Vanadium redox flow batteries: Potentials and challenges of an emerging storage technology

open4noIn this paper an overview of Vanadium Redox Flow Battery technologies, architectures, applications and power electronic interfaces is given. These systems show promising features for energy storage in smart grid applications, where the intermittent power produced by renewable sources must meet strict load requests and economical opportunities. This paper reviews the vanadium-based technology for redox flow batteries and highlights its strengths and weaknesses, outlining the research lines that aim at taking it to full commercial success.openSpagnuolo, Giovanni, Guarnieri, Massimo; Mattavelli, Paolo; Petrone, Giovanni;Guarnieri, Massimo; Mattavelli, Paolo; Petrone, Giovanni; Spagnuolo, Giovann

A Real Multitechnology Microgrid in Venice: A Design Review

Electrical grids are evolving rapidly toward smart, self-regulating systems capable of managing distributed generation from intermittent renewable sources. Apart from hydroelectric, the large majority of them are photovoltaic (PV) systems grasping the fluctuating solar radiation and wind turbines (WT) capturing fickle wind energy, but other sources, which are at different stages of development, also generate energy with predictable or unpredictable intermittency. Several investigations have highlighted that, when power production from intermittent sources exceeds 20% of the total generation, the grid may face instabilities that can evolve into blackouts. Energy storage (ES) is a measure to balance source-load mismatches and to avoid such occurrence, but it can also provide a number of additional services which are part of the smart-grid paradigm. The operation of energy storage systems (ESSs) depends on the interface converters that manage the power flow and on the supervisors that control them according to the ESS, grid, and load features. Furthermore, the transmission system operator (TSO) may impose constraints on the ESS operation such as the obligation of contributing to primary regulation. Several numerical analyses have been developed to investigate the behavior of electrical grids provided with energy generation from renewable sources and energy storage, either islanded or connected to the national/transnational grid (macrogrid)

Design and analysis of flow control algorithms for data networks

Thesis (M.S.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 1997.Includes bibliographical references (leaves 110-112).by Paolo L. Naváez Guarnieri.M.S

Glioblastoma Models Reveal the Connection between Adult Glial Progenitors and the Proneural Phenotype

Tumor heterogeneity is a major obstacle for finding effective treatment of Glioblastoma (GBM). Based on global expression analysis, GBM can be classified into distinct subtypes: Proneural, Neural, Classical and Mesenchymal. The signatures of these different tumor subtypes may reflect the phenotypes of cells giving rise to them. However, the experimental evidence connecting any specific subtype of GBM to particular cells of origin is lacking. In addition, it is unclear how different genetic alterations interact with cells of origin in determining tumor heterogeneity. This issue cannot be addressed by studying end-stage human tumors.To address this issue, we used retroviruses to deliver transforming genetic lesions to glial progenitors in adult mouse brain. We compared the resulting tumors to human GBM. We found that different initiating genetic lesions gave rise to tumors with different growth rates. However all mouse tumors closely resembled the human Proneural GBM. Comparative analysis of these mouse tumors allowed us to identify a set of genes whose expression in humans with Proneural GBM correlates with survival.This study offers insights into the relationship between adult glial progenitors and Proneural GBM, and allows us to identify molecular alterations that lead to more aggressive tumor growth. In addition, we present a new preclinical model that can be used to test treatments directed at a specific type of GBM in future studies

Direct effects of estrogens on cholinergic primary neurons from the human fetal nucleus basalis of Meynert

Epidemiological studies have indicated that Alzheimer’s disease (AD) is more common in females and that post-menopausal women are at increased risk than their male counterpart, thus suggesting that estrogens could play a protective role to counteract neurodegenerative processes (1). However, the mechanisms underlying this association remain to be clarified. Since the nucleus basalis of Meynert (nbM) is the major source of cholinergic innervation selectively vulnerable to degeneration in AD, our study is aimed at investigating the effects of estrogens on human cholinergic primary neurons (hfCNs) isolated from the nbM of 12-week old fetuses. The primary culture obtained was immunophenotyped with flow cytometry and resulted almost totally positive (97±2 %) for the neuronal marker MAP2 and for the choline acetyltransferase (ChAT). We demonstrated that hfCNs express receptors for hormones of the reproductive axis (ERs, LHR, GnRHR). In particular, besides to classical estrogen receptors (ERa and ERb), hfCNs express the transmembrane receptor GPR30, which is known to mediate rapid non-genomic estrogen actions. Increasing concentrations of 17-β estradiol (E2, 0.1-100 nM) determined a dose-dependent significant increase in cell number after 24h exposure, which was antagonized by tamoxifen treatment. In addition, E2 exposure determined a significant increase in ChAT expression, thus indicating a direct positive effect of E2 on cholinergic phenotype. Given that substantial evidence now indicates that estrogens exert an anti-inflammatory activity even in the central nervous system (2), we exposed hfCN cells to the proinflammatory cytokine TNFα. E2 treatment (1nM) was able to significantly counteract the TNFα-induced nuclear NF-kB p65 translocation. Interestingly, this effect was mimicked by G1, a GPR30 agonist, and abolished by pretreating cells with the GPR30 antagonist G15, but not by tamoxifen, which usually antagonizes classical ERs. Overall, our results indicate that estrogens exert direct neuroprotective mechanisms on hfCNs through the activation of either classical (trophic) and non-classical (anti-inflammatory) receptors

Mechanisms of endothelial cell dysfunction in cystic fibrosis

Although cystic fibrosis (CF) patients exhibit signs of endothelial perturbation, the functions of the cystic fibrosis conductance regulator (CFTR) in vascular endothelial cells (EC) are poorly defined. We sought to uncover biological activities of endothelial CFTR, relevant for vascular homeostasis and inflammation. We examined cells from human umbilical cords (HUVEC) and pulmonary artery isolated from non-cystic fibrosis (PAEC) and CF human lungs (CF-PAEC), under static conditions or physiological shear. CFTR activity, clearly detected in HUVEC and PAEC, was markedly reduced in CF-PAEC. CFTR blockade increased endothelial permeability to macromolecules and reduced trans‑endothelial electrical resistance (TEER). Consistent with this, CF-PAEC displayed lower TEER compared to PAEC. Under shear, CFTR blockade reduced VE-cadherin and p120 catenin membrane expression and triggered the formation of paxillin- and vinculin-enriched membrane blebs that evolved in shrinking of the cell body and disruption of cell-cell contacts. These changes were accompanied by enhanced release of microvesicles, which displayed reduced capability to stimulate proliferation in recipient EC. CFTR blockade also suppressed insulin-induced NO generation by EC, likely by inhibiting eNOS and AKT phosphorylation, whereas it enhanced IL-8 release. Remarkably, phosphodiesterase inhibitors in combination with a β2 adrenergic receptor agonist corrected functional and morphological changes triggered by CFTR dysfunction in EC. Our results uncover regulatory functions of CFTR in EC, suggesting a physiological role of CFTR in the maintenance EC homeostasis and its involvement in pathogenetic aspects of CF. Moreover, our findings open avenues for novel pharmacology to control endothelial dysfunction and its consequences in CF

Physical activity modify skeletal muscle fiber types in an animal model of metabolic syndrome

Metabolic Syndrome (MetS) is a cluster of clinical conditions, associated to an increased cardiovascular risk, as well as to hypogonadism in males. Lifestyle modification (including physical exercise, PhyEx) may be beneficial for the condition. Skeletal muscles (SkM) are some of the most highly plastic tissues, able of remodeling in response to use, disuse and disease. In particular, transformations of fiber type may occur in response to physiological milieu to induce functional adaptations. This study is aimed at investigating in experimental MetS, high fat diet-induced in male rabbits [1], the effect of PhyEx on hormonal and metabolic parameters, as well as on SkM composition. Control and MetS rabbits were exercise-trained to run on a treadmill for 12 weeks. Quadriceps femoris samples were collected for histomorphological and gene expression analyses. We found that exercise resistance was significantly reduced in MetS rabbits, as demonstrated by the significant reduction of both running time and distance, compared to control group. MetS rabbits also exhibited the lowest quadriceps mass. Fiber typing by PAS-staining showed a pronounced shift from slower type I to faster type II fibers in MetS group in response to PhysEx, suggesting that MetS condition addressed SkM function towards anaerobic metabolism. Accordingly, extracellular lactate levels were significantly increased and mitochondrial respiration-related genes reduced in SkM of MetS rabbits respect to controls. Interestingly, PhyEx significantly counteracted MetS-related testosterone deficiency and hypercholesterolemia. In conclusion, our results indicate that dysmetabolic milieu induces a reduced proportion of fatigue-resistant type I fibers in response to PhysEx, which however resulted beneficial for MetS condition

Nerve growth factor-promotes primary cilium assembly in cholinergic neurons from the human basal forebrain

The primary cilium is a non-motile sensory antenna protruding from the surface of nearly all cells of the body, able to mediate the cellular response to extracellular signals. Although many of its functions remain to be clarified, it has been recently shown a role in neurogenesis [1]. In this study we evaluated the presence of the primary cilium in neurons isolated from the human fetal nucleus basalis of Meynert (hfnbM), a basal forebrain region crucially involved in the cholinergic transmission required for learning and memory. The hfnbM cells are characterized by the expression of cholinergic markers, such as choline acetyl transferase (ChAT) and also express the primary cilium, which, in basal conditions, was detected in the 17% of cells. It is known that nerve growth factor (NGF) supports survival, maintenance, connectivity and function of the brain cholinergic neurons. Indeed, we demonstrated that hfnbM cells respond to NGF in terms of proliferation, neurite formation and ChAT expression. Interestingly, NGF exposure significantly increased the percentage of ciliated cells (34.9%±1.8%). Given the known adverse effect of systemic chronic inflammation in the pathogenesis of neurodegenerative diseases, such as Alzheimer’s disease, characterized by the loss of nbM neurons, we exposed our cells to tumor necrosis factor-α (TNF-α). We observed that TNF-α significantly reduced the number of ciliated cells (4.3%±2%). Our results strongly suggest for the first time that primary cilia may be involved in the NGF-driven maturation of human nbM cholinergic neurons and suggest that the deleterious effects of neuroinflammation may be linked to an altered formation of the primary cilium