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If judged against prevailing understandings of community schools (CSs) in the scholarly literature, all Romanian schools should qualify as CSs in light of the regulatory framework. However, few Romanian schools are genuinely CSs. This article describes a recent NGO-led initiative to assist Romanian schools in becoming CSs and explores the nature of this transformation and its outcomes through a case study using a range of primary data, including the school's project reports about activities undertaken, direct observation, and in-depth interview material with relevant stakeholders at the end of the project. After describing the sequence of interventions undertaken as part of the NGO-led project, the article moves on to explore the ways in which school leadership, involved parents, and other local actors reflected on the nature and implications of the school's transformation into a CS in light of the defining characteristics of a CS, beyond superficial compliance with national legal requirements. The article suggests that, in addition to the collaborative process of continuous improvement based on systematic self-assessment using collectively negotiated standards, continued community-wide involvement, and the use of the school as a community resource and venue, one of the politically most relevant aspects of the analyzed school's transformation has been the school's willingness to showcase its approach to policy makers. This is particularly important and welcome in a context in which policy making has been known to be centralized; ad hoc; and, often, detached from schools' resources, needs, and capacities.

Background: Depression has been shown to have adverse effects on blood pressure (BP) and is associated with high blood pressure variability (BPV). In turn, high short-term BPV has been related to eventual cardiovascular risk. But it is not clear how early in adulthood the detrimental effects of depression on BPV may be discerned, if being at high risk for depression also compromises BPV, and whether the clinical features of depression moderate its adverse effects. We investigated these three issues among young adults using an office-like setting. Methods: In total, 218 subjects with a history of childhood-onset major depressive episodes (probands), 206 never-depressed full biological siblings of the probands (high-risk siblings), and 166 emotionally healthy unrelated controls received a psychiatric evaluation and three standardized-sitting BP measurements 5 min apart. Short-term BPV was defined as the maximum difference between measures (range) for each case. The statistical methods included analyses of variance/covariance, chi-square tests, and multiple regression. Results: Systolic and diastolic BP decreased over consecutive measurements (p < 0.001). After controlling for age, the probands, siblings, and controls did not differ significantly in terms of BPV. However, the number of lifetime depressive episodes did predict the diastolic BP range (p = 0.005): probands with the highest number of depressive episodes had the largest short-term diastolic BPV. Conclusions: On a group level, the adverse effects on BPV of having experienced or being at high risk for depression are not yet evident during young adulthood. However, the number of major depressive episodes, which is an index of lifetime depression burden, predicts higher BPV. Thus, BPV monitoring for young adults with clinical depression histories could be part of an early intervention program to reduce the risk of eventual cardiovascular disease. [ABSTRACT FROM AUTHOR]

Respiratory sinus arrhythmia (RSA) is an index of parasympathetic nervous system activity reflecting respiratory influences on heart rate. This influence is typically measured as high frequency heart rate variability (HF‐HRV) or root mean square of successive differences (RMSSD) of adjacent inter‐beat intervals. Examining the long‐term stability of its measurement is important as levels of resting RSA have been conceptualized as a marker of individual differences; in particular, of an individual's autonomic regulation and affect‐related processes, including emotion regulation. At present, it is not known if resting RSA levels reflect stable differences over a long‐term period (i.e., >1 year). Even less is known about how RSA stability differs as a function of depression history and whether it relates to depression risk trajectories. In the present study, we examined the 1.5‐year test–retest reliability of resting RSA using the intraclass correlation coefficient (ICC) in 82 adults: n = 41 with a history of depression (ever‐depressed); n = 41 controls with no depression history (never‐depressed). HF‐HRV was fairly stable in both groups (ever‐depressed ICC = 0.55, never‐depressed ICC = 0.54). RMSSD was also fairly stable in ever‐depressed adults (ICC = 0.57) and never‐depressed controls (ICC = 0.40). ICC values for both indices did not differ between groups per overlapping 95% confidence intervals. Therefore, RSA stability as assessed by both frequency (HF‐HRV) and time domain (RMSSD) measures was not attenuated by a depression history. Implications and the need for future research are discussed. Researchers commonly utilize resting levels of parasympathetically‐mediated heart rate variability (e.g., HF‐HRV, RMSSD) to assess emotion regulation in healthy and clinical samples, particularly depression. However, little is known about its long‐term stability, and even less so in the presence of psychopathology. Our findings indicate that resting HF‐HRV and RMMSD are fairly stable indices of RSA over a period of 1.5 years, on average, among adults with and without a history of depression. [ABSTRACT FROM AUTHOR]

Background: Offspring of depressed parents are at greatly increased risk for mood disorders. Among potential mechanisms of risk, recent studies have focused on information processing anomalies, such as attention and memory biases, in the offspring of depressed parents. In this study we examined another information processing domain, perceptual sensitivity to emotion cues in facial expressions, as a potential mechanism of risk that characterizes the offspring of depressed parents. Methods: The study included 64 children at familial-risk for depression and 40 low-risk peers between the ages 7 and 13 (M[subscript age] = 9.51; SD = 2.27). Participants were presented with pictures of facial expressions that varied in emotional intensity from neutral to full-intensity sadness or anger (i.e., emotion recognition), or pictures of faces morphing from anger to sadness (emotion discrimination). After each picture was presented, children indicated whether the face showed a specific emotion (i.e., sadness, anger) or no emotion at all (neutral) using a forced choice paradigm. We examined group differences in the intensity of emotion that suggested greater sensitivity to specific emotions. Results: In the emotion recognition task, boys (but not girls) at familial-risk for depression identified sadness at significantly lower levels of emotional intensity than did their low-risk peers. The high and low-risk groups did not differ with regard to identification of anger. In the emotion discrimination task, both groups displayed over-identification of sadness in ambiguous mixed faces but high-risk youth were less likely to show this labeling bias than their peers. Conclusion: Our findings are consistent with the hypothesis that enhanced perceptual sensitivity to subtle traces of sadness in facial expressions may be a potential mechanism of risk among boys at familial-risk for depression. This enhanced perceptual sensitivity does not appear to be due to biases in the labeling of ambiguous faces. (Contains 1 table and 3 figures.)

This study examined the relations of school-age children's depressive symptoms, frontal EEG asymmetry, and maternal history of childhood-onset depression (COD). Participants were 73 children, 43 of whom had mothers with COD. Children's EEG was recorded at baseline and while watching happy and sad film clips. Depressive symptoms were measured using parent-report of Children's Depression Inventory. The key findings are the interaction effects between baseline and film frontal EEG asymmetry on child depressive symptoms. Specifically, relative right frontal EEG asymmetry while watching happy or sad film clip was associated with elevated depressive symptoms for children who also exhibited right frontal EEG asymmetry at baseline. Results suggest that right frontal EEG asymmetry that is consistent across situations may be an marker of depression-prone children.

Background: Although low positive affect (PA) and high negative affect (NA) have been posited to predispose to depressive disorders, little is known about the developmental trajectories of these affects in children at familial risk for mood disorders. Methods: We examined 202 offspring of mothers who had a history of juvenile-onset unipolar depressive disorder (n = 60) or no history of major psychopathology (n = 80). Offspring participated in up to seven annual, structured laboratory tasks that were designed to elicit PA and NA. Results: Growth curve analyses revealed that PA increased linearly and similarly for all children from late infancy through age 9. However, there also were individual differences in early PA. Relative to control peers, offspring of mothers with lifetime unipolar depression had consistently lower levels of PA, and this association remained significant even when controlling for current maternal depression and maternal affect displays. Growth curve analyses also revealed a significant linear decrease in NA in children across time; however, there was no significant inter-individual variation either in early NA or rate of change in NA. Conclusion: Attenuated PA (rather than excessive NA) may be an early vulnerability factor for eventual unipolar depressive disorder in at-risk children and may represent one pathway through which depression is transmitted.

Background: Given the long-term morbidity of juvenile-onset major depressive disorder (MDD), it is timely to consider whether more effort should be dedicated to its primary and secondary prevention. Methods: We reviewed studies of prodromal symptoms that may herald a first episode pediatric MDD and considered whether that literature has made an impact on secondary prevention (efforts to prevent progression from symptoms to full disorder). We also reviewed studies of children at familial risk for MDD that addressed atypical affectivity and the regulation of sad, dysphoric affect (mood repair) and related physiological systems, and considered whether research in those areas has made an impact on primary prevention of pediatric MDD (efforts to prevent the disorder). Results: A compelling body of literature indicates that depressive symptoms in youngsters predict subsequent MDD across the juvenile (and early adult) years and that any combination of several symptoms for at least one week is informative in that regard. These findings are echoed in the case selection criteria used by many secondary prevention programs. Convergent findings also indicate that (compared to typical peers) young offspring at familial risk for depression manifest low positive affectivity and compromised mood repair, along with signs of dysfunction in three intertwined physiological systems that contribute to affectivity and mood repair (the hypothalamic-pituitary-adrenal (HPA) axis, cerebral hemispheric asymmetry, and cardiac vagal control). While all these affect-related parameters are suitable for case selection and as intervention targets, they have not yet made an impact on primary prevention programs. Conclusions: According to recent meta-analyses, attempts to prevent pediatric depression have not lived up to expectations. Based on our review, possible reasons for this include: (a) the use of case selection criteria that yield samples heterogeneous with regard to whether the symptoms are truly prodromal to an episode of MDD or are trait-like (which could affect response to the intervention), (b) failure to fully capitalize on the broad-ranging literature on vulnerability to pediatric MDD, as evidenced by the infrequent use of family history of depression (a robust index of vulnerability) or combined indices of vulnerability for case selection, and (c) lack of synchrony between dimensions of vulnerability and the content of the prevention program, as indicated by the overwhelming use of cognitive-behavioral interventions, irrespective of subjects' age, developmental readiness, and whether or not they evidenced the relevant cognitive vulnerability. Prevention trials of pediatric MDD could benefit from new approaches to case selection that combine various indices of vulnerability, more effective use of existing findings, and new or modified interventions that are developmentally sensitive.

Background: This study examined preschoolers' emotion regulation (ER) strategies and the association with temperament, maternal interactive style, and maternal history of childhood-onset depression (COD). Methods: Participants were 62 children and their mothers, 37 of whom had mothers with COD. Children's ER was assessed using a disappointment paradigm; temperament assessment also was laboratory-based. Results: Maternal COD was inversely related to offspring's active ER and positive mood. Among children of COD mothers, behavioral inhibition was associated with passive regulation and sadness, and maternal positivity toward these children was associated with child active ER and positive mood. Conclusion: Behavioral inhibition may place children of COD mothers at risk for developing maladaptive ways of regulating negative emotion, whereas mothers' positivity may serve as a protective factor for them.

Although major depressive disorder (MDD) is associated with suicidal behaviors, some depressed individuals are not suicidal and others evidence various forms of suicidality. We thus investigated whether aspects of temperament and self-regulation of dysphoria represent risk factors for DSM-IV suicidality (recurrent thoughts of death, recurrent suicidal ideation, suicidal plan, and suicide attempt) in depressed youths. Using a sample of children with MDD (N = 407; ages 7-14 years), recruited from clinical sites across Hungary, we tested the hypotheses that: (a) suicidality is related to higher levels of trait negative emotionality as well as more maladaptive and fewer adaptive regulatory responses to dysphoria and (b) as the severity of suicidal behavior increases, levels of trait negative emotionality and dysfunctional emotion regulation also increase. We also explored if other aspects of temperament relate to suicidality. Children's DSM-IV diagnoses were based on semi-structured interviews and best-estimate psychiatric consensus. Parents independently provided ratings of their children's temperament, and children separately completed an inventory of emotion regulation (ER). Using multivariate models, we failed to confirm the hypothesized relations of negative trait emotionality and suicidality, but confirmed that high maladaptive and low adaptive ER response tendencies increase the odds of suicidal behaviors, above and beyond the risk posed by depressive illness severity. Unplanned interaction terms between temperament dimensions (other than negative emotionality) and ER suggested that at some high-extremes of temperament, ER has no impact on suicidality but in their absence, adaptive ER lowers the risk of suicidality. The practical implications of the findings are discussed.

Objective: To pilot test the acceptability and efficacy of contextual emotion-regulation therapy (CERT), a new, developmentally appropriate intervention for childhood depression, which focuses on the self-regulation of dysphoria. Method: Two samples of convenience (n = 29, n = 2) served to verify some CERT constructs; it was then operationalized in a treatment manual. To pilot test CERT, 20 children (ages 7-12; 35% girls) with "DSM" dysthymic disorder (mean duration 24.4 months) entered an open, 30-session, 10-month, 4-phase trial, with 6- and 12-month follow-up. Assessments included independent clinical evaluations and self-rated questionnaires. Results: Fifteen children completed therapy, four were administratively terminated and one dropped out. Completers did not clinically differ from the rest, but they were more likely to have better educated and less depressed mothers and intact families. At the end of treatment, 53% of the completers had full and 13% partial remission of dysthymia (remission from superimposed major depression was 80%). By 6- and 12-month follow-up, 79% and 92% had full remission of dysthymia (p less than 0.0001). Self-reported depressive and anxiety symptoms significantly declined by the end of treatment (p less than 0.001) and remained so throughout follow-up. Conclusions:: CERT enables clinicians to "match" the intervention to children's emotion regulatory needs and symptoms and was readily accepted by families. The promising results suggest the need for a randomized trial. (Contains 1 table and 1 figure.)

Loss-of-function mutations of the KCNJ2 gene encoding for the inward rectifier potassium channel subunit Kir2.1 cause Andersen-Tawil Syndrome (ATS), a rare genetic disorder characterised by periodic paralysis, ventricular arrhythmias, and dysmorphic features. Clinical manifestations of the disease appear to vary greatly with the nature of mutation, therefore, functional characterisation of ATS-causing mutations is of clinical importance. In this study, we describe the identification and functional analysis of a novel KCNJ2 mutation, Val302del, identified in a patient with ATS. Heterologously expressed wild type (WT) and Val302del mutant alleles showed similar subcellular distribution of the Kir2.1 protein with high intensity labelling from the membrane region, demonstrating normal membrane trafficking of the Val302del Kir2.1 variant. Cells transfected with the WT allele displayed a robust current with strong inward rectification, while no current above background was detected in cells expressing the Val302del Kir2.1 subunit. Co-transfection of CHO cells with the WT and the Val302del Kir2.1 revealed a dose-dependent inhibitory effect of the Val302del Kir2.1 mutant subunit on WT Kir2.1 currents. These observations indicate that the WT and the Val302del mutant subunits co-assemble in the cell membrane and that the mutation affects potassium conductivity and (or) gating of the WT/Val302del heteromeric Kir2.1 channels. Key words: Andersen-Tawil Syndrome, KCNJ2 mutation, KCNJ2 gene, inward rectifier potassium channel, Kir2.1 subunit. Les mutations associees a une perte fonctionnelle du gene KCNJ2 codant la sous-unite Kir2.1 du canal potassique a rectification entrante causent le syndrome d'Andersen-Tawil, un trouble genetique rare associe a une paralysie periodique, des arythmies ventriculaires et des caracteristiques dysmorphiques. Les manifestations cliniques de la maladie semblent varier largement selon la nature de la mutation: la caracterisation fonctionnelle des mutations responsables du syndrome d'Andersen-Tawil revet une importance clinique. Dans le cadre de ces travaux, nous decrivons l'identification et l'analyse fonctionnelle de Val302del, une nouvelle mutation du gene KCNJ2 identifiee chez un patient atteint du syndrome d'Andersen-Tawil. Les distributions infracellulaires de la proteine Kir2.1 dans des alleles de type sauvages et portant la mutation Val302del--exprimes de maniere heterologue--etaient similaires et presentaient un marquage a haute intensite de la region membranaire, ce qui montre que la variante Val302del de la proteine Kir2.1 est associee a un trafic membranaire normal. Le courant rectificateur entrant des cellules transfectees avec l'allele de type sauvage etait puissant, alors que celui des cellules exprimant la mutation Val302del de la sous-unite Kir2.1 ne depassait pas le courant de base. La cotransfection de cellules d'ovaires de hamster chinois avec le Kir2.1 de type sauvage et le Kir2.1 de type Val302del a revele un effet inhibiteur de la sous-unite mutante de Kir2.1 (Val302del), dans une mesure proportionnelle a la dose, sur les courants associes au Kir2.1 de type sauvage. Ces observations indiquent que les sous-unites de type sauvage et presentant la mutation Val302del s'assemblent dans la membrane cellulaire et que la mutation affecte la conductivite des canaux potassiques ou la fonction d'ouverture des canaux Kir2.1 heteromeriques de type sauvage/Val302del. [Traduit par la Redaction] Mots-cles: syndrome d'Andersen-Tawil, mutation du gene KCNJ2, gene KCNJ2, canal potassique rectificateur entrant, sous-unite Kir2.1., Introduction Andersen-Tawil Syndrome (ATS) is a rare and unique genetic disorder characterised by a triad of clinical manifestations: periodic paralysis, ventricular arrhythmias, and dysmorphic features that include cranial, facial, and [...]

The objective of this study was to provide evidence that gap junctions are involved in the delayed antiarrhythmic effect of cardiac pacing. Twenty-four dogs were paced through the right ventricle (4x5 min, rate of 240 beats/min) 24 h prior to a 25 min occlusion of the left anterior descending coronary artery. Some of these paced dogs were infused with 50 (n = 7) or 100 µmol/L (n = 7) of the gap junction uncoupler carbenoxolone (CBX), prior to and during the occlusion. Ten sham-paced dogs, subjected only to occlusion, served as the controls. Cardiac pacing markedly reduced the number of ectopic beats and episodes of ventricular tachycardia (VT), as well the incidence of VT and ventricular fibrillation during occlusion. The changes in severity of ischaemia and tissue electrical resistance were also less marked compared with the unpaced controls. Pacing also preserved the permeability of gap junctions, the phosphorylation of connexin43, and the structural integrity of the intercalated discs. The closing of gap junctions with CBX prior to and during ischaemia markedly attenuated or even abolished these protective effects of pacing. Conclusion: Our results support the previous findings that gap junctions play a role in the delayed antiarrhythmic effect of cardiac pacing. Key words: arrhythmias, carbenoxolone, gap junction, cardioprotection, ischaemia-reperfusion. Le but de la presente etude est de fournir des donnees probantes indiquant que les jonctions gap jouent un role dans l'effet antiarythmique retarde de la stimulation electrique cardiaque. Vingt-quatre chiens ont ete soumis a une stimulation electrique du ventricule droit (4x5 min, frequence de 240 battements/min) 24 h avant une occlusion de 25 min de l'artere interventriculaire anterieure. Chez certains des chiens soumis a la stimulation electrique, le carbenoxolone, un decoupleur des jonctions gap, a ete perfuse a des concentrations de 50 p.mol/L (n = 7) et de 100 µmol/L (n = 7) avant et pendant l'occlusion coronarienne. Dix chiens'sham'soumis uniquement a l'occlusion coronarienne ont servi de temoins. La stimulation electrique du creur a nettement diminue le nombre de battements ectopiques et d'episodes de tachycardie ventriculaire, ainsi que la frequence d'apparition de tachycardies et de fibrillations ventriculaires pendant l'occlusion coronarienne. En outre, nous avons observe moins de variations marquees de la gravite de l'ischemie et de la resistance electrique tissulaire que chez les temoins non stimules. La stimulation electrique a aussi preserve la permeabilite des jonctions gap, la phosphorylation de la connexine43 et l'integrite de la structure des disques intercalates. La fermeture des jonctions gap induite par la carbenoxolone avant et pendant l'ischemie a nettement attenue ou meme annule les effets protecteurs de la stimulation electrique. Conclusion: Les resultats de la presente etude s'ajoutent aux resultats precedents qui indiquent que les jonctions gap jouent un role dans l'apparition des effets antiarythmiques retardes de la stimulation electrique du creur. [Traduit par la Redaction] Mots-cles: arythmies, carbenoxolone, jonction gap, cardioprotection, ischemie-reperfusion., Introduction There is substantial evidence for the hypothesis that the electrical uncoupling of cells through gap junctions plays an essential role in the generation of severe ventricular arrhythmias that occur [...]

In their article, Drs. Patalay and Demkowicz raise important questions about research regarding the sex/gender gap in depression rates. However, their perspective on this topic is rather polarizing and yields statements of questionable accuracy. In this Commentary, I respond to several statements in the Article, which I consider potentially misleading. My goal is to present a broader perspective on sex/gender and depression and encourage further discussion of this important topic. [ABSTRACT FROM AUTHOR]

The combination of technologies and efficient urban planning makes up the smart city concept. Over the last 20 years, the geomatics industry has provided city planners with invaluable geospatial data that has helped them understand the environmental, social and economic profiles of buildings, streets and entire neighbourhoods. Smart cities, with their endless source of live sensors, will simply accelerate the process. In this actual context, combining the geomatics and smart cities technology industries will provide mutual co-benefits. Processing this vast amount of geo-linked information is the next frontier in efficient urban planning, enabling city officials diagnose and predict current and future urban phenomena. In essence, the smart city concept is based on geospatial data to enhance the understanding of complex urban systems. It is important that city manager scan quickly obtain relevant information about the urban infrastructure and urban services, as well as stakeholders (citizens) feedback. [ABSTRACT FROM AUTHOR]

Assessed the intellectual development and academic achievement of 87 diabetic children during the first 6 years of their illness. At the initial diagnosis, intellectual performance and school grades were in the average range. Over time, verbal intellectual performance and school grades declined, whereas nonverbal intellectual performance improved slightly. (BC)