L’effetto della liberalizzazione ferroviaria sulle politiche di prezzo delle compagnie aeree e ferroviarie. Evidenze preliminari sui principali collegamenti ad Alta Velocità in Italia

Il mercato italiano del trasporto ferroviario passeggeri è stato recentemente caratterizzato dall'ingresso di un nuovo operatore nel settore dell'Alta Velocità, Nuovo Trasporto Viaggiatori (NTV). L'ingresso di NTV ha stimolato sia la concorrenza intramodale con l’incumbent Trenitalia sia la concorrenza intermodale con le compagnie aeree. Il presente lavoro si propone di studiare le strategie di pricing nel mercato del trasporto passeggeri, con il duplice l'obiettivo di esplorare l'effetto della concorrenza intramodale sulle tariffe degli operatori ferroviari - applicate sulle principali rotte Italiane servite dall’Alta Velocità (AV) - e di analizzare l'effetto della concorrenza intermodale sulle strategie di prezzo delle compagnie aeree. I risultati dell'analisi evidenziano che le due compagnie ferroviarie che operano nel segmento AV pongono in essere una politica di prezzo strategica, sebbene eterogenea fra le rotte. Inoltre, le compagnie aeree riducono in misura consistente le tariffe quando operano in concorrenza diretta con i servizi ad AV

The impact of open access on intra- and inter-modal rail competition. A national level analysis in Italy

During 2012 the Italian passenger market has experienced the entry of a new operator, Nuovo Trasporto Viaggiatori (NTV) on the high speed rail (HSR) market segment, in competition with the incumbent Trenitalia. The Italian market is the first and most extensive case in Europe where two railway companies compete for HSR services on open access basis. In this paper we empirically explore the competitive effects of the newcomer’s entry in the passenger market tackling two issues. First, we study price and capacity effects of the stemming intra-modal competition. Second, we measure the impact of inter-modal competition by HSR on airline pricing behaviour. The results show that the two railway companies engage in strategic pricing, although to a different degree on different routes and that capacity and frequency are strategic variables. We also find that airlines significantly reduce fares when flights are in direct competition with HSR services

An experience of collaboration using a PaaS for the smarter university model

In this paper we continue our previous research on the development of the current model of higher education, which pointed out that the labor market is looking for people with competencies and skills reflecting a T-shape model. As a consequence, universities should include a wider mix of disciplines in the curricula of their courses. Hence, to overcome existing criticisms and to provide some suggestions on how to enhance universities' performances, we thought of education as a process with inputs, outputs, and relevant dependencies. We called such a university a “smarter university” in which knowledge is a common heritage of teachers and students. In our research the smarter university model is based on a smart-city-like model, due to the fact that next generation networks and relevant services are going to be more and more integrated with existing infrastructure and information management systems. Thus, it is mandatory that smart solutions are the most prominent assets of modern university environments to improve the effectiveness of higher education. In this paper, we report the experimental results from a specific case study of collaboration between industry and university, which could be used as a refer- ence for the definition of patterns to be applied in the redesign of the current education systems, even though the experiment refers to a technological application scenario

Immunohistochemical Localisation of PDE5 in Rat Lung during Pre- and Postnatal Development

In mammalian lung, at the transition to extrauterine life, NO/cGMP signal transduction system is known to play crucial roles in the regulation of vascular resistance and is supposed to act in angiogenesis. PDE5, which is the most abundant cGMP metabolizing enzyme within the lung, is highly expressed in the perinatal period, but its localisation in the different pulmonary cells is still poorly known. In our research, PDE5 immunohistochemical distribution was investigated in foetal and neonatal rat lung. The highest expression of PDE5 was found in cells randomly located in the stroma; in newborns, in particular, many cells in the intersaccular walls were heavily labelled, while much lower staining levels were shown by smooth myocytes belonging to vessels and airways. On the basis of their immunoreactivity for α-SM actin and/or desmin, most of the heavily PDE5-positive cells were identified as interstitial myofibroblasts and transitional pericytes, while only a few were interpreted as interstitial lipofibroblasts

Intentional Minds: A Philosophical Analysis of Intention Tested through fMRI Experiments Involving People with Schizophrenia, People with Autism, and Healthy Individuals

In this paper we show how we empirically tested one of the most relevant topics in philosophy of mind through a series of fMRI experiments: the classification of different types of intention. To this aim, firstly we trace a theoretical distinction among private, prospective, and communicative intentions. Second, we propose a set of predictions concerning the recognition of these three types of intention in healthy individuals, and we report the experimental results corroborating our theoretical model of intention. Third, we derive from our model predictions relevant for the domain of psychopathological functioning. In particular, we treat the cases of both hyper-intentionality (as in paranoid schizophrenia) and hypo-intentionality (as in autistic spectrum disorders). Our conclusion is that the theoretical model of intention we propose contributes to enlarge our knowledge on the neurobiological bases of intention processing, in both healthy people and in people with impairments to the neurocognitive system that underlies intention recognition

HIV Modifies the m6A and m5C Epitranscriptomic Landscape of the Host Cell

The study of RNA modifications, today known as epitranscriptomics, is of growing interest. The N6-methyladenosine (m6A) and 5-methylcytosine (m5C) RNA modifications are abundantly present on mRNA molecules, and impact RNA interactions with other proteins or molecules, thereby affecting cellular processes, such as RNA splicing, export, stability, and translation. Recently m6A and m5C marks were found to be present on human immunodeficiency (HIV) transcripts as well and affect viral replication. Therefore, the discovery of RNA methylation provides a new layer of regulation of HIV expression and replication, and thus offers novel array of opportunities to inhibit replication. However, no study has been performed to date to investigate the impact of HIV replication on the transcript methylation level in the infected cell. We used a productive HIV infection model, consisting of the CD4+ SupT1 T cell line infected with a VSV-G pseudotyped HIVeGFP-based vector, to explore the temporal landscape of m6A and m5C epitranscriptomic marks upon HIV infection, and to compare it to mock-treated cells. Cells were collected at 12, 24, and 36 h post-infection for mRNA extraction and FACS analysis. M6A RNA modifications were investigated by methylated RNA immunoprecipitation followed by high-throughput sequencing (MeRIP-Seq). M5C RNA modifications were investigated using a bisulfite conversion approach followed by high-throughput sequencing (BS-Seq). Our data suggest that HIV infection impacted the methylation landscape of HIV-infected cells, inducing mostly increased methylation of cellular transcripts upon infection. Indeed, differential methylation (DM) analysis identified 59 m6A hypermethylated and only 2 hypomethylated transcripts and 14 m5C hypermethylated transcripts and 7 hypomethylated ones. All data and analyses are also freely accessible on an interactive web resource (http://sib-pc17.unil.ch/HIVmain.html). Furthermore, bothm6A andm5Cmethylations were detected on viral transcripts and viral particle RNA genomes, as previously described, but additional patterns were identified. This work used differential epitranscriptomic analysis to identify novel players involved in HIV life cycle, thereby providing innovative opportunities for HIV regulation

Endogenous CCL2 neutralization restricts HIV-1 replication in primary human macrophages by inhibiting viral DNA accumulation

Macrophages are key targets of HIV-1 infection. We have previously described that the expressionof CC chemokine ligand 2 (CCL2) increases during monocyte differentiation to macrophages and it is furtherup-modulated by HIV-1 exposure. Moreover, CCL2 acts as an autocrine factor that promotes viral replication ininfected macrophages. In this study, we dissected the molecular mechanisms by which CCL2 neutralization inhibitsHIV-1 replication in monocyte-derived macrophages (MDM), and the potential involvement of the innate restrictionfactors protein sterile alpha motif (SAM) histidine/aspartic acid (HD) domain containing 1 (SAMHD1) and apolipoproteinB mRNA-editing, enzyme-catalytic, polypeptide-like 3 (APOBEC3) family members.Results:CCL2 neutralization potently reduced the number of p24 Gag+cells during the course of either productive orsingle cycle infection with HIV-1. In contrast, CCL2 blocking did not modify entry of HIV-1 based Virus Like Particles, thusdemonstrating that the restriction involves post-entry steps of the viral life cycle. Notably, the accumulation of viralDNA, both total, integrated and 2-LTR circles, was strongly impaired by neutralization of CCL2. Looking for correlates ofHIV-1 DNA accumulation inhibition, we found that the antiviral effect of CCL2 neutralization was independent of themodulation of SAMHD1 expression or function. Conversely, a strong and selective induction of APOBEC3A expression,to levels comparable to those of freshly isolated monocytes, was associated with the inhibition of HIV-1 replicationmediated by CCL2 blocking. Interestingly, the CCL2 neutralization mediated increase of APOBEC3A expression was typeI IFN independent. Moreover, the transcriptome analysis of the effect of CCL2 blocking on global gene expressionrevealed that the neutralization of this chemokine resulted in the upmodulation of additional genes involved in thedefence response to viruses.Conclusions:Neutralization of endogenous CCL2 determines a profound restriction of HIV-1 replication in primaryMDM affecting post-entry steps of the viral life cycle with a mechanism independent of SAMHD1. In addition, CCL2blocking is associated with induction of APOBEC3A expression, thus unravelling a novel mechanism which mightcontribute to regulate the expression of innate intracellular viral antagonistsin vivo. Thus, our study may potentially leadto the development of new therapeutic strategies for enhancing innate cellular defences against HIV-1 and protecting macrophages from infection