplished by sparse optoacoustic sensing with high contrast, ∼115-µm spatial and submillisecond temporal resolution. We extract accurate dispersion and phase velocity maps of the cardiac waves and reveal vortex-like patterns associated with mechanical phase singularities that occur during arrhythmic events induced via burst ventricular electric stimulation. The newly introduced cardiac mapping approach is a bold step toward deciphering the complex mechanisms underlying cardiac arrhythmias and enabling precise therapeutic interventions

LightSpeed: A Compact, High-Speed Optical-Link-Based 3D Optoacoustic Imager

Wide-scale adoption of optoacoustic imaging in biology and medicine critically depends on availability of affordable scanners combining ease of operation with optimal imaging performance. Here we introduce LightSpeed: a low-cost real-time volumetric handheld optoacoustic imager based on a new compact software-defined ultrasound digital acquisition platform and a pulsed laser diode. It supports the simultaneous signal acquisition from up to 192 ultrasound channels and provides a hig-bandwidth direct optical link (2x 100G Ethernet) to the host-PC for ultra-high frame rate image acquisitions. We demonstrate use of the system for ultrafast (500Hz) 3D human angiography with a rapidly moving handheld probe. LightSpeed attained image quality comparable with a conventional optoacoustic imaging systems employing bulky acquisition electronics and a Q-switched pulsed laser. Our results thus pave the way towards a new generation of compact, affordable and high-performance optoacoustic scanners

The AP-1 transcription factor Fosl-2 drives cardiac fibrosis and arrhythmias under immunofibrotic conditions

Fibrotic changes in the myocardium and cardiac arrhythmias represent fatal complications in systemic sclerosis (SSc), however the underlying mechanisms remain elusive. Mice overexpressing transcription factor Fosl-2 (Fosl-2$^{tg}$) represent animal model of SSc. Fosl-2$^{tg}$ mice showed interstitial cardiac fibrosis, disorganized connexin-43/40 in intercalated discs and deregulated expression of genes controlling conduction system, and developed higher heart rate (HR), prolonged QT intervals, arrhythmias with prevalence of premature ventricular contractions, ventricular tachycardias, II-degree atrio-ventricular blocks and reduced HR variability. Following stimulation with isoproterenol Fosl-2$^{tg}$ mice showed impaired HR response. In contrast to Fosl-2$^{tg}$, immunodeficient Rag2$^{-/-}$Fosl-2$^{tg}$ mice were protected from enhanced myocardial fibrosis and ECG abnormalities. Transcriptomics analysis demonstrated that Fosl-2-overexpression was responsible for profibrotic signature of cardiac fibroblasts, whereas inflammatory component in Fosl-2$^{tg}$ mice activated their fibrotic and arrhythmogenic phenotype. In human cardiac fibroblasts FOSL-2-overexpression enhanced myofibroblast signature under proinflammatory or profibrotic stimuli. These results demonstrate that under immunofibrotic conditions transcription factor Fosl-2 exaggerates myocardial fibrosis, arrhythmias and aberrant response to stress