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Dive into the research topics where Yoichi Kawanishi is active.

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Featured researches published by Yoichi Kawanishi.


European Neuropsychopharmacology | 2007

CLOCK gene T3111C polymorphism is associated with Japanese schizophrenics: A preliminary study

T. Takao; H. Tachikawa; Yoichi Kawanishi; Katsuyoshi Mizukami; Takashi Asada

The CLOCK gene has attracted attention due to its influence on the circadian rhythm, as well as its impacts on the dopaminergic system. We conducted a preliminary study to examine whether the T3111C single nucleotide polymorphism of the CLOCK gene is associated with the development of schizophrenia by examining samples from schizophrenics (n=145) and normal controls (n=128). Both genotype and allele frequencies were significantly different between schizophrenics and controls (p=0.022, p=0.015, respectively). Schizophrenics had a significantly higher frequency of the C allele compared to controls (odds ratio 1.76, 95% CI 1.12-2.75). In particular, disorganized and residual type schizophrenics had significantly higher C allele frequencies than controls (p=0.004 and p=0.037, respectively). Our results suggest that the T3111C polymorphism of the CLOCK gene is associated with schizophrenia. It is important to explore the association between CLOCK and dopamine function, and to examine the impact of CLOCK on phenotypes such as symptoms and drug response in patients with schizophrenia.


BMC Psychiatry | 2001

The (CTG)n polymorphism in the NOTCH4 gene is not associated with schizophrenia in Japanese individuals

Koubun Imai; Shoji Harada; Yoichi Kawanishi; Hirokazu Tachikawa; Takehito Okubo; Toshihito Suzuki

BackgroundThe human NOTCH4 gene is a candidate gene for schizophrenia due to its chromosomal location and neurobiological roles. In a British linkage study, NOTCH4 gene polymorphisms were highly associated with schizophrenia. In a Japanese case-control association study, however, these polymorphisms did not show significant associations with schizophrenia. We conducted a case-control study with Japanese subjects to explore an association between the triplet repeat polymorphism in the NOTCH4 gene and schizophrenia, including subtypes of schizophrenia, longitudinal disease course characteristics, and a positive family history for psychoses.MethodsWe examined the (CTG)n repeat polymorphism in the NOTCH4 gene among 100 healthy Japanese individuals and 102 patients with schizophrenia (22 paranoid, 38 disorganized, 29 residual, 64 episodic, 31 continuous, 42 with prominent negative symptoms, and 46 with positive family histories) using a polymerase chain reaction-based, single-strand conformational polymorphism analysis.ResultsFive different alleles consisting of 6, 9, 10, 11, and 13 repeats of CTG (Leu) in patients with schizophrenia, and 4 alleles consisting of 6, 9, 10, and 11 repeats in controls were found. No significant differences in genotype or allele frequencies of repeat numbers were found between controls and patients. In addition, there were no associations between the polymorphism and schizophrenia subtypes, longitudinal disease course characteristics, or positive family history of the patients.ConclusionsOur data suggest a lack of association between the NOTCH4 gene triplet repeat polymorphism and schizophrenia in Japanese individuals.


European Journal of Pharmacology | 2000

Pharmacogenomics and schizophrenia

Yoichi Kawanishi; Hirokazu Tachikawa; Toshihito Suzuki

Although antipsychotic drugs are effective in alleviating schizophrenic symptoms, individual differences in patient response suggest that genetic components play a major role, and pharmacogenetic studies have indicated the possibility for a more individually based pharmacotherapy. The new field of pharmacogenomics, which focuses on genetic determinants of drug response at the level of the entire human genome, is important for development and prescription of safer and more effective individually tailored drugs. DNA microarray (DNA chip) analysis enables genome-wide scanning, using the high-density single nucleotide polymorphisms map. Pharmacogenomics will aid in understanding how genetics influence disease development and drug response, and contribute to discovery of new treatments. The rate of discovery of those polymorphisms will depend on the quality of the drug response phenotype. Prospective genotyping of schizophrenic patients for the many genes at the level of the drug target, drug metabolism, and disease pathways will contribute to individualized therapy matching the patients unique genetic make-up with an optimally effective drug.


Journal of Human Genetics | 1999

Novel variants in the promoter region of the CREB gene in schizophrenic patients

Yoichi Kawanishi; Shoji Harada; Hirokazu Tachikawa; Takehito Okubo; Hiroyasu Shiraishi

AbstractCyclic AMP-responsive element-binding protein (CREB) is one of the messenger molecules involved in intracellular signal transduction pathways used by most dopamine and serotonin receptor subtypes. In addition, CREB stimulates the expression of a number of genes, alterations in the expression of which may be associated with schizophrenia. The promoter region of the human CREB gene was therefore analyzed to identify genetic variants that may lead to the modification of CREB expression and contribute to schizophrenia. Eighty unrelated schizophrenics and 100 healthy controls were screened for genetic variants of the CREB gene by SSCP analysis, followed by direct sequencing of PCR products. Two novel variants (−933T→C and −413G→A) were found only in schizophrenics. A patient with the −933T→C variant had unusual clinical characteristics in addition to typical schizophrenic symptoms.


Neuropsychobiology | 2001

Polymorphism of the 5`-Upstream Region of the Human SNAP-25 Gene:An Association Analysis with Schizophrenia

Hirokazu Tachikawa; Shoji Harada; Yoichi Kawanishi; Takehito Okubo; Toshihito Suzuki

Recent studies have suggested that synaptic abnormalities may be part of the pathophysiology of schizophrenia. SNAP-25 (synaptosomal-associated protein of 25 kD) is one of the synaptic proteins responsible for presynaptic neurotransmission, axonal elongation and synaptogenesis. Genetic variation in the 5′-upstream region of the SNAP-25 gene was analyzed in 87 unrelated schizophrenic patients and 100 healthy controls. A novel polymorphic (TAAA)n tandem repeat was identified in the 5′-upstream region. There were no significant differences between the patient and the control groups in the distribution of repeat numbers of alleles or genotypes. In addition, no associations were found between the polymorphism for subtypes, longitudinal courses or positive family history of the patients. Our results suggest that polymorphisms in the 5′-upstream region of the SNAP-25 gene have no association with schizophrenia.


Psychiatry and Clinical Neurosciences | 2000

Tardive dystonia provoked by concomitantly administered risperidone

Hirokazu Tachikawa; Toshihito Suzuki; Yoichi Kawanishi; Masashi Hori; Takafumi Hori; Hiroyasu Shiraishi

Abstract Two cases of tardive dystonia are reported. The first case was an 18‐year‐old schizophrenic woman suffering from parkinsonism and hypotension induced by antipsychotic drugs. Risperidone (4 mg/day) was added to her drug regimen and after increasing the dosage to 6 mg/day, she began to exhibit retrocollis. The second case was a 61‐year‐old woman who had schizophrenia and tardive dyskinesia. After replacing chlorpromazine (75 mg/day) with risperidone (4 mg/day), she began to exhibit retrocollis. The retrocollis in both cases was considered to be tardive dystonia provoked by risperidone administered concomitantly with other antipsychotics. Risperidone is reported to produce few extrapyramidal symptoms, but these cases suggested that changing from other drugs to risperidone, or rapidly increasing risperidone dosage, may provoke tardive syndrome.


Neuropsychobiology | 2001

Polymorphisms in the promoter and coding regions of the synapsin III gene. A lack of association with schizophrenia.

Koubun Imai; Shoji Harada; Yoichi Kawanishi; Hirokazu Tachikawa; Takehito Okubo; Toshihito Suzuki

The human synapsin III gene, located on chromosome 22q12–13, has previously been reported to indicate a susceptibility for schizophrenia. Noval rare variants (Thr136Thr in exon 3, Pro468Ser, Glu525Gln and Pro534Leu in exon 12, and 1769 G/C in the untranslated region of exon 13) were found in addition to the polymorphic variant (–196 G/A in the promoter region). No significant differences in genotypic or allelic frequencies of the –196 G/A polymorphism were found between 87 unrelated schizophrenic patients and 100 healthy controls, even when the patients were diagnostically subdivided into subtypes and course specifiers. Furthermore, allelic frequencies of the GATG repeat in intron 1 were not significantly different between the patients and the controls. These results suggest that synapsin III gene polymorphisms are not associated with schizophrenia.


Journal of Human Genetics | 2000

Novel polymorphisms of the AP-2 gene (6p24): analysis of association with schizophrenia.

Yoichi Kawanishi; Shoji Harada; Hirokazu Tachikawa; Takehito Okubo; Hiroyasu Shiraishi

AbstractThe transcription factor activator protein 2 (AP-2) gene is a possible candidate gene for schizophrenia, since it maps near D6S470, a marker on chromosome 6p24 that provided evidence of linkage to schizophrenia. In the present study we analyzed the promoter region and the whole coding region of the human AP-2 gene in order to identify genetic variations that may lead to the modification of AP-2 expression or the alteration of protein function, contributing to schizophrenia or particular schizophrenic phenotypes. Genomic DNA was isolated from the whole blood samples of 87 unrelated schizophrenics and 100 healthy controls. Polymerase chain reaction (PCR) was performed, using 15 primer sets that spanned the promoter region and the whole coding region, and amplified products were screened by single-strand conformational polymorphism (SSCP) analysis. Aberrant SSCP patterns were analyzed by direct sequencing. Three novel polymorphisms were found in the promoter region; two relatively common (−90G→C, −803G→T) and one rare (−1769G→A). Polymorphic status at both loci suggested strong linkage disequilibrium between the −90G and −803G alleles, and between the −90C and −803T alleles. Although no significant differences in genotypic and allelic frequencies at the −90 and −803 loci were found between patients and controls, significant differences in the distribution of genotypes at the −90 (P = 0.008) and −803 (P = 0.037) loci were observed in patients with an episodic course compared with controls. However, the difference for the −803 locus was not significant after Bonferroni correction for multiple comparisons. Our data provided no direct evidence of an association between schizophrenia and the polymorphisms of the AP-2 gene, although the positive result at the −90 locus in schizophrenics with an episodic course is potentially interesting.


Journal of Human Genetics | 2001

Association analysis of polymorphisms in the prepronociceptin gene and schizophrenia

Koubun Imai; Shoji Harada; Yoichi Kawanishi; Hirokazu Tachikawa; Takehito Okubo; Toshihito Suzuki

AbstractThe human prepronociceptin (ppNoc) gene is located on chromosome 8p21, and several linkage studies have suggested that the susceptibility locus for schizophrenia is present in this chromosomal region. We investigated genetic variations in the promoter and coding regions of the ppNoc gene to determine if there may be an association between naturally occurring mutations and the manifestation of schizophrenia. Association analyses for the variations found were conducted between 87 unrelated schizophrenic patients and 100 healthy controls. Polymorphisms were found at both the –503 locus (G/A) in the promoter region and the 353 locus (Ala118Gly) in exon 3. Additionally, rare variants were identified at the –261 locus (A/G) in the promoter region, the 515 locus (Gln172Arg) in exon 3, and the 561 locus (G/A) in the untranslated region of exon 3. A significant difference was observed in allele frequency at the 353 locus between controls and patients with continuous-course schizophrenia (P = 0.0237), and between patients with and without prominent negative symptoms (P = 0.0201). However, neither difference was significant after Bonferroni correction. In addition, there were no significant differences in genotype and allele frequencies at either the –503 or 353 locus between the control group and patients with schizophrenia. These results suggest that ppNoc gene polymorphisms have no association with schizophrenia.


Psychiatry and Clinical Neurosciences | 1995

A clinical case of neuro-Behçet syndrome without mucocutaneo-ocular symptoms: relationship with brain stem encephalitis.

Yoichi Kawanishi; Takafumi Hori; Toshihito Suzuki; Katsuyoshi Mizukami; Megumi Sasaki; Hiroyasu Shiraishi

Abstract The case of a 50 year old man with personality changes, dementia, and brain stem symptoms is presented. Magnetic resonance imaging (MRI) disclosed high signal areas mainly in the brain stem. Both a positive skin prick test and an HLA‐B51 were demonstrated. These clinical findings were suggestive of neuro‐Behçet syndrome, although there were no mucocutaneo‐ocular symptoms characteristically associated with this disease. The relationship between neuro‐Behçet syndrome and brain stem encephalitis, including a discrimination from multiple sclerosis, is discussed.

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