Crowd-sensing our Smart Cities: a Platform for Noise Monitoring and Acoustic Urban Planning

Environmental pollution and the corresponding control measurements put in place to tackle it play a significant role in determining the actual quality of life in modern cities. Amongst the several pollutant that have to be faced on a daily basis, urban noise represent one of the most widely known for its already ascertained health-related issues. However, no systematic noise management and control activities are performed in the majority of European cities due to a series of limiting factors (e.g., expensive monitoring equipment, few available technician, scarce awareness of the problem in city managers). The recent advances in the Smart City model, which is being progressively adopted in many cities, nowadays offer multiple possibilities to improve the effectiveness in this area. The Mobile Crowd Sensing paradigm allows collecting data streams from smartphone built-in sensors on large geographical scales at no cost and without involving expert data captors, provided that an adequate IT infrastructure has been implemented to manage properly the gathered measurements. In this paper, we present an improved version of a MCS-based platform, named City Soundscape, which allows exploiting any Android-based device as a portable acoustic monitoring station and that offers city managers an effective and straightforward tool for planning Noise Reduction Interventions (NRIs) within their cities. The platform also now offers a new logical microservices architecture

The human gene SLC25A29, of solute carrier family 25, encodes a mitochondrial transporter of basic amino acids

The human genome encodes 53 members of the solute carrier family 25 (SLC25), also called the mitochondrial carrier family, many of which have been shown to transport carboxylates, amino acids, nucleotides, and cofactors across the inner mitochondrial membrane, thereby connecting cytosolic and matrix functions. In this work, a member of this family, SLC25A29, previously reported to be a mitochondrial carnitine/acylcarnitine- or ornithine-like carrier, has been thoroughly characterized biochemically. The SLC25A29 gene was overexpressed in Escherichia coli, and the gene product was purified and reconstituted in phospholipid vesicles. Its transport properties and kinetic parameters demonstrate that SLC25A29 transports arginine, lysine, homoarginine, methylarginine and, to a much lesser extent, ornithine and histidine. Carnitine and acylcarnitines were not transported by SLC25A29. This carrier catalyzed substantial uniport besides a counter-exchange transport, exhibited a high transport affinity for arginine and lysine, and was saturable and inhibited by mercurial compounds and other inhibitors of mitochondrial carriers to various degrees. The main physiological role of SLC25A29 is to import basic amino acids into mitochondria for mitochondrial protein synthesis and amino acid degradation

The Risky-Opportunity Analysis Method (ROAM) to Support Risk-Based Decisions in a Case-Study of Critical Infrastructure Digitization

none4Ali Aghazadeh Ardebili; Elio Padoano; Antonella Longo; Antonio FicarellaAGHAZADEH ARDEBILI, Ali; Padoano, Elio; Longo, Antonella; Ficarella, Antoni

Machine Learning approach towards real time assessment of hand-arm vibration risk

In industry 4,0, the establishment of an interconnected environment where human operators cooperate with the machines offers the opportunity for substantially improving the ergonomics and safety conditions of the workplace. This topic is discussed in the paper referring to the vibration risk, which is a well-known cause of work-related pathologies. A wearable device has been developed to collect vibration data and to segment the signals obtained in time windows. A machine learning classifier is then proposed to recognize the worker’s activity and to evaluate the exposure to vibration risks. The experimental results demonstrate the feasibility and effectiveness of the methodology proposed

A child with hyperferritinemia: Case report

Hereditary hyperferritinemia cataract syndrome (HHCS) is a rare condition caused by mutations in the gene coding for the light chain of ferritin; it does not lead to iron overload, but it is associated with the risk of developing a bilateral nuclear cataract also in childhood. On the contrary, a raise of serum ferritin levels is a common finding in pediatrics. We describe here a case of HHCS that offers some interesting clues for the daily practice. Our patient is a 6 year old Italian boy who came to our attention after some time of diagnostic uncertainties because of persistently high levels of ferritin with no apparent cause. We were guided to the suspect of this syndrome by the family history (5 members with various degrees of cataract developed in first infancy). High levels of serum ferritin and specific genetic testing (mutation A37C) confirmed the diagnosis. This case underlines the need of considering rare genetic syndromes, including hereditary hyperferritinemia cataract syndrome, in the differential diagnosis of raised serum ferritin in children and the importance of paying attention to family history in considering a patient with isolated raised levels of serum ferritin

Genome Mining of Plant NPFs Reveals Varying Conservation of Signature Motifs Associated With the Mechanism of Transport

Nitrogen is essential for all living species and may be taken up from the environment in different forms like nitrate or peptides. In plants, members of a transporter family named NPFs transport nitrate and peptides across biological membranes. NPFs are phylogenetically related to a family of peptide transporters (PTRs) or proton-coupled oligopeptide transporters (POTs) that are evolutionarily conserved in all organisms except in Archaea. POTs are present in low numbers in bacteria, algae and animals. NPFs have expanded in plants and evolved to transport a wide range of substrates including phytohormones and glucosinolates. Functional studies have shown that most NPFs, like POTs, operate as symporters with simultaneous inwardly directed movement of protons. Here we focus on four structural features of NPFs/POTs/PTRs that have been shown by structural and functional studies to be essential to proton-coupled symport transport. The first two features are implicated in proton binding and transport: a conserved motif named ExxER/K, located in the first transmembrane helix (TMH1) and a D/E residue in TMH7 that has been observed in some bacterial and algal transporters. The third and fourth features are two inter-helical salt bridges between residues on TMH1 and TMH7 or TMH4 and TMH10. To understand if the mechanism of transport is conserved in NPFs with the expansion to novel substrates, we collected NPFs sequences from 42 plant genomes. Sequence alignment revealed that the ExxER/K motif is not strictly conserved and its conservation level is different in the NPF subfamilies. The proton binding site on TMH7 is missing in all NPFs with the exception of two NPFs from moss. The two moss NPFs also have a positively charged amino acid on TMH1 that can form the salt bridge with the TMH7 negative residue. None of the other NPFs we examined harbor residues that can form the TMH1–TMH7 salt bridge. In contrast, the amino acids required to form the TMH4–TMH10 salt bridge are highly conserved in NPFs, with some exceptions. These results support the need for further biochemical and structural studies of individual NPFs for a better understanding of the transport mechanism in this family of transporters

Changes in membrane lipids drive increased endocytosis following Fas ligation

Once activated, some surface receptors promote membrane movements that open new portals of endocytosis, in part to facilitate the internalization of their activated complexes. The prototypic death receptor Fas (CD95/Apo1) promotes a wave of enhanced endocytosis that induces a transient intermixing of endosomes with mitochondria in cells that require mitochondria to amplify death signaling. This initiates a global alteration in membrane traffic that originates from changes in key membrane lipids occurring in the endoplasmic reticulum (ER). We have focused the current study on specific lipid changes occurring early after Fas ligation. We analyzed the interaction between endosomes and mitochondria in Jurkat T cells by nanospray-Time-of-flight (ToF) Mass Spectrometry. Immediately after Fas ligation, we found a transient wave of lipid changes that drives a subpopulation of early endosomes to merge with mitochondria. The earliest event appears to be a decrease of phosphatidylcholine (PC), linked to a metabolic switch enhancing phosphatidylinositol (PI) and phosphoinositides, which are crucial for the formation of vacuolar membranes and endocytosis. Lipid changes occur independently of caspase activation and appear to be exacerbated by caspase inhibition. Conversely, inhibition or compensation of PC deficiency attenuates endocytosis, endosome-mitochondria mixing and the induction of cell death. Deficiency of receptor interacting protein, RIP, also limits the specific changes in membrane lipids that are induced by Fas activation, with parallel reduction of endocytosis. Thus, Fas activation rapidly changes the interconversion of PC and PI, which then drives enhanced endocytosis, thus likely propagating death signaling from the cell surface to mitochondria and other organelles

delivering collaborative web labs as a service for engineering education

As Internet speed grows up and academic networks reach more users, engineering schools take interest in online laboratories as a mean to increase the spectrum of offered services and to reduce costs by sharing expensive lab equipments. In this perspective, online labs must comply both with the scientific and pedagogic requirements coming from the lab users (students, researchers, â?¦) and with the requirements coming from the administrative and technical staff in charge to manage and deliver the lab services. In this paper we describe a system architecture based on both the classes of requirements and discuss the main results achieved implementing a prototype of the proposed architecture in a real academic scenario

supporting continuous improvement in care management with bpm

The present work analyzes the results of an Italian care management project, called Leonardo, promoted by Apulia Region, in the south of Italy, in partnership with Pfizer. The work starts from the consideration that care management represents an innovation in the management of the chronic diseases because it introduces a new model in the organization of healthcare services. Such a model needs gradual refinements in a continuous improvement perspective, in order to be effective. The proposed approach is about the adoption of a Business Process Modelling technique to "model" all phases and activities of the care management process as developed in Leonardo Project. Then this model is used to define the key performance indicators, to analyze the Leonardo Project results and to enhance the underlying care management process. Specific attention has been dedicated to analyze the impact of the software proposed by Pfizer and used to support the care managers and the family doctors in the Leonardo Project. The process model, in fact, helped us to identify several limitations related to the adopted software and to formulate the correct requirements to overcome these issues. In other words, the paper aims to illustrate how tools borrowed from enterprise modelling domain can help to identify and overcome the weaknesses of a care management process and to design more effective software tools in a continuous refinement cycle

Complex phenotype in an Italian family with a novel mutation in SPG3A.

Mutations in the SPG3A gene represent a significant cause of autosomal dominant hereditary spastic paraplegia with early onset and pure phenotype. We describe an Italian family manifesting a complex phenotype, characterized by cerebellar involvement in the proband and amyotrophic lateral sclerosis-like syndrome in her father, in association with a new mutation in SPG3A. Our findings further widen the notion of clinical heterogeneity in SPG3A mutations