Miracle-dz/UniFAR-FTUs huggingface dataset:
Posture Recognition Using the Interdistances Between Wearable Devices

Recognition of user's postures and activities is particularly important, as it allows applications to customize their operations according to the current situation. The vast majority of available solutions are based on wearable devices equipped with accelerometers and gyroscopes. In this article, a different approach is explored: The posture of the user is inferred from the interdistances between the set of devices worn by the user. Interdistances are first measured by using ultra-wideband transceivers operating in two-way ranging mode and then provided as input to a classifier that estimates current posture. An experimental evaluation shows that the proposed method is effective (up to $\sim 98.2\%$ accuracy), especially when using a personalized model. The method could be used to enhance the accuracy of activity recognition systems based on inertial sensors.
Bcl-2 Independence of Flavopiridol-induced Apoptosis

The new chemotherapeutic agent, flavopiridol, presently in clinical trials, has been extensively studied yet little is known about its mechanism of action. In this study we show that the induction of apoptosis by flavopiridol is largely independent of Bcl-2. This is indicated by the observation that neither overexpression nor the antisense oligonucleotide-mediated down-regulation of Bcl-2 had any effect on flavopiridol-induced cell killing. Our results suggest that flavopiridol can induce apoptosis through different pathways of caspase activation with caspase 8 playing a pivotal role. In human lung carcinoma cells, which contain high levels of endogenous Bcl-2 and lack procaspase 8, flavopiridol treatment leads to mitochondrial depolarization in the absence of cytochrome c release, followed by the activation of caspase 3 and cell death. These results clearly differ from observations made with other anti-tumor drugs and might explain, at least in part, the unusual anti-tumor properties of flavopiridol.
Gabapentin in the treatment of fibromyalgia: a randomized, double-blind, placebo-controlled, multicenter trial.

OBJECTIVE To assess the efficacy and safety of gabapentin in patients with fibromyalgia. METHODS A 12-week, randomized, double-blind study was designed to compare gabapentin (1,200-2,400 mg/day) (n=75 patients) with placebo (n=75 patients) for efficacy and safety in treating pain associated with fibromyalgia. The primary outcome measure was the Brief Pain Inventory (BPI) average pain severity score (range 0-10, where 0=no pain and 10=pain as bad as you can imagine). Response to treatment was defined as a reduction of >or=30% in this score. The primary analysis of efficacy for continuous variables was a longitudinal analysis of the intent-to-treat sample, with treatment-by-time interaction as the measure of effect. RESULTS Gabapentin-treated patients displayed a significantly greater improvement in the BPI average pain severity score (P=0.015; estimated difference between groups at week 12=-0.92 [95% confidence interval -1.75, -0.71]). A significantly greater proportion of gabapentin-treated patients compared with placebo-treated patients achieved response at end point (51% versus 31%; P=0.014). Gabapentin compared with placebo also significantly improved the BPI average pain interference score, the Fibromyalgia Impact Questionnaire total score, the Clinical Global Impression of Severity, the Patient Global Impression of Improvement, the Medical Outcomes Study (MOS) Sleep Problems Index, and the MOS Short Form 36 vitality score, but not the mean tender point pain threshold or the Montgomery Asberg Depression Rating Scale. Gabapentin was generally well tolerated. CONCLUSION Gabapentin (1,200-2,400 mg/day) is safe and efficacious for the treatment of pain and other symptoms associated with fibromyalgia.
Unemployment, wages and pensions

Abstract Empirical evidence has shown the existence of a negative relationship between the rates of unemployment and real wages. If pensions are computed according to the wages that workers have contributed, then the unemployment rates during working life may also influence the pensions to which they are entitled. Using data from 2005 to 2012 for the Spanish social security system, we estimate that the unemployment elasticity of real pension is −0.135. A 1% increase in unemployment rate is associated with a reduction in pension equal to 0.135%. In ‘normal times’, this value could be considered modest, but the Great Recession has increased dramatically the rate of unemployment. In 2012, the rate of unemployment in Spain had increased to 25.7% and in 2015, it had diminished to 20.9%. It is estimated that unemployment rate will not be returned to figures existing before the crisis until middle of the next decade. Moreover, the current reforms in social security systems could interact with the future effects of the current rates of unemployment and cause future pensions to be significantly lower than those estimated by individuals. The economic welfare of the future cohorts of retirees would then be significantly worsened.
Quality of life of patients with esophageal replacement for congenital and acquired esophageal anomalies.

AIM To assess the long-term quality of life (QoL) and symptoms experienced by patients who underwent esophageal replacement for congenital and acquired children esophageal pathology. MATERIAL AND METHODS The study group comprised 71 patients divided into 2 groups, group I: 34 patients who underwent gastric tube esophagoplasty, and group II: 37 patients who underwent colic tube esophagoplasty. QoL score was assessed using a 24-item original questionnaire covering aspects of eating, disease-specific symptoms, physical and psychological development, and social integration. RESULTS QoL scores based on patient and parental responses were very close. Long-term postoperative functional outcomes for the two groups were comparable. CONCLUSIONS The QoL scores and general life status were not influenced by the used technique and this pathology should be approached according to the particularity of each case and surgeon's personal experience and preference.
The Eaf3/5/7 Subcomplex Stimulates NuA4 Interaction with Methylated Histone H3 Lys-36 and RNA Polymerase II*

NuA4 is the only essential lysine acetyltransferase complex in Saccharomyces cerevisiae, where it has been shown to stimulate transcription initiation and elongation. Interaction with nucleosomes is stimulated by histone H3 Lys-4 and Lys-36 methylation, but the mechanism of this interaction is unknown. Eaf3, Eaf5, and Eaf7 form a subcomplex within NuA4 that may also function independently of the lysine acetyltransferase complex. The Eaf3/5/7 complex and the Rpd3C(S) histone deacetylase complex have both been shown to bind di- and trimethylated histone H3 Lys-36 stimulated by Eaf3. We investigated the role of the Eaf3/5/7 subcomplex in NuA4 binding to nucleosomes. Different phenotypes of eaf3/5/7Δ mutants support functions for the complex as both part of and independent of NuA4. Further evidence for Eaf3/5/7 within NuA4 came from mutations in the subcomplex leading to ∼40% reductions in H4 acetylation in bulk histones, probably caused by binding defects to both nucleosomes and RNA polymerase II. In vitro binding assays showed that Eaf3/5/7 specifically stimulates NuA4 binding to di- and trimethylated histone H3 Lys-36 and that this binding is important for NuA4 occupancy in transcribed ORFs. Consistent with the role of NuA4 in stimulating transcription elongation, loss of EAF5 or EAF7 resulted in a processivity defect. Overall, these results reveal the function of Eaf3/5/7 within NuA4 to be important for both NuA4 and RNA polymerase II binding.
The Term Structure of Currency Carry Trade Risk Premia

Fixing the investment horizon, the returns to currency carry trades decrease as the maturity of the foreign bonds increases. Across developed countries, the local currency term premia, which increase with the maturity of the bonds, offset the currency risk premia. Similarly, in the time-series, the predictability of foreign bond returns in dollars declines with the bonds’ maturities. Leading no-arbitrage models in international finance do not match the downward term structure of currency carry trade risk premia. We derive a simple preference-free condition that no-arbitrage models need to reproduce in the absence of carry trade risk premia on long-term bonds. (JEL E43, G12, G15)
Benefits of the Balancing Act: Motherhood, Employment and Mental Health

Benefits of the Balancing Act: Motherhood, Employment and Mental Health Katrina Leupp Chair of the Supervisory Committee: Professor Becky Pettit Department of Sociology Variant findings on the benefits and strains of combining employment and family roles encourage investigation into the mechanisms and conditions under which employment improves the well-being of individuals who perform the greatest amounts of family caregiving labor-mothers caring for children. In this dissertation, I explore the effects of employment on depressive symptoms in light of gendered parental responsibilities. Two possible mechanisms through which employment may confer mental health benefits are explored: identity accumulation, and for married women, gains in relative spousal resources. First, motivated by symbolic interaction perspectives on identity, I examine how the mental health effects of employment for mothers vary according to their attitudes about the compatibility of employment and childrearing. Secondly, I draw on household bargaining and resource perspectives to examine whether the increase in relative spousal earnings generated by employment are associated with fewer depressive symptoms among married women. Finally, I approach the social roles of parenthood and employment from a life course perspective, considering their effects on the distribution of depressive symptoms by age for men and women. These analyses enrich understandings of how and when employment improves mental well-being, and highlight the force of gendered parental responsibilities in shaping the effects of work and family roles.
The impact of dietary and lifestyle risk factors on risk of colorectal cancer: A quantitative overview of the epidemiological evidence

Colorectal cancer is a major cause of cancer mortality and is considered to be largely attributable to inappropriate lifestyle and behavior patterns. The purpose of this review was to undertake a comparison of the strength of the associations between known and putative risk factors for colorectal cancer by conducting 10 independent meta‐analyses of prospective cohort studies. Studies published between 1966 and January 2008 were identified through EMBASE and MEDLINE, using a combined text word and MESH heading search strategy. Studies were eligible if they reported estimates of the relative risk for colorectal cancer with any of the following: alcohol, smoking, diabetes, physical activity, meat, fish, poultry, fruits and vegetables. Studies were excluded if the estimates were not adjusted at least for age. Overall, data from 103 cohort studies were included. The risk of colorectal cancer was significantly associated with alcohol: individuals consuming the most alcohol had 60% greater risk of colorectal cancer compared with non‐ or light drinkers (relative risk 1.56, 95% CI 1.42–1.70). Smoking, diabetes, obesity and high meat intakes were each associated with a significant 20% increased risk of colorectal cancer (compared with individuals in the lowest categories for each) with little evidence of between‐study heterogeneity or publication bias. Physical activity was protective against colorectal cancer. Public‐health strategies that promote modest alcohol consumption, smoking cessation, weight loss, increased physical activity and moderate consumption of red and processed meat are likely to have significant benefits at the population level for reducing the incidence of colorectal cancer. © 2009 UICC
Proteomic identification of proteins translocated to membrane microdomains upon treatment of fibroblasts with the glycosphingolipid, C8‐β‐D‐lactosylceramide

Plasma membrane (PM) microdomains, including caveolae and other cholesterol‐enriched subcompartments, are involved in the regulation of many cellular processes, including endocytosis, attachment and signaling. We recently reported that brief incubation of human skin fibroblasts with the synthetic glycosphingolipid, D‐erythro‐octanoyl‐lactosylceramide (C8‐D‐e‐LacCer), stimulates endocytosis via caveolae and induces the appearance of micron‐size microdomains on the PM. To further understand the effects of C8‐D‐e‐LacCer treatment on PM microdomains, we used a detergent‐free method to isolate microdomain‐enriched membranes from fibroblasts treated ±C8‐D‐e‐LacCer, and performed 2‐DE and mass spectrophotometry to identify proteins that were altered in their distribution in microdomains. Several proteins were identified in the microdomain‐enriched fractions, including lipid transfer proteins and proteins related to the functions of small GTPases. One protein, Rho‐associated protein kinase 2 (ROCK2), was verified by Western blotting to occur in microdomain fractions and to increase in these fractions after D‐e‐LacCer treatment. Immunofluorescence revealed that ROCK2 exhibited an increased localization at or near the PM in C8‐D‐e‐LacCer‐treated cells. In contrast, ROCK2 distribution in microdomains was decreased by treatment of cells with C8‐L‐threo‐lactosylceramide, a glycosphingolipid with non‐natural stereochemistry. This study identifies new microdomain‐associated proteins and provides evidence that microdomains play a role in the regulation of the Rho/ROCK signaling pathway.
Impact of Device Layout and Annealing Process During the Passivation of Interface States in Presence of Silicon Nitride Layers

This paper reports the experimental evidence of anomalous electrical characteristics of large test structures for the characterization of both silicon-oxide-nitride-oxide-silicon (SONOS) and MOS gate stacks featuring nitride caps. The anomaly has been studied on devices featuring different layouts and it has been attributed to the property of silicon nitride layers to block the diffusion of hydrogen used for the passivation of the Si/SiO2 interface dangling bonds. Since the hydrogen passivation can occur only from the lateral sides of the device, our findings imply restrictions on the dimensions and on the layout of the test structures used to study the electrical properties of the gate stacks in SONOS or in large MOS devices featuring protective nitride caps.
Extracellular Matrix Secretion by Cardiac Fibroblasts: Role of MicroRNA-29b and MicroRNA-30c

Rationale: MicroRNAs (miRNAs), in particular miR-29b and miR-30c, have been implicated as important regulators of cardiac fibrosis. Objective: To perform a proteomics comparison of miRNA effects on extracellular matrix secretion by cardiac fibroblasts. Methods and Results: Mouse cardiac fibroblasts were transfected with pre-/anti-miR of miR-29b and miR-30c, and their conditioned medium was analyzed by mass spectrometry. miR-29b targeted a cadre of proteins involved in fibrosis, including multiple collagens, matrix metalloproteinases, and leukemia inhibitory factor, insulin-like growth factor 1, and pentraxin 3, 3 predicted targets of miR-29b. miR-29b also attenuated the cardiac fibroblast response to transforming growth factor-&bgr;. In contrast, miR-30c had little effect on extracellular matrix production but opposite effects regarding leukemia inhibitory factor and insulin-like growth factor 1. Both miRNAs indirectly affected cardiac myocytes. On transfection with pre–miR-29b, the conditioned medium of cardiac fibroblasts lost its ability to support adhesion of rat ventricular myocytes and led to a significant reduction of cardiac myocyte proteins (&agr;-actinin, cardiac myosin-binding protein C, and cardiac troponin I). Similarly, cardiomyocytes derived from mouse embryonic stem cells atrophied under pre–miR-29 conditioned medium, whereas pre–miR-30c conditioned medium had a prohypertrophic effect. Levels of miR-29a, miR-29c, and miR-30c, but not miR-29b, were significantly reduced in a mouse model of pathological but not physiological hypertrophy. Treatment with antagomiRs to miR-29b induced excess fibrosis after aortic constriction without overt deterioration in cardiac function. Conclusions: Our proteomic analysis revealed novel molecular targets of miRNAs that are linked to a fibrogenic cardiac phenotype. Such comprehensive screening methods are essential to define the concerted actions of miRNAs in cardiovascular disease.
Aerosolized Phosphoinositide 3-Kinase γ/δ Inhibitor TG100-115 [3-[2,4-Diamino-6-(3-hydroxyphenyl)pteridin-7-yl]phenol] as a Therapeutic Candidate for Asthma and Chronic Obstructive Pulmonary Disease

Phosphatidylinositol 3-kinases (PI3Ks) are key elements in the signaling cascades that lie downstream of many cellular receptors. In particular, PI3K δ and γ isoforms contribute to inflammatory cell recruitment and subsequent activation. For this reason, in a series of preclinical studies, we tested the potential of a recently developed small-molecule inhibitor of these two isoforms, TG100-115 [3-[2,4-diamino-6-(3-hydroxyphenyl)pteridin-7-yl]phenol], as a form of anti-inflammatory therapy for respiratory diseases such as asthma and chronic obstructive pulmonary disease (COPD). To determine pharmacokinetic profiles, aerosolized formulations of the drug were delivered to mice by a nose-only inhalation route, yielding high pulmonary TG100-115 levels with minimal systemic exposure. Safety assessments were favorable, with no clinical or histological changes noted after 21 days of daily dosing. In a murine asthma model, aerosolized TG100-115 markedly reduced the pulmonary eosinophilia and the concomitant interleukin-13 and mucin accumulation characteristic of this disease. As a functional benefit, interventional dosing schedules of this inhibitor also reduced airway hyper-responsiveness. To model the pulmonary neutrophilia characteristic of COPD, mice were exposed to either intranasal lipopolysaccharide or inhaled smoke. Aerosolized TG100-115 again inhibited these inflammatory patterns, most notably in the smoke model, where interventional therapy overcame the steroid-resistant nature of the pulmonary inflammation. In conclusion, aerosolized TG100-115 displays pharmacokinetic, safety, and biological activity profiles favorable for further development as a therapy for both asthma and COPD. Furthermore, these studies support the hypothesis that PI3K δ and γ are suitable molecular targets for these diseases.
Effect of augmentation with olanzapine in outpatients with depression in partial remission with melancholic features: Consecutive case series

The aim of the present 12‐week, open‐label study was to investigate the effect of olanzapine augmentation in outpatients with depression with melancholic features who demonstrated partial response to standard antidepressants but who were reluctant to change antidepressants. The subjects consisted of 22 outpatients meeting the DSM‐IV‐TR criteria for major depression. Olanzapine was initially added at 2.5 mg/day and the dose was adjusted according to the clinical condition. Data were analyzed using an intention‐to‐treat methodology. A paired t‐test was used to compare total Montgomery Asberg Depression Rating Scale (MADRS) scores before treatment, at baseline (prior to olanzapine), and 4, 8, and 12 weeks after starting olanzapine. Of 22 enrolled patients, 20 completed the trial. The mean (±SD) MADRS score was 17.1 ± 1.0 at baseline and decreased significantly to 8.1 ± 3.2 at 4 weeks after the administration of olanzapine. This significant reduction continued until 12 weeks, when the mean MADRS score was 4.9 ± 2.9, indicating full remission. These results suggest that olanzapine augmentation may be useful for patients with depression in partial remission. A controlled, double‐blind trial, however, is needed to confirm these preliminary findings.
Evidence for a founder effect of the MPL-S505N mutation in eight Italian pedigrees with hereditary thrombocythemia

Hereditary thrombocythemia is a rare disease characterized by increased megakaryopoiesis and overproduction of platelets. Germline mutations have been identified in the genes for thrombopoietin (THPO) and its receptor, MPL. This study suggests that the recurrent MPL (S505N) mutation found in eight Italian families with hereditary thrombocythemia is likely due to a founder effect. Background Hereditary thrombocythemia is a rare disease characterized by increased megakaryopoiesis and overproduction of platelets. Germ line mutations have been identified in the genes for thrombopoietin (THPO) and its receptor, MPL. A clustering of familial cases with the MPL-G1073A mutation that results in a serine to asparagine substitution (S505N) has been recently reported in Italy. Here we performed haplotype analysis in nine families (eight Italian and one Japanese) with hereditary thrombocythemia carrying the MPL-S505N mutation in the MPL gene. Design and Methods The MPL gene was examined by genomic DNA sequencing. Haplotype analysis was performed using microsatellites and single nucleotide polymorphisms. Results Analysis of microsatellite markers and single nucleotide polymorphisms in the eight Italian families with hereditary thrombocythemia revealed the presence of a common haplotype compatible with a founder effect, which may have originated 23 generations ago. This haplotype was rarely observed in 132 unrelated individuals and was absent in a Japanese family with the MPL-S505N mutation. Conclusions The recurrent MPL-S505N mutation found in the eight Italian families with hereditary thrombocythemia is likely due to a founder effect.
Construction and validation of the chronic acquired polyneuropathy patient‐reported index (CAP‐PRI): A disease‐specific, health‐related quality‐of‐life instrument

Introduction: Generic health‐related quality‐of‐life (HRQOL) patient‐reported outcome measures have been used in patients with chronic immune‐mediated polyneuropathies. We have created a disease‐specific HRQOL instrument. Methods: The chronic acquired polyneuropathy patient‐reported index (CAP‐PRI) was developed and validated in multiple steps. Items were initially generated through patient and specialist input. The performance of the preliminary 20 items was analyzed via a prospective, 5‐center study involving chronic immune‐mediated polyneuropathy patients. Results: Data analysis suggested modification to a 15‐item scale with 3 response categories rather than 5. The final CAP‐PRI was validated in another prospective, 5‐center study. The CAP‐PRI appeared to be a unidimensional outcome measure that fit the Rasch model in our multicenter cohort. It correlated appropriately with outcome measures commonly used in this patient population. Conclusions: The CAP‐PRI is a simple disease‐specific HRQOL measure that appears to be useful for clinical care and possibly also for clinical trials. Muscle Nerve 54: 9–17, 2016