Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 9 de 9
Filtrar
Mais filtros

Base de dados
País/Região como assunto
Tipo de documento
País de afiliação
Intervalo de ano de publicação
1.
Mol Psychiatry ; 28(9): 3851-3855, 2023 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-37845495

RESUMO

Life threatening trauma and the development of PTSD during childhood, may each associate with transcriptional perturbation of immune cell glucocorticoid reactivity, yet their separable longer term contributions are less clear. The current study compared resting mononuclear cell gene expression levels of the nuclear receptor, subfamily 3, member 1 (NR3C1) coding the glucocorticoid receptor, its trans-activator spindle and kinetochore-associated protein 2 (SKA2), and its co-chaperon FKBP prolyl isomerase 5 (FKBP5), between a cohort of young adults first seen at the Hadassah Emergency Department (ED) after surviving a suicide bombing terror attack during childhood, and followed longitudinally over the years, and matched healthy controls not exposed to life threatening trauma. While significant reductions in mononuclear cell gene expression levels were observed among young adults for all three transcripts following early trauma exposure, the development of subsequent PTSD beyond trauma exposure, accounted for a small but significant portion of the variance in each of the three transcripts. Long-term perturbation in the expression of immune cell glucocorticoid response transcripts persists among young adults who develop PTSD following life threatening trauma exposure in childhood, denoting chronic dysregulation of immune stress reactivity.


Assuntos
Transtornos de Estresse Pós-Traumáticos , Suicídio , Humanos , Adulto Jovem , Proteínas Cromossômicas não Histona , Glucocorticoides , Receptores de Glucocorticoides/genética , Receptores de Glucocorticoides/metabolismo , Transtornos de Estresse Pós-Traumáticos/genética , Transtornos de Estresse Pós-Traumáticos/metabolismo , Criança
2.
Mol Psychiatry ; 26(11): 6680-6687, 2021 11.
Artigo em Inglês | MEDLINE | ID: mdl-33981010

RESUMO

Childhood adversity (CA) may alter reactivity to stress throughout life, increasing risk for psychiatric and medical morbidity, yet long-term correlates of milder CA levels among high functioning healthy adolescents are less studied. The current study examined the prevalence and impact of CA exposure among a cohort of healthy motivated elite parachute unit volunteers, prospectively assessed at rest and at the height of an intensive combat-simulation exposure. We found significantly reduced gene expression levels in resting mononuclear cell nuclear receptor, subfamily 3, member 1 (NR3C1), and its transactivator spindle and kinetochore-associated protein 2 (SKA2), that predict blunted cortisol reactivity to combat-simulation stress among CA exposed adolescents. Long-term alterations in endocrine immune indices, subjective distress, and executive functions persist among healthy high functioning adolescents following milder CA exposure, and may promote resilience or vulnerability to later real-life combat exposure.


Assuntos
Experiências Adversas da Infância , Militares , Adolescente , Proteínas Cromossômicas não Histona/metabolismo , Humanos , Hidrocortisona/metabolismo , Receptores de Glucocorticoides/genética , Receptores de Glucocorticoides/metabolismo , Estresse Psicológico/metabolismo
3.
Eat Weight Disord ; 25(6): 1821-1825, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31667778

RESUMO

OBJECTIVE: Uric acid (UA) is increasingly recognized as having important physiological roles and associated with several peripheral and central pathophysiological outcomes, and might play a role in eating disorders (ED) pathogenesis. We investigated whether UA levels are altered among adolescents with ED. METHODS: Morning salivary UA concentrations were compared between adolescents referred to treatment at the Herman Dana Center receiving a DSM-V diagnosis of an ED and matched healthy controls. RESULTS: Salivary UA was significantly elevated among ED compared with control values (ED mean 3.9 ± 1.2 mg/dl, control mean 2.9 ± 1.9 mg/dl, t = - 3.13 df = 81, p = 0.003). DISCUSSION: Salivary UA is elevated among adolescents with ED. Further studies are required to replicate and extend this finding and evaluate its generalizability as a state or trait marker as regards ED subtypes, other body fluids (plasma and cerebrospinal fluid), and recovery or premorbid stages, as well as its putative mechanistic relevance to ED. LEVEL OF EVIDENCE: Level III, case-control analytic study.


Assuntos
Anorexia Nervosa , Bulimia Nervosa , Transtornos da Alimentação e da Ingestão de Alimentos , Adolescente , Estudos de Casos e Controles , Manual Diagnóstico e Estatístico de Transtornos Mentais , Transtornos da Alimentação e da Ingestão de Alimentos/diagnóstico , Humanos , Ácido Úrico
4.
Neuropsychobiology ; 76(3): 130-135, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-29949798

RESUMO

BACKGROUND AND AIM: Long-term immune alterations have been proposed to play a mechanistic role in posttraumatic stress disorder (PTSD) as well as in its associated increase in medical morbidity and mortality. Better characterization of altered immune function may help identify diagnostic and prognostic biomarkers and potentially targets for preventive intervention. METHODS: As part of an ongoing study, we conducted a preliminary case-control comparison of resting immune inflammatory profiles between terror victims treated in childhood at the emergency department over the previous decade, who developed chronic PTSD upon long-term follow-up, and healthy controls. RESULTS: Our preliminary results in a subsample of this ongoing study support and extend elevated resting levels of granulocyte colony-stimulating factor, interleukin-4, and regulated on activation, normal T cell expressed and secreted in childhood onset chronic PTSD. CONCLUSION: Chronic immune alterations may participate in inflammatory activation and signal to the CNS through the neurovascular unit, as well as modulate the neuroendocrine axis. Better characterization and understanding of these preliminary findings may point to diagnostic and prognostic biomarkers and potentially elucidate mechanistic involvement of immune activation in PTSD.

5.
J Inherit Metab Dis ; 33(4): 429-36, 2010 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-20549363

RESUMO

Anderson-Fabry disease (AFD) is an X-linked inherited lysosomal storage disorder disease caused by a deficiency in the activity of the alpha-galactosidase enzyme. We investigated neuropsychological and psychiatric function in AFD patients. We studied 16 AFD patients, aged 7 to 61 years. Intelligence, language, vision-spatial abilities, memory, sensorimotor abilities, and attention and executive functions were tested with a computerized test battery as well as standard paper and pencil tests. The results were compared to known age-based norms. In addition, all patients were screened for lifelong DSM-IV Axis-I and Axis-II psychiatric diagnoses, and 4 were interviewed by a psychiatrist. Performance on most cognitive measures was within average range. All measures of information processing speed were significantly reduced, as were some measures of executive functions. Ten out of 16 patients met DSM-IV criteria for Axis I or Axis II diagnoses at some point in their lives. This preliminary study delineates a psychiatric and cognitive phenotype in AFD patients and contributes to the growing field of characterizing behavioral phenotypes of patients with genetic diseases. We suggest that psychiatric and neuro-psychological evaluation be included in the patient's evaluation.


Assuntos
Transtornos Cognitivos/etiologia , Transtornos Cognitivos/fisiopatologia , Doença de Fabry/complicações , Doença de Fabry/psicologia , Adolescente , Adulto , Atenção , Criança , Feminino , Humanos , Testes de Inteligência , Masculino , Memória , Pessoa de Meia-Idade , Testes Neuropsicológicos , Projetos Piloto , Desempenho Psicomotor
6.
J Pediatr Surg ; 53(8): 1526-1531, 2018 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-29129330

RESUMO

INTRODUCTION: Surgical procedures involve traumatic stress. Children may develop chronic psychological distress and dysfunction after surgery, with consequent reluctance to comply with medical follow-up care. A literature review of this topic shows that it has been understudied. Our study aims to assess the frequency and characteristics of symptoms of persistent psychological distress in children following surgery, which have not been documented before, in order to promote its awareness and its early identification. METHODS: Parents of 79 children (aged 1-6) that were hospitalized in a pediatric surgical ward, comprising a representative sample, completed three validated questionnaires assessing their children's psychological symptoms 3-5months after the hospitalization. RESULTS: A significant portion of children suffer from psychological distress 3-5months after hospitalization. Moreover, 10.39% of the children exhibited symptoms of PTSD, and 28.6% of parents reported that the child's distress causes dysfunction. Additionally, our findings emphasize the parents' concerns regarding the child's behavior, function, and health following hospitalization. CONCLUSION: Since a significant prevalence of hospitalization-related traumatic stress is documented, the awareness to it has to be improved, in order to reduce its frequency and increase adherence to medical follow-up care. TYPE OF STUDY: Prognosis study. LEVEL OF EVIDENCE: 1.


Assuntos
Transtornos de Estresse Pós-Traumáticos/epidemiologia , Estresse Psicológico/epidemiologia , Procedimentos Cirúrgicos Operatórios/psicologia , Adolescente , Criança , Comportamento Infantil , Pré-Escolar , Feminino , Hospitalização/estatística & dados numéricos , Humanos , Lactente , Masculino , Pais/psicologia , Prevalência , Fatores de Risco , Transtornos de Estresse Pós-Traumáticos/etiologia , Estresse Psicológico/etiologia , Inquéritos e Questionários
7.
Isr J Psychiatry Relat Sci ; 40(1): 57-66, 2003.
Artigo em Inglês | MEDLINE | ID: mdl-12817670

RESUMO

Attention Deficit and Hyperactivity Disorder (ADHD) is a common idiopathic childhood neurodevelopmental disorder, exacting a significant clinical and public health toll. It impairs schooling and social adaptation, resulting in high rates of depression, conduct disorder, school dropouts, and substance abuse, and necessitating exposure of many children to prolonged courses of stimulant psychotropic medication. Although the biological basis of ADHD is unknown, it has been shown to possess considerable heritability. Candidate gene association studies proved to be a productive strategy leading to replicated association findings of genetic loci contributing to susceptibility to ADHD. Based on the mechanism of action of stimulant drugs effective in the alleviation of ADHD symptoms, current association studies have focused mainly on dopaminergic genes. Promising exploratory findings have also been reported for genes affecting other neurotransmitter systems. The current article reviews the rationale, methodology, and main findings in the field, and outlines future directions. Locating the actual genes mediating ADHD susceptibility will have far reaching implications for understanding the pathophysiology of ADHD as well as for understanding mechanisms of therapeutic drug action and genetic determinants of response.


Assuntos
Transtorno do Deficit de Atenção com Hiperatividade/genética , Glicoproteínas de Membrana , Proteínas de Membrana Transportadoras , Proteínas do Tecido Nervoso , Proteínas de Saccharomyces cerevisiae , Transtorno do Deficit de Atenção com Hiperatividade/tratamento farmacológico , Transtorno do Deficit de Atenção com Hiperatividade/metabolismo , Estimulantes do Sistema Nervoso Central/uso terapêutico , Criança , Proteínas de Ligação a DNA/genética , Dopamina/genética , Dopamina/metabolismo , Proteínas da Membrana Plasmática de Transporte de Dopamina , Humanos , Metilfenidato/uso terapêutico , Repetições Minissatélites/genética , Polimorfismo Genético/genética
8.
Isr J Psychiatry Relat Sci ; 47(1): 72-82, 2010.
Artigo em Inglês | MEDLINE | ID: mdl-20686202

RESUMO

Major depressive disorder (MDD) is a heterogeneous, highly prevalent, and moderately heritable disorder. A complex and diverse genetic-environmental interplay converges to set apart a significant minority that is susceptible to MDD, from among those who experience shorter lived and less recurrent intensive and incapacitating forms of sadness. The major technological advances of deciphering the human genome reference sequence and its common gene variations are beginning to allow cost effective genetic studies of unprecedented scale, applying increasingly denser genome wide mapping to increasingly larger case control samples. This effort is now at the initial stages of unraveling the genetic architecture of several complex phenotypes. Despite a tardy beginning, MDD genetic research is maturing from modest scale candidate gene association studies to include family-based linkage studies, and will soon allow genome wide case control association studies. Replicated risk conferring gene variants discovered so far exert a modest effect size that appears to contribute to overt phenotype expression in the context of a highly intricate concert of interrelated epigenetic and epistatic modifiers. The unraveling of additional previously unimplicated MDD risk conferring genes, that will throw light on molecular mechanisms mediating such susceptibilities, is necessary for progressing beyond current generation monoamine modulating antidepressant drugs. The review outlines basic concepts and current progress briefly overviews major replicated gene findings that to date mostly stem from hypotheses driven candidates, and ends with a discussion of current directives, including sample size and phenotype considerations and advancement of systematic studies of the functional significance of implicated gene variants, beyond their current exploratory stage.


Assuntos
Transtorno Depressivo Maior/genética , Frequência do Gene , Variação Genética , Receptor trkC/genética , Proteínas da Membrana Plasmática de Transporte de Serotonina/genética , Transtorno Depressivo Maior/psicologia , Família/psicologia , Predisposição Genética para Doença , Genoma Humano , Estudo de Associação Genômica Ampla , Humanos , Fenótipo , Fatores de Risco , Índice de Gravidade de Doença
9.
Int J Eat Disord ; 37(4): 357-9, 2005 May.
Artigo em Inglês | MEDLINE | ID: mdl-15856493

RESUMO

OBJECTIVE: The current study described a subgroup of children presenting with obesity and comorbid attention deficit/hyperactivity disorder (AD/HD) and assessed a possible casual relationship. METHOD: School-aged children hospitalized for obesity (body mass index [BMI] >85%) in a tertiary referral center underwent extensive evaluations and were prospectively assessed for comorbid AD/HD. RESULTS: During a 4-year period, 32 obese school-aged children were hospitalized and 26 were included in the current study. We found that over one half (57.7%) suffered from comorbid AD/HD. DISCUSSION: AD/HD shows a high comorbidity among obese hospitalized children. The characteristic difficulty in regulation found in AD/HD may be a risk factor for the development of abnormal eating behaviors leading to obesity. We suggest that obese children should be screened routinely for AD/HD.


Assuntos
Transtorno do Deficit de Atenção com Hiperatividade/epidemiologia , Obesidade Mórbida/epidemiologia , Adolescente , Criança , Criança Hospitalizada/estatística & dados numéricos , Comorbidade , Feminino , Humanos , Israel/epidemiologia , Masculino , Prevalência , Fatores de Risco
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA