Constructing lists to construct categories

The aim of this paper is to analyze list constructions as linguistic tools to build categories in discourse, identifying the inferential processes leading from list constructions to categorization and examining the semantic and morphosyntactic elements that activate abstractive reasoning within lists. Based on real occurrences of lists in written and spoken Italian, we will first of all propose a crucial distinction between exhaustive and non-exhaustive lists, arguing that (non-)exhaustivity determines the layer at which the construction of a category occurs, namely the layer of presupposition or the \u2018what-is-said\u2019 part of the utterance. We will then focus on non-exhaustive lists, arguing that they directly communicate a bottom-up, exemplar-driven abstraction, characterized by the presence of an inherently indexical reference (i.e. reference to further Xs characterized by some underlying Property P), which will lead us to call it \u2018indexical categorization\u2019. The linguistic analysis of how indexical categorization is expressed in discourse will show a major distinction between (i) elements characterized by an indexical semantics, which trigger the abstraction process, and (ii) elements providing semantic clues towards the correct construction of the indexical category. We will conclude by taking a broader perspective and by explaining the patterns observed for indexical categorization in the light of the wider process of online reference construction

Non-exhaustive connectives

This paper provides the first cross-linguistic study on non-exhaustive connectives. After defining non-exhaustivity and briefly exploring the range of linguistic strategies encoding it across languages, the methodology underlying the study will be discussed. Based on the analysis of 35 languages, for which at least one non-exhaustive connective was found, it will be argued that non-exhaustive connectives exhibit quite homogenous distributional properties and derive from a restricted set of recurrent diachronic sources. Speakers are indeed likely to mobilize i) elements already encoding or implying non-exhaustivity, ii) elements expressing an epistemic condition of uncertainty, or iii) elements expressing exemplification

Symptom Dimensions as Predictors of Clinical Outcome, Duration of Hospitalization, and Aggressive Behaviours in Acutely Hospitalized Patients with Psychotic Exacerbation

In the present study we extract clusters of symptoms in acute hospitalized psychotic patients during a re-exacerbation phase, using factor analysis of BPRS-E. We aim to investigate the relative contribution of each symptom dimension in predicting the severity of symptoms at discharge, the length of acute hospitalization, and the occurrence of aggressive behaviours during acute hospitalization. The data are drawn from a prospective, naturalistic, observational study of 183 patients with Psychotic Disorders consecutively admitted to a psychiatric ward, during a re-exacerbation phase. General symptomatology has been measured through BPRS-E at admission and at discharge. Statistical analyses include principal component analysis and multiple linear regression

Phonon dispersion and low energy anomaly in CaC6_6

We report measurements of phonon dispersion in CaC$_6$ using inelastic X-ray and neutron scattering. We find good overall agreement, particularly in the 50 meV energy region, between experimental data and first-principles density-functional-theory calculations. However, on the longitudinal dispersion along the $(1 1 1)$ axis of the rhombohedral representation, we find an unexpected anti-crossing with an additional longitudinal mode, at about 11 meV. At a comparable energy, we observe also unexpected intensity on the in-plane direction. These results resolve the previous incorrect assignment of a longitudinal phonon mode to a transverse mode in the same energy range. By calculating the electron susceptibility from first principles we show that this longitudinal excitation is unlikely to be due to a plasmon and consequently can probably be due to defects or vacancies present in the sample.Comment: Accepted for publication in Physical Review

Simultaneous gut colonization by Klebsiella grimontii and Escherichia coli co-possessing the blaKPC-3-carrying pQil plasmid.

Only two plasmid-mediated carbapenemases (KPC-2 and VIM-1) are reported in Klebsiella grimontii. Here, we report two blaKPC-3-positive isolates that were identified as K. oxytoca and E. coli by MALDI-TOF MS in the same rectal swab. Whole-genome sequencing indicated that K. oxytoca was actually K. grimontii of ST391, whereas E. coli was of ST10. In both, blaKPC-3 was carried by a pQil conjugative plasmid. The core-genome analysis identified additional blaKPC-positive K. grimontii strains from public databases, most of which were misidentified as K. oxytoca. Since K. grimontii represents an emerging reservoir of resistance traits, routine tools should improve their ability to detect this species

Galectin-3: An early predictive biomarker of modulation of airway remodeling in patients with severe asthma treated with omalizumab for 36 months

Background: Bronchial asthma is a heterogeneous disease characterized by three cardinal features: chronic inflammation, variable airflow obstruction, and airway hyperresponsiveness. Asthma has traditionally been defined using nonspecific clinical and physiologic variables that encompass multiple phenotypes and are treated with nonspecific anti-inflammatory therapies. Based on the modulation of airway remodeling after 12 months of anti-immunoglobulin E (IgE) treatment, we identified two phenotypes (omalizumab responder, OR; and non-omalizumab responder, NOR) and performed morphometric analysis of bronchial biopsy specimens. We also found that these two phenotypes were correlated with the presence/absence of galectin-3 (Gal-3) at baseline (i.e., before treatment). The aims of the present study were to investigate the histological and molecular effects of long-term treatment (36 months) with anti-IgE and to analyze the behavior of OR and NOR patients. Methods: All patients were treated with the monoclonal antibody anti-IgE omalizumab for 36 months. The bronchial biopsy specimens were evaluated using morphometric, eosinophilic, and proteomic analysis (MudPIT). New data were compared with previous data, and unsupervised cluster analysis of protein profiles was performed. Results: After 36 months of treatment with omalizumab, reduction of reticular basement membrane (RBM) thickness was confirmed in OR patients (Gal-3-positive at baseline); similarly, the protein profiles (over 500 proteins identified) revealed that, in the OR group, levels of proteins specifically related to fibrosis and inflammation (e.g., smooth muscle and extracellular matrix proteins (including periostin), Gal-3, and keratins decreased by between 5- and 50-fold. Eosinophil levels were consistent with molecular data and decreased by about tenfold less in ORs and increased by twofold to tenfold more in NORs. This tendency was confirmed (p < 0.05) based on both fold change and DAVE algorithms, thus indicating a clear response to anti-IgE treatment in Gal-3-positive patients. Conclusions: Our results showed that omalizumab can be considered a disease-modifying treatment in OR. The proteomic signatures confirmed the presence of Gal-3 at baseline to be a biomarker of long-term reduction in bronchial RBM thickness, eosinophilic inflammation, and muscular and fibrotic components in omalizumab-treated patients with severe asthma. Our findings suggest a possible relationship between Gal-3 positivity and improved pulmonary function

Mechanisms of Resistance to Immunotherapy in Hepatocellular Carcinoma

: Systemic treatment for advanced hepatocellular carcinoma (HCC) has been revolutionized over the last few years following the approval of immune checkpoint inhibitors (ICI). Despite the promising survival extension seen with ICI combination regimens, responses are not universally seen and the optimal partner for programmed cell death 1 pathway inhibitors remains to be identified. Even fewer encouraging results have been demonstrated with ICI used for monotherapy. Several mechanisms of resistance have been described so far, involving characteristics of cancer cells (intrinsic mechanisms) and of the surrounding tumor microenvironment (extrinsic mechanisms). Factors related to therapy may also contribute to the development of resistance. Increasing research efforts are being dedicated to the discovery of novel approaches and targets to overcome resistance, some of which may be introduced into clinic in the future. Herein we describe a selection of resistance mechanisms that have been involved in impairing response to ICI and propose potential therapeutic approaches to overcome resistance

SETBP1 induces transcription of a network of development genes by acting as an epigenetic hub

SETBP1 variants occur as somatic mutations in several hematological malignancies such as atypical chronic myeloid leukemia and as de novo germline mutations in the Schinzel-Giedion syndrome. Here we show that SETBP1 binds to gDNA in AT-rich promoter regions, causing activation of gene expression through recruitment of a HCF1/KMT2A/PHF8 epigenetic complex. Deletion of two AT-hooks abrogates the binding of SETBP1 to gDNA and impairs target gene upregulation. Genes controlled by SETBP1 such as MECOM are significantly upregulated in leukemias containing SETBP1 mutations. Gene ontology analysis of deregulated SETBP1 target genes indicates that they are also key controllers of visceral organ development and brain morphogenesis. In line with these findings, in utero brain electroporation of mutated SETBP1 causes impairment of mouse neurogenesis with a profound delay in neuronal migration. In summary, this work unveils a SETBP1 function that directly affects gene transcription and clarifies the mechanism operating in myeloid malignancies and in the Schinzel- Giedion syndrome caused by SETBP1 mutations.Peer reviewe