Search PubMed⌕ Search

Biomedical subjects

S Nanko

Publications and source records attributed to S Nanko.

At least 91 records · Page 5Linked to original sources
PubMed1994

Failure to find linkage between a functional polymorphism in the dopamine D4 receptor gene and schizophrenia.

We report the results of a linkage study in 24 families multiply affected with schizophrenia using a polymorphic DNA sequence encoding the third cytoplasmic loop of the dopamine D4 receptor. Two-point LOD score analyses with a range of single gene models ranging from near dominant to near recessive revealed no evidence for linkage. In addition, we examined the data by non-parametric sib-pair analysis and found no excess sharing of alleles between affected sib-pairs. We therefore conclude that mutations within the dopamine D4 receptor gene do not have a major aetiological role in schizophrenia in our collection of pedigrees.

Alleles↗
PubMed1994

Changes of immunological functions after acute exacerbation in schizophrenia.

We investigated the changes of immunological functions in 14 schizophrenic patients (DSM-III-R; six men and eight women) who were hospitalized due to acute exacerbation of schizophrenia. The following immunological functions were studied on admission, 4 and 8 weeks after admission: serum immunoglobulins (Ig)G, A, and M; serum complement CH50; lymphocyte responses to mitogens (phytohemagglutinin, concanavalin A, and pokeweed mitogen); lymphocyte subpopulations (CD3%, 4%, 8%, 16%, 20%, 25%, and 56%); and natural killer cell (NK) activity. Psychological status of the patients, which was assessed by using Brief Psychiatric Rating Scale, improved gradually after admission. Changes in immune functions were analyzed using one-way analysis of variance and a randomized block analysis of variance with multiple comparison. NK activity on admission was significantly lower than those at 4 and 8 weeks after admission (p < .03). Serum IgG levels on admission and at 4 weeks after admission were significantly decreased as compared with those at 8 weeks after admission (p < .05); they were also lower than those in controls (p < .05). CD56% on admission and CD25% 4 weeks after admission were significantly increased as compared with controls (p < .05). These results indicate that several immunological functions might change related to time course after acute exacerbation. It is suggested that clinical conditions be carefully taken into consideration to evaluate immunological studies in schizophrenia.

Acute Disease↗
PubMed1994

Linkage studies between affective disorder and dopamine D2, D3, and D4 receptor gene loci in four Japanese pedigrees.

Dopamine antagonists are effective in the treatment of episodes of acute mania. Conversely, drugs which increase dopamine activity can induce a switch to mania. Therefore, disturbances in dopamine transmission and dopamine receptors might be implicated in the pathophysiology of bipolar affective disorder. We have carried out linkage studies between the susceptibility gene for effective disorder and polymorphisms of dopamine DRD2, DRD3, and DRD4 receptor genes in four Japanese pedigrees. Linkages of both DRD2 and DRD3 have been excluded, at least for dominant and intermediate models. The result for DRD2 was consistent with previous studies. For DRD3 this is the first exclusion of affective disorder from this locus in the 3q13.3 where DRD3 has been localized. On the other hand, our data could not exclude linkage of DRD4.

Adolescent↗
PubMed1994

HLA-DR types in Japanese schizophrenics: analysis by group-specific PCR amplification.

An association of HLA-DR8 and DR1 with DSM-III schizophrenia has been reported in Japan (Miyanaga et al. (1984) Biol. Psychiatr. 19, 121-129). To further investigate this preliminary finding, we compared HLA-DR types in 44 unrelated Japanese schizophrenics (DSM-III-R) with those in 51 unrelated, healthy Japanese volunteers. Group-specific PCR amplification was used in the determination of HLA-DR in the patients. No significant difference was observed in the frequency of any DR types between patients and controls, after statistical correction for multiple testing. However, the frequency of DR1 in our patients (23%) and controls (10%) was almost the same as those in the previous report (22% vs. 10%), which means that there is a suggestive trend which could become significant if numbers were larger. It is argued that an exact determination of HLA-DR by DNA typing is important in current HLA studies of schizophrenia.

Adult↗
PubMed1994

Neurotrophin-3 gene polymorphism associated with schizophrenia.

The recent possible neurodevelopmental etiology of schizophrenia makes the neurotrophin-3 (NT-3) gene an interesting candidate locus. We studied the allelic distributions of dinucleotide repeat polymorphism at the NT-3 gene locus in 70 patients with schizophrenia and in 70 controls. A highly significant difference between the two groups was observed at the allele A3. Even Bonferroni's correction was used, the difference was still significant. Individuals with homozygous or heterozygous for the allele A3 had a 2.4-fold increased risk of schizophrenia. Determination of NT-3 genotype may help to identify those at greater risk of schizophrenia. Furthermore, this finding supports evidence implicating neurodevelopmental deficit in the pathogenesis of this disorder.

Adult↗
PubMed1993

Failure to find linkage between schizophrenia and genetic markers on chromosome 21.

We sought evidence for the involvement of mutations in the amyloid precursor protein gene (APP) in the pathogenesis of schizophrenia in two ways. First, linkage analysis was performed in a sample of 24 families multiply affected with schizophrenia. The genotypes were studied for GT12 (D21S210), a highly polymorphic microsatellite marker at the APP locus. Second, we used single strand conformation analysis (SSCA) to screen for mutations in exon 17 of APP in one affected member from each family and in a sample of 44 unrelated patients. In addition, we looked for linkage between schizophrenia and a series of highly polymorphic markers situated at approximately 20cM intervals along the long arm of chromosome 21. We were unable to find evidence for linkage to GT12 or the other markers studied. SSCA did not reveal any mutations in exon 17 of AP. We conclude that mutations within APP are an unlikely cause of schizophrenia. Moreover, this study provides no evidence for a major gene for schizophrenia on chromosome 21, and linkage can be excluded from much of this region under some genetic models.

Adult↗
PubMed1993

A study of the association between schizophrenia and the dopamine D3 receptor gene.

A study of the genetic association between schizophrenia and a BalI polymorphism in exon 1 of the dopamine D3 (DRD3) gene, a candidate gene for schizophrenia, was conducted. The polymorphism was examined in 91 patients whose symptoms satisfied DSM-III-R for schizophrenia and 90 controls. There were no significant differences between the groups in allele frequencies or genotype counts. Contrary to a previous report, the patients were no more likely to be homozygous than controls. Moreover, no association with the presence of illness could be demonstrated when the patients were grouped according to sex, age of onset, history of admission to psychiatric institutions or positive family history.

Adult↗
PubMed1993

A case of schizophrenia with a dicentric Y chromosome.

A case of DSM-III-R schizophrenia with a dicentric Y chromosome (46,X,dic(Y)(q11)) is reported. Structural chromosome abnormalities such as this case may provide clues to finding regions of the genome etiologically involved in schizophrenia.

Chromosome Banding↗
PubMed1993

No evidence for a point mutation at codon 713 and 717 of amyloid precursor protein gene in Japanese schizophrenics.

A point mutation at codon 717 of amyloid precursor protein (APP) gene has been demonstrated to play an important pathogenic role in some cases of familial Alzheimer's disease (FAD). Recently, a single case of chronic schizophrenia with a point mutation at codon 713 of APP gene which sits very close to the mutation in FAD was reported. We screened for these two kinds of mutations in 39 schizophrenic patients using polymerase chain reaction (PCR) and restriction enzyme technique. A mutation of codon 713 creates a MaeIII restriction site and that of codon 717 creates a BclI site. Enzyme digestion with amplified PCR product revealed no restriction site in all subjects. None of our subjects had either of these two kinds of mutations. Our findings support the hypothesis that the case of a mutation at codon 713 of APP gene is a natural non-pathogenic variant and, as well as a mutation at codon 717, has no relation with the genetic predisposition to schizophrenia.

Adult↗
PubMed1993

Schizophrenia with pericentric inversion of chromosome 9: a case report.

A case of schizophrenia according to the DSM-III-R criteria with pericentric inversion of chromosome 9 was reported. This case and the review of the literature indicate that the pericentric region of chromosome 9 might be one of the potential regions of interest for linkage analysis of psychiatric disorders.

Chromosome Banding↗
PubMed1993

Life events and depression in Japan.

The relationship of life events to the onset of depression as well as the relationship between positive family history and reactivity to stress were investigated. Our results indicated that life stress in general plays an important role for women in the onset of depression and that undesirable events and problems of work specifically play a role in the onset of depression. The dichotomy of reactive and endogenous depression was not supported based on our result that no relationship was observed between the presence of familial loading and reactivity to stress.

Adult↗