Family dissolution and labour supply decisions over the life cycle

Life-history data can clarify the consequences of household split and divorce on the probability of working. Indeed, employment choices are affected by the occurrence of family dissolution episodes. The effect is stronger for women. The magnitude of this effect increases with the presence of children

Divorce and well-being. Disentangling the role of stress and socio economic status

We investigate the happiness variations associated with divorce by drawing data from a retrospective panel dataset based on the third wave of the Survey of Health, Ageing and Retirement in Europe (SHARE) and covering 14 European countries. This dataset proposes as a powerful tool to control for reporting style heterogeneity in happiness self-evaluations. Indeed, in addition to individual fixed-effects, we control for full migration trajectories in order to remove bias in well-being evaluations produced by cross-country heterogeneity in the cultural norms and societal values individuals have been exposed during their life-cycle. Happiness is found to increase in the period after divorce for both men and women. We show that this pattern goes through a decrease in stress and financial hardship

INSTITUCIONALIZAÇÃO DA ASSEMBLEIA LEGISLATIVA DO ESTADO DE SÃO PAULO (ALESP): EVIDÊNCIAS DE UM PARLAMENTO SUBNACIONAL BRASILEIRO

O artigo procura mensurar o grau de institucionalização da Assembleia Legislativa do Estado de São Paulo (ALESP) no período recente a partir de indicadores consagrados da literatura em ciência política. Além de uma breve revisão teórica sobre o conceito, são apresentados resultados empíricos que demonstram crescente institucionalização deste Poder Legislativo subnacional. Ao final, são discutidas as implicações destes achados a partir da crítica à própria noção de institucionalização e de sua aplicação para a compreensão da dinâmica do sistema político e federativo brasileiros. 

Boosting 5G mm-Wave IAB Reliability with Reconfigurable Intelligent Surfaces

The introduction of the mm-Wave spectrum into 5G NR promises to bring about unprecedented data throughput to future mobile wireless networks but comes with several challenges. Network densification has been proposed as a viable solution to increase RAN resilience, and the newly introduced IAB is considered a key enabling technology with compelling cost-reducing opportunities for such dense deployments. Reconfigurable Intelligent Surfaces (RIS) have recently gained extreme popularity as they can create Smart Radio Environments by EM wave manipulation and behave as inexpensive passive relays. However, it is not yet clear what role this technology can play in a large RAN deployment. With the scope of filling this gap, we study the blockage resilience of realistic mm-Wave RAN deployments that use IAB and RIS. The RAN layouts have been optimised by means of a novel mm-Wave planning tool based on MILP formulation. Numerical results show how adding RISs to IAB deployments can provide high blockage resistance levels while significantly reducing the overall network planning cost

Ranolazine Attenuates Trastuzumab-Induced Heart Dysfunction by Modulating ROS Production

The ErbB2 blocker trastuzumab improves survival in oncologic patients, but can cause cardiotoxicity. The late Na+ current inhibitor ranolazine has been shown to counter experimental HF, including doxorubicin cardiotoxicity (a condition characterized by derangements in redox balance), by lowering the levels of reactive oxygen species (ROS). Since ErbB2 can modulate ROS signaling, we tested whether trastuzumab cardiotoxicity could be blunted by ranolazine via redox-mediated mechanisms. Trastuzumab decreased fractional shortening and ejection fraction in mice, but ranolazine prevented heart dysfunction when co-administered with trastuzumab. Trastuzumab cardiotoxicity was accompanied by elevations in natriuretic peptides and matrix metalloproteinase 2 (MMP2) mRNAs, which were not elevated with co-treatment with ranolazine. Trastuzumab also increased cleavage of caspase-3, indicating activation of the proapoptotic machinery. Again, ranolazine prevented this activation. Interestingly, Neonatal Rat Ventricular Myocytes (NRVMs), labeled with MitoTracker Red and treated with trastuzumab, showed only a small increase in ROS compared to baseline conditions. We then stressed trastuzumab-treated cells with the beta-agonist isoproterenol to increase workload, and we observed a significant increase of probe fluorescence, compared with cells treated with isoproterenol alone, reflecting induction of oxidative stress. These effects were blunted by ranolazine, supporting a role for INa inhibition in the regulation of redox balance also in trastuzumab cardiotoxicity

A chemical threshold controls nanocrystallization and degassing behaviour in basalt magmas

An increasing number of studies are being presented demonstrating that volcanic glasses can be heterogeneous at the nanoscale. These nano-heterogeneities can develop both during viscosity measurements in the laboratory and during magma eruptions. Our multifaceted study identifies here total transition metal oxide content as a crucial compositional factor governing the tendency of basalt melts and glasses towards nanolitization: at both anhydrous and hydrous conditions, an undercooled trachybasalt melt from Mt. Etna readily develops nanocrystals whose formation also hampers viscosity measurements, while a similar but FeO- and TiO2-poorer basalt melt from Stromboli proves far more stable at similar conditions. We therefore outline a procedure to reliably derive pure liquid viscosity without the effect of nanocrystals, additionally discussing how subtle compositional differences may contribute to the different eruptive styles of Mt. Etna and Stromboli

MiR-221/222 target the DNA methyltransferase MGMT in glioma cells

Glioblastoma multiforme (GBM) is one of the most deadly types of cancer. To date, the best clinical approach for treatment is based on administration of temozolomide (TMZ) in combination with radiotherapy. Much evidence suggests that the intracellular level of the alkylating enzyme O6-methylguanine-DNA methyltransferase (MGMT) impacts response to TMZ in GBM patients. MGMT expression is regulated by the methylation of its promoter. However, evidence indicates that this is not the only regulatory mechanism present. Here, we describe a hitherto unknown microRNA-mediated mechanism of MGMT expression regulation. We show that miR-221 and miR-222 are upregulated in GMB patients and that these paralogues target MGMT mRNA, inducing greater TMZ-mediated cell death. However, miR-221/miR-222 also increase DNA damage and, thus, chromosomal rearrangements. Indeed, miR-221 overexpression in glioma cells led to an increase in markers of DNA damage, an effect rescued by re-expression of MGMT. Thus, chronic miR-221/222-mediated MGMT downregulation may render cells unable to repair genetic damage. This, associated also to miR-221/222 oncogenic potential, may poor GBM prognosis

RYK promotes the stemness of glioblastoma cells via the WNT/ \u3b2-catenin pathway

Glioblastoma multiforme (GBM) is characterized by a strong self-renewal potential and a poor differentiation state. Since receptor-like tyrosine kinase (RYK) activates the WNT/\u3b2-catenin pathway essential for cancer stem cell maintenance, we evaluated its contribution in conferring stemness to GBM cells. Here, we report that Ryk (related-to-receptor tyrosine kinase), an atypical tyrosine kinase receptor, is upregulated in samples from GBM patients as well as in GSCs. Ryk overexpression confers stemness properties to GBM cells through the modulation of the canonical Wnt signaling and by promoting the activation of pluripotency-related transcription factor circuitry and neurosphere formation ability. In contrast, siRNA-mediated knockdown of Ryk expression suppresses this stem-like phenotype. Rescue experiments reveal that stemness-promoting activity of Ryk is attributable, at least in part, to \u3b2-catenin stabilization. Furthermore, Ryk overexpression improves cell motility and anchorage independent cell growth. Taken together, our findings demonstrate that Ryk promotes stem cell-like and tumorigenic features to glioma cells its essential for the maintenance of GSCs and could be a target of novel therapies

miR-340 predicts glioblastoma survival and modulates key cancer hallmarks through down-regulation of NRAS

Glioblastoma is the most common primary brain tumor in adults; with a survival rate of 12 months from diagnosis. However, a small subgroup of patients, termed long-term survivors (LTS), has a survival rate longer then 12–14 months. There is thus increasing interest in the identification of molecular signatures predicting glioblastoma prognosis and in how to improve the therapeutic approach. Here, we report miR-340 as prognostic tumor-suppressor microRNA for glioblastoma. We analyzed microRNA expression in > 500 glioblastoma patients and found that although miR-340 is strongly down-regulated in glioblastoma overall, it is up-regulated in LTS patients compared to short-term survivors (STS). Indeed, miR-340 expression predicted better prognosis in glioblastoma patients. Coherently, overexpression of miR-340 in glioblastoma cells was found to produce a tumor-suppressive activity. We identified NRAS mRNA as a critical, direct target of miR-340: in fact, miR-340 negatively influenced multiple aspects of glioblastoma tumorigenesis by down-regulating NRAS and downstream AKT and ERK pathways. Thus, we demonstrate that expression of miR-340 in glioblastoma is responsible for a strong tumor-suppressive effect in LTS patients by down-regulating NRAS. miR-340 may thus represent a novel marker for glioblastoma diagnosis and prognosis, and may be developed into a tool to improve treatment of glioblastoma

MiR-221 promotes stemness of breast cancer cells by targeting DNMT3b

Cancer stem cells (CSCs) are a small part of the heterogeneous tumor cell population possessing self-renewal and multilineage differentiation potential as well as a great ability to sustain tumorigenesis. The molecular pathways underlying CSC phenotype are not yet well characterized. MicroRNAs (miRs) are small noncoding RNAs that play a powerful role in biological processes. Early studies have linked miRs to the control of self-renewal and differentiation in normal and cancer stem cells. We aimed to study the functional role of miRs in human breast cancer stem cells (BCSCs), also named mammospheres. We found that miR-221 was upregulated in BCSCs compared to their differentiated counterpart. Similarly, mammospheres from T47D cells had an increased level of miR-221 compared to differentiated cells. Transfection of miR-221 in T47D cells increased the number of mammospheres and the expression of stem cell markers. Among miR-221's targets, we identified DNMT3b. Furthermore, in BCSCs we found that DNMT3b repressed the expression of various stemness genes, such as Nanog and Oct 3/4, acting on the methylation of their promoters, partially reverting the effect of miR-221 on stemness. We hypothesize that miR-221 contributes to breast cancer tumorigenicity by regulating stemness, at least in part through the control of DNMT3b expression