Smart cities and the urban digital divide

The debate on urban smartness as an instrument for managing more efficient cities has been revolving around the notion that Smart Cities might be causing an increase in inequalities. This effect would be caused by the role played in smart urban transformations by Multi-National Corporations, which would be influencing local policymakers’ agendas. In this work we empirically verify whether smart urban characteristics are associated with an increase in urban inequalities along the digital divide dimension among urban dwellers. To this aim, we exploit a large database of 181 European cities, with data on smart urban characteristics, along with measures of the digital divide obtained with the use of survey data carried out at the European Union level. Results show a negative causal relation between the level of urban smartness and the digital divide within-EU cities. Our findings are robust to a number of robustness checks

Industrial Clusters and Innovation: An Evaluation and Implications for Economic Cohesion

Texto dispoñible en galego, español e inglésEste traballo estuda o papel dos clusters industriais para fomentar a innovación rexional e a cohesión económica en Europa. A partir dunha visión de conxunto dos clusters industriais na UE, na que se destacan as fortalezas e debilidades das aglomeracións de empresas, investigamos empiricamente a forma en que os clusters e as características rexionais afectan ao investimento en I+D e ao output de innovación e, así mesmo, investigamos o papel que desempeñan no impulso da cohesión económica. Atopamos que a existencia e o tamaño dos clusters rexionais fomentan de maneira significativa a innovación rexional en Europa. Porén, ten importancia a industria na que se especializan as distintas rexións. En particular, a especialización en clusters de tecnoloxía media-alta e alta parece crear unha contorna máis favorable para a innovación e para a I+D. Por último, a presenza de clusters nunha rexión asóciase positivamente con maiores niveis de empregoEste trabajo estudia el papel de los clusters industriales para fomentar la innovación regional y la cohesión económica en Europa. A partir de una visión de conjunto de los clusters industriales en la UE, en la que se destacan las fortalezas y debilidades de las aglomeraciones de empresas, investigamos empíricamente la forma en que los clusters y las características regionales afectan a la inversión en I+D y al output de innovación y, asimismo, investigamos el papel que desempeñan en el impulso de la cohesión económica. Encontramos que la existencia y el tamaño de los clusters regionales fomentan de manera significativa la innovación regional en Europa. Sin embargo, tiene importancia la industria en la que se especializan las distintas regiones. En particular, la especialización en clusters de tecnología media-alta y alta parece crear un entorno más favorable para la innovación y la I+D. Por último, la presencia de clusters en una región se asocia positivamente con mayores niveles de empleoThis paper studies the role of industrial clusters in stimulating regional innovation and economic cohesion in Europe. Starting from an overview of industrial clusters in the EU, in which we highlight the strengths and weaknesses of agglomerations of firms, we empirically investigate how cluster and regional characteristics influence R&D investment and innovation output and the role they play in fostering economic cohesion. We find that the presence and size of clusters significantly enhance regional innovation in Europe; however, the industry in which regions specialize matters. In particular, specialization in medium- high and high-technology clusters seems to create a better environment for innovation and R&D. Finally, the presence of clusters in a region is positively associated with higher levels of employmentS

ERα-LBD, an isoform of estrogen receptor alpha, promotes breast cancer proliferation and endocrine resistance

Estrogen receptor alpha (ER alpha) drives mammary gland development and breast cancer (BC) growth through an evolutionarily conserved linkage of DNA binding and hormone activation functions. Therapeutic targeting of the hormone binding pocket is a widely utilized and successful strategy for breast cancer prevention and treatment. However, resistance to this endocrine therapy is frequently encountered and may occur through bypass or reactivation of ER-regulated transcriptional programs. We now identify the induction of an ER alpha isoform, ER alpha-LBD, that is encoded by an alternative ESR1 transcript and lacks the activation function and DNA binding domains. Despite lacking the transcriptional activity, ER alpha-LBD is found to promote breast cancer growth and resistance to the ER alpha antagonist fulvestrant. ER alpha-LBD is predominantly localized to the cytoplasm and mitochondria of BC cells and leads to enhanced glycolysis, respiration and stem-like features. Intriguingly, ER alpha-LBD expression and function does not appear to be restricted to cancers that express full length ER alpha but also promotes growth of triple-negative breast cancers and ER alpha-LBD transcript (ESR1-LBD) is also present in BC samples from both ER alpha(+) and ER alpha(-) human tumors. These findings point to ER alpha-LBD as a potential mediator of breast cancer progression and therapy resistance

CYP17, GSTP1, PON1 and GLO1 gene polymorphisms as risk factors for breast cancer: an Italian case-control study

<p>Abstract</p> <p>Background</p> <p>Estrogens, environmental chemicals with carcinogenic potential, as well as oxidative and carbonyl stresses play a very important role in breast cancer (BC) genesis and progression. Therefore, polymorphisms of genes encoding enzymes involved in estrogen biosynthesis pathway and in the metabolic activation of pro-carcinogens to genotoxic intermediates, such as cytochrome P450C17α (CYP17), endogenous free-radical scavenging systems, such as glutathione S-transferase (GSTP1) and paraoxonase 1 (PON1), and anti-glycation defenses, such as glyoxalase I (GLO1), could influence individual susceptibility to BC. In the present case-control study, we investigated the possible association of CYP17 A1A2, GSTP1 ILE105VAL, PON1 Q192R or L55M, and GLO1 A111E polymorphisms with the risk of BC.</p> <p>Methods</p> <p>The above-said five polymorphisms were characterized in 547 patients with BC and in 544 healthy controls by PCR/RFLP methods, using DNA from whole blood. To estimate the relative risks, Odds ratios and 95% confidence intervals were calculated using unconditional logistic regression after adjusting for the known risk factors for BC.</p> <p>Results</p> <p>CYP17 polymorphism had no major effect in BC proneness in the overall population. However, it modified the risk of BC for certain subgroups of patients. In particular, among premenopausal women with the A1A1 genotype, a protective effect of later age at menarche and parity was observed. As to GSTP1 and PON1 192 polymorphisms, the mutant Val and R alleles, respectively, were associated with a decreased risk of developing BC, while polymorphisms in PON1 55 and GLO1 were associated with an increased risk of this neoplasia. However, these findings, while nominally significant, did not withstand correction for multiple testing.</p> <p>Conclusion</p> <p>Genetic polymorphisms in biotransformation enzymes CYP17, GSTP1, PON1 and GLO1 could be associated with the risk for BC. Although significances did not withstand correction for multiple testing, the results of our exploratory analysis warrant further studies on the above mentioned genes and BC.</p

Noncomparabilities & Non Standard Logics

Many normative theories set forth in the welfare economics, distributive justice and cognate literatures posit noncomparabilities or incommensurabilities between magnitudes of various kinds. In some cases these gaps are predicated on metaphysical claims, in others upon epistemic claims, and in still others upon political-moral claims. I show that in all such cases they are best given formal expression in nonstandard logics that reject bivalence, excluded middle, or both. I do so by reference to an illustrative case study: a contradiction known to beset John Rawls\u27s selection and characterization of primary goods as the proper distribuendum in any distributively just society. The contradiction is avoided only by reformulating Rawls\u27s claims in a nonstandard form, which form happens also to cohere quite attractively with Rawls\u27s intuitive argumentation on behalf of his claims

Association of kidney disease measures with risk of renal function worsening in patients with type 1 diabetes

Background: Albuminuria has been classically considered a marker of kidney damage progression in diabetic patients and it is routinely assessed to monitor kidney function. However, the role of a mild GFR reduction on the development of stage 653 CKD has been less explored in type 1 diabetes mellitus (T1DM) patients. Aim of the present study was to evaluate the prognostic role of kidney disease measures, namely albuminuria and reduced GFR, on the development of stage 653 CKD in a large cohort of patients affected by T1DM. Methods: A total of 4284 patients affected by T1DM followed-up at 76 diabetes centers participating to the Italian Association of Clinical Diabetologists (Associazione Medici Diabetologi, AMD) initiative constitutes the study population. Urinary albumin excretion (ACR) and estimated GFR (eGFR) were retrieved and analyzed. The incidence of stage 653 CKD (eGFR &lt; 60 mL/min/1.73 m2) or eGFR reduction &gt; 30% from baseline was evaluated. Results: The mean estimated GFR was 98 \ub1 17 mL/min/1.73m2 and the proportion of patients with albuminuria was 15.3% (n = 654) at baseline. About 8% (n = 337) of patients developed one of the two renal endpoints during the 4-year follow-up period. Age, albuminuria (micro or macro) and baseline eGFR &lt; 90 ml/min/m2 were independent risk factors for stage 653 CKD and renal function worsening. When compared to patients with eGFR &gt; 90 ml/min/1.73m2 and normoalbuminuria, those with albuminuria at baseline had a 1.69 greater risk of reaching stage 3 CKD, while patients with mild eGFR reduction (i.e. eGFR between 90 and 60 mL/min/1.73 m2) show a 3.81 greater risk that rose to 8.24 for those patients with albuminuria and mild eGFR reduction at baseline. Conclusions: Albuminuria and eGFR reduction represent independent risk factors for incident stage 653 CKD in T1DM patients. The simultaneous occurrence of reduced eGFR and albuminuria have a synergistic effect on renal function worsening

Coulomb dissociation of N 20,21

Neutron-rich light nuclei and their reactions play an important role in the creation of chemical elements. Here, data from a Coulomb dissociation experiment on N20,21 are reported. Relativistic N20,21 ions impinged on a lead target and the Coulomb dissociation cross section was determined in a kinematically complete experiment. Using the detailed balance theorem, the N19(n,γ)N20 and N20(n,γ)N21 excitation functions and thermonuclear reaction rates have been determined. The N19(n,γ)N20 rate is up to a factor of 5 higher at

Analysis of shared common genetic risk between amyotrophic lateral sclerosis and epilepsy

Because hyper-excitability has been shown to be a shared pathophysiological mechanism, we used the latest and largest genome-wide studies in amyotrophic lateral sclerosis (n = 36,052) and epilepsy (n = 38,349) to determine genetic overlap between these conditions. First, we showed no significant genetic correlation, also when binned on minor allele frequency. Second, we confirmed the absence of polygenic overlap using genomic risk score analysis. Finally, we did not identify pleiotropic variants in meta-analyses of the 2 diseases. Our findings indicate that amyotrophic lateral sclerosis and epilepsy do not share common genetic risk, showing that hyper-excitability in both disorders has distinct origins