Early maladaptive schemas and symptoms of psychopathology in children in residential care.

According to schema theory, early maladaptive schemas (EMS) contribute to the onset and development of psychopathology. Given that research on EMS in children is limited, the contribution of the present study is that it investigates the role of EMS in psychopathology in children living in residential care. Participants of the present study were children who lived in residential care and were referred for assessment to the Day Center "The House of the Child" run by the Organisation "The Smile of the Child". The study sample comprised of 75 children (35 boys, 40 girls), mean age 12.7 years old. The Greek version of the Achenbach Child Behavior Checklist was completed by the child's caregiver, whereas the Greek version of the Schema Questionnaire for Children was administered to children. The research questions were explored by implementing both variable-focused (multiple regression) as well as person-focused (cluster analysis) techniques. The Confirmatory Factor Analysis conducted in the Schema Questionnaire for Children showed acceptable goodness of fit indices. The Vulnerability schema was found to be the highest scoring schema. Social isolation was a strong predictor for most indicators of psychopathology (internalizing and externalizing). Strong predictor for the Symptoms of Withdrawal, Anxiety/Depression, Social Problems and Thought Problems was the EMS of Failure. Hierarchical cluster analysis on schemas revealed two strong clusters, one with low scores and one with high scores in most EMS. In the cluster with high levels of EMS, Emotional deprivation, Failure, Defectiveness, Social isolation and Abandonment showed the highest scores. In this cluster, children presented statistically significant burdened indicators in externalizing psychopathology. Our hypotheses that EMS and, especially, schemas related to the domains of Disconnection/Rejection and Impaired Autonomy/Performance would be predictive indicators of psychopathology were confirmed. Cluster analysis confirmed the above findings and highlighted the role of schemas Emotional deprivation and Defectiveness in the emergence of psychopathology symptoms. The results of the current study highlight the importance of assessing EMS in children who live in residential care and could inform the development of appropriate intervention programs in this population to prevent the establishment of psychopathology.

Effects of dipeptidyl peptidase-4 (DPP-4) inhibition on angiogenesis and hypoxic injury in type 2 diabetes.

AIMS: We examined whether, in diabetic Ob/Ob mice, the dipeptidyl peptidase-4 (DPP-4) inhibitor (PKF275-055), an antihyperglycemic drug, that inhibits the biological inactivation of SDF-1 (stromal cell-derived factor-1), may increase endothelial progenitor cells (EPCs) mobilization and incorporation, which, in turn, may regenerate capillaries and reduce myocardial ischemia induced by strenuous exercise. MAIN METHODS: Half of sixteen control and Ob/Ob mice and eight Ob/Ob mice treated with PKF275-055 for four weeks underwent a forced swim protocol. Oral glucose tolerance, circulating EPCs, capillary ultrastructure and density, hypoxic areas and SDF-1 localization in myocardium were measured. KEY FINDINGS: Ob/Ob mice were glucose intolerant, had a significant low number of circulating EPCs and myocardial capillaries compared to lean controls. The DPP-4 inhibitor significantly improved their glucose tolerance, doubled the number of circulating EPCs, stimulated the formation of functional vessels and SDF-1 localization in the endothelium of myocardial capillaries and arterioles. Cardiac hypoxia after forced swim in Ob/Ob mice was significantly reduced when they were treated with the DPP-4 inhibitor. SIGNIFICANCE: DPP-4 inhibition may re-establish an adequate capillary network in the myocardium of diabetic Ob/Ob mice by the mobilization and SDF-1-mediated incorporation of EPCs and, consequently, reducing the susceptibility to myocardial ischemic injury provoked by strenuous exercise.

Selection of potential predictors of worsening heart failure: rational and design of the SELENE HF study.

BACKGROUND: Heart failure is a leading cause of hospitalization and a significant medical burden in our society. Implantable medical devices are nowadays established therapies in heart failure patients that not only provide cardiac resynchronization therapy (CRT) and implantable cardioverter defibrillators (ICDs) therapy but are also able to continuously and remotely monitor diagnostic information of various physiologic parameters. The value of combining individual diagnostic variables to predict worsening of heart failure is still largely unclear but could eventually become a valuable tool towards a better heart failure management. METHODS: SELENE HF (Selection of potential predictors of worsening Heart Failure) is an observational, multicentre study designed to prospectively collect follow-up and home monitoring data trends from a population of individuals with ICDs with or without resynchronization therapy (CRT-D), to document heart failure hospitalizations and deaths and to correlate these events with Home Monitoring data in order to identify the combination with the greatest sensitivity and specificity in predicting heart failure events.The purpose of this study is to describe the design of the study focusing on the Heart Failure Predicting model and statistical approach that will be used to analyse the data. CONCLUSION: The results of the SELENE HF study could help to select and define potential predictors of worsening heart failure in patients with remotely monitored ICD or CRT-D devices. TRIAL REGISTRATION: ClinicalTrials.gov Identifier NCT01836510.

Placental HIFs as markers of cerebral hypoxic distress in fetal mice.

Reduced oxygen supply during the pre- and perinatal period often leads to acquired neonatal brain damage. So far, there are no reliable markers available to assess the hypoxic cerebral damage and the resulting prognosis during the immediate postnatal period. Thus we aimed to determine whether the hypoxia-inducible transcription factors (HIF-1 and HIF-2) and/or their target genes in the placenta represent reliable indicators of hypoxic distress of the developing brain during systemic hypoxia at the end of gestation. To this end, pregnant mice were exposed to systemic hypoxia (inspired O2 fraction: 6%, 6 h) at gestational day 20. This hypoxic exposure significantly increased HIF-1alpha and HIF-2alpha protein levels in brain and placental tissue. Compared with normoxic controls, an increase of HIF-1alpha-immunoreactive neurons and HIF-2alpha-positive glial cells and vascular endothelial cells was observed in hypoxic cerebral cortex and hippocampus. In placenta, HIF-1alpha and HIF-2alpha were expressed in labyrinthine layer with increased staining intensity during hypoxia compared with normoxia. Significant upregulation of VEGF mRNA and protein in brain and placenta, as well as erythropoietin protein in placenta, indicated activity of the HIF system upon fetal hypoxia. Notably, hypoxia did not affect expression of the HIF target genes inducible nitric oxide synthase and GLUT-1. Taken together, at gestational day 20, systemic hypoxia led to upregulation of HIF-alpha in mouse brain that was temporally paralleled in placenta, implying that alpha-subunits of both HIF-1 and HIF-2 are indeed early markers of hypoxic distress in vivo. If our data reflect the situation in humans, analysis of the placenta will allow early identification of the hypoxic brain distress occurring near birth.