Functionalized carbon nanotubes as a filler for dielectric elastomer composites with improved actuation performance

Among the broad class of electro-active polymers, dielectric elastomer actuators represent a rapidly growing technology for electromechanical transduction. In order to further develop this applied science, the high driving voltages currently needed must be reduced. For this purpose, one of the most widely considered approaches is based on making elastomeric composites with highly polarizable fillers in order to increase the dielectric constant while maintaining both low dielectric losses and high-mechanical compliance. In this work, multi-wall carbon nanotubes were first functionalized by grafting either acrylonitrile or diurethane monoacrylate oligomers, and then dispersed into a polyurethane matrix to make dielectric elastomer composites. The procedures for the chemical functionalization of carbon nanotubes and proper characterizations of the obtained products are provided in detail. The consequences of the use of chemically modified carbon nanotubes as a filler, in comparison to using unmodified ones, were studied in terms of dielectric, mechanical and electromechanical response. In particular, an increment of the dielectric constant was observed for all composites throughout the investigated frequency spectrum, but only in the cases of modified carbon nanotubes did the loss factor remain almost unchanged with respect to the simple matrix, indicating that conductive percolation paths did not arise in such systems. An effective improvement in the actuation strain was observed for samples loaded with functionalized carbon nanotubes

Crack growth behavior of SBR, NR and BR rubber compounds: comparison of Pure-Shear versus Strip Tensile test

Fatigue crack growth experiments on different carbon black–filled rubber compounds have been carried out to evaluate the influence of pure-shear and strip tensile testing mode by using sine and pulse as waveforms. In a previous set of experimental investigations regarding the influence of both waveform and tested material, it was found that the mode I of crack opening sometimes propagates too quickly to be properly monitored in tests involving strip-tensile specimens. An alternative test methodology based on pure-shear test mode has been investigated, optimizing both the shape of the specimen and the test equipment. Data obtained from the different compound formulations were consistent with the theoretical background and resulted in similar ranking of compound crack growth resistance for the two testing modes; in addition, pure-shear mode showed a higher sensitivity to formula variations

Renal progenitor cells revert LPS-induced endothelial-to-mesenchymal transition by secreting CXCL6, SAA4, and BPIFA2 antiseptic peptides

Endothelial dysfunction is a hallmark of LPS-induced acute kidney injury (AKI). Endothelial cells (ECs) acquired a fibroblast-like phenotype and contributed to myofibroblast generation through the endothelial-to-mesenchymal transition (EndMT) process. Of note, human adult renal stem/progenitor cells (ARPCs) enhance the tubular regenerative mechanism during AKI but little is known about their effects on ECs. Following LPS exposure, ECs proliferated, decreased EC markers CD31 and vascular endothelial cadherin, and up-regulated myofibroblast markers, collagen I, and vimentin. The coculture with ARPCs normalized the EC proliferation rate and abrogated the LPS-induced EndMT. The gene expression analysis showed that most of the genes modulated in LPS-stimulated ARPCs belong to cell activation and defense response pathways. We showed that the ARPC-specific antifibrotic effect is exerted by the secretion of CXCL6, SAA4, and BPIFA2 produced after the anaphylatoxin stimulation. Next, we investigated the molecular signaling that underlies the ARPC protective mechanism and found that renal progenitors diverge from differentiated tubular cells and ECs in myeloid differentiation primary response 88-independent pathway activation. Finally, in a swine model of LPS-induced AKI, we observed that activated ARPCs secreted CXCL6, SAA4, and BPIFA2 as a defense response. These data open new perspectives on the treatment of both sepsis- and endotoxemia-induced AKI, suggesting an underestimated role of ARPCs in preventing endothelial dysfunction and novel strategies to protect the endothelial compartment and promote kidney repair.-Sallustio, F., Stasi, A., Curci, C., Divella, C., Picerno, A., Franzin, R., De Palma, G., Rutigliano, M., Lucarelli, G., Battaglia, M., Staffieri, F., Crovace, A., Pertosa, G. B., Castellano, G., Gallone, A., Gesualdo, L. Renal progenitor cells revert LPS-induced endothelial-to-mesenchymal transition by secreting CXCL6, SAA4, and BPIFA2 antiseptic peptides

Design, fabrication and characterization of composite piezoelectric ultrafine fibers for cochlear stimulation

Sensorineural hearing loss, primed by dysfunction or death of hair cells in the cochlea, is the main cause of severe or profound deafness. Piezoelectric materials work similarly to hair cells, namely, as mechano-electrical transducers. Polyvinylidene fluoride (PVDF) films have demonstrated potential to replace the hair cell function, but the obtained piezoresponse was insufficient to stimulate effectively the auditory neurons. In this study, we reported on piezoelectric nanocomposites based on ultrafine PVDF fibers and barium titanate nanoparticles (BTNPs), as a strategy to improve the PVDF performance for this application. BTNP/PVDF fiber meshes were produced via rotating-disk electrospinning, up to 20/80 weight composition. The BTNP/PVDF fibers showed diameters ranging in 0.160-1.325 μm. Increasing collector velocity to 3000 rpm improved fiber alignment. The piezoelectric β phase of PVDF was well expressed following fabrication and the piezoelectric coefficients increased according to the BTNP weight ratio. The BTNP/PVDF fibers were not cytotoxic towards cochlear epithelial cells. Neural-like cells adhered to the composite fibers and, upon mechanical stimulation, showed enhanced viability. Using BTNP filler for PVDF matrices, in the form of aligned ultrafine fibers, increased the piezoresponse of PVDF transducers and favored neural cell contact. Piezoelectric nanostructured composites might find application in next generation cochlear implants

Detecting cryptic clinically relevant structural variation in exome-sequencing data increases diagnostic yield for developmental disorders.

Structural variation (SV) describes a broad class of genetic variation greater than 50 bp in size. SVs can cause a wide range of genetic diseases and are prevalent in rare developmental disorders (DDs). Individuals presenting with DDs are often referred for diagnostic testing with chromosomal microarrays (CMAs) to identify large copy-number variants (CNVs) and/or with single-gene, gene-panel, or exome sequencing (ES) to identify single-nucleotide variants, small insertions/deletions, and CNVs. However, individuals with pathogenic SVs undetectable by conventional analysis often remain undiagnosed. Consequently, we have developed the tool InDelible, which interrogates short-read sequencing data for split-read clusters characteristic of SV breakpoints. We applied InDelible to 13,438 probands with severe DDs recruited as part of the Deciphering Developmental Disorders (DDD) study and discovered 63 rare, damaging variants in genes previously associated with DDs missed by standard SNV, indel, or CNV discovery approaches. Clinical review of these 63 variants determined that about half (30/63) were plausibly pathogenic. InDelible was particularly effective at ascertaining variants between 21 and 500 bp in size and increased the total number of potentially pathogenic variants identified by DDD in this size range by 42.9%. Of particular interest were seven confirmed de novo variants in MECP2, which represent 35.0% of all de novo protein-truncating variants in MECP2 among DDD study participants. InDelible provides a framework for the discovery of pathogenic SVs that are most likely missed by standard analytical workflows and has the potential to improve the diagnostic yield of ES across a broad range of genetic diseases

Contribution of retrotransposition to developmental disorders.

Mobile genetic Elements (MEs) are segments of DNA which can copy themselves and other transcribed sequences through the process of retrotransposition (RT). In humans several disorders have been attributed to RT, but the role of RT in severe developmental disorders (DD) has not yet been explored. Here we identify RT-derived events in 9738 exome sequenced trios with DD-affected probands. We ascertain 9 de novo MEs, 4 of which are likely causative of the patient's symptoms (0.04%), as well as 2 de novo gene retroduplications. Beyond identifying likely diagnostic RT events, we estimate genome-wide germline ME mutation rate and selective constraint and demonstrate that coding RT events have signatures of purifying selection equivalent to those of truncating mutations. Overall, our analysis represents a comprehensive interrogation of the impact of retrotransposition on protein coding genes and a framework for future evolutionary and disease studies

Vitamin D receptor ChIP-seq in primary CD4+ cells: relationship to serum 25-hydroxyvitamin D levels and autoimmune disease

PMCID: PMC3710212This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited

Cardiac magnetic resonance predictors of left ventricular remodelling following acute ST elevation myocardial infarction: The VavirimS study

Left ventricular (LV) remodelling (REM) ensuing after ST-elevation myocardial infarction (STEMI), has typically been studied by echocardiography, which has limitations, or cardiac magnetic resonance (CMR) in early phase that may overestimate infarct size (IS) due to tissue edema and stunning. This prospective, multicenter study investigated LV-REM performing CMR in the subacute phase, and 6 months after STEMI