ABSTRACT
Adolescence, period of transition from childhood to adulthood, is time with changes in social, psychological, behavioral, and physical situations. These changes combined with the cultural, social and family backgrounds' adolescents, can lead to social problems such as social deviations [delinquency].This study aims to compare the components of perceived social support and early maladaptive schemas in adolescents [male and female] delinquent and non-delinquent. This research was based on comparative and causal method. In this research, 100 delinquent adolescents [80 male and 20 female] using convenience sampling method and 100 non-delinquent adolescents [80 male and 20 female] using Cluster sampling method were selected. They completed the Multidimensional Scale of Perceived Social Support [MSPSS] questionnaires and Young Schema Questionnaire-Short Form [YSQ-SF]. Data analysis was performed via descriptive statistics [Mean and SD.] and analytic methods such as independent T-test. Delinquent adolescents had higher mean of early maladaptive schemas and instead had lower level of social support. In addition, delinquent boys had higher early maladaptive schemas mean compared to non-delinquent boys and they had different levels of social support. There was a significant difference in perceived social support between delinquent and non-delinquent girls. Also, there was a significant difference between early maladaptive schemas of delinquent and non-delinquent girls. The findings showed the importance of providing background for strengthening of social support. Identification of early maladaptive schemas as patterns of emotional and cognitive damage in adolescence can be useful to provide appropriate psychological services to improve the quality of life and increased health-related behaviors of delinquent individual
ABSTRACT
Schizophrenia is a severe psychiatric disorder that has a lifetime prevalence of 1% in the most studied population. Schizophrenia is a multifactorial disorder that is characterized by the contribution of multiple susceptibility genes that could act in conjunction with epigenetic processes and environmental factors. Linkage and association studies have shown a number of candidate risk genes including Nerugulin 1, Disrupted in schizophrenia, Disbyndin and Epsin 4 that have associated with schizophrenia. However, their biological function remains elusive. 'Disrupted in schizophrenia 1' [DISC1], a gene locus originally identified at the first in a large Scottish family, showing a heavy burden of major mental illnesses associated with a balanced t[1;11][q42.1;q14.3] chromosome translocation. Substantial genetic and biological research on DISC1 has been displayed in past decade that DISC1 is now recognized as a genetic risk factor for a spectrum of psychiatric disorders and it impacts on many aspects of central nervous system [CNS] function, including neurodevelopment, neurosignaling, and synaptic functioning. Evidences emerged from genetic studies have shown a relationship between DISC1 and quantitative traits, including working memory, cognitive aging, gray matter volume in the prefrontal cortex, and abnormalities in hippocampal structures as well as function. DISC1 interacts with numerous proteins, also involved in neuronal migration, neurite outgrowth, cytoskeletal modulation, and signal transduction, some of which have been reported as independent genetic susceptibility factors for psychiatric morbidity. Here, we studied association of genetic variants of several susceptibility genes to schizophrenia, specially DISC1 and its intractor proteins and their effect on functional and structural of the brain in human and in the mouse
ABSTRACT
The 3-hydroxy-3-methylglutaryl-coenzyme A [HMG-CoA] reductase inhibitors [statins] have revolutionized the treatment of hypercholesterolemia. Some evidence indicated the role of nodal refractoriness and concealed conduction in anticipating the ventricular rate during atrial fibrillation. Recent evidence has indicated that statins can reduce the incidence of both supraventricular and ventricular arrhythmias. The aim of the present study is to investigate adenosine A1 receptor role on simvastatin protective effects on atrioventricular nodal properties in isolated atrial fibrillation model of rabbit heart. The present study was performed in cardiovascular research center of Golestan University of Medical Sciences in 2012. Recovery and atrial fibrillation protocols were used to study electrophysiological properties of atrioventricular node in 5 groups of male Newsland rabbits [n=40]. Extracellular recording was carried out from transitional cells of posterior and anterior extension of AV-node and upper part of atrium and its bundle. All stimuli protocols repeated in the presence of adenosine A1 receptor agonist and antagonist [dipridamole and CPX] alone or with simvastatin on isolated perfused atrio-nodal preparation. Extracellular field potential recording was sampled during specific stimulation protocols. Significant inhibition was observed in basic node properties such as wenckebach prolongation, functional refractory period, effective refractory period and atrioventricular node conduction time with simvastatin [P<0.05]. Simvastatin prolonged His-His interval and increased number of concealed beat in atrial fibrillation protocol [P<0.05]. The simvastatin protective effects on atrioventricular nodal properties were intensified by dipridamole as an adenosine A1 receptor agonist [P<0.05], but CPX as an adenosine A1 receptor antagonist could only dampen them [P>0.05]. Our results showed that the use of adenosine agonist increased simvastatin effects on electrophysiological properties of atrioventricular node, but its antagonist could not prevent these effects. This may indicate simvastatin protective mechanism on atrioventricular node electrophysiological properties without adenosine direct involvement