134,018 research outputs found
Introduzione
No full textIn età moderna e contemporanea il Mediterraneo ha rappresentato uno dei crocevia più importanti dell’economia mondiale, e la sua popolazione ne ha utilizzato le acque, che si insinuano profondamente tra coste, promontori e arcipelaghi, per operare un’efficace redistribuzione dei prodotti provenienti dai tre continenti che su di esso si affacciano. La navigazione ha consentito nel corso dei secoli l’integrazione dei mercati e ha favorito l’urbanizzazione, incentivando la specializzazione e la divisione del lavoro. Intorno alla metà dell’Ottocento, l’intensificazione degli scambi legati alla rivoluzione dei trasporti marittimi e all’adozione di politiche liberiste ha incrementato la portata dei flussi commerciali. L’apertura del Canale di Suez ha, inoltre, restituito nuova vitalità al Mediterraneo all’interno del sistema degli scambi internazionali.
Alla luce di tali considerazioni, le relazioni contenute in questo volume si raccolgono intorno a tre filoni di ricerca: le reti marittime come punto di riferimento per gli scambi commerciali, le aree portuali come fulcro dello sviluppo economico e, infine, il contributo dei servizi e del turismo all’incremento dei rapporti economici tra le diverse aree del Mediterraneo
The Crisis in Italy. Anthropological Insights on Changes of Work, Enterprise and Life Horizons
No full textIntroduction [to Positioning the self and others. Linguistic Perspectives]
No full textThis chapter introduces to main topics of the volume, which aims to focus specifically on the linguistic means used to index the relationship between the self and other(s) in different types of communicative activity. The volume makes no claims to exhaustivity. The linguistic features which primarily emerged as relevant from the different contributions are : a) T/V address terms and vocatives, b) pragmatic markers c) code switching/code choice and d) orthography. These elements relate, in the case of a), to the conventionalised encoding of social hierarchies and power relations, in the case of b), to stance-taking and social indexicalisation and, in the case of c) and d), to more broadly circulating language ideologies
Synergistic combination of N-acetylcysteine and ribavirin to protect from lethal influenza viral infection in a mouse model
No full text: Oxidative stress is implicated in the pathogenesis of pulmonary damage during viral infections. In a previous study we observed a significant improvement of survival of influenza-infected mice with NAC, 1g/kg divided in two daily administrations, for 8 days including a pretreatment on day 1 before infection. In order to test NAC in a more realistic model, we studied the effect of combined treatment with NAC and the antiviral drug, ribavirin. Since in the present work we wanted to test a possible synergistic effect by combination of NAC and ribavirin, we used a different NAC's treatment regimen (1 g/kg, once a day for 4 days) that, alone, did not significantly protect mice from death. Mice (12 per group) infected intranasally with a lethal dose of influenza A virus APR/8. NAC was given as a single daily dose of 1000 mg/kg starting from 4 h after infection and until day 4 after infection, in association with ribavirin (100 mg/kg, i.p.). End-point evaluation was 14-day survival. With this schedule survival in infected mice was 17%, it was not significantly changed by NAC (25%). Survival increased to 58% with ribavirin and to 92% (n=12) with a combined treatment with ribavirin and NAC. This suggest that antioxidant therapy can increase survival by either improving the defenses against virus or by protecting from the pathogenesis of lung inflammation
Parkinson’s Disease, Parkinsonisms, and Mitochondria: the Role of Nuclear and Mitochondrial DNA
No full textPurpose of Review: Overwhelming evidence indicates that mitochondrial dysfunction is a central factor in Parkinson’s disease (PD) pathophysiology. This paper aims to review the latest literature published, focusing on genetic defects and expression alterations affecting mitochondria-associated genes, in support of their key role in PD pathogenesis. Recent Findings: Thanks to the use of new omics approaches, a growing number of studies are discovering alterations affecting genes with mitochondrial functions in patients with PD and parkinsonisms. These genetic alterations include pathogenic single-nucleotide variants, polymorphisms acting as risk factors, and transcriptome modifications, affecting both nuclear and mitochondrial genes. Summary: We will focus on alterations of mitochondria-associated genes described by studies conducted on patients or on animal/cellular models of PD or parkinsonisms. We will comment how these findings can be taken into consideration for improving the diagnostic procedures or for deepening our knowledge on the role of mitochondrial dysfunctions in PD
Demystifying Oxidative Stress
No full text: The hypothesis that reactive oxygen species (ROS) can be not just associated with but causally implicated in disease was first made in 1956, but so far, the oxidative stress theory of disease has not led to major therapeutic breakthrough, and the use of antioxidant is now confined to the field of complementary medicine. This chapter reviews the lack of high-level clinical evidence for the effectiveness of antioxidants in preventing disease and the epistemological problems of the oxidative stress theory of disease. We conclude on possible ways forward to test this hypothesis with approaches that take into account personalized medicine. The previous oxidative stress model has helped neither to diagnose nor to treat possibly ROS-related or ROS-dependent diseases. The redox balance concept that low ROS levels are beneficial or tolerable and high levels are disease triggers and best reduced is apparently wrong. Physiological ROS signalling may become dysfunctional or a disease trigger by at least five mechanisms: a physiological source may appear at an unphysiological site, a physiological source may be underactivated (less common) or overactivated (more common), a new source may appear, a physiological source may be overactivated or underactivated, and a toxifying enzyme may convert an ROS signal molecule into a more reactive molecule. The latter three mechanisms may reach a physiological or nonphysiological target. All of these dysregulations may be the direct and essential cause of a disease (rarely the case) or just a secondary epiphenomenon, which will disappear once the non-ROS-related cause of the disease is cured (much more common). Importantly, these mechanisms are the same for almost every signalling system. Causal target validation (sources, toxifiers and targets) is essential in order to identify effective drugs and therapies for ROSopathies
Disease-modifying drugs in Alzheimer's disease
No full textAlzheimer's disease (AD) is an age-dependent neurodegenerative disorder and the most common cause of dementia. The early stages of AD are characterized by short-term memory loss. Once the disease progresses, patients experience difficulties in sense of direction, oral communication, calculation, ability to learn, and cognitive thinking. The median duration of the disease is 10 years. The pathology is characterized by deposition of amyloid beta peptide (so-called senile plaques) and tau protein in the form of neurofibrillary tangles. Currently, two classes of drugs are licensed by the European Medicines Agency for the treatment of AD, ie, acetylcholinesterase inhibitors for mild to moderate AD, and memantine, an N-methyl-D-aspartate receptor antagonist, for moderate and severe AD. Treatment with acetylcholinesterase inhibitors or memantine aims at slowing progression and controlling symptoms, whereas drugs under development are intended to modify the pathologic steps leading to AD. Herein, we review the clinical features, pharmacologic properties, and cost-effectiveness of the available acetylcholinesterase inhibitors and memantine, and focus on disease-modifying drugs aiming to interfere with the amyloid beta peptide, including vaccination, passive immunization, and tau deposition
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