RESUMO
BACKGROUND: Growing evidence indicates that if disruptive behavior is left unidentified and untreated, a significant proportion of these problems will persist and may develop into problems linked with delinquency, substance abuse, and violence. Research is needed to develop valid and reliable measures of disruptive behavior to assist recognition and impact of treatments on disruptive behavior. The aim of this study was to develop and evaluate the psychometric properties of a scale for disruptive behavior in adolescents. METHODS: Six hundred high school students (50% girls), ages ranged 15-18 years old, selected through multi stage random sampling. Psychometrics of the disruptive behavior scale for adolescents (DISBA) (Persian version) was assessed through content validity, explanatory factor analysis (EFA) using Varimax rotation and confirmatory factor analysis (CFA). The reliability of this scale was assessed via internal consistency and test-retest reliability. RESULTS: EFA revealed four factors accounting for 59% of observed variance. The final 29-item scale contained four factors: (1) aggressive school behavior, (2) classroom defiant behavior, (3) unimportance of school, and (4) defiance to school authorities. Furthermore, CFA produced a sufficient Goodness of Fit Index > 0.90. Test-retest and internal consistency reliabilities were acceptable at 0.85 and 0.89, respectively. CONCLUSIONS: The findings from this study suggest that the Iranian version of DISBA questionnaire has content validity. Further studies are needed to evaluate stronger psychometric properties for DISBA.
Assuntos
Distonia/diagnóstico , Fosfolipases A2 do Grupo VI/genética , Transtornos Heredodegenerativos do Sistema Nervoso/diagnóstico , Distúrbios do Metabolismo do Ferro/diagnóstico , Distrofias Neuroaxonais/diagnóstico , Adulto , Consanguinidade , Distonia/etiologia , Distonia/genética , Distonia/fisiopatologia , Olho/fisiopatologia , Transtornos Heredodegenerativos do Sistema Nervoso/complicações , Transtornos Heredodegenerativos do Sistema Nervoso/genética , Transtornos Heredodegenerativos do Sistema Nervoso/fisiopatologia , Humanos , Distúrbios do Metabolismo do Ferro/complicações , Distúrbios do Metabolismo do Ferro/genética , Distúrbios do Metabolismo do Ferro/fisiopatologia , Masculino , Distrofias Neuroaxonais/complicações , Distrofias Neuroaxonais/genética , Distrofias Neuroaxonais/fisiopatologia , Torcicolo/fisiopatologia , Adulto JovemRESUMO
Complement C3 glomerulopathy refers to a disease process in which abnormal control of complement activation or degradation results in predominant C3 fragment deposition within the glomerulus and causes glomerular damage. Abnormal control of the complement alternative pathway is a well-established risk factor for the occurrence of C3 glomerulonephritis. It is the first reported case in Iran with multiple mutations in complement factor H, with one of these mutations we have expected in hemolytic uremic syndrome rather than C3 glomerulopathy Genetic analysis showed that the molecular abnormalities of factor H led to complement factor H malfunction that were polymorphous and not restricted to the C-terminal domains of the protein.
Assuntos
Síndrome Hemolítico-Urêmica Atípica/etiologia , Complemento C3/genética , Glomerulonefrite/genética , Glomérulos Renais/patologia , Adulto , Ativação do Complemento , Fator H do Complemento/deficiência , Fator H do Complemento/genética , Via Alternativa do Complemento , Feminino , Glomerulonefrite/complicações , Glomerulonefrite/patologia , Humanos , Irã (Geográfico) , MutaçãoRESUMO
Uromodulin (UMOD) gene mutation causes autosomal dominant Uromodulin-Associated Kidney Disease (UAKD), which in turn leads to end-stage renal disease. This is the first case report of a family with UAKD caused by a novel de novo mutation (E197X) in the UMOD gene. This case is a 28-year-old man with severely reduced kidney function [1]. No similar case was reported in his family history. This report highlights and reminds the importance of genetic screening in young patients involving kidney dysfunction, as the UAKD and some other kidney genetic diseases may be late-onset.
