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The CERN IT provides a set of Hadoop clusters featuring more than 5 PBytes of raw storage with different open-source, user-level tools available for analytical purposes. The CMS experiment started collecting a large set of computing meta-data, e.g. dataset, file access logs, since 2015. These records represent a valuable, yet scarcely investigated, set of information that needs to be cleaned, categorized and analyzed. CMS can use this information to discover useful patterns and enhance the overall efficiency of the distributed data, improve CPU and site utilization as well as tasks completion time. Here we present evaluation of Apache Spark platform for CMS needs. We discuss two main use-cases CMS analytics and ML studies where efficient process billions of records stored on HDFS plays an important role. We demonstrate that both Scala and Python (PySpark) APIs can be successfully used to execute extremely I/O intensive queries and provide valuable data insight from collected meta-data.

Red wine polyphenols inhibit chemically-induced oxidative DNA damage in vivo in experimental animals through a mechanism which is still unclear. On this basis, we tried to clarify the mechanisms of inhibition of DNA oxidation in vitro by wine extracts containing monomeric and polymeric phenols (WE) and monomer-free complex polyphenols and tannins (WCPT) from red wine. Oxidative DNA damage was induced by incubating DNA with GSH/Fe3+ or cumene hydroperoxide (CumOOH) in vitro and using 8-OH-2-deoxyguanosine (8-OHdG) levels as a measure of DNA oxidation. Levels of 8-OHdG were determined by HPLC coupled with electrochemical detector (ESA). WCPT and WE, at microM concentrations, reduced concentration-dependently oxidative DNA damage induced by GSH/Fe3+. WCPT and WE also reduced DNA oxidation by CumOOH. In conclusion, complex polyphenols and tannin extracts from red wine, with or without small molecular phenols, prevent oxidative DNA damage through a dual mechanism, iron binding and direct free radical scavenging.

Background Impulse control disorders (ICDs) are frequently encountered in Parkinson’s disease (PD). Objectives We aimed to assess whether clonidine, an α2-adrenergic receptor agonist, would improve ICDs. Methods We conducted a multicentre trial in five movement disorder departments. Patients with PD and ICDs ( n  = 41) were enrolled in an 8-week, randomised (1:1), double-blind, placebo-controlled study of clonidine (75 μg twice a day). Randomisation and allocation to the trial group were carried out by a central computer system. The primary outcome was the change at 8 weeks in symptom severity using the Questionnaire for Impulsive-Compulsive Disorders in Parkinson’s Disease–Rating Scale (QUIP-RS) score. A reduction of the most elevated subscore of the QUIP-RS of more than 3 points without any increase in the other QUIP-RS dimension defined success. Results Between 15 May 2019 and 10 September 2021, 19 patients in the clonidine group and 20 patients in the placebo group were enrolled. The proportion difference of success in reducing QUIP-RS at 8 weeks, was 7% (one-sided upper 90% CI 27%) with 42.1% of success in the clonidine group and 35.0% in the placebo group. Compared to patients in the placebo group, patients in the clonidine group experienced a greater reduction in the total QUIP-RS score at 8 weeks (11.0 points vs. 3.6). Discussion Clonidine was well tolerated but our study was not enough powerful to demonstrate significant superiority compared to placebo in reducing ICDs despite a greater reduction of total QUIP score at 8 weeks. A phase 3 study should be conducted. Trial Registration The study was registered (NCT03552068) on clinicaltrials.gov on June 11, 2018.

The COVID-19 pandemic continues to affect millions of people globally, with increasing reports of neurological manifestations but limited data on their incidence and associations with outcome. To determine the neurological phenotypes, incidence, and outcomes among adults hospitalized with COVID-19. This cohort study included patients with clinically diagnosed or laboratory-confirmed COVID-19 at 28 centers, representing 13 countries and 4 continents. The study was performed by the Global Consortium Study of Neurologic Dysfunction in COVID-19 (GCS-NeuroCOVID) from March 1 to September 30, 2020, and the European Academy of Neurology (EAN) Neuro-COVID Registry (ENERGY) from March to October 2020. Three cohorts were included: (1) the GCS-NeuroCOVID all COVID-19 cohort (n = 3055), which included consecutive hospitalized patients with COVID-19 with and without neurological manifestations; (2) the GCS-NeuroCOVID COVID-19 neurological cohort (n = 475), which comprised consecutive patients hospitalized with COVID-19 who had confirmed neurological manifestations; and (3) the ENERGY cohort (n = 214), which included patients with COVID-19 who received formal neurological consultation. Clinically diagnosed or laboratory-confirmed COVID-19. Neurological phenotypes were classified as self-reported symptoms or neurological signs and/or syndromes assessed by clinical evaluation. Composite incidence was reported for groups with at least 1 neurological manifestation. The main outcome measure was in-hospital mortality. Of the 3055 patients in the all COVID-19 cohort, 1742 (57%) were men, and the mean age was 59.9 years (95% CI, 59.3-60.6 years). Of the 475 patients in the COVID-19 neurological cohort, 262 (55%) were men, and the mean age was 62.6 years (95% CI, 61.1-64.1 years). Of the 214 patients in the ENERGY cohort, 133 (62%) were men, and the mean age was 67 years (95% CI, 52-78 years). A total of 3083 of 3743 patients (82%) across cohorts had any neurological manifestation (self-reported neurological symptoms and/or clinically captured neurological sign and/or syndrome). The most common self-reported symptoms included headache (1385 of 3732 patients [37%]) and anosmia or ageusia (977 of 3700 patients [26%]). The most prevalent neurological signs and/or syndromes were acute encephalopathy (1845 of 3740 patients [49%]), coma (649 of 3737 patients [17%]), and stroke (222 of 3737 patients [6%]), while meningitis and/or encephalitis were rare (19 of 3741 patients [0.5%]). Presence of clinically captured neurologic signs and/or syndromes was associated with increased risk of in-hospital death (adjusted odds ratio [aOR], 5.99; 95% CI, 4.33-8.28) after adjusting for study site, age, sex, race, and ethnicity. Presence of preexisting neurological disorders (aOR, 2.23; 95% CI, 1.80-2.75) was associated with increased risk of developing neurological signs and/or syndromes with COVID-19. In this multicohort study, neurological manifestations were prevalent among patients hospitalized with COVID-19 and were associated with higher in-hospital mortality. Preexisting neurological disorders were associated with increased risk of developing neurological signs and/or syndromes in COVID-19.

Time-dependent phenomena, such as creep of concrete, induce stress/strain redistributions in post-tensioned concrete bridges that must be taken into account during their design. The underestimation of time-dependent effects can negatively influence the load-deformation behavior of this bridge typology, leading to unexpected deformations of the deck, serviceability issues, and collapses. Numerical models able to simulate time-dependent phenomena should also be used to properly conduct the structural assessment of existing post-tensioned concrete bridges. However, before the introduction of specific materials’ constitutive laws to account for time-dependent phenomena, numerical models should be calibrated and validated according to the information gathered by testing the structures they represent, to carry out reliable numerical simulations. The paper presents the preliminary results obtained from the structural assessment of a post-tensioned concrete box girder bridge with vertically prestressed internal structural joints, which exhibits marked deflections of the box girder. A numerical model of the case study bridge was constructed, hence non-destructive and partially destructive tests were carried out on the structure to characterize its structural response. Overall, the resulting numerical model represents a solid basis for conducting more advanced analyses, such as those investigating the influence of time-dependent phenomena on the long-term structural response of the structure.

Apathy is a disabling symptom in Parkinson’s disease (PD). The effect of dopaminergic treatment on apathy is inconsistent, depending on the stage of the disease, the type of apathy and strongly influenced by placebo effect. Our study assessed the evolution of a cohort of 86 de novo, drug naive PD patients for 4 years, after dopaminergic treatment introduction. The main objective of the study was the change of apathy from baseline to follow-up and secondary outcomes were the change of other neuropsychiatric symptoms. At 4 years there was an improvement of apathy ( p  = 0.002), mainly driven by improvement of baseline apathy ( p  = 0.001). This was associated with an improvement of anxiety ( p  = 0.001), an increase in hyperdopaminergic behavior including nocturnal hyperactivity with consecutive diurnal sleepiness ( p  = 0.001 and p  < 0.001), independently of the presence of apathy at baseline. These findings confirm, in a large real-life cohort, that dopaminergic treatment improves motivational apathy in early PD.

ObjectivesTo explore the impact of sex and age on relationship between prodromal constipation and disease phenotype in Parkinson’s disease at early stages.MethodsA total of 385 Parkinson’s disease patients from the PRIAMO study were classified according to the presence of prodromal constipation and followed for 24 months. Multivariable mixed-effect models were applied. All analyses were performed separately for sex (64.1% men) and median age (different by sex: 67 years-old in men and 68 years-old in women).ResultsAs for sex, prodromal constipation was associated with greater odds of attention/memory complaints and apathy symptoms in women only. As for age, prodromal constipation was associated with lower cognitive and higher apathy scores in older patients only.ConclusionsProdromal constipation anticipates lower cognitive performances and more severe apathy since the earliest stages in women and older patients. Sex- and age-related heterogeneity of prodromal markers of Parkinson’s disease may impact disease phenotype.

ObjectiveTo evaluate the prevalence of psychosis associated with Parkinson's disease (PSY-PD) in its early stages, its incidence over a 24 month follow-up period and the association with motor and non-motor clinical features.MethodsPRIAMO is a 2 year longitudinal observational study that has enrolled patients with parkinsonism in 55 Italian centres. A cohort of 495 patients with early disease stage PD (baseline Hoehn and Yahr score ≤2, disease's duration (median) 3.4 years) were followed for 2 years. PSY-PD was evaluated by means of a clinician rated questionnaire and defined as the presence of at least one of the following symptoms occurring for at least 1 month: illusions, hallucinations, jealousy ideas and persecutory ideas. Patients with and without PSY-PD were compared on several clinical variables, encompassing motor and non-motor features.ResultsThe prevalence of PSY-PD at baseline was 3%; the incidences at 12 and 24 months were 5.2% and 7.7%, respectively. Longer disease duration and prescription of dopamine agonists at baseline were associated with the development of PSY-PD over the 24 month period. At this follow-up time, worse disease severity, decline in cognitive performances, presence of depressive symptoms and anxiety were more frequently observed in PSY-PD.ConclusionsPsychotic type symptoms may occur in the early stages of PD although less frequently than in later stages. Beyond dopaminergic treatment, there are disease related factors, such as disease severity and the occurrence of cognitive and depressive symptoms, which may underlie the onset of psychotic type symptoms from the earliest stages.

Background Sudden cardiac death occurs commonly in the end-stage renal disease population receiving dialysis, with 25% dying of sudden cardiac death over 5 years. Despite this high risk, surprisingly few prospective studies have studied clinical- and dialysis-related risk factors for sudden cardiac death and arrhythmic precursors of sudden cardiac death in end-stage renal disease. Methods/Design We present a brief summary of the risk factors for arrhythmias and sudden cardiac death in persons with end-stage renal disease as the rationale for the Predictors of Arrhythmic and Cardiovascular Risk in End Stage Renal Disease (PACE) study, a prospective cohort study of patients recently initiated on chronic hemodialysis, with the overall goal to understand arrhythmic and sudden cardiac death risk. Participants were screened for eligibility and excluded if they already had a pacemaker or an automatic implantable cardioverter defibrillator. We describe the study aims, design, and data collection of 574 incident hemodialysis participants from the Baltimore region in Maryland, U.S.A.. Participants were recruited from 27 hemodialysis units and underwent detailed clinical, dialysis and cardiovascular evaluation at baseline and follow-up. Cardiovascular phenotyping was conducted on nondialysis days with signal averaged electrocardiogram, echocardiogram, pulse wave velocity, ankle, brachial index, and cardiac computed tomography and angiography conducted at baseline. Participants were followed annually with study visits including electrocardiogram, pulse wave velocity, and ankle brachial index up to 4 years. A biorepository of serum, plasma, DNA, RNA, and nails were collected to study genetic and serologic factors associated with disease. Discussion Studies of modifiable risk factors for sudden cardiac death will help set the stage for clinical trials to test therapies to prevent sudden cardiac death in this high-risk population.

Background End-stage kidney disease (ESKD) is a significant public health concern disproportionately affecting African Americans (AAs). Type 2 diabetes (T2D) is the leading cause of ESKD in the USA, and efforts to uncover genetic susceptibility to diabetic kidney disease (DKD) have had limited success. A prior genome-wide association study (GWAS) in AAs with T2D-ESKD was expanded with additional AA cases and controls and genotypes imputed to the higher density 1000 Genomes reference panel. The discovery analysis included 3432 T2D-ESKD cases and 6977 non-diabetic non-nephropathy controls ( N  = 10,409), followed by a discrimination analysis in 2756 T2D non-nephropathy controls to exclude T2D-associated variants. Results Six independent variants located in or near RND3/RBM43 , SLITRK3 , ENPP7 , GNG7 , and APOL1 achieved genome-wide significant association ( P  < 5 × 10 −8 ) with T2D-ESKD. Following extension analyses in 1910 non-diabetic ESKD cases and 908 non-diabetic non-nephropathy controls, a meta-analysis of 5342 AA all-cause ESKD cases and 6977 AA non-diabetic non-nephropathy controls revealed an additional novel all-cause ESKD locus at EFNB2 (rs77113398; P  = 9.84 × 10 –9 ; OR = 1.94). Exclusion of APOL1 renal-risk genotype carriers identified two additional genome-wide significant T2D-ESKD-associated loci at GRAMD3 and MGAT4C . A second variant at GNG7 (rs373971520; P  = 2.17 × 10 –8 , OR = 1.46) remained associated with all-cause ESKD in the APOL1 -negative analysis. Conclusions Findings provide further evidence for genetic factors associated with advanced kidney disease in AAs with T2D.