L^p(R^n)-continuity of translation invariant anisotropic pseudodifferential operators: a necessary condition

We consider certain anisotropic translation invariant pseudodifferential operators, belonging to a class denoted by $\mathrm{op}(\mathcal{M}^{\lambda}_{\psi})$, where $\lambda$ and $\psi=(\psi_1,\dots,\psi_n)$ are the "order" and "weight" functions, defined on $\mathbb{R}^n$, for the corresponding space of symbols. We prove that the boundedness of a suitable function $F_p\colon\mathbb{R}^n\to[0,+\infty)$, $1<p<\infty$, associated with $\lambda$ and $\psi$, is necessary to let every element of $\mathrm{op}(\mathcal{M}^{\lambda}_{\psi})$ be a $L^p(\mathbb{R}^n)$-multiplier. Additionally, we show that some results known in the literature can be recovered as special cases of our necessary condition.Comment: 16 pages, mistakes and typos correctio

Content addressable memory project

The progress on the Rutgers CAM (Content Addressable Memory) Project is described. The overall design of the system is completed at the architectural level and described. The machine is composed of two kinds of cells: (1) the CAM cells which include both memory and processor, and support local processing within each cell; and (2) the tree cells, which have smaller instruction set, and provide global processing over the CAM cells. A parameterized design of the basic CAM cell is completed. Progress was made on the final specification of the CPS. The machine architecture was driven by the design of algorithms whose requirements are reflected in the resulted instruction set(s). A few of these algorithms are described

A perturbed MicroRNA expression pattern characterizes embryonic neural stem cells derived from a severe mouse model of spinal muscular atrophy (SMA)

Spinal muscular atrophy (SMA) is an inherited neuromuscular disorder and the leading genetic cause of death in infants. Despite the disease-causing gene, survival motor neuron (SMN1), encodes a ubiquitous protein, SMN1 deficiency preferentially affects spinal motor neurons (MNs), leaving the basis of this selective cell damage still unexplained. As neural stem cells (NSCs) are multipotent self-renewing cells that can differentiate into neurons, they represent an in vitro model for elucidating the pathogenetic mechanism of neurodegenerative diseases such as SMA. Here we characterize for the first time neural stem cells (NSCs) derived from embryonic spinal cords of a severe SMNΔ7 SMA mouse model. SMNΔ7 NSCs behave as their wild type (WT) counterparts, when we consider neurosphere formation ability and the expression levels of specific regional and self-renewal markers. However, they show a perturbed cell cycle phase distribution and an increased proliferation rate compared to wild type cells. Moreover, SMNΔ7 NSCs are characterized by the differential expression of a limited number of miRNAs, among which miR-335-5p and miR-100-5p, reduced in SMNΔ7 NSCs compared to WT cells. We suggest that such miRNAs may be related to the proliferation differences characterizing SMNΔ7 NSCs, and may be potentially involved in the molecular mechanisms of SMA

A surge of late-occurring meiotic double-strand breaks rescues synapsis abnormalities in spermatocytes of mice with hypomorphic expression of SPO11

Meiosis is the biological process that, after a cycle of DNA replication, halves the cellular chromosome complement, leading to the formation of haploid gametes. Haploidization is achieved via two successive rounds of chromosome segregation, meiosis I and II. In mammals, during prophase of meiosis I, homologous chromosomes align and synapse through a recombination-mediated mechanism initiated by the introduction of DNA double-strand breaks (DSBs) by the SPO11 protein. In male mice, if SPO11 expression and DSB number are reduced below heterozygosity levels, chromosome synapsis is delayed, chromosome tangles form at pachynema, and defective cells are eliminated by apoptosis at epithelial stage IV at a spermatogenesis-specific endpoint. Whether DSB levels produced in Spo11 (+/-) spermatocytes represent, or approximate, the threshold level required to guarantee successful homologous chromosome pairing is unknown. Using a mouse model that expresses Spo11 from a bacterial artificial chromosome, within a Spo11 (-/-) background, we demonstrate that when SPO11 expression is reduced and DSBs at zygonema are decreased (approximately 40 % below wild-type level), meiotic chromosome pairing is normal. Conversely, DMC1 foci number is increased at pachynema, suggesting that under these experimental conditions, DSBs are likely made with delayed kinetics at zygonema. In addition, we provide evidences that when zygotene-like cells receive enough DSBs before chromosome tangles develop, chromosome synapsis can be completed in most cells, preventing their apoptotic elimination

Sistema de seguimiento solar para paneles fotovoltaicos

El objetivo del presente trabajo es desarrollar un seguidor solar de dos ejes para ser aplicado a panales fotovoltaicos. Esta aplicación permite que el panel incremente su producción en un 20 a 30%, dependiendo del mes y la hora del día. El sistema desarrollado contempla 5 modos de funcionamiento. Se utilizó una placa Arduino Mega ya que esta satisface los requerimientos de memoria y potencia de cálculo requeridos. Se usaron sensores LDR para el posicionamiento; además, el sistema contempla la posibilidad de conectarse mediante telefonía celular. Para el modelo a escala se usaron servomotores marca Tower Pro modelo SG90 por sus bajos requerimientos energéticos que permiten modularizar el sistema. Se realizaron simulaciones donde el error resultante es inferior al 1% para el posicionamiento y el aumento de energía producida está dentro de los valores esperados. Se proponen mejoras en el software de manera de hacerlo más accesible.The objective of the present work is to develop a two axis solar tracker to be applied to photovoltaic panels. This application allows the panel to increase its production by 20 to 30%, depending on the month and the time of day. The developed system contemplates 5 modes of operation. An Arduino Mega board was used as it satisfies the required memory and computing power requirements. LDR sensors were used for positioning; In addition, the system contemplates the possibility of connecting by cellular telephony. For the scale model, a Tower Pro model SG90 servomotors are used for their low energy requirements that allow modularizing the system. Simulations were carried out where the error was less than 1% for the positioning and the increase of the energy produced within the expected values. Improvements are proposed in the software in order to make it more accessible.Asociación Argentina de Energías Renovables y Medio Ambiente (ASADES

SMA human iPSC-derived motor neurons show perturbed differentiation and reduced miR-335-5P expression

Spinal Muscular Atrophy (SMA) is a neuromuscular disease caused by mutations in the Survival Motor Neuron 1 gene, resulting in very low levels of functional Survival of Motor Neuron (SMN) protein. SMA human induced Pluripotent Stem Cells (hiPSCs) represent a useful and valid model for the study of the disorder, as they provide in vitro the target cells. MicroRNAs (miRNAs) are often reported as playing a key role in regulating neuronal differentiation and fate specification. In this study SMA hiPSCs have been differentiated towards early motor neurons and their molecular and immunocytochemical profile were compared to those of wild type cells. Cell cycle proliferation was also evaluated by fluorescence-activated cell sorting (FACS). SMA hiPSCs showed an increased proliferation rate and also higher levels of stem cell markers. Moreover; when differentiated towards early motor neurons they expressed lower levels of NCAM and MN specific markers. The expression of miR-335-5p; already identified to control self-renewal or differentiation of mouse embryonic stem cells (mESCs); resulted to be reduced during the early steps of differentiation of SMA hiPSCs compared to wild type cells. These results suggest that we should speculate a role of this miRNA both in stemness characteristic and in differentiation efficiency of these cells

Human induced pluripotent stem cells for monogenic disease modelling and therapy

Recent and advanced protocols are now available to derive human induced pluripotent stem cells (hiPSCs) from patients affected by genetic diseases. No curative treatments are available for many of these diseases; thus, hiPSCs represent a major impact on patient' health. hiPSCs represent a valid model for the in vitro study of monogenic diseases, together with a better comprehension of the pathogenic mechanisms of the pathology, for both cell and gene therapy protocol applications. Moreover, these pluripotent cells represent a good opportunity to test innovative pharmacological treatments focused on evaluating the efficacy and toxicity of novel drugs. Today, innovative gene therapy protocols, especially gene editing-based, are being developed, allowing the use of these cells not only as in vitro disease models but also as an unlimited source of cells useful for tissue regeneration and regenerative medicine, eluding ethical and immune rejection problems. In this review, we will provide an up-to-date of modelling monogenic disease by using hiPSCs and the ultimate applications of these in vitro models for cell therapy. We consider and summarize some peculiar aspects such as the type of parental cells used for reprogramming, the methods currently used to induce the transcription of the reprogramming factors, and the type of iPSC-derived differentiated cells, relating them to the genetic basis of diseases and to their inheritance model