Schizophrenia, obsessive-compulsive and autistic disorders are traditionally considered as three separate psychiatric conditions each with specific symptoms and pattern of brain alterations. This view can be challenged since these three conditions have the same neurobiological origin, stemming from a common root of a unique neurodevelopmental tree. The aim of this meta-analytic study was to determine, from a neuroimaging perspective, whether i) white matter and gray matter alterations are specific for the three different spectrum disorders, and the nosographical differentiation of three spectra is supported by different patterns of brain alterations. ii) it might be possible to define new spectra starting from specific brain damage. iii) it is possible to detect a “brain damage network” (a connecting link between the damaged areas that relates areas constantly involved in the disorder). Three main findings emerged from our meta-analysis: The three psychiatric spectra do not appear to have their own specific damage. It is possible to define two new damage clusters. The first includes substantial parts of the salience network, and the second is more closely linked to the auditory-visual, auditory and visual somatic areas. It is possible to define a "Damage Network" and to infer a hierarchy of brain substrates in the pattern of propagation of the damage. These results suggest the presence of a common pattern of damage in the three pathologies plus a series of variable alterations that, rather than support the sub-division into three spectra, highlight a two-cluster parcellation with an input-output and more cognitive clusters.

Based on 368.5 pb −1 of e + e − collision data collected at center-of-mass energies 4.914 and 4.946 GeV by the BESIII detector, the e + e − → φχc1(3872) process is searched for the first time. No significant signal is observed and the upper limits at the 90% confidence level on the product of the Born cross section σ(e + e − → φχc1(3872)) and the branching fraction B[χc1(3872) → π + π − J/ψ] at 4.914 and 4.946 GeV are set to be 0.85 and 0.96 pb, respectively. These measurements provide useful information for the production of the χc1( 3872) at e + e − collider and deepen our understanding about the nature of this particle.

A search for the hadronic decays of the h c meson to the final states ppπ + π − π 0 , ppη, and ppπ 0 via the process ψ(3686) → π 0 h c is performed using (4.48 ± 0.03) × 10 8 ψ(3686) events collected with the BESIII detector. The decay channel h c → ppη is observed for the first time with a significance greater than 5σ and a branching fraction of (6.41 ± 1.74 ± 0.53 ± 1.00) × 10 −4 , where the uncertainties are statistical, systematic, and that from the branching fraction of ψ(3686) → π 0 h c . Strong evidence for the decay h c → ppπ + π − π 0 is found with a significance of 4.9σ and a branching fraction of (3.84 ± 0.83 ± 0.69 ± 0.58) × 10 −3 . The significances include systematic uncertainties. No clear signal of the decay h c → ppπ 0 is found, and an upper limit of 6.59 × 10 −4 on its branching fraction is set at the 90% confidence level.

The present review aimed to analyze the scientific literature untill 2010 about the theories of Obsessive Compulsive Disorder in order to make clear how a biological and cognitive hypotheses might be integrated in a comprehensive point of view. In the analysis, at biological level were included neuroanatomic and neurophysiologic models and animal models; instead at cognitive level were included different theories of Salwoskies, Van den Hout, Mancini e Rachman. Biological, cognitive, and behavioral elements of the theories have to be clearly distinguished between specific and general conditions, as do critical past events and current trigger conditions. The theories compared were drawn from the neurobiological, cognitive, and behavioral literature that proposed empirical supported models. We conclude that there are substantive differences among the cognitive theories and between the biological theories reviewed. However, cognitive and biological theories appear to be compatible in principle. It is not clear whether substantive differences among theories are due to the existence of subtypes of OCD or due to the predominance of multifactorial cause. It is argued that current treatment methods imply particular theories, and that particular patterns of success and failure can be understood in relation to theory through the methods we have employed.