Riis Cassidy (spongepasta1)

eclines transiently after surgery.The brain continuously receives diverse information about the external environment and changes in the homeostatic state. The attribution of salience determines which stimuli capture attention and, therefore, plays an essential role in regulating emotions and guiding behaviors. Although the thalamus is included in the salience network, the neural mechanism of how the thalamus contributes to salience processing remains elusive. In this mini-review, we will focus on recent advances in understanding the specific roles of distinct thalamic nuclei in salience processing. We will summarize the functional connections between thalamus nuclei and other key nodes in the salience network. We will highlight the convergence of neural circuits involved in reward and pain processing, arousal, and attention control in thalamic structures. We will discuss how thalamic activities represent salience information in associative learning and how thalamic neurons modulate adaptive behaviors. Lastly, we will review recent studies which investigate the contribution of thalamic dysfunction to aberrant salience processing in neuropsychiatric disorders, such as drug addiction, posttraumatic stress disorder (PTSD), and schizophrenia. Based on emerging evidence from both human and rodent research, we propose that the thalamus, different from previous studies that as an information relay, has a broader role in coordinating the cognitive process and regulating emotions. Neurotensin and xenin are two closely related anorexigenic neuropeptides synthesized in the small intestine that exert diverse peripheral and central functions. Both act via the neurotensin-1-receptor. In animal models of obesity reduced central concentrations of these peptides have been found. Dysregulations of the acute and chronic stress response are associated with development and maintenance of obesity. Until now, associations of both peptides with stress, anxiety, depressiveness, and eating disorder symptoms have not been investigated. The aim of the present study was to examine associations of neurotensin and xenin with these psychological characteristics under conditions of obesity. From 2010 to 2016 we consecutively enrolled 160 inpatients (63 men and 97 women), admitted due to obesity and its mental and somatic comorbidities. Blood withdrawal und psychometric tests (PSQ-20, GAD-7, PHQ-9, and EDI-2) occurred within one week after admission. We measured levels of neurotensin and xenin in plasma byelated with perceived stress, anxiety, depressiveness, and eating disorder symptoms. These associations could be influenced by higher prevalence of mental disorders in women and by sex hormones. In men, no correlations were observed, which points toward a sex-dependent regulation. Neurotensin and xenin plasma levels of female obese patients are positively correlated with perceived stress, anxiety, depressiveness, and eating disorder symptoms. NCGC00186528 These associations could be influenced by higher prevalence of mental disorders in women and by sex hormones. In men, no correlations were observed, which points toward a sex-dependent regulation.Angelman syndrome (AS) is caused by loss of information from the 15q11.2-13 region on the maternal chromosome with striking phenotypic difference from Prader-Willi syndrome in which information is lost from the same region on the paternal chromosome. Motivation for social contact and sensory seeking behaviors are often noted as characteristics of the phenotype of AS and it has been argued that the strong drive for social contact supports a kinship theory interpretation of genomic imprinting. In this study we developed an experimental paradigm for quantifying the motivation for social contact in AS and examined differences across the genetic subtypes that cause AS [deletion, imprinting centre defect (ICD), uniparental disomy and UBE3A mutation]. Using single case experimental designs we exam