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There have been considerable recent advances in understanding the genetic architecture of psychiatric disorders as well as the underlying neurocircuitry. However, there is little work on the concordance of genetic variations that increase risk for cross-disorder vulnerability, and those that influence subcortical brain structures. We undertook a genome-wide investigation of the genetic overlap between cross-disorder vulnerability to psychiatric disorders (p-factor) and subcortical brain structures.

Summary statistics were obtained from the PGC cross-disorder genome-wide association study (GWAS) (N
= 232,964, N
= 494,162) and the CHARGE-ENIGMA subcortical brain volumes GWAS (N=38,851). SNP effect concordance analysis (SECA) was used to assess pleiotropy and concordance. Linkage Disequilibrium (LD) Score Regression and ρ-HESS were used to assess genetic correlation and conditional false discovery (cFDR) was used to identify variants associated with p-factor, conditional on the variants association with surainstem volumes, are consistent with previous work. cFDR results highlight actin binding and neuron regulation as key underlying mechanisms. Further fine-grained delineation of these mechanisms is needed to advance the field.
Military combat trauma is often associated with negative outcomes, including high rates of posttraumatic stress disorder (PTSD). Less is known, however, about whether military combat trauma may foster posttraumatic growth (PTG), which has been observed in relation to other trauma types, in representative samples of veterans.

We analyzed data from veterans who participated in the National Health and Resilience in veterans Study who reported a military-related trauma (n=210). Participants completed measures of trauma history, combat exposure, PTSD symptoms, PTG, functioning, and quality of life (QOL). Bivariate correlations, regression analyses, analyses of covariance, and fit of linear and quadratic functions were used to examine relationships between PTSD symptom clusters, PTG and its subdomains, and functioning.

Number of deployments (β=0.23) and lifetime PTSD symptom severity (β=0.19), particularly re-experiencing symptoms (β=0.37), were independently associated with greater PTG. An inverted-U-shaped quadratic function provided the best fit for the relationship between PTSD symptoms and PTG (R
=0.22). Greater PTG was associated with greater mental functioning (β=0.15) and QOL (β=0.24).

The inability to make casual inferences in this cross-sectional study; possible bias related to self-report measures; and the lengthy time period between index trauma and assessment of PTSD and PTG.

PTG is relatively common among combat veterans, particularly among those with PTSD, and is associated with better mental functioning and QOL. Positive psychology interventions to bolster PTG may help promote functional outcomes in this population.
PTG is relatively common among combat veterans, particularly among those with PTSD, and is associated with better mental functioning and QOL. Positive psychology interventions to bolster PTG may help promote functional outcomes in this population.
Insomnia and affective temperaments influence depressive symptoms in the general population. However, the ways in which the interaction between insomnia and affective temperaments affects depressive symptoms remains unknown. We studied the moderating effects of affective temperaments on the relationship between insomnia and depressive symptoms in adult community volunteers.

The participants were recruited from a community in Japan (n=525). GSK2256098 molecular weight The Athens Insomnia Scale; Temperament Evaluation of Memphis, Pisa, Paris, and San Diego Auto-questionnaire version; and Patient Health Questionnaire-9 were used to evaluate insomnia, affective temperaments, and depressive symptoms, respectively. A hierarchical multiple regression analysis were conducted to evaluate the interactions.

Insomnia significantly and positively interacted with cyclothymic, depressive, and anxious temperaments with regard to depressive symptoms, while insomnia significantly and negatively interacted with hyperthymic temperament on depressive ore, it may be useful to consider affective temperaments while dealing with depressive symptoms associated with insomnia.
Alterations in positive valence systems and social processes, including low reward responsiveness and high rejection sensitivity, have been observed in depression. Most reward research focuses on the monetary domain, but social reward responsiveness may be particularly relevant to understanding the etiology of depression, especially in combination with other social processes. Pathways to depression are complex, and research testing interactions between multiple factors is needed. The present study examined the interactive effects of reward responsiveness and rejection sensitivity on depressive symptoms using both social and monetary reward electroencephalogram (EEG) tasks.

Emerging adults (N=120) completed peer interaction and monetary incentive delay tasks while EEG data were recorded, as well as self-report measures of rejection sensitivity and depressive symptoms.

The interaction between social reward responsiveness and self-reported rejection sensitivity was significantly associated with depressive rch. With extension to longitudinal studies and clinical samples, the present findings may inform understanding of targets for intervention.
There areassociations between maternal mental health (anxiety and depression), maternal-infant bonding, and infant temperament.However, few studies have examined these variables simultaneously, and none have applied a parallel mediation analysis to consider maternal mental health as an explanatory variable.We aimed to examine these relationships, and whether mental health (anxiety and/or depression) mediates the observed association between maternal-infant bonding and infant temperament.

Mothers with babies between zero and twelve months (N=527) were recruited to a cross-sectional online survey containing a battery of psychometric measures.

Correlation analyses examined relationships between the predictor (maternal-infant bonding), outcome (infant temperament), and mediator (maternal mental health; anxiety and/or depression).All associations were highly significant (p<.001). A parallel mediation (anxiety and/or depression) model was conducted, showing a significant indirect effect of maternal-infant r, only anxiety mediated the relationship between bonding and temperament. Healthcare professionals should consider the role of maternal anxiety when working with mothers who present with relational issues or report their infant as excessively challenging. These results signify the need to address maternal anxious and depressive symptoms as distinct issues considering their differential effects on parenting behaviour.
Bipolar disorder (BD) is highly heritable and often severe, particularly when illness onset occurs early in life. There is limited knowledge regarding the clinical and neurostructural correlates of family history of BD among youth with BD.

Clinical characteristics were evaluated in 197 youth with BD, ages 13-20 years, including 87 with familial BD and 110 with non-familial BD. Structural neuroimaging was examined in a subsample of familial BD (n=39), non-familial BD (n=42), and healthy control (HC, n=58) youth. Region of interest (ROI) analyses of anterior cingulate cortex (ACC), inferior frontal gyrus (IFG), and amygdala were complemented by whole-brain vertex-wise analyses.

Youth with familial BD had more family history of other psychiatric disorders, less severe worst manic episode, and less treatment with lithium, selective serotonin reuptake inhibitor (SSRI) antidepressants, and any lifetime psychiatric medications. None of these findings survived after correction for multiple comparisons. There were no significant between-group differences in ROI analyses. In whole-brain analyses, significant differences in cortical thickness were as follows familial and non-familial BD < HC in left precentral gyrus and right inferior parietal lobe; familial BD < HC in left superior frontal gyrus; non-familial BD < HC in right precentral gyrus.

Relatives did not complete full diagnostic interviews.

There were relatively few differences in clinical and neurostructural correlates related to family history of BD in youth with BD. Current findings suggest that family history of BD is not a strong contributor to the clinical or neuroimaging phenotypes in youth with BD.
There were relatively few differences in clinical and neurostructural correlates related to family history of BD in youth with BD. Current findings suggest that family history of BD is not a strong contributor to the clinical or neuroimaging phenotypes in youth with BD.
Childhood maltreatment are well-established risk factors for adolescent psychopathology. Positive childhood experiences (PCEs) known protective factors. However, few studies have simultaneously investigated childhood maltreatment and PCEs in the context of longitudinal study. The aim of this paper was to assess the buffering effect of PCEs in adolescence in the association between chronic childhood maltreatment and psychological symptoms in adolescence.

Data were from an ongoing longitudinal study with 2288 children aged 8.15 y at baseline who were recruited from 3 large elementary schools in China. Participants were followed up for four waves across 6 years. The associations between re-victimization and poly-victimization with adolescent psychopathological symptoms across different PCEs contexts were explored.

Poly-victimization was highly predictive of depressive symptoms, oppositional defiant disorder and conduct disorder. PCEs may mitigate the negative effect of chronic childhood maltreatment on adogies for providing intervention and support to best help reduce the psychopathology burden for children.
Cognitive-behavioral therapy (CBT) is the gold-standard psychotherapeutic treatment for pediatric negative valence disorders. However, some youths do not respond optimally to treatment, which may be due to variations in neural functioning.

We systematically reviewed functional magnetic resonance imaging studies in youths with negative valence disorders to identify pre- and post-treatment neural correlates of CBT response.

A total of 21 studies were identified, of overall weak to moderate quality. The most consistent findings across negative valence disorders consisted of associations of treatment response with pre- and post-treatment task-based activation and/or functional connectivity within and between the prefrontal cortex, the medial temporal lobe, and other limbic regions. Associations of CBT response with baseline and/or post-treatment activity in the striatum, precentral and postcentral gyri, medial and posterior cingulate cortices, and parietal cortex, connectivity within and between the default-mode, cognitive control, salience, and frontoparietal networks, and metrics of large-scale brain network organization, were also reported, although less consistently.

The poor quality and limited number of studies and the important heterogeneity of study designs and results considerably limit the conclusions that can be drawn from this literature.

Despite these limitations, these findings provide preliminary evidence suggesting youths presenting certain patterns of brain function may respond better to CBT, whereas others may benefit from alternative or augmented forms of treatment.
Despite these limitations, these findings provide preliminary evidence suggesting youths presenting certain patterns of brain function may respond better to CBT, whereas others may benefit from alternative or augmented forms of treatment.
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