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Attention-Deficit/Hyperactivity Disorder (ADHD) is closely linked to the development of conduct problems during socialization in early life and to an increased risk for antisocial activities and delinquency over the lifespan. The interaction between ADHD and common comorbid disorders like substance use disorders as well as changing environmental conditions could mediate the course of antisocial and delinquent behavior with increasing age. However, this complex interaction is only partially understood so far. This review presents current knowledge about the association of ADHD with antisociality and the development of delinquent behavior. Thereby, the relationships between ADHD, conduct disorder and antisocial personality disorder in offenders are discussed, as well as the impact of comorbid psychiatric disorders and psychosocial conditions on offending behavior. Also, treatment studies in offender populations with ADHD are presented. Although our understanding of the role of ADHD in the development of criminal behavior has substantially improved during the last two decades, more research is needed to further elucidate the mechanisms generating unfavorable outcomes and to engender adequate treatment strategies for this population at risk. Moreover, more attention is needed on children with conduct problems in order to avoid antisocial or delinquent behaviors over the lifespan.Palagi et al. (Neurosci. Biobehav. Rev. 111149-165, 2020) propose a multidisciplinary approach to the study of spontaneous mimicry, focusing on comparative research on facial mimicry and contagious yawning. In doing so, the authors highlight connections between these behaviors and emotional contagion. The aim of this commentary is to critically evaluate the link between contagious yawning and emotional contagion, address the role of attention in contagious yawning, and promote further research examining the sensory and perceptual factors driving variability in contagious yawning. Contrary to the position of Palagi et al., a strong matching between emotional contagion and contagious yawning has not been established. Variation in contagious yawning appears to be driven by biased attentional processes and yawn detection rather than emotional sharing.The aim of this paper is to leverage the free-energy principle and its corollary process theory, active inference, to develop a generic, generalizable model of the representational capacities of living creatures; that is, a theory of phenotypic representation. Given their ubiquity, we are concerned with distributed forms of representation (e.g., population codes), whereby patterns of ensemble activity in living tissue come to represent the causes of sensory input or data. The active inference framework rests on the Markov blanket formalism, which allows us to partition systems of interest, such as biological systems, into internal states, external states, and the blanket (active and sensory) states that render internal and external states conditionally independent of each other. In this framework, the representational capacity of living creatures emerges as a consequence of their Markovian structure and nonequilibrium dynamics, which together entail a dual-aspect information geometry. This entails a modest representational capacity internal states have an intrinsic information geometry that describes their trajectory over time in state space, as well as an extrinsic information geometry that allows internal states to encode (the parameters of) probabilistic beliefs about (fictive) external states. Building on this, we describe here how, in an automatic and emergent manner, information about stimuli can come to be encoded by groups of neurons bound by a Markov blanket; what is known as the neuronal packet hypothesis. As a concrete demonstration of this type of emergent representation, we present numerical simulations showing that self-organizing ensembles of active inference agents sharing the right kind of probabilistic generative model are able to encode recoverable information about a stimulus array.Pathological dissociation is a severe, debilitating and transdiagnostic psychiatric symptom. This review identifies biomarkers of pathological dissociation in a transdiagnostic manner to recommend the most promising research and treatment pathways in support of the precision medicine framework. A total of 205 unique studies that met inclusion criteria were included. Studies were divided into four biomarker categories, namely neuroimaging, psychobiological, psychophysiological and genetic biomarkers. The dorsomedial and dorsolateral prefrontal cortex, bilateral superior frontal regions, (anterior) cingulate, posterior association areas and basal ganglia are identified as neurofunctional biomarkers of pathological dissociation and decreased hippocampal, basal ganglia and thalamic volumes as neurostructural biomarkers. Increased oxytocin and prolactin and decreased tumor necrosis factor alpha (TNF-α) are identified as psychobiological markers. Psychophysiological biomarkers, including blood pressure, heart rate and skin conductance, were inconclusive. For the genetic biomarker category studies related to dissociation were limited and no clear directionality of effect was found to warrant identification of a genetic biomarker. Recommendations for future research pathways and possible clinical applicability are provided.Over the last decade, precision medicine and immunotherapeutic approaches have become increasingly popular in oncology. read more Early clinical trials reported promising results, but response rates in phase III clinical trials have been suboptimal. Knowledge gained from subsequent translational studies indicates the importance of targeting the tumour microenvironment to overcome resistance to immunotherapy. In this era of precision medicine, it is crucial to consider inter- as well as intratumoural heterogeneity. Single-cell analysis is a cutting-edge technology that enables us to better define the tumour cell community and to identify potential targets for immunotherapy or combination treatments. This review focuses on single-cell analysis in the context of immunotherapy in liver cancer, including the rationale behind studying hepatocellular carcinoma biology at a single-cell level. Single-cell technologies have the potential to revolutionise our understanding of resistance mechanisms and to guide drug discovery efforts, leading to further advances in personalised medicine.
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