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Biomedical subjects

N Takei

Publications and source records attributed to N Takei.

At least 127 records · Page 7Linked to original sources
PubMed1995

Prenatal exposure to influenza epidemics and risk of mental retardation.

This study was undertaken to determine whether prenatal exposure to influenza epidemics increases the risk of mental handicap. The monthly birth frequencies of 827 first-admission individuals (mean age at admission 13 years) with a primary diagnosis of non-specific mental retardation, discharged from psychiatric hospitals in England and Wales, were examined in relation to the monthly death rates from influenza over the period 1953-1980. The relative risk of developing mental handicap when exposed to influenza epidemics during mid-gestation was assessed by a generalized linear model. Increased death rates from influenza, a measure of prevalence of the infection, were significantly associated with an increase in births of mentally handicapped individuals 6 months later. For every 1000 female deaths from influenza there was a 17% increase in births of mentally handicapped individuals 6 months later. Maternal exposure to influenza at approximately the third to fourth month of gestation may be risk factor for developing mental handicap.

Adult↗
PubMed1995

Neurotrophic and neuroprotective effects of neuron-specific enolase on cultured neurons from embryonic rat brain.

We previously reported that the gamma gamma-isozyme of enolase, NSE), one of the glycolytic enzymes, promoted the survival of embryonic rat neocortical neurons in culture, but alpha alpha-isozyme (non-neuronal enolase) had no effect. In the present study, the neurotrophic effects of NSE on cultured mesencephalic and spinal neurons from rat embryo were examined. NSE promoted the survival of neurons not only in neocortical cultures but also in mesencephalic and spinal cord cultures. Furthermore, NSE showed neuroprotective action on cultured neocortical neurons in a low-oxygen atmosphere. By contrast, non-neuronal enolase did not show any neurotrophic or neuroprotective activities. To clarify the mechanism of the neurotrophic effect of NSE, the binding of NSE to cultured neurons was determined by radio-receptor assay using 125I-labelled NSE. The specific binding, which was dose-dependent, saturable, and calcium-dependent, could be detected. These results suggest that NSE has neurotrophic and neuroprotective effects on rather a broad spectrum of neurons in the central nervous system. The existence of specific binding of NSE to cultured neurons suggests the possibility that receptor-like or carrier-like molecules on the neuronal surface are involved in the neurotrophic activity of NSE.

Animals↗
PubMed1995

Gender differences in schizophrenia: hormonal effect or subtypes?

Compared with their male counterparts, females with schizophrenia, on average, show better premorbid functioning, later onset, and a more benign course of illness. They are also more likely to have a family history of schizophrenia and/or affective illness, to exhibit "atypical" and affective features, and to show a seasonal pattern of hospital admission that mimics that of patients with mania. However, there exists a paradox. Although schizophrenia in females has much in common with affective disorder, the "schizophrenogenic" effect of maternal influenza also appears to be more significant in female than in male schizophrenia. Perhaps females with a predisposition to affective psychosis who have also been subject to the effects of maternal viral infection during gestation develop some subtle neurodevelopmental damage that renders their psychosis schizophrenia-like.

Female↗
PubMed1995

No association between prenatal exposure to influenza and autism.

We examined the relationship between the number of autistic patients, obtained from the register of the National Autism Society (NAS), born each month between January 1953 and December 1988 in England, and the occurrence of influenza epidemics one to nine months before birth. The relative risk of developing autism, for exposure to influenza during gestation, was assessed by a Poisson regression model. Our results indicate that exposure to influenza epidemics during gestation is not associated with autism.

Adolescent↗
PubMed1995

Maternal influenza, obstetric complications, and schizophrenia.

OBJECTIVE: Epidemiologic studies have reported an association between prenatal exposure to influenza and adult schizophrenia. The authors studied this association in individual patients with schizophrenia and also investigated the relationship of obstetric complications, another postulated risk factor, to adult schizophrenia. METHOD: Using a structured interview instrument, the authors assessed infections during pregnancy, obstetric complications, gestational age, and birth weight by interviewing the mothers of 121 patients with DSM-III-R schizophrenia. RESULTS: Significantly more infections were reported in the second trimester of the patients' gestations than in the combined first and third trimesters. Influenza accounted for 70% of second-trimester infections. Patients with schizophrenia whose mothers reported having influenza during the second trimester were almost five times more likely to experience at least one definite obstetric complication than were patients who were not exposed to influenza during the second trimester; the exposed patients weighed a mean of 210 g less at birth than the unexposed patients. CONCLUSIONS: Maternal influenza during the second trimester may impair fetal growth and predispose to obstetric complications and lower birth weight in a proportion of individuals destined to develop schizophrenia.

Adult↗
PubMed1995

Schizophrenia following in utero exposure to the 1957 influenza epidemics in Japan.

OBJECTIVE: Studies in Finland, England, and Denmark have reported that individuals exposed to the 1957 A2 influenza pandemic during their second trimester in utero are at greater risk for later schizophrenia. However, other studies in England, the United States, and Holland reported no such association. The authors' goal was to shed light on these conflicts. METHOD: They compared the number of individuals who later developed schizophrenia who were born in the 5 months after the peak prevalence of three distinct 1957 influenza epidemics in Japan with the mean number of individuals who later developed schizophrenia who were born in the corresponding months of the 4 years surrounding the epidemics. RESULTS: A significantly greater number of females but not males who later developed schizophrenia were born during the risk exposure months than in the non-risk-exposure months. CONCLUSIONS: These findings, although weak, lend support to the claim that in utero exposure to influenza epidemics is a risk factor for adult schizophrenia.

Adult↗
PubMed1995

Regional cerebral blood flow in obsessive-compulsive disordered patients at rest. Differential correlates with obsessive-compulsive and anxious-avoidant dimensions.

BACKGROUND: We tested whether cortical and subcortical regional cerebral blood flow (rCBF) differs between patients with obsessive-compulsive disorder (OCD) and healthy controls. We then explored the relationship between rCBF and OCD mental state. METHOD: Thirty out-patients from the Maudsley Hospital with OCD as defined in DSM-III-R were scanned at rest using brain-dedicated, high-resolution, single photon emission tomography. RCBF was measured as uptake of 99mTc-HMPAO in 15 regions of interest and compared with rCBF data in 30 healthy people matched for age, sex and handedness. Symptom ratings were obtained using standard measures on the scanning day. Principal components factor analysis identified two distinct clinical dimensions: obsessive-compulsive (OC) and anxious-avoidant (AA). These were correlated with patients' rCBF measurements, using Spearman's rank correlation coefficient, and multiple regression coefficients calculated. RESULTS: We found significant reductions in rCBF measurements of OCD patients compared with resting, healthy controls (F = 1.92, P = 0.04) in seven brain regions: the right and left superior frontal cortex, right inferior frontal cortex, left temporal cortex, left parietal cortex, right caudate nucleus and right thalamus. Regional differences were not secondary to generalised reduction in patients' brain perfusion. Reduced blood flow to the right inferior frontal cortex correlated significantly with illness severity (r = 0.37, P = 0.02). There was no relationship with age, age-of-onset, sex, handedness, depression or medication status. OC clinical dimension, concerning obsessions, compulsions and low mood, was significantly negatively correlated with left inferior frontal, medial frontal and right parietal rCBF. AA dimension, concerning anxiety and avoidance, was significantly positively associated with left and right superior frontal, right inferior frontal, medial frontal cortical, and right and left caudate and thalamic rCBF. CONCLUSIONS: rCBF differs significantly between resting OCD patients and healthy controls, and separate clinical dimensions are associated with functionally distinct rCBF patterns.

Adult↗
PubMed1995

[Augmentation of clonidine on Bezold-Jarisch reflex control of renal sympathetic nerve activity in cats].

The present study was undertaken to examine the possible augmentation of clonidine on the control of renal sympathetic nerve activity by Bezold-Jarisch reflex in anesthetized cats. Veratrine (3-20 micrograms/kg) produced dose-dependent decreases in arterial blood pressure (BP), heart rate (HR) and renal sympathetic nerve activity (RNA). Clonidine (3 micrograms/kg) resulted in decreases in BP, HR and RNA. Clonidine significantly potentiated the influence of Bezold-Jarisch reflex on RNA, but did not potentiate the influence of Bezold-Jarisch reflex on BP and HR. Bezold-Jarisch reflex gain calculated as percent inhibition of renal sympathetic nerve activity divided by decreases in mean blood pressure was significantly higher after the administration of clonidine.

Animals↗
PubMed1994

Ca2+ ionophore-induced apoptosis on cultured embryonic rat cortical neurons.

The neurotoxicity of ionomycin, a Ca2+ ionophore, was investigated in cultured cortical neurons from embryonic rats. While about 90% of neurons survived 2 h after exposure to ionomycin, the surviving neurons had decreased by about 30 to 40% at 16 h. Both RNA and protein synthesis inhibitors blocked this neurotoxicity. Furthermore, c-Fos immunoreactive neurons increased not only in number but also in the intensity of immunoreactivity. These results suggest that ionomycin-induced neuronal cell death is an active process which requires de novo transcription and translation. In addition, the ultrastructural changes, such as shrinkage of cell body, compaction of nucleus, condensation of chromatin, and membrane blebbing, were observed by electron microscopy. These morphological changes are indexes of apoptosis. Furthermore, DNA fragmentation, a biochemical marker of apoptosis, was also observed. All the results suggest that ionomycin-induced neuronal cell death is apoptotic.

Animals↗
PubMed1994

Neurotrophic effects of annexin V on cultured neurons from embryonic rat brain.

Recombinant human annexin V showed survival promoting activity in embryonic rat neocortical and mesencephalic neurons in vitro. The neurotrophic effect was observed from a relatively low dose and in a dose-dependent manner. The neurotrophic activity of annexin V was completely blocked by anti-annexin V antibody. Northern blot analysis demonstrated that annexin V mRNA is expressed in non-neuronal cells in the CNS. These results suggest that annexin V plays certain roles in the CNS as a paracrine-type neurotrophic factor.

Amino Acid Sequence↗
PubMed1994

Prenatal exposure to influenza and the development of schizophrenia: is the effect confined to females?

The question of whether prenatal exposure to influenza epidemics is associated with an increased risk of later schizophrenia remains controversial. The authors examined this relationship, using data on the dates of birth and gender of 3,827 schizophrenic patients born in England and Wales between 1938 and 1965 and first admitted to hospitals in the 1980s, the numbers of live births between 1938 and 1965, and the numbers of deaths attributed to influenza between 1937 and 1965. The analysis showed that females, but not males, exposed to influenza epidemics 5 months before birth had a significantly greater rate of adult schizophrenia.

Adult↗
PubMed1994

The relationship of schizophrenic births to 16 infectious diseases.

BACKGROUND: Recently, several investigators have reported an association between influenza epidemics and increased birth rates of 'preschizophrenic' individuals some four to six months later. Here we examine whether maternal exposure to other infectious diseases can also predispose the foetus to later schizophrenia. METHOD: Two independent sets of dates of birth of first admission schizophrenic patients, born between 1938 and 1965 in England and Wales, were obtained from the Mental Health Enquiry in England and Wales. Data on the number of deaths per month from 16 infectious diseases between 1937 and 1965 in England and Wales were also collected. We used a Poisson regression model to examine the relationship between deaths from infectious diseases and schizophrenic births. RESULTS: In the two separate data sets, increased national deaths from bronchopneumonia preceded, by three and five months respectively, increased numbers of schizophrenic births. We did not find any other significant associations between schizophrenic births and any of the other 15 infectious diseases. CONCLUSIONS: The association between deaths from bronchopneumonia and increased schizophrenic births some months later may be a reflection of the fact that bronchopneumonia deaths increase markedly during influenza epidemics.

Adult↗