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Biomedical subjects

N Takei

Publications and source records attributed to N Takei.

At least 73 records · Page 4Linked to original sources
PubMed1999

Factor analysis of symptoms in schizophrenia: differences between White and Caribbean patients in Camberwell.

BACKGROUND: The incidence of schizophrenia among African-Caribbeans living in Britain has been frequently reported to be increased. We sought to determine whether the symptom profile in schizophrenic patients from this group differed from that of their White counterparts. METHODS: Factor analysis was applied to symptom data obtained by the Present State Examination (PSE) from a group of White (N = 96) and Afro-Caribbean (N = 64) patients who satisfied Research Diagnostic Criteria criteria for broad schizophrenia. We identified six symptom dimensions: mania, depression, first-rank delusions, other delusions, hallucinations and one which comprised both manic and catatonic symptoms. RESULTS: The only difference between the two ethnic groups was seen on the mixed mania-catatonia dimension with the Afro-Caribbean group being over-represented. There were no other significant differences between the groups. Discriminant analysis, however, revealed no significant differences between the groups in any dimension. CONCLUSIONS: These results indicate that there are no differences between White and African-Caribbean patients with schizophrenia in terms of the core symptoms of the disorder, however, the African-Caribbean patients may present with more symptoms of a mixed affective nature.

Adolescent↗
PubMed1999

Urbanization and risk for schizophrenia: does the effect operate before or around the time of illness onset?

BACKGROUND: Higher level of urbanicity of place of birth and of place of residence at the time of illness onset has been shown to increase the risk for adult schizophrenia. However, because urban birth and urban residence are strongly correlated, no conclusions can be drawn about the timing of the risk-increasing effect. The current study discriminated between any effect of urbanization before and around the time of illness onset. METHODS: All individuals born between 1972 and 1978 were followed up through the Dutch National Psychiatric Case Register for first admission for schizophrenia until 1995 (maximum age 23 years). Exposure status was defined by a combination of place of birth and place of residence at the time of illness onset in the three most densely populated provinces of the Netherlands (the 'Randstad', exposed) or in all other areas (the 'non-Randstad', non-exposed). The risk for schizophrenia was examined in four different exposure groups: non-exposed born and non-exposed resident (NbNr, reference category), non-exposed born and exposed resident (NbEr), exposed born and non-exposed resident (EbNr) and exposed born and exposed resident (EbEr). RESULTS: The greatest risk for schizophrenia was found in the EbNR group, without evidence for any additive effect of urban residence (rate ratio (RR) for narrow schizophrenia in EbNr group, 2.05 (95 % CI 1.18-3-57); in EbEr group, 1.96 (95% CI, 1.55-2.46)). Individuals who were not exposed at birth, but became so later in life, were not at increased risk of developing schizophrenia (RR for narrow schizophrenia in NbEr group, 0.79 (0.46-1.36)). CONCLUSION: The results suggest that environmental factors associated with urbanization increase the risk for schizophrenia before rather than around the time of illness onset.

Adolescent↗
PubMed1999

Schizophrenia and complications of pregnancy and labor: an individual patient data meta-analysis.

Several epidemiological studies have reported an association between complications of pregnancy and delivery and schizophrenia, but none have had sufficient power to examine specific complications that, individually, are of low prevalence. We, therefore, performed an individual patient meta-analysis using the raw data from case control studies that used the Lewis-Murray scale. Data were obtained from 12 studies on 700 schizophrenia subjects and 835 controls. There were significant associations between schizophrenia and premature rupture of membranes, gestational age shorter than 37 weeks, and use of resuscitation or incubator. There were associations of borderline significance between schizophrenia and birthweight lower than 2,500 g and forceps delivery. There was no significant interaction between these complications and sex. We conclude that some abnormalities of pregnancy and delivery may be associated with development of schizophrenia. The pathophysiology may involve hypoxia and so future studies should focus on the accurate measurement of this exposure.

Case-Control Studies↗
PubMed1999

Regulation of nerve growth factor release by nitric oxide through cyclic GMP pathway in cortical glial cells.

In the present study, we found that S-nitroso-N-acetyl-DL-penicillamine, a spontaneous nitric oxide (NO) generator, dose-dependently inhibited basal nerve growth factor (NGF) release from mixed glial cells. To elucidate the function of endogenous NO in the regulation of NGF release, the mixed glial cells were stimulated with lipopolysaccharide (LPS) or LPS plus interferon-gamma (IFNgamma). The results showed that LPS alone induced NGF release and moderate NO production. However, costimulation with LPS plus IFNgamma greatly enhanced NO production but significantly suppressed LPS-induced NGF release. When N(G)-monomethyl-L-arginine, an NOS inhibitor, was added to the culture, the suppression of NGF release by IFNgamma was significantly reduced. Quantitative reverse transcription-polymerase chain reaction demonstrated S-nitroso-N-acetyl-DL-penicillamine was also able to inhibit the LPS-induced NGF mRNA expression. To understand the different contributions of astroglia and microglia to this phenomenon, both cell types were purified. We found purified astroglia produced high amounts of NGF but low amounts of NO. However, purified microglia produced a large amount of NO but very low amounts of NGF after stimulation with LPS or LPS plus IFNgamma. Our data also indicated the second messenger cyclic GMP, but not cyclic AMP, was able to inhibit basal NGF release. In vivo experiments confirmed that NGF protein level was significantly enhanced in rats treated with L-N(omega)-nitro-arginine methyl ester and in endothelial NO synthase mutant mice. Taken together, we conclude NO derived mainly from microglia down-regulates NGF release from astroglia at the transcriptional level by stimulating cyclic GMP pathway.

Animals↗
PubMed1998

Developmental regulation of pituitary adenylate cyclase activating polypeptide (PACAP) and its receptor 1 in rat brain: function of PACAP as a neurotrophic factor.

To function as a trophic factor PACAP and PACAP-R must be expressed in the nervous system during early development. We report here on the distribution of PACAP mRNA in the developing nervous system of the rat and compare its expression with that of PACAP-R. We discuss primary neuron culture experiments that study the neurotrophic activity of PACAP. Experimental results that indicate the presence of PACAP and its receptor in the developing nervous system, together with the observed neuropeptide activity on various populations of neurons, support the view that PACAP exhibits important neurotrophic activities comparable to those of the classical neurotrophic factors.

Animals↗
PubMed1998

Neurotrophic and neuroprotective effects of pituitary adenylate cyclase-activating polypeptide (PACAP) on mesencephalic dopaminergic neurons.

The neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) is present in many regions of the adult and developing brain as are receptors for PACAP. PACAP stimulates different signalling cascades in neurons, involving cAMP, MAP kinase, and calcium. These characteristics suggest that PACAP may influence neuronal development. Here we have studied the effects of PACAP on mesencephalic dopaminergic neurons using primary cultures from embryonic rats. PACAP increased the number of tyrosine hydroxylase (TH)-immunoreactive neurons, elevated TH protein, and enhanced tritiated dopamine uptake in these cultures. Moreover, PACAP counteracted the effects of 6-hydroxydopamine treatments, which induce cell death of dopaminergic neurons. In situ hybridisation showed that both PACAP and PACAP receptor type 1 are present in developing and adult rat mesencephalon. These results show that PACAP has a neurotrophic action on dopaminergic neurons and partially protects them against 6-OHDA induced neurotoxicity.

Animals↗
PubMed1998

Brain-derived neurotrophic factor induces rapid and transient release of glutamate through the non-exocytotic pathway from cortical neurons.

There is increasing interest in the involvement of neurotrophins in neural transmission and plasticity. Thus, we investigated the effects of brain-derived neurotrophic factor (BDNF) on glutamate release from cortical neurons. Treatment of cultured cortical neurons with BDNF induced rapid and transient release of glutamate. This effect was suggested to be mediated by TrkB activation because K252a inhibited the release of glutamate and BDNF phosphorylated TrkB within 30 s. BDNF-induced glutamate release was observed even when using Ca2+-free assay buffer but was inhibited by BAPTA-AM, a cell-permeable Ca2+ chelator. Therefore, BDNF-induced glutamate release was independent of extracelluar Ca2+ but dependent on intracellular Ca2+. Because normal neurotransmitter release is exocytotic, the involvement of the exocytotic pathway in BDNF-induced glutamate release was examined. As botulinum toxin is known to cleave exocytosis-associated proteins, thereby inhibiting exocytosis, it was applied to neurons prior to the release assay. Although botulinum toxin B cleaved VAMP2 and inhibited Ca2+-triggered glutamate release, it did not inhibit the BDNF-induced release of glutamate. These results strongly suggested that BDNF induces rapid and transient release of glutamate from cortical neurons through a non-exocytotic pathway.

Animals↗
PubMed1998

Pituitary adenylate cyclase-activating polypeptide (PACAP) protects dorsal root ganglion neurons from death and induces calcitonin gene-related peptide (CGRP) immunoreactivity in vitro.

Pituitary adenylate cyclase-activating polypeptide (PACAP) is a recently discovered neuropeptide which is present both in the central and peripheral nervous system of adult rats. Here we show that PACAP is also expressed by dorsal root ganglion sensory neurons of embryonic and newborn rats. To characterize the effects of PACAP on dorsal root ganglion (DRG) neurons, dissociated cultures were established and incubated in the absence or presence of this neuropeptide. The results show that PACAP increases the survival of cultured DRG neurons, and the effect was comparable to that of nerve growth factor (NGF). In DRG explants, PACAP induces the immunoreactivity for the neuropeptide calcitonin gene-related peptide (CGRP). PACAP also promoted the outgrowth of neurites in the DRG cultures. The present results show that PACAP acts as a trophic factor for DRG neurons and that it is able to modulate the expression of another neuropeptide in the ganglia. The presence of PACAP in normal DRG and after nerve lesions suggests that PACAP acts in a autocrine/paracrine manner possibly in conjunction with other neurotrophic factors such as nerve growth factor.

Animals↗
PubMed1998

Neurological abnormalities in familial and sporadic schizophrenia.

Neurological assessment was carried out on patients with schizophrenia from multiply and singly affected families, their relatives, and a normal control group (214 subjects). A systematic examination was used in which abnormal signs were divided into 'primary' and 'integrative' signs. Primary signs were elicited by a standard clinical neurological examination and included signs of focal damage to nuclei and tracts, whilst integrative signs were selected as reflecting distributed brain function. The assessments were carried out to test the hypotheses that (i) neurological abnormalities are present in schizophrenia, (ii) the pattern of abnormality is different in familial and sporadic schizophrenic subjects, and (iii) the well relatives of familial (but not sporadic) schizophrenic subjects will show neurological abnormalities. An excess of primary signs compared with the controls was demonstrated in the sporadic schizophrenic group only. Both the familial schizophrenics and their first-degree relatives (but not their sporadic counterparts) showed an increase in integrative signs. The results support the existence of different mechanisms of underlying brain dysfunction in familial and sporadic schizophrenia.

Adult↗
PubMed1998

Minor physical anomalies in familial and sporadic schizophrenia: the Maudsley family study.

OBJECTIVES: (1) To test the hypothesis that minor physical anomalies are increased in patients with schizophrenia and (2) to investigate differences in the prevalence of minor physical anomalies in patients with familial and sporadic schizophrenia and their first degree relatives. METHODS: A weighted Waldrop assessment was carried out on 214 subjects in five groups: schizophrenic patients from multiply affected families; first degree relatives of these familial schizophrenic patients; sporadic schizophrenic patients; first degree relatives of these sporadic schizophrenic patients, and normal controls. Broad and narrow criteria for abnormality were defined based on the distribution of minor physical anomalies in the control group. RESULTS: (1) The total schizophrenic group did not have a significant increase in minor physical anomalies using a narrow criterion of abnormality, but did when a broader criterion was used. (2) A significant increase in the proportion of subjects with an abnormally high number of minor physical abnormalities was shown in the group of sporadic schizophrenic patients (uncorrected p<0.01). Separate analyses for males and females showed a significant increase in the male sporadic group (uncorrected p<0.05), and a smaller non-significant increase in the female sporadic group. Neither the familial schizophrenic group nor either group of first degree relatives showed any significant increases in the proportion of patients with high abnormality scores. CONCLUSION: This work supports prenatal developmental abnormality as a mechanism for sporadic, but not familial, schizophrenia.

Adult↗
PubMed1998

First episodes of psychosis in Afro-Caribbean and White people. An 18-year follow-up population-based study.

BACKGROUND: There have been few prospective studies of the long-term outcome of psychosis in people of Afro-Caribbean origin in the UK. METHOD: We followed-up a population-based, consecutive series of 34 Afro-Caribbean and 54 White people with psychosis who had been extensively investigated during their first admission in 1973/74. Diagnoses were made by direct interview using the Present State Examination at both first admission and follow-up. RESULTS: Ninety-seven percent of the original sample were traced. A slightly greater proportion of the Afro-Caribbean people were assigned to the S+ Catego class (schizophrenia), both on first assessment and at follow-up. No difference was found between the two groups in the consistency of diagnosis over the 18 years or in the proportion of patients considered psychotic but Afro-Caribbean people tended to have fewer negative symptoms at follow-up. There were striking differences between the two groups in their experience of psychiatric care; Afro-Caribbean people were more likely to have been readmitted, to have experienced longer hospitalisations, and to have undergone more involuntary admissions than their White counterparts. CONCLUSIONS: Afro-Caribbean people who met clinical and research criteria for schizophrenia had a less satisfactory experience of, and response to, psychiatric care over 18 years than their White counterparts.

Adolescent↗
PubMed1998

SPET study of verbal fluency in schizophrenia and epilepsy.

BACKGROUND: The association between temporal lobe epilepsy and schizophrenia suggests that the critical abnormality may be pathology within the temporal lobes. People with schizophrenia-like psychosis of epilepsy (SLPE) provide a useful group in which to examine the importance of temporal and frontal lobe dysfunction in schizophrenia. METHOD: A verbal fluency activation paradigm and a 99mTc HMPAO SPET were used to study frontotemporal function in people with SLPE (n = 12), schizophrenia (n = 11) and epilepsy (n = 16). RESULTS: People with SLPE differed from both other groups by showing lower blood flow in the left superior temporal gyrus during performance of a verbal fluency task compared with a word repetition task (F = 5.4, P = 0.01). During the verbal fluency task people with primary schizophrenia showed a greater increase in blood flow in anterior cingulate (F = 4.5, P = 0.02) than the other two groups. There were no between-group differences in frontal brain regions. CONCLUSION: Our findings support an association between left temporal lobe abnormality and SLPE. The different patterns of activation observed in people with primary schizophrenia and SLPE suggests that different pathophysiological mechanisms may operate in these two groups. In SLPE the pathophysiology may be relatively confined to the dominant temporal lobe.

Adult↗
PubMed1998

Brain changes in schizophrenia. Volumetric MRI study of families multiply affected with schizophrenia--the Maudsley Family Study 5.

BACKGROUND: Structural brain abnormalities have been reported in schizophrenia. We tested the hypothesis that these abnormalities represented a marker for the genetic liability to schizophrenia in a sample of people with schizophrenia and their relatives from families multiply affected with the disorder. METHOD: We compared 31 people with schizophrenia, 57 relatives and 39 unrelated control subjects. Volumetric measurement of brain structures was carried out using stereological principles from three-dimensional reconstructed magnetic resonance images. RESULTS: Subjects with schizophrenia had larger lateral ventricles than their relatives and the normal control subjects. Relatives who were 'presumed obligate carriers' had larger left lateral ventricles than other relatives and the control subjects. Subjects with schizophrenia showed smaller whole brain and cerebellar volumes and larger lateral ventricles than their age- and gender-matched unaffected siblings. CONCLUSIONS: In families multiply affected with schizophrenia lateral ventricular enlargement distinguishes people with schizophrenia and presumed obligate carriers from other relatives and unrelated control subjects. These changes may be a marker for a genetic liability to schizophrenia.

Adult↗
PubMed1998

Roles of neurotrophins on synaptic development and functions in the central nervous system.

Evidence is emerging to suggest that in addition to their "classical" neurotrophic involvement in the regulation of the differentiation, maturation and survival of neurons, neurotrophins play crucial roles in neural transmission and succeeding activity-dependent plasticity of synapses. Here we discuss: 1) the regulated synthesis and secretion of neurotrophins in response to neural activity, 2) the short- and long-term effects of neurotrophins on neural transmission, and 3) the neurotrophin-induced rearrangement of synaptic networks.

Brain↗
PubMed1997

Maternal exposure to influenza and paranoid schizophrenia.

Previous research has suggested that schizophrenics exposed to influenza in the second trimester have more delusions of jealousy, delusions of reference and suspiciousness. We therefore hypothesised that the risk-increasing effect of in utero exposure to influenza would be particularly demonstrable in paranoid schizophrenia. We studied patients with an ICD diagnosis of schizophrenia in England and Wales who were born each month between 1923 and 1965 (N = 17,247. Chi-square test for trend showed that an increase in influenza exposure level during the fifth month of gestation was accompanied by an increase in the proportion of patients with paranoid schizophrenia. However, logistic regression analysis including sex, seasonality and birth period in the model resulted in the loss of any significant association between in utero exposure to influenza and the development of paranoid schizophrenia, the loss of this significance being mainly accounted for by birth period. Therefore, the association in utero exposure to influenza and subsequent development of paranoid schizophrenia we hypothesised was not supported by our data.

Adult↗