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1.
BMC Psychiatry ; 22(1): 146, 2022 02 24.
Artigo em Inglês | MEDLINE | ID: mdl-35209866

RESUMO

BACKGROUND: Somatic depression (SD) is different from non-somatic depression (NSD), and insular subregions have been associated with somatic symptoms. However, the pattern of damage in the insular subregions in SD remains unclear. The aim of this study was to use functional connectivity (FC) analyses to explore the bilateral ventral anterior insula (vAI), bilateral dorsal anterior insula (dAI), and bilateral posterior insula (PI) brain circuits in SD patients. METHODS: The study included 28 SD patients, 30 NSD patients, and 30 matched healthy control (HC) subjects. All participants underwent 3.0 T resting state functional magnetic resonance imaging. FC analyses were used to explore synchronization between insular subregions and the whole brain in the context of depression with somatic symptoms. Pearson correlation analyses were performed to assess relationships between FC values in brain regions showing significant differences and the total and factor scores on the 17-item Hamilton Rating Scale for Depression (HAMD17). RESULTS: Compared with the NSD group, the SD group showed significantly decreased FC between the left vAI and the right rectus gyrus, right fusiform gyrus, and right angular gyrus; between the right vAI and the right middle cingulate cortex, right precuneus, and right superior frontal gyrus; between the left dAI and the left fusiform gyrus; and between the right dAI and the left postcentral gyrus. Relative to the NSD group, the SD group exhibited increased FC between the left dAI and the left fusiform gyrus. There were no differences in FC between bilateral PI and any brain regions among the SD, NSD, and HC groups. Within the SD group, FC values between the left vAI and right rectus gyrus were positively correlated with cognitive impairment scores on the HAMD17; FC values between the right vAI and right superior frontal gyrus were positively related to the total scores and cognitive impairment scores on the HAMD17 (p < 0.05, uncorrected). CONCLUSIONS: Aberrant FC between the anterior insula and the frontal and limbic cortices may be one possible mechanism underlying SD.


Assuntos
Disfunção Cognitiva , Sintomas Inexplicáveis , Encéfalo , Depressão , Humanos , Imageamento por Ressonância Magnética/métodos
2.
Zhong Nan Da Xue Xue Bao Yi Xue Ban ; 33(4): 316-20, 2008 Apr.
Artigo em Chinês | MEDLINE | ID: mdl-18460775

RESUMO

OBJECTIVE: To investigate whether there is association between the-2548G/A functional polymorphism in the promoter region of leptin gene and weight gain following antipsychotic agents (APS) acute treatment in schizophrenic patients. METHODS: Eight-four Chinese Han untreated schizophrenia patients in 70 nuclear families were recruited. The polymorphism of leptin gene was determined with PCR-RFLP technique. Body weight was measured in the patients on admission the and after 10 weeks treatment with risperidone or chlorpromazine. RESULTS: There was an average (8.00+/-6.13)% increases in baseline weight after the 10 week treatment. There were significant differences in the distribution of allele frequencies (chi2=4.031, P=0.045) between the patients with weight changed >or=7% and <7% subgroups. Family-based association analysis further confirmed the above significant finding by transmission disequilibrium test but not by quantitative trait transmission disequilibrium test. CONCLUSION: The finding confirms that the-2548G/A polymorphism in promoter region of leptin gene is associated with APS-induced weight gain.


Assuntos
Antipsicóticos/uso terapêutico , Leptina/genética , Polimorfismo de Fragmento de Restrição , Esquizofrenia/tratamento farmacológico , Aumento de Peso/efeitos dos fármacos , Adolescente , Adulto , Saúde da Família , Feminino , Genótipo , Humanos , Masculino , Reação em Cadeia da Polimerase , Regiões Promotoras Genéticas/genética , Esquizofrenia/genética , Esquizofrenia/fisiopatologia , Aumento de Peso/genética
3.
Zhonghua Yi Xue Za Zhi ; 87(5): 315-20, 2007 Jan 30.
Artigo em Chinês | MEDLINE | ID: mdl-17456359

RESUMO

OBJECTIVE: To study the physiologic base of voice familiarity (VF) and the mechanism of auditory verbal hallucination (AVH) in the patients with schizophrenia (SCH). METHODS: Twenty-six schizophrenic patients, 13 with and 13 without AVH, and 13 healthy control subjects were instructed to passively listen to familiar or unfamiliar voices and to give their judgment and underwent event-related functional magnetic resonance imaging (efMRI) based on blood oxygenation level-dependent (BOLD) signal efficacy. The functional images were collected by using a 1.5-T MRI and were analyzed by using statistical parametric mapping 2 (SPM2). RESULTS: The total score of positive symptoms of the SCH patients with AVH was (45.5 +/- 13.2), significantly higher than that of the SCH patients without AVH [(22.2 +/- 6.7), P < 0.05]. In comparison with unfamiliar voices, familiar voices elicited greater responses in the left superior temporal gyrus, right frontal lobe and limbic lobe among the SCH patients with AVH (P < 0.005, K(E) > 10). IN comparison with healthy control group, when the patients with AVH discriminated the familiar voices their left precuneus lobes were activated more significantly, and when they discriminated unfamiliar voices their right frontal lobes were activated more significantly (P < 0.005, K(E) > 10). In comparison with the SCH patients without AVH when the SCH patients with AVH discriminated the familiar voices their right frontal lobe were activated more significantly (P < 0.005, K(E) > 10), however, when they discriminated unfamiliar voices there was not significantly difference in the activation of the right frontal lobe between these groups. CONCLUSION: The efMRI results of the inter-group comparison support the inner speech disorder hypothesis that the activation of inner speech in the SCH patients with AVH inhibits the activation of external voice on the corresponding cerebral areas. In addition, hallucinating patients may have significant change of VF neurocognitive model.


Assuntos
Percepção Auditiva/fisiologia , Alucinações/fisiopatologia , Imageamento por Ressonância Magnética/métodos , Esquizofrenia/fisiopatologia , Adulto , Atenção/fisiologia , Humanos , Masculino , Testes Neuropsicológicos , Psicologia do Esquizofrênico
4.
Zhonghua Yi Xue Yi Chuan Xue Za Zhi ; 22(5): 575-6, 2005 Oct.
Artigo em Chinês | MEDLINE | ID: mdl-16215954

RESUMO

OBJECTIVE: To investigate whether the -1438G/A polymorphism in the promoter region of 5-HTR2A gene associates with the weight gain following antipsychotic agents (APS) acute treatment in schizophrenic patients. METHODS: Eighty-four Chinese Han patients with schizophrenia at the first onset were recruited from among 70 nuclear families. The polymorphism of 5-HTR2A gene was determined with PCR-RFLP technique. Body weight was measured in the patients on admission after 10 weeks of treatment with risperidone or chlorpromazine. RESULTS: There were no statistically significant differences in the distribution frequencies of genotype (chi2: 0.172, v1, P > 0.05) and allele (chi2: 0.121, v1, P > 0.05) of -1438G/A polymorphism of 5-HTR2A gene between subgroups (weight gain >or= 7% or < 7%). Likewise, there was no significant difference in weight gain between genotype groups. By means of transmission disequilibrium test and quantitative transmission disequilibrium test, no significant association between the -1438G/A polymorphism of 5-HTR2A gene and weight gain was observed. CONCLUSION: 5-HTR2A gene -1438G/A polymorphism was probably not associated with APS-induced weight gain in Chinese Han patients with schizophrenia in this study.


Assuntos
Antipsicóticos/uso terapêutico , Polimorfismo Genético , Regiões Promotoras Genéticas/genética , Receptor 5-HT2A de Serotonina/genética , Aumento de Peso/efeitos dos fármacos , Adulto , Clorpromazina/uso terapêutico , Feminino , Frequência do Gene , Genótipo , Humanos , Masculino , Reação em Cadeia da Polimerase , Polimorfismo de Fragmento de Restrição , Risperidona/uso terapêutico , Esquizofrenia/tratamento farmacológico , Esquizofrenia/genética , Esquizofrenia/fisiopatologia , Aumento de Peso/genética
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