Relation between EEG source functional connectivity and the negative symptom severity in schizophrenia: a preliminary report from a multicentre study

IntroductionNeural dysconnectivity is hypothesized to be a key element in pathophysiology of schizophrenia. However, the relation of disordered connectivity with the different clinical characteristics of the syndrome is not fully elucidated.ObjectivesThe current research investigated the relations between resting-state EEG Source Functional Connectivity (EEG-SFC) and the two main clusters of negative symptoms derived from the Brief Negative Symptom Scale, the Expressive Deficit (ED) and the Avolition (AV), in subjects with schizophrenia (SCZ) enrolled to the multicentre study of the Italian Network for Research on Psychoses.MethodsOut of 97 chronic, stabilized SCZ included, we selected subjects according the lower and the upper quartile of the ED and AV value distribution: 25 were in upper and 24 in the lower quartile of ED (respectively, HIGH-ED and LOW-ED); 27 were in upper and 24 in the lower quartile of AV (respectively, HIGH-AV and LOW-AV). Fifty-five healthy controls (HC) were included, comparable to SCZ for gender, age and educational level. EEG-SFC analysis was based on the lagged phase synchronization (LPS) computed by eLORETA from 5 minutes resting-state EEG recordings in eyes closed condition. LPS indices were determined for each spectrum band and between all 28 regions of interest (ROI) pairs. Group differences were significant for corrected P-value &lt; 0.05.ResultsSCZ had higher theta band LPS than HC. Respect to LOW-ED, HIGH-ED showed significant increased alpha LPS in fronto-cingulate, para-hippocampal and insular inter-hemispheric ROI pairs. No significant difference emerged between HIGH-AV and LOW-AV.ConclusionsSubgrouping SCZ according to negative symptom severity reveals heterogeneous patterns of resting-state LPS connectivity.Disclosure of interestThe authors have not supplied their declaration of competing interest.</jats:sec

Dry acellular oesophageal matrix prepared by supercritical carbon dioxide

The research leading to these results received funding from Cassa di Risparmio di Trento e Rovereto (CaRiTRo) within the research project “Supercritical decellularization of engineered tissues for clinical application”, biomedical science section, 2013. PDC is supported by NIHR Professorship and the Catapult Cell Therapy, UK. NMP is supported by the European Research Council (ERC StG Ideas 2011 BIHSNAM no. 279985 on ‘Bio-Inspired hierarchical super-nanomaterials’, ERC PoC 2013 KNOTOUGH no. 632277 on ‘Super-tough knotted fibres’, ERC PoC 2015 SILKENE no. 693670 on ’Bionic silk with graphene or other nanomaterials spun by silkworms’) and by the European Commission under the Graphene Flagship (WP14 ‘Polymer Composites’, no. 696656). NE thanks Lorenza Lazzari for the donation of BM-MSCs from the Cell Factory Bank (Milan-Italy)

Transcriptional Control in Cardiac Progenitors: Tbx1 Interacts with the BAF Chromatin Remodeling Complex and Regulates Wnt5a

Mutations of the Wnt5a gene, encoding a ligand of the non-canonical Wnt pathway, and the Ror2 gene, encoding its receptor, have been found in patients with cardiac outflow tract defects. We found that Wnt5a is expressed in the second heart field (SHF), a population of cardiac progenitor cells destined to populate the cardiac outflow tract and the right ventricle. Because of cardiac phenotype similarities between Wnt5a and Tbx1 mutant mice, we tested potential interactions between the two genes. We found a strong genetic interaction in vivo and determined that the loss of both genes caused severe hypoplasia of SHF–dependent segments of the heart. We demonstrated that Wnt5a is a transcriptional target of Tbx1 and explored the mechanisms of gene regulation. Tbx1 occupies T-box binding elements within the Wnt5a gene and interacts with the Baf60a/Smarcd1 subunit of a chromatin remodeling complex. It also interacts with the Setd7 histone H3K4 monomethyltransferase. Tbx1 enhances Baf60a occupation at the Wnt5a gene and enhances its H3K4 monomethylation status. Finally, we show that Baf60a is required for Tbx1–driven regulation of target genes. These data suggest a model in which Tbx1 interacts with, and probably recruits a specific subunit of, the BAF complex as well as histone methylases to activate or enhance transcription. We speculate that this may be a general mechanism of T-box function and that Baf60a is a key component of the transcriptional control in cardiac progenitors

Increasing along rays vector functions

The class of increasing along rays functions is generalized to consider vector valued functions. A general approach through scalarization is used and minimal properties for the scalarization are given. The class of vector increasing along rays functions introduced is compared with the scalar one to prove similar properties hold. The relation with convex and generalized convex functions is preserved for the vector valued counterpart