Structure functions for light nuclei

We discuss the nuclear EMC effect with particular emphasis on recent data for light nuclei including 2H, 3He, 4He, 9Be, 12C and 14N. In order to verify the consistency of available data, we calculate the \chi^2 deviation between different data sets. We find a good agreement between the results from the NMC, SLAC E139, and HERMES experiments. However, our analysis indicates an overall normalization offset of about 2% in the data from the recent JLab E03-103 experiment with respect to previous data for nuclei heavier than 3He. We also discuss the extraction of the neutron/proton structure function ratio F2n/F2p from the nuclear ratios 3He/2H and 2H/1H. Our analysis shows that the E03-103 data on 3He/2H require a renormalization of about 3% in order to be consistent with the F2n/F2p ratio obtained from the NMC experiment. After such a renormalization, the 3He data from the E03-103 data and HERMES experiments are in a good agreement. Finally, we present a detailed comparison between data and model calculations, which include a description of the nuclear binding, Fermi motion and off-shell corrections to the structure functions of bound proton and neutron, as well as the nuclear pion and shadowing corrections. Overall, a good agreement with the available data for all nuclei is obtained.Comment: 18 pages, 7 figures, 5 tables, final version published in Phys. Rev.

The fifth most prevalent disease is being neglected by public health organisations

The progress towards reduction of global mortality has produced an epidemiological transition towards non-fatal diseases, which challenge the ability of the world’s population to live in full health. Although traumatic dental injuries are not lethal, their treatment is more expensive (US$2 000 000–5 000 000 per million inhabitants) and time-consuming than that of all the other bodily injuries, making dental rehabilitation less likely among disadvantaged individuals. Since untreated traumatic dental injuries have a negative social, functional, and emotional effect in children and adolescents, differences in treatment of these injuries between children from different countries and social classes produce disparities in their quality of life

Cultural heritage and sustainable development targets : a possible harmonisation? Insights from the European Perspective

The Agenda 2030 includes a set of targets that need to be achieved by 2030. Although none of the 17 Sustainable Development Goals (SDGs) focuses exclusively on cultural heritage, the resulting Agenda includes explicit reference to heritage in SDG 11.4 and indirect reference to other Goals. Achievement of international targets shall happen at local and national level, and therefore, it is crucial to understand how interventions on local heritage are monitored nationally, therefore feeding into the sustainable development framework. This paper is focused on gauging the implementation of the Sustainable Development Goals with reference to cultural heritage, by interrogating the current way of classifying it (and consequently monitoring). In fact, there is no common dataset associated with monitoring SDGs, and the field of heritage is extremely complex and diversified. The purpose for the paper is to understand if the taxonomy used by different national databases allows consistency in the classification and valuing of the different assets categories. The European case study has been chosen as field of investigation, in order to pilot a methodology that can be expanded in further research. A cross‐comparison of a selected sample of publicly accessible national cultural heritage databases has been conducted. As a result, this study confirms the existence of general harmonisation of data towards the achievement of the SDGs with a broad agreement of the conceptualisation of cultural heritage with international frameworks, thus confirming that consistency exists in the classification and valuing of the different assets categories. However, diverse challenges of achieving a consistent and coherent approach to integrating culture in sustainability remains problematic. The findings allow concluding that it could be possible to mainstream across different databases those indicators, which could lead to depicting the overall level of attainment of the Agenda 2030 targets on heritage. However, more research is needed in developing a robust correlation between national datasets and international targets

BCI-assisted training for upper limb motor rehabilitation: estimation of effects on individual brain connectivity and motor functions

The aim of the study is to quantify individual changes in scalp connectivity patterns associated to the affected hand movement in stroke patients after a 1-month training based on BCIsupported motor imagery to improve upper limb motor recovery. To perform the statistical evaluation between pre- and post-training conditions at the single subject level, a resampling approach was applied to EEG datasets acquired from 12 stroke patients during the execution of a motor task with the stroke affected hand before and after the rehabilitative intervention. Significant patterns of the network reinforced after the training were extracted and a significant correlation was found between indices related to the reinforced pattern and the clinical outcome indicated by clinical scales

Determination of Strange Sea Quark Distributions from Fixed-target and Collider Data

We present an improved determination of the strange sea distribution in the nucleon with constraints coming from the recent charm production data in neutrino-nucleon deep-inelastic scattering by the NOMAD and CHORUS experiments and from charged current inclusive deep-inelastic scattering at HERA. We demonstrate that the results are consistent with the data from the ATLAS and the CMS experiments on the associated production of $W^\pm$-bosons with $c$-quarks. We also discuss issues related to the recent strange sea determination by the ATLAS experiment using LHC collider data.Comment: 23 pages, 14 figure

A Comprehensive Analysis of Multilayer Community Detection Algorithms for Application to EEG-Based Brain Networks

Modular organization is an emergent property of brain networks, responsible for shaping communication processes and underpinning brain functioning. Moreover, brain networks are intrinsically multilayer since their attributes can vary across time, subjects, frequency, or other domains. Identifying the modular structure in multilayer brain networks represents a gateway toward a deeper understanding of neural processes underlying cognition. Electroencephalographic (EEG) signals, thanks to their high temporal resolution, can give rise to multilayer networks able to follow the dynamics of brain activity. Despite this potential, the community organization has not yet been thoroughly investigated in brain networks estimated from EEG. Furthermore, at the state of the art, there is still no agreement about which algorithm is the most suitable to detect communities in multilayer brain networks, and a way to test and compare them all under a variety of conditions is lacking. In this work, we perform a comprehensive analysis of three algorithms at the state of the art for multilayer community detection (namely, genLouvain, DynMoga, and FacetNet) as compared with an approach based on the application of a single-layer clustering algorithm to each slice of the multilayer network. We test their ability to identify both steady and dynamic modular structures. We statistically evaluate their performances by means of ad hoc benchmark graphs characterized by properties covering a broad range of conditions in terms of graph density, number of clusters, noise level, and number of layers. The results of this simulation study aim to provide guidelines about the choice of the more appropriate algorithm according to the different properties of the brain network under examination. Finally, as a proof of concept, we show an application of the algorithms to real functional brain networks derived from EEG signals collected at rest with closed and open eyes. The test on real data provided results in agreement with the conclusions of the simulation study and confirmed the feasibility of multilayer analysis of EEG-based brain networks in both steady and dynamic conditions

ROLE OF SPHINGOSINE-1-PHOSPATE PATHWAY IN INTESTINAL EPITHELIAL CELLS AND ITS INVOLVEMENT IN INTESTINAL TUMORIGENESIS.

Title: Role of Sphingosine-1-phosphate pathway in intestinal epithelial cells and its involvement in intestinal tumorigenesis. Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid metabolite, involved in several cellular processes. S1P is both an intracellular second messenger and the ligand of five EDG family G protein-coupled receptors 1-5 (S1PR1-5). S1PRs are widely expressed on many cell types of different tissues including the gut. However, so far there are no evidences about which S1P receptor is expressed on intestinal epithelial layer. Therefore, the first proposal of this project is to characterize the S1P pathway on intestinal epithelial cells and to explore the physiological functions of the S1PRs on intestinal epithelial cells. I characterized the expression of the ubiquitous expressed S1P receptors S1PR1, S1PR2 and S1PR3 on human and murine primary intestinal epithelial cells isolated from healthy controls by qRT-PCR and western blot. Interestingly, both the analyses revealed that the S1PR2 is the most abundantly expressed S1PR in the colonic epithelium, among the three S1PRs analyzed. Consequentially, I decided to focus specifically on S1PR2 for the study of the physiological functions of the S1PRs in the epithelium. Recently, in vitro studies have been highlighted the capacity of S1P to enhance epithelial barrier function suggesting this pathway as new potential target of intestinal barrier restoration (Vetrano et al., 2011; Greenspoon et al., 2011). However, so far there are no evidences of which receptor mediates this effect. Since the expression of the S1PR1 and S1PR3 transcript is very low also in the human epithelial cell line Caco-2, whereas the S1PR2 transcript is constitutively expressed, I assessed the hypothesis of the S1PR2 involvement in the S1P-mediated regulation of the epithelial barrier permeability. I evaluated the intestinal permeability in vivo in S1pr2 knock out mice (S1P2-/-) at baseline and after DSS-induced colitis by the Evans Blue method. Surprisingly, no difference in terms of intestinal permeability and susceptibility to DSS-induced colitis was found between S1P2-/- and WT mice. In line with this, the expression of tight junction (TJ) proteins at baseline in S1P2-/- mice was comparable to WT mice thus excluding direct defects of the epithelial junction proteins in absence of S1PR2. Several studies reported that the S1P signalling controls the cell growth and few papers bring to light the anti-proliferative role of the S1PR2 in vitro and in vivo in different cell lines (Ikeda et al., 2003; Goparaju et al., 2005). Therefore, it was of interest to analyse the role of S1PR2 in the proliferation of the colonic epithelial cells. I evaluated the proliferation in vitro and in vivo respectively in Caco-2 cell line under the treatment with different concentrations of S1PR2 inhibitor and in S1P2-/- mice by BrdU incorporation assay. Both analyses have showed an increase in the epithelial proliferation rate in absence of S1PR2. Since the abnormal proliferation is associated with tumor development and the S1P2 acts as a tumor suppressor in different types of tumors, I tested whether the loss of S1PR2 could be a pro-tumorigenic key for the development of colorectal cancer. To this end, a AOM/DSS model of colitis associated cancer was induced in S1P2-/- and WT mice. All mice were treated with a single injection of azoxymethane (AOM) (10mg/Kg) a known cancerogenic agent, followed by four cycles of DSS (2,5%). During the experiment, the animals were monitored for body weight loss, rectal bleeding and fecal consistency, and analyzed by endoscopic procedure to monitor the tumor growth in vivo. Interestingly, although no differences in terms of grade and extension of intestinal inflammation were observed between two groups, S1PR2 mice were characterized by a higher number of tumors compared to WT mice. These results were confirmed by three independent experiments thus indicating a crucial role of S1PR2 in the intestinal tumorigenesis. The incidence of high grade adenomas is higher and the few carcinomas observed are bigger in s1pr2-/- compared with wild type mice. These observations indicate that the loss of S1PR2 leads to an increased onset and a faster progression of colorectal cancers. No difference in the clinical parameters of inflammation (body weight loss, disease activity index, colon length and Rachmilewitz score) has been observed between S1PR2 knockout and wild type mice, suggesting that the increase in the cancer development does not depend on a higher inflammatory response in the S1P2-/- mice. The analysis of tumors in the Apcmin/+ genetic model of intestinal and colon cancer further confirms this hypothesis. Indeed, I observed a higher incidence and size of tumors in the colon of s1pr2-/-/Apcmin/+ mice compared to s1pr2+/+/Apcmin/+ controls and, while control mice mainly develop few adenomas, almost all the tumors observed in S1PR2-null mice are carcinomas. Overall these data point out a protective role of S1PR2 during the development of the colorectal cancer, both spontaneous and inflammation-driven. By immunohistochemistry staining and western blot, I observed a strong decrease of the S1PR2 expression both in early staged human carcinomas and in the murine adenomatous polyps and adenocarcinomas of both AOM/DSS and genetic models, suggesting that S1PR2 down-regulation is an early event required for the development of colorectal cancers. Since the pharmacological inhibition of S1PR2 increases the proliferation of epithelial cells in vitro and the expression of S1P2 is mainly observed in the differentiated epithelial cells localized in the upper region of the crypts in the colon and at the top of the crypts and in the villi in the small intestine, I investigated whether S1PR2 is involved in the regulation of the intestinal epithelial cell differentiation. To verify this hypothesis, I took advantage from the mini-gut culture system and I observed that the pharmacological inhibition of S1PR2 during the early phases of the organoid development blocks the complete formation of the branches and keep the organoids in a round shape and undifferentiated. Interestingly, the organoids treated with S1PR2 inhibitor show an enrichment of stem cell markers such as Lgr5 and Olfm4 compared to untreated organoids. This finding raises the unrknown role of S1PR2 in determining the differentiation of the intestinal epithelial cells, thus suggesting the S1PR2 as a master player in the maintenance of the crypt-villus differentiation axis. Overall these results suggest that the loss of S1PR2 affects the differentiation of epithelial cells promoting their proliferative potential. Taken together these results suggest that S1PR2 functions as a negative regulator of epithelial cell proliferation in the colon and may contrast tumorigenesis by promoting epithelial cells differentiation and impeding their malignant transformation