Contextualized property market models vs. Generalized mass appraisals: An innovative approach

The present research takes into account the current and widespread need for rational valuation methodologies, able to correctly interpret the available market data. An innovative automated valuation model has been simultaneously implemented to three Italian study samples, each one constituted by two-hundred residential units sold in the years 2016-2017. The ability to generate a "unique" functional form for the three different territorial contexts considered, in which the relationships between the influencing factors and the selling prices are specified by different multiplicative coefficients that appropriately represent the market phenomena of each case study analyzed, is the main contribution of the proposed methodology. The method can provide support for private operators in the assessment of the territorial investment conveniences and for the public entities in the decisional phases regarding future tax and urban planning policies

S100B protein as a therapeutic target in multiple sclerosis: The S100B inhibitor arundic acid protects from chronic experimental autoimmune encephalomyelitis

S100B is an astrocytic protein behaving at high concentration as a damage-associated molecular pattern molecule. A direct correlation between the increased amount of S100B and inflammatory processes has been demonstrated, and in particular, the inhibitor of S100B activity pentamidine has been shown to ameliorate clinical scores and neuropathologic-biomolecular parameters in the relapsing-remitting experimental autoimmune encephalomyelitis mouse model of multiple sclerosis. This study investigates the effect of arundic acid (AA), a known inhibitor of astrocytic S100B synthesis, in the chronic experimental autoimmune encephalomyelitis, which is another mouse model of multiple sclerosis usually studied. By the daily evaluation of clinical scores and neuropathologic-molecular analysis performed in the spinal cord, we observed that the AA-treated group showed lower severity compared to the vehicle-treated mice, particularly in the early phase of disease onset. We also observed a significant reduction of astrocytosis, demyelination, immune infiltrates, proinflammatory cytokines expression and enzymatic oxidative reactivity in the AA-treated group. Overall, our results reinforce the involvement of S100B in the development of animal models of multiple sclerosis and propose AA targeting the S100B protein as a focused potential drug to be considered for multiple sclerosis treatment

Ligand engagement of Toll-like receptors regulates their expression in cortical microglia and astrocytes

BACKGROUND: Toll-like receptor (TLR) activation on microglia and astrocytes are key elements in neuroinflammation which accompanies a number of neurological disorders. While TLR activation on glia is well-established to up-regulate pro-inflammatory mediator expression, much less is known about how ligand engagement of one TLR may affect expression of other TLRs on microglia and astrocytes. METHODS: In the present study, we evaluated the effects of agonists for TLR2 (zymosan), TLR3 (polyinosinic-polycytidylic acid (poly(I:C)), a synthetic analogue of double-stranded RNA) and TLR4 (lipopolysaccaride (LPS)) in influencing expression of their cognate receptor as well as that of the other TLRs in cultures of rat cortical purified microglia (>99.5 %) and nominally microglia-free astrocytes. Elimination of residual microglia (a common contaminant of astrocyte cultures) was achieved by incubation with the lysosomotropic agent L-leucyl-L-leucine methyl ester (L-LME). RESULTS: Flow cytometric analysis confirmed the purity (essentially 100 %) of the obtained microglia, and up to 5 % microglia contamination of astrocytes. L-LME treatment effectively removed microglia from the latter (real-time polymerase chain reaction). The three TLR ligands robustly up-regulated gene expression for pro-inflammatory markers (interleukin-1 and interleukin-6, tumor necrosis factor) in microglia and enriched, but not purified, astrocytes, confirming cellular functionality. LPS, zymosan and poly(I:C) all down-regulated TLR4 messenger RNA (mRNA) and up-regulated TLR2 mRNA at 6 and 24 h. In spite of their inability to elaborate pro-inflammatory mediator output, the nominally microglia-free astrocytes (>99 % purity) also showed similar behaviours to those of microglia, as well as changes in TLR3 gene expression. LPS interaction with TLR4 activates downstream mitogen-activated protein kinase and nuclear factor-κB signalling pathways and subsequently causes inflammatory mediator production. The effects of LPS on TLR2 mRNA in both cell populations were antagonized by a nuclear factor-κB inhibitor. CONCLUSIONS: TLR2 and TLR4 activation in particular, in concert with microglia and astrocytes, comprise key elements in the initiation and maintenance of neuropathic pain. The finding that both homologous (zymosan) and heterologous (LPS, poly(I:C)) TLR ligands are capable of regulating TLR2 gene expression, in particular, may have important implications in understanding the relative contributions of different TLRs in neurological disorders associated with neuroinflammation

Farsighted Stable Sets

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Privacy accountability and penalties for IoT firms

Internet of things (IoT) business partnership are formed by technological partners and traditional manufacturers. IoT sensors and devices capture data from manufacturers' products. Data enforce product/service innovation thanks to data sharing among companies. However, data sharing among firms increases the risk of data breaches. The latter is due to two phenomena: information linkage and privacy interdependency. Data Protection Authorities (DPA) protect data users' rights and fine firms if there is an infringement of privacy laws. DPA sanction the responsible for the infringement of privacy laws. We present two different business scenarios: the first occurs when each firm is a data owner; the second occurs when only the manufacturer is the data owner. For both scenarios, we present two fair penalty schemes that suggest the following: total amount of the fine; and how to share the fine among participants. Penalties critically vary at how innovation networks are structured in IoT industries. Our penalties provide incentives to data sharing since they redistribute firms' responsibility against data breaches. Our penalties may mitigate the risk on the manufacturer if is the unique responsible for data handling

Accountability and Penalties for IoT Firms.

Internet of things (IoT) business partnership are formed by technological partners and traditional manufacturers. IoT sensors and devices capture data from manufacturers' products. Data enforce product/service innovation thanks to data sharing among companies. However, data sharing among firms increases the risk of data breaches. The latter is due to two phenomena: information linkage and privacy interdependency. Data Protection Authorities (DPA) protect data users' rights and fine firms if there is an infringement of privacy laws. DPA sanction the responsible for the infringement of privacy laws. We present two different business scenarios: the first occurs when each firm is a data owner; the second occurs when only the manufacturer is the data owner. For both scenarios, we present two fair penalty schemes that suggest the following: total amount of the fine; and how to share the fine among participants. Penalties critically vary at how innovation networks are structured in IoT industries. Our penalties provide incentives to data sharing since they redistribute firms' responsibility against data breaches. Our penalties may mitigate the risk on the manufacturer if is the unique responsible for data handling