Tribological Properties of SiNx Films on PH Stainless Steel with and Without Nitriding as a Pre-treatment

AbstractIn this work, the tribological behavior and adhesion of SiNx films deposited by PACVD on nitrided and non-nitrided Corraẍ PH stainless steel were evaluated. The films were characterized by FTIR and EDS, hardness was assessed with a nanoindenter and the microstructure was analyzed by Optical Microscopy, SEM and FIB. To evaluate the tribological behavior, fretting and linear sliding tests were performed using WC and alumina balls as counterparts, and the adhesion of the SiNx films was characterized using the Scratch Test and Rockwell C indentation methods. Erosion tests were conducted in sea water and sand flux. Corrosion behavior was evaluated by the Salt Spray Fog Test. The film reached a hardness of 2300 HV and a thickness of about 1.4 microns. The duplex coated sample had a better tribological behavior than the simple coated sample, the nitrided layer allowed a graded interlayer which improved the wear resistance. Regarding the film adhesion, the duplex coating had an acceptable adhesion; the nitrided layer reduced the interface stress and enhanced the adhesion. Additionally, the films evidenced good corrosion resistance in a saline environment

Production of isotopically enriched high molecular weight hyaluronic acid and characterization by solid-state NMR

Hyaluronic acid (HA) is a naturally occurring polysaccharide that is abundant in the extracellular matrix (ECM) of all vertebrate cells. HA-based hydrogels have attracted great interest for biomedical applications due to their high viscoelasticity and biocompatibility. In both ECM and hydrogel applications, high molecular weight (HMW)-HA can absorb a large amount of water to yield matrices with a high level of structural integrity. To understand the molecular underpinnings of structural and functional properties of HA-containing hydrogels, few techniques are available. Nuclear magnetic resonance (NMR) spectroscopy is a powerful tool for such studies, e.g. 13C NMR measurements can reveal the structural and dynamical features of (HMW) HA. However, a major obstacle to 13C NMR is the low natural abundance of 13C, necessitating the generation of HMW-HA that is enriched with 13C isotopes. Here we present a convenient method to obtain 13C- and 15N-enriched HMW-HA in good yield from Streptococcus equi subsp. zooepidemicus. The labeled HMW-HA has been characterized by solution and magic angle spinning (MAS) solid-state NMR spectroscopy, as well as other methods. These results will open new ways to study the structure and dynamics of HMW-HA-based hydrogels, and interactions of HMW-HA with proteins and other ECM components, using advanced NMR techniques. </p

Protofilament structure and supramolecular polymorphism of aggregated mutant huntingtin exon 1

Huntington's disease is a progressive neurodegenerative disease caused by expansion of the polyglutamine domain in the first exon of huntingtin (HttEx1). The extent of expansion correlates with disease progression and formation of amyloid-like protein deposits within the brain. The latter display polymorphism at the microscopic level, both in cerebral tissue and in vitro. Such polymorphism can dramatically influence cytotoxicity, leading to much interest in the conditions and mechanisms that dictate the formation of polymorphs. We examine conditions that govern HttEx1 polymorphism in vitro, including concentration and the role of the non-polyglutamine flanking domains. Using electron microscopy, we observe polymorphs that differ in width and tendency for higher-order bundling. Strikingly, aggregation yields different polymorphs at low and high concentrations. Narrow filaments dominate at low concentrations that may be more relevant in vivo. We dissect the role of N- and C-terminal flanking domains using protein with the former (httNT or N17) largely removed. The truncated protein is generated by trypsin cleavage of soluble HttEx1 fusion protein, which we analyze in some detail. Dye binding and solid-state NMR studies reveal changes in fibril surface characteristics and flanking domain mobility. Higher-order interactions appear facilitated by the C-terminal tail, while the polyglutamine forms an amyloid core resembling those of other polyglutamine deposits. Fibril-surface-mediated branching, previously attributed to secondary nucleation, is reduced in absence of httNT. A new model for the architecture of the HttEx1 filaments is presented and discussed in context of the assembly mechanism and biological activity

Recubrimientos Superficiales Aplicados mediante el Proceso de Plasma

The need for new materials with very specific functional properties, and the tools for your mechanical conformation, have risen greatly the cost of the machining processes, and the cost of the finished parts. Surface coatings, allow to obtain the required mechanical properties, on a base material of low cost and easy machining. The plasma coating processes produce improved behavior surfaces and have among others the following advantages:•Allow higher quality results, and in many cases unique properties compared to other conventional technologies.•There are not contaminants; make efficient use of energy apply to more materials and have high operational safety.•They apply to the component, tool or part of piece when they are finished, namely, that is part of the final manufacturing step, and therefore directly influence elements that already have a high added value.La necesidad de nuevos materiales con propiedades funcionales muy específicas y las herramientas para su conformación mecánica han encarecido enormemente muchos procesos de mecanizado y el costo de las piezas terminadas. Los recubrimientos superficiales permiten la obtención de las propiedades mecánicas requeridas sobre un material de base de bajo costo y fácil mecanizado. Los procesos de recubrimientos por plasma producen mejoras en el comportamiento de las superficies y tienen, entre otras, las ventajas siguientes: •Permiten obtener resultados de calidad superior y en muchos casos propiedades únicas frente a otras tecnologías convencionales.•No son contaminantes; hacen uso eficiente de la energía; son aplicables a mayor cantidad de materiales y tienen máxima seguridad operativa.•Se aplican al componente, herramienta o pieza cuando ya están terminados, es decir, forman parte de la última etapa de fabricación y, por lo tanto, influyen directamente sobre elementos que ya tienen alto valor agregado

Effect of butanol and salt concentration on solid-state nanopores resistance

The objective of this study was to demonstrate the possibility of using 1-butanol to detect in a reliable way the open pore current of pyramidal solid-state nanopores produced in silicon wafers. The nanopores were produced through controlled pore formation by neutralizing an etchant (KOH) with a strong acid (HCl). Since nanopores produced by this method have a larger depth than those made in nanometer thick membranes, they behave as nanochannels. As a consequence, the open pore current detection is more challenging. Thus, we report that low amounts of butanol considerably aid in the detection of the open pore current of nanopores.Fil: Vega, M.. Universidad Tecnológica Nacional. Facultad Regional Haedo; ArgentinaFil: Perez, Maximiliano Sebastian. Universidad Tecnológica Nacional. Facultad Regional Haedo; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Granell, Pablo Nicolás. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Golmar, Federico. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Wloka, C.. University of Groningen; Países BajosFil: Maglia, G.. University of Groningen; Países BajosFil: Dieguez, M.J.. Instituto Nacional de Tecnología Agropecuaria; ArgentinaFil: Del Valle, E.M.. Universidad de Salamanca; EspañaFil: Lasorsa, Carlos Alberto. Universidad Tecnológica Nacional. Facultad Regional Haedo; ArgentinaFil: Lerner, Betiana. Universidad Tecnológica Nacional. Facultad Regional Haedo; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentin

A protein kinase a-independent pathway controlling aquaporin 2 trafficking as a possible cause for the syndrome of inappropriate antidiuresis associated with polycystic kidney disease 1 haploinsufficiency.

Renal water reabsorption is controlled by vasopressin (AVP) which binds to V2 receptors resulting in PKA activation, phosphorylation of AQP2 at serine 256 (pS256) and translocation to the plasma membrane. Besides S256, AVP causes dephosphorylation of S261. Recent studies showed that cyclin-dependent kinases can phosphorylate S261 AQP2 peptides in vitro. In an attempt to investigate the possible role of cdks on AQP2 phosphorylation, we identified a new PKA-independent pathway regulating AQP2 trafficking. In ex-vivo kidney slices and MDCK-AQP2 cells, R-roscovitine, a specific cdks inhibitor, increased pS256 and decreased pS261. The changes in AQP2 phosphorylation were paralleled by an increase in cell surface AQP2 expression and osmotic water permeability in the absence of forskolin stimulation. Of note, R-roscovitine didn’t alter cAMP-dependent PKA activity. Because phosphorylation results from the balance between kinase and phosphatase activity, we evaluated the possible contribution of protein phosphatases PP1, PP2A and PP2B. Of these, R-roscovitine treatment specifically reduced PP2A protein expression and activity in MDCK cells. Interestingly, in PKD1+/- mice displaying a syndrome of inappropriate antidiuresis with high level of pS256 despite unchanged AVP and cAMP, we found a reduced PP2A expression and activity and reduced pS261. Similarly to what previously found in PKD1+/- mice, R-roscovitine treatment caused a significant decrease in intracellular calcium in MDCK cells. Our data indicate that a reduced activity of PP2A, secondary to reduced intracellular Ca2+ levels, promotes AQP2 trafficking independently of the AVP-PKA axis. This pathway may be relevant for explaining pathological states characterized by inappropriate AVP secretion and positive water balance

Verificación de las Curvas de Paschen y la Ley de Peek en microionizadores por descarga luminiscente

En este trabajo analizamos el sistema de ionización por descarga luminiscente para su utilización como fuente de iones en un equipo de identificación de compuestos químicos tipo IMS. Se realizaron modelos de descarga corona implementados con tecnología MEMS (Sistemas Micro-electro Mecánicos). Se propone que en la escala micrométrica es posible mejorar rendimientos, confiabilidad y demandas operativas. Así se redujo la tensión de la fuente de alimentación a menos de 1kV.Centro de Técnicas Analógico-Digitale

Deficiency of Mitochondrial Aspartate-Glutamate Carrier 1 Leads to Oligodendrocyte Precursor Cell Proliferation Defects Both In Vitro and In Vivo

Aspartate-Glutamate Carrier 1 (AGC1) deficiency is a rare neurological disease caused by mutations in the solute carrier family 25, member 12 (SLC25A12) gene, encoding for the mitochondrial aspartate-glutamate carrier isoform 1 (AGC1), a component of the malate-aspartate NADH shuttle (MAS), expressed in excitable tissues only. AGC1 deficiency patients are children showing severe hypotonia, arrested psychomotor development, seizures and global hypomyelination. While the effect of AGC1 deficiency in neurons and neuronal function has been deeply studied, little is known about oligodendrocytes and their precursors, the brain cells involved in myelination. Here we studied the effect of AGC1 down-regulation on oligodendrocyte precursor cells (OPCs), using both in vitro and in vivo mouse disease models. In the cell model, we showed that a reduced expression of AGC1 induces a deficit of OPC proliferation leading to their spontaneous and precocious differentiation into oligodendrocytes. Interestingly, this effect seems to be related to a dysregulation in the expression of trophic factors and receptors involved in OPC proliferation/differentiation, such as Platelet-Derived Growth Factor \u3b1 (PDGF\u3b1) and Transforming Growth Factor \u3b2s (TGF\u3b2s). We also confirmed the OPC reduction in vivo in AGC1-deficent mice, as well as a proliferation deficit in neurospheres from the Subventricular Zone (SVZ) of these animals, thus indicating that AGC1 reduction could affect the proliferation of different brain precursor cells. These data clearly show that AGC1 impairment alters myelination not only by acting on N-acetyl-aspartate production in neurons but also on OPC proliferation and suggest new potential therapeutic targets for the treatment of AGC1 deficiency

Histone Acetylation Defects in Brain Precursor Cells: A Potential Pathogenic Mechanism Causing Proliferation and Differentiation Dysfunctions in Mitochondrial Aspartate-Glutamate Carrier Isoform 1 Deficiency

Mitochondrial aspartate-glutamate carrier isoform 1 (AGC1) deficiency is an ultra-rare genetic disease characterized by global hypomyelination and brain atrophy, caused by mutations in the SLC25A12 gene leading to a reduction in AGC1 activity. In both neuronal precursor cells and oligodendrocytes precursor cells (NPCs and OPCs), the AGC1 determines reduced proliferation with an accelerated differentiation of OPCs, both associated with gene expression dysregulation. Epigenetic regulation of gene expression through histone acetylation plays a crucial role in the proliferation/differentiation of both NPCs and OPCs and is modulated by mitochondrial metabolism. In AGC1 deficiency models, both OPCs and NPCs show an altered expression of transcription factors involved in the proliferation/differentiation of brain precursor cells (BPCs) as well as a reduction in histone acetylation with a parallel alteration in the expression and activity of histone acetyltransferases (HATs) and histone deacetylases (HDACs). In this study, histone acetylation dysfunctions have been dissected in in vitro models of AGC1 deficiency OPCs (Oli-Neu cells) and NPCs (neurospheres), in physiological conditions and following pharmacological treatments. The inhibition of HATs by curcumin arrests the proliferation of OPCs leading to their differentiation, while the inhibition of HDACs by suberanilohydroxamic acid (SAHA) has only a limited effect on proliferation, but it significantly stimulates the differentiation of OPCs. In NPCs, both treatments determine an alteration in the commitment toward glial cells. These data contribute to clarifying the molecular and epigenetic mechanisms regulating the proliferation/differentiation of OPCs and NPCs. This will help to identify potential targets for new therapeutic approaches that are able to increase the OPCs pool and to sustain their differentiation toward oligodendrocytes and to myelination/remyelination processes in AGC1 deficiency, as well as in other white matter neuropathologies