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Di solito, il compito attribuito all’incipit di un’introduzione è quello di fornire al lettore una definizione sintetica ed efficace del principale oggetto di analisi di un testo. Nel caso della smart city l’impresa appare, secondo gli autori, quasi sisifea. L’espressione smart city non rimanda a un concetto universalmente condiviso ma, a partire dagli anni Novanta, è stata generica- mente utilizzata per riferirsi a uno spazio urbano all’interno del quale, grazie alla rivoluzione delle ICT (Information and Communication Technologies), i cittadini possono usufruire di maggiori servizi erogati in tempi rapidi. Se nel villaggio globale teorizzato da McLuhan (1967) la comunicazione era soprattutto unidirezionale dal centro alla periferia, come nel caso della televisione, dei giornali e delle radio, nell’epoca della smart city l’informatica diffusa sembra essere in grado di sviluppare una struttura connettiva multidirezionale che garantisce scambi costanti di dati e una sovrapposizione tra spazi fisici e virtuali (Ratti 2017). Il modello ideale di smart city prevede infatti la diffusione nel tessuto urbano di sensori (quali rilevatori divelocità, videocamere, misuratori dell’aria o del traffico) che sono in grado di registrare informazioni, trasmetterle e, soprattutto, analizzarle attraverso algoritmi. L’interazione di questi sensori con i dati forniti dai cittadini, magari attraverso i loro dispositivi smart di uso quotidiano, garantirebbe una fruizione degli spazi pubblici capace di adattarsi in tempo reale alle esigenze degli utenti. In questo senso, la smartness2 delle città migliorerebbe la vita degli abitanti in diversi ambiti (Mosannenzadeh, Vettorato 2014; Papa, Gargiulo, Battara 2016)): dalla mobilità e trasporto pubblico alla gestione e distribuzione dell’energia, dalla sicurezza alla gestione ambientale e alla comunicazione.

Questo articolo riflette sul contributo che lo sguardo antropologico può apportare al dibattito interdisciplinare attorno alla smart city e sui quadri interpretativi attraverso i quali approcciarsi etnograficamente all’integrazione delle tecnologie dell’informazione e della comunicazione nel tessuto cittadino. Il testo ricostruisce il dibattito attorno alla nuova policy urbana, mettendo in luce la contrapposizione tra coloro che vedono nella smart city una risposta ai bisogni di inclusione sociale, sostenibilità ambientale e sviluppo economico, e quegli studi critici che ne mettono in luce le potenziali forme di controllo ed esclusione. Il saggio sottolinea come entrambe le posizioni si fondino su uno sguardo in gran parte interno al momento della progettazione e suggerisce di non restare abbagliati dall’autorappresentazione del nuovo paradigma urbano come forza omogeneizzante e globalizzante. Attraverso l’analisi di alcuni lavori etnografici, il testo sottolinea l’importanza di sviluppare un approccio teorico e metodologico “non-smart-centrico” che possa (ri)comprendere le dinamiche di smartizzazione all’interno di più lunghi e sedimentati processi di costruzione della località, facendo emergere gli immaginari prodotti dalle politiche smart, gli usi informali e imprevisti delle tecnologie e il modo in cui questi contribuiscono a ridefinire il senso dei luoghi. This article reflects on the contribution that cultural anthropology brings to the interdisciplinary debate on the smart city, and the analytical frameworks through which we can investigate through ethnography the dissemination of information and communication technologies within urban spaces. The essay retraces the debate on new urban policies, and highlights the dichotomy between those for whom the smart city is an instrument of social inclusion, environmental sustainability and economic development, and those who see its potential forms of control and exclusion. We argue that both tendencies share an analytical approach mainly focused on the moment of planning, which is unable to escape from the self-representation of the new urban paradigm as a globalizing and homogenizing force. Drawing from ethnographic cases, the article argues for a “non smart-centered” approach to investigate urban smartization in the context of long-term processes of place-making. This would shed light on the imaginaries produced by smart policies, ICT’s informal and unpredictable uses and the ways these (re-)shape senses of locality

Background: Dietary habits during pregnancy have been inconsistently linked to childhood acute myeloid leukemia (AML), given the putative intrauterine onset of the disease as a result of triggering events during the critical period of fetal hematopoiesis. We investigated the potential association of maternal coffee and tea consumption during pregnancy with childhood AML risk, pooling primary data from eight case-control studies participating in the Childhood Leukemia International Consortium. Methods: Information on coffee and/or tea consumption was available for 444 cases and 1255 age- and sex-matched controls, on coffee consumption for 318 cases and 971 controls and on tea consumption for 388 cases and 932 controls. Categories for cups of daily coffee/tea consumption were created in order to explore potential dose-response associations. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using logistic regression. Results: Associations were found neither in the analysis on coffee or tea nor in the analysis on coffee only consumption (any versus no). A positive association with increasing coffee intake was observed (>1 cup per day; OR: 1.40, 95% CI: 1.03–1.92, increment of one cup per day; OR: 1.18, 95% CI: 1.01–1.39). No associations were observed with tea consumption. Interaction analyses showed non-significant associations between coffee/tea and smoking. Hyperdiploidy was inversely associated with tea consumption, with other cytogenetic markers having no association with coffee/tea. Conclusion: Given the widespread consumption of caffeinated beverages among pregnant women, our finding is of important public health relevance, suggesting adverse effects of maternal coffee consumption during pregnancy in the offspring. © 2019

IMPORTANCE Molecular diagnosis is difficult to achieve in disease groups with a highly heterogeneous genetic background, such as cerebellar ataxia (CA). In many patients, candidate gene sequencing or focused resequencing arrays do not allow investigators to reach a genetic conclusion. OBJECTIVES To assess the efficacy of exome-targeted capture sequencing to detect mutations in genes broadly linked to CA in a large cohort of undiagnosed patients and to investigate their prevalence. DESIGN, SETTING, AND PARTICIPANTS Three hundred nineteen index patients with CA and without a history of dominant transmission were included in the this cohort study by the Spastic Paraplegia and Ataxia Network. Centralized storage was in the DNA and cell bank of the Brain and Spine Institute, Salpetriere Hospital, Paris, France. Patients were classified into 6 clinical groups, with the largest being those with spastic ataxia (ie, CA with pyramidal signs [n = 100]). Sequencing was performed from January 1, 2014, through December 31, 2016. Detected variants were classified as very probably or definitely causative, possibly causative, or of unknown significance based on genetic evidence and genotype-phenotype considerations. MAIN OUTCOMES AND MEASURES Identification of variants in genes broadly linked to CA, classified in pathogenicity groups. RESULTS The 319 included patients had equal sex distribution (160 female [50.2%] and 159 male patients [49.8%]; mean [SD] age at onset, 27.9 [18.6] years). The age at onset was younger than 25 years for 131 of 298 patients (44.0%) with complete clinical information. Consanguinity was present in 101 of 298 (33.9%). Very probable or definite diagnoses were achieved for 72 patients (22.6%), with an additional 19 (6.0%) harboring possibly pathogenic variants. The most frequently mutated genes were SPG7 (n = 14), SACS (n = 8), SETX (n = 7), SYNE1 (n = 6), and CACNA1A (n = 6). The highest diagnostic rate was obtained for patients with an autosomal recessive CA with oculomotor apraxia-like phenotype (6 of 17 [35.3%]) or spastic ataxia (35 of 100 [35.0%]) and patients with onset before 25 years of age (41 of 131 [31.3%]). Peculiar phenotypes were reported for patients carrying KCND3 or ERCC5 variants. CONCLUSIONS AND RELEVANCE Exome capture followed by targeted analysis allows the molecular diagnosis in patients with highly heterogeneous mendelian disorders, such as CA, without prior assumption of the inheritance mode or causative gene. Being commonly available without specific design need, this procedure allows testing of a broader range of genes, consequently describing less classic phenotype-genotype correlations, and post hoc reanalysis of data as new genes are implicated in the disease. © 2018 American Medical Association. All rights reserved.

BACKGROUND AND PURPOSE: Duchenne muscular dystrophy (DMD), caused by dystrophin deficiency, results in chronic inflammation and irreversible skeletal muscle degeneration. Moreover, the associated impairment of autophagy greatly contributes to the aggravation of muscle damage. We explored the possibility of using non-euphoric compounds present in Cannabis sativa, cannabidiol (CBD), cannabidivarin (CBDV) and tetrahydrocannabidivarin (THCV), to reduce inflammation, restore functional autophagy and positively enhance muscle function in vivo. EXPERIMENTAL APPROACH: Using quantitative PCR, western blots and [Ca2+ ]i measurements, we explored the effects of CBD and CBDV on the differentiation of both murine and human skeletal muscle cells as well as their potential interaction with TRP channels. Male dystrophic mdx mice were injected i.p. with CBD or CBDV at different stages of the disease. After treatment, locomotor tests and biochemical analyses were used to evaluate their effects on inflammation and autophagy. KEY RESULTS: CBD and CBDV promoted the differentiation of murine C2C12 myoblast cells into myotubes by increasing [Ca2+ ]i mostly via TRPV1 activation, an effect that undergoes rapid desensitization. In primary satellite cells and myoblasts isolated from healthy and/or DMD donors, not only CBD and CBDV but also THCV promoted myotube formation, in this case, mostly via TRPA1 activation. In mdx mice, CBD (60 mg·kg-1 ) and CBDV (60 mg·kg-1 ) prevented the loss of locomotor activity, reduced inflammation and restored autophagy. CONCLUSION AND IMPLICATIONS: We provide new insights into plant cannabinoid interactions with TRP channels in skeletal muscle, highlighting a potential opportunity for novel co-adjuvant therapies to prevent muscle degeneration in DMD patients.[object Object]

The associations between childhood acute lymphoblastic leukemia (ALL) and several factors related to early stimulation of the immune system, that is, farm residence and regular contacts with farm animals (livestock, poultry) or pets in early childhood, were investigated using data from 13 case–control studies participating in the Childhood Leukemia International Consortium. The sample included 7847 ALL cases and 11,667 controls aged 1–14 years. In all studies, the data were obtained from case and control parents using standardized questionnaires. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by unconditional logistic regression adjusted for age, sex, study, maternal education, and maternal age. Contact with livestock in the first year of life was inversely associated with ALL (OR = 0.65, 95% CI: 0.50, 0.85). Inverse associations were also observed for contact with dogs (OR = 0.92, 95% CI: 0.86, 0.99) and cats (OR = 0.87, 95% CI: 0.80, 0.94) in the first year of life. There was no evidence of a significant association with farm residence in the first year of life. The findings of these large pooled and meta-analyses add additional evidence to the hypothesis that regular contact with animals in early childhood is inversely associated with childhood ALL occurrence which is consistent with Greaves’ delayed infection hypothesis. © 2018 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.

Purpose: The early onset of childhood acute lymphoblastic leukemia (ALL) suggests that critical exposures occurring during pregnancy may increase risk. We investigated the effects of maternal coffee and tea consumption during pregnancy on ALL risk by pooling data from eight case–control studies participating in the Childhood Leukemia International Consortium. Method: Data on maternal coffee intake were available for 2,552 cases and 4,876 controls, and data on tea intake were available for 2,982 cases and 5,367 controls. Coffee and tea intake was categorized into 0, > 0–1, > 1–2, and > 2 cups/day, and covariates were combined and harmonized. Data on genetic variants in NAT2, CYP1A1, and NQO1 were also available in a subset. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using unconditional logistic regression, and linear trends across categories were assessed. Results: No association was seen with ‘any’ maternal coffee consumption during pregnancy, but there was evidence of a positive exposure–response; the pooled OR for > 2 cups/day versus none was 1.27 (95% CI 1.09–1.43), p trend = 0.005. No associations were observed with tea consumption. No interactions were seen between coffee or tea intake and age, maternal smoking or genotype, and there was little or no evidence that associations with coffee or tea differed among cases with and without chromosomal translocations. Conclusions: Despite some limitations, our findings suggest that high coffee intake during pregnancy may increase risk of childhood ALL. Thus, current advice to limit caffeine intake during pregnancy to reduce risk of preterm birth may have additional benefits. © 2018, Springer International Publishing AG, part of Springer Nature.