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1.
J Dev Behav Pediatr ; 31(7): 545-54, 2010 Sep.
Article in English | MEDLINE | ID: mdl-20729761

ABSTRACT

OBJECTIVE: The aims of this study were to review studies on the molecular genetics of child temperament and prospectively analyze infant temperament as a function of the interaction between infant and mother: 5-HTT, DRD4, and MAO-A functional polymorphisms and the mother's emotional state. METHOD: A prospective study of 317 newborns and their mothers was performed. Infant temperament and the mother's anxiety and confidence in caregiving were evaluated at 8 and 32 weeks after childbirth using the Mother and Baby Scale. The mother's emotional state was evaluated using the Edinburgh Postpartum Depression Scale and the State-Trait Anxiety Inventory. These variables were correlated with 5-HTTLPR and Stin2 variants in the 5-HTT gene and the DRD4 variable number tandem repeats Exon 3 and MAO-A variable number tandem repeats genotypes of both the infants and their mothers. RESULTS: The irritability scores of infants with the 5-HTTLPR s allele showed a linear relationship with their mothers' anxiety of caregiving at 8 (p = .011) and 32 weeks (p = .001), whereas the irritability of infants carrying the HTTLPR ll genotype was independent of their mothers' anxiety. CONCLUSIONS: The review of the literature in this field and the results of this study support that the 5-HTTLPR polymorphism moderates the influence of the mother's anxiety on infant irritability.


Subject(s)
Anxiety/genetics , Infant Behavior/psychology , Mother-Child Relations , Mothers/psychology , Serotonin Plasma Membrane Transport Proteins/genetics , Temperament , Adult , Anxiety/psychology , Environment , Female , Genetic Predisposition to Disease , Humans , Infant, Newborn , Male , Maternal Behavior/psychology , Monoamine Oxidase/genetics , Polymorphism, Genetic , Postpartum Period , Pregnancy , Prospective Studies , Receptors, Dopamine D4/genetics , Risk Factors , Time Factors
2.
Rev. neurol. (Ed. impr.) ; 50(6): 325-332, 16 mar., 2010. tab, ilus
Article in Spanish | IBECS | ID: ibc-86815

ABSTRACT

Introducción. Estudiar el papel del gen del transportador de serotonina (SLC6A4) en el procesado emocional de las alucinaciones auditivas podría ser muy importante para entender mejor su fisiopatología. Además, este gen ya se ha relacionado previamente con trastornos emocionales. El objetivo fue evaluar la relación entre polimorfismos del gen SLC6A4 y diferentes aspectos de las alucinaciones auditivas en la esquizofrenia, con una especial consideración hacia la respuesta emocional frente a las alucinaciones auditivas. Sujetos y métodos. Se compararon dos muestras de 224 pacientes con alucinaciones auditivas y 346 sujetos sanos. La evaluación de las alucinaciones auditivas en los pacientes psicóticos se realizó mediante la escala para la valoración de los síntomas psicóticos (PSYRATS). Varios polimorfismos situados en el gen SLC6A4 se genotiparon y analizaron a través de comparaciones de casos y controles y análisis de asociación con diferentes parámetros clínicos de las alucinaciones auditivas. Resultados. No se encontraron diferencias entre pacientes y controles para ninguno de los polimorfismos analizados (p > 0,05). Sin embargo, la evaluación de los ítems de la escala PSYRATS mostró que los alelos de baja expresión del polimorfismo 5-HTTLPR se asociaban con niveles más altos de ansiedad (p = 0,049, corregido para el ítem ‘intensidad de la ansiedad’). Además, se observó una tendencia a asociación con el parámetro ‘repercusión’ (p = 0,06, corregido). Estos ítems se relacionan con la dimensión emocional de las alucinaciones auditivas. No se observó, en cambio, asociación conparámetros relacionados con otras dimensiones de dichas alucinaciones. Conclusiones. Nuestros resultados apoyan el posible papel del transportador de serotonina en la respuesta emocional de los pacientes con alucinaciones auditivas (AU)


Introduction. To study the role of the serotonin transporter gene (SLC6A4) in the emotional processing of auditory hallucinations it can be particularly important to better understand the pathophysiology of auditory hallucinations. Moreover, a polymorphism located in this gene (5-HTTLPR) has been previously associated with different disorders related to altered emotional responses. The aim of this study was to evaluate the relationship between different polymorphisms of the SLC6A4 gene and different aspects of auditory hallucinations in schizophrenic patients, with a special consideration toward the emotional response to auditory hallucinations. Subjects and methods. Two samples of 224 patients with auditory hallucinations and 346 healthy subjects were studied. AH were assessed in patients through the PSYRATS scale for auditory hallucinations. Several polymorphisms located within the SLC6A4 gene were analysed through case-control comparisons as well as association analyses with different parameters of auditory hallucinations. Results. No differences were found between patients and controls for any of the analysed polymorphisms (p > 0.05). However, the evaluation of auditory hallucinations parameters showed that the low expressing alleles of the 5-HTTLPR polymorphism were associated with higher levels of intensity of the distress caused by auditory hallucinations (p = 0.049 corrected for the item ‘intensity of distress’). There was also a trend with the parameter ‘disruption’ (p = 0.06 corrected). These two items of the PSYRATS scale are directly related to the emotional dimension of auditory hallucinations. In contrast, we did not observe any association with items related to other dimensions of auditory hallucinations. Conclusions. Our results support a possible role of the serotonin transporter in the emotional response to auditory hallucinations (AU)


Subject(s)
Humans , Hallucinations/genetics , Serotonin , Neurotransmitter Transport Proteins/genetics , Psychotic Disorders/genetics , Polymorphism, Genetic , Genetic Markers , Genetic Predisposition to Disease , Case-Control Studies
3.
Cell Host Microbe ; 4(4): 337-49, 2008 Oct 16.
Article in English | MEDLINE | ID: mdl-18854238

ABSTRACT

The requirements for in vivo steady state differentiation of IL-17-producing T-helper (Th17) cells, which are potent inflammation effectors, remain obscure. We report that Th17 cell differentiation in the lamina propria (LP) of the small intestine requires specific commensal microbiota and is inhibited by treating mice with selective antibiotics. Mice from different sources had marked differences in their Th17 cell numbers and animals lacking Th17 cells acquired them after introduction of bacteria from Th17 cell-sufficient mice. Differentiation of Th17 cells correlated with the presence of cytophaga-flavobacter-bacteroidetes (CFB) bacteria in the intestine and was independent of toll-like receptor, IL-21 or IL-23 signaling, but required appropriate TGF-beta activation. Absence of Th17 cell-inducing bacteria was accompanied by increase in Foxp3+ regulatory T cells (Treg) in the LP. Our results suggest that composition of intestinal microbiota regulates the Th17:Treg balance in the LP and may thus influence intestinal immunity, tolerance, and susceptibility to inflammatory bowel diseases.


Subject(s)
Bacteria/immunology , Cell Differentiation , Interleukin-17/biosynthesis , Intestinal Mucosa/immunology , Intestine, Small/immunology , T-Lymphocytes, Helper-Inducer/immunology , Animals , Anti-Bacterial Agents/administration & dosage , Bacteria/drug effects , Mice , Mice, Inbred C57BL , Mice, Knockout , Mucous Membrane , T-Lymphocyte Subsets/immunology , T-Lymphocytes, Regulatory/immunology
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