Anàlisi traductològica de Ulysses/Ulisses

Treball final de Grau en Traducció i Interpretació. Codi: TI0983. Curs acadèmic 2014-2015La curiositat per Joyce em va guiar al seu Ulysses per fer aquest TFG, i per realitzar aquesta tasca faltava la figura d’un traductor, que en aquest cas és Joaquim Mallafrè. En aquest treball, l’anàlisi traductològica consisteix en una anàlisi qualitativa de la traducció de Mallafrè que se centrarà en tres aspectes principals que ell també analitza en el seu llibre Llengua de tribu i llengua de polis, el qual ha sigut una font de documentació molt important per entendre la seua manera de traduir. Aquestes tres qüestions són les al·lusions intertextuals, els jocs de paraules i els registres que apareixen en les vint primeres pàgines del primer capítol. A més a més, farem un breu repàs de Joyce i de la seua obra, Ulysses, així com també de Mallafrè i de la seua concepció de la traducció literària, que després ens ajudarà a entendre la seua metodologia durant la traducció de l’Ulisses

Preliminary Report on the Study of Beam-Induced Background Effects at a Muon Collider

Physics at a multi-TeV muon collider needs a change of perspective for the detector design due to the large amount of background induced by muon beam decays. Preliminary studies, based on simulated data, on the composition and the characteristics of the particles originated from the muon decays and reaching the detectors are presented here. The reconstruction performance of the physics processes $H\to b\bar b$ and $Z\to b\bar b$ has been investigated for the time being without the effect of the machine induced background. A preliminary study of the environment hazard due to the radiation induced by neutrino interactions with the matter is presented using the FLUKA simulation program

DNA replication determines timing of mitosis by restricting CDK1 and PLK1 activation

To maintain genome stability, cells need to replicate their DNA before dividing. The kinases CDK1 and PLK1 drive mitotic entry and become active when bulk DNA synthesis is completed at the S/G2 transition. Here, we have tested the hypothesis that DNA replication controls activation of mitotic kinases. Using an optimized double-degron system, we find that human cells unable to initiate DNA replication in S-phase promptly activate CDK1 and PLK1 and prematurely enter mitosis. In the presence of DNA replication, inhibition of CHK1 and p38 leads to premature activation of CDK1 and PLK1. While CDK2 activity promotes DNA replication, activation of CDK1 in S-phase induces severe replication stress. We propose that mitotic kinase activation is governed by a CDK2- and DNA replication-dependent feed-forward loop that ensures timely cell division while preserving genome stability. DNA replication thus functions as a break that coordinates cell cycle activities and determines cell cycle duration

Nanobubbles at GPa Pressure under Graphene

We provide direct evidence that irradiation of a graphene membrane on Ir with low-energy Ar ions induces formation of solid noble-gas nanobubbles. Their size can be controlled by thermal treatment, reaching tens of nanometers laterally and height of 1.5 nm upon annealing at 1080 \ub0C. Ab initio calculations show that Ar nanobubbles are subject to pressures reaching tens of GPa, their formation being driven by minimization of the energy cost of film distortion and loss of adhesion

Impacts on biodiversity from codend and fisher selection in bottom trawl fishing

Fisheries have important impacts on marine biodiversity. In this work, combined information on the abundance, species richness, diversity indices, species composition, trophic level and vulnerability index were examined for the first-time to detect differences in five units related to trawl fishing: the fish assemblage entering the trawl codend, and the escaping, retained, discarded and landed fractions, derived by the gear and fisher selection practices. The work was based on a case study conducted in the Mediterranean Sea, using three different meshes in the trawl codend (40mm-40D and 50mm-50D diamond meshes, and 40 mm-40S square meshes) and a cover of the codends with small mesh size. In general, trawl fishing produces an escaping fraction that was always lower in abundance, richness, and vulnerability index, similar in diversity indices and trophic level, and different in species composition compared to the fish assemblage entering the codend. In almost all cases, fishers selected as landings a fraction that was the lowest in diversity indices, and the highest in trophic level. In contrast, fishers discarded a fraction that was the highest in diversity and vulnerability index, and the lowest in trophic level. Although the three codends did not differ significantly in the fraction of escapees in terms of diversity indices, trophic level, and vulnerability index, the 40S codend showed a significantly higher percentage in the escaping number of species and individuals, and less differences in the species composition; in addition, lower percentage in abundance of discards and higher of landings in the retained catch (0.6:1) than did the other two codends (0.9:1). It was suggested that an urgent modification of the trawl for the elimination of the discarded highly vulnerable species (e.g. Elasmobranchs) is needed, and that trawl species-selectivity should be improved by allowing escape or avoiding catch of the discarded fraction to minimize biodiversity losses.publishedVersio

National Health Care Network for children with oral clefts: organization, functioning, and preliminary outcomes

Introduction. Oral clefts are major congenital anomalies that may affect the lip and/or palate, and that may also involve the nose and nostrils. In Argentina, their prevalence is approximately 15 per 10 000 births. In 2015, the Ministry of Health of Argentina created a national health care network for children with oral clefts in Argentina through the joint work with the National Registry of Congenital Anomalies (Red Nacional de Anomaliás Congénitas, RENAC) (coordinating center for the national network) and the SUMAR Program. The objective of this study was to describe the health care network and its preliminary outcomes. Population and methods. A total of 61 centers that provided a comprehensive treatment for oral clefts or in collaboration with other centers were identified and accredited. Maternity centers were connected with treating centers grouped in health care network nodes. Results. In the period between March 2015 and February 2016, 550 newborn infants who were exclusively covered by the public health care system were identified. Among these, 18% had a cleft lip; 62%, cleft lip and palate; and 20%, cleft palate only; 75% were isolated cases and 25%, in association with other congenital anomalies. Conclusion. Approximately 70% of children were assessed by a certified treating institution and are receiving treatment. The network seeks to improve data systematization, include the largest number of centers possible, strengthen interdisciplinary team work, and promote highquality standards for treatments.Fil: Cassinelli, Agustina. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorios e Institutos de Salud "Dr. Carlos G. Malbrán". Centro Nacional de Genética Médica; ArgentinaFil: Pauselli, Nadia. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorios e Institutos de Salud "Dr. Carlos G. Malbrán". Centro Nacional de Genética Médica; ArgentinaFil: Piola, Agustina. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorios e Institutos de Salud "Dr. Carlos G. Malbrán". Centro Nacional de Genética Médica; ArgentinaFil: Martinelli, Claudia. Ministerio de Salud de la Nación; ArgentinaFil: Alves De Azevedo, José L.. Ministerio de Salud de la Nación; ArgentinaFil: Bidondo, Mariá P.. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorios e Institutos de Salud "Dr. Carlos G. Malbrán". Centro Nacional de Genética Médica; ArgentinaFil: Groisman, Boris. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorios e Institutos de Salud "Dr. Carlos G. Malbrán". Centro Nacional de Genética Médica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Barbero, Pablo Miguel. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorios e Institutos de Salud "Dr. Carlos G. Malbrán". Centro Nacional de Genética Médica; ArgentinaFil: Liascovich, Rosa. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorios e Institutos de Salud "Dr. Carlos G. Malbrán". Centro Nacional de Genética Médica; ArgentinaFil: Sala, Ana. Ministerio de Salud de la Nación; Argentin

New generation implantable cardiac rhythm devices allow safe radiotherapy treatments: A large single centre study

n/

Follow-Up Study Confirms the Presence of Gastric Cancer DNA Methylation Hallmarks in High-Risk Precursor Lesions

Intestinal metaplasia confers an increased risk of progression to gastric cancer. However, some intestinal metaplasia patients do not develop cancer. The development of robust molecular biomarkers to stratify patients with advanced gastric precursor lesions at risk of cancer progression will contribute to guiding programs for prevention. Starting from a genome-wide methylation study, we have simplified the detection method regarding candidate-methylation tests to improve their applicability in the clinical environment. We identified CpG methylation at the ZNF793 and RPRM promoters as a common event in intestinal metaplasia and intestinal forms of gastric cancer. Furthermore, we also showed that Helicobacter pylori infection influences DNA methylation in early precursor lesions but not in intestinal metaplasia, suggesting that therapeutic strategies to prevent epigenome reprogramming toward a cancer signature need to be adopted early in the precursor cascade. To adopt prevention strategies in gastric cancer, it is imperative to develop robust biomarkers with acceptable costs and feasibility in clinical practice to stratified populations according to risk scores. With this aim, we applied an unbiased genome-wide CpG methylation approach to a discovery cohort composed of gastric cancer (n = 24), and non-malignant precursor lesions (n = 64). Then, candidate-methylation approaches were performed in a validation cohort of precursor lesions obtained from an observational longitudinal study (n = 264), with a 12-year follow-up to identify repression or progression cases. H. pylori stratification and histology were considered to determine their influence on the methylation dynamics. As a result, we ascertained that intestinal metaplasia partially recapitulates patterns of aberrant methylation of intestinal type of gastric cancer, independently of the H. pylori status. Two epigenetically regulated genes in cancer, RPRM and ZNF793, consistently showed increased methylation in intestinal metaplasia with respect to earlier precursor lesions. In summary, our result supports the need to investigate the practical utilities of the quantification of DNA methylation in candidate genes as a marker for disease progression. In addition, the H. pylori-dependent methylation in intestinal metaplasia suggests that pharmacological treatments aimed at H. pylori eradication in the late stages of precursor lesions do not prevent epigenome reprogramming toward a cancer signature

A Mendelian randomization study of circulating uric acid and type 2 diabetes

We aimed to investigate the causal effect of circulating uric acid concentrations on type 2 diabetes risk. A Mendelian randomization study was performed using a genetic score with 24 uric acid associated loci. We used data of the EPIC-InterAct case-cohort study, comprising 24,265 individuals of European ancestry from eight European countries. During a mean (SD) follow-up of 10 (4) years, 10,576 verified incident type 2 diabetes cases were ascertained. Higher uric acid associated with higher diabetes risk following adjustment for confounders, with a HR of 1.20 (95%CI: 1.11,1.30) per 59.48 µmol/L (1 mg/dL) uric acid. The genetic score raised uric acid by 17 µmol/L (95%CI: 15,18) per SD increase, and explained 4% of uric acid variation. Using the genetic score to estimate the unconfounded effect found that a 59.48 µmol/L higher uric acid concentration did not have a causal effect on diabetes (HR 1.01, 95%CI: 0.87,1.16). Including data from DIAGRAM consortium, increasing our dataset to 41,508 diabetes cases, the summary OR estimate was 0.99 (95%CI: 0.92, 1.06). In conclusion, our study does not support a causal effect of circulating uric acid on diabetes risk. Uric acid lowering therapies may therefore not be beneficial in reducing diabetes risk