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N Takei

Publications and source records attributed to N Takei.

At least 145 records · Page 8Linked to original sources
PubMed1993

Microglial conditioned medium promotes survival and development of cultured mesencephalic neurons from embryonic rat brain.

We previously reported that microglial conditioned medium (Mic-CM) has a neurotrophic effect on cultured rat neocortical neurons [Nakajima et al. (1989): Biomed Res 10:411-423]. In order to investigate the interaction between microglia and neurons in more detail, we determined the effects of Mic-CM on the primary cultured mesencephalic neurons from 16-day embryonic rats. The addition of Mic-CM to the culture medium significantly enhanced the survivability of neurons and promoted neurite extension in a low cell-density culture condition. In a high cell-density culture condition, Mic-CM markedly increased dopamine uptake, which was quantified by assessing the specific [3H]dopamine uptake, and also increased the dopamine content of cultured cells. Furthermore, the number of mesencephalic dopaminergic neurons, which was determined by quantitative analysis of tyrosine hydroxylase (TH)-immunoreactive cells, increased significantly in the presence of Mic-CM. These results suggest that Mic-CM enhances survival or maturation of TH-positive neurons present in cultures of the embryonic mesencephalon and that these neurotrophic effects may be due to a diffusible factor(s) from microglia.

Animals↗
PubMed1993

Effect of direct current stimulation on triradiate physeal cartilage. In vivo study in young rabbits.

Electrical stimulation with 8 microA direct current was applied to the triradiate physeal cartilage of young rabbits for periods of 3, 4, and 5 weeks. The effect was evaluated by morphometric measurement and histological observation. We tried to improve some previously described technical problems (e.g., movement of electrode during experiment) in this model of the growing acetabulum. Statistically significant differences in acetabular depth were found between the experimental and the control side in the 3-week group, but no obvious differences were found among the other measurements. Characteristic thickening of the growing physeal cartilage, especially proliferating cells, was found in the stimulated sides. Electricity affects the cell behavior in the triradiate physeal cartilage as well as the growth plate of long bone, but further study is still necessary to find more appropriate conditions to gain actual growth.

Acetabulum↗
PubMed1993

Does prenatal influenza divert susceptible females from later affective psychosis to schizophrenia?

We examined the relationship between influenza epidemics and the number of schizophrenic and affective psychotic individuals born each month between 1938 and 1965 in England and Wales. Increased death rates from influenza were followed 5 months later by a significant increase in schizophrenic births and a concurrent fall in the number of births of affective psychotic individuals. When the sexes were examined separately, both the positive effect of influenza on schizophrenic births and its negative effect on affective psychotic births were evident for females but not for males. Furthermore, during February to June in high influenza years, there was an inverse relationship between the number of female schizophrenic and affective psychotic births. The explanation for these surprising findings may be that prenatal exposure to influenza impairs the neurodevelopment of some females with a predisposition to affective psychosis, in such a way that their later illness shows schizophrenic rather than affective features.

Adult↗
PubMed1993

[Schizophrenia following prenatal exposure to influenza during second trimester].

Mednick et al and O'Callaghan et al have recently reported that individuals exposed to the 1957 A2 influenza pandemic during their second trimester in utero are at risk for later schizophrenia. In this study, we determined whether their findings could be reproducible in a Japanese sample. In Japan, there were two waves of the 1957 A2 influenza pandemic; the first occurred from June to July, and the second from November to December. In addition, an epidemic of influenza A/B mixed type prevailed from January to February 1957. We obtained information on all dates of birth of 1187 individuals born between June 1955 and May 1960, who were treated for schizophrenia during the study period. November 1991 to September 1992, at 18 mental hospitals around Tokyo metropolitan areas. Hospital clinical diagnosis was used. We defined the index year from June 1957, beginning the first wave of the pandemic, to May 1958. We compared the number of schizophrenic births in each month of the index year with the average number of births in the corresponding month of the two years before, and following, the index year. The observed number of births in June 1957 and April 1958 were found to be significantly high compared with the average number of births for the corresponding month in the four control years. The 63% excess of schizophrenic births in June 1957 ensued about 5 months after the peak of influenza A/B mixed type epidemic; there was also 49% increase in births about 5 months after the second wave of the pandemic. Given that full term delivery occurred in our sample (ie, 9 months pregnancy), our results support the view of Mednick et al and O'Callaghan et al that maternal exposure to influenza in the mid-pregnancy increases the risk of developing schizophrenia.

Disease Outbreaks↗
PubMed1992

Genes, viruses and neurodevelopmental schizophrenia.

Recent neuroimaging and neuropathological studies suggest a developmental origin for schizophrenia. Some cases may, therefore, be caused by a genetic defect in the specification of brain development. Early environmental hazards such as obstetric complications, and maternal exposure during pregnancy to influenza epidemics, have also been found to increase the risk of later schizophrenia. The relationship between the prevalence of influenza and birth date has been found more consistently for female than male schizophrenics. Female schizophrenia is also associated with a higher risk of schizophrenia in first degree relatives. This raises the question of whether part of the genetic predisposition to schizophrenia may comprise an abnormal reaction to maternal influenza.

Brain Damage, Chronic↗
PubMed1992

Schizophrenia following pre-natal exposure to influenza epidemics between 1939 and 1960.

We examined the relationship between the dates of births of schizophrenic patients admitted to hospitals for the first time in England and Wales between 1970 and 1979, and the occurrence of influenza epidemics between 1939 and 1960. Our results indicate that exposure to influenza epidemics between the third and seventh month of gestation is associated with schizophrenia in adult life. The hypothesis that maternal viral infection is an important cause of schizophrenia can explain many aspects of the enigmatic epidemiology of the condition.

Adult↗
PubMed1992

Seasonality of admissions in the psychoses: effect of diagnosis, sex, and age at onset.

A summer peak was found in first admissions to hospitals in England and Wales between 1976 and 1986 for both affective psychoses and schizophrenia, but not for neurotic conditions or personality disorders. There was no significant relationship between age at first admission and season of admission. The summer peak was most prominent for mania, where it was present in both sexes; for schizophrenia, it was present only in females. These findings suggest that schizophrenia in females, and mania in both sexes, have some aetiological or precipitating factor in common.

Adult↗
PubMed1992

[An autopsy case of spinal subdural abscess in the aged--comparative study with neuroradiological findings].

An 82-year-old woman without previous medical problem noticed vague back pain on December 31, 1989, and was admitted to a hospital because she developed a fever, a rapidly progressive weakness followed by anesthesia of the lower extremities and sphincter disturbance. On myelography and myelo-CT, the spinal cord appeared to be displaced by an extramedullary mass which partially blocked the subdural space at the level of T-9 to L-1. When transferred to our hospital on January 8, 1990, she was febrile and complaining of headache with meningeal signs. Percussion tenderness was present at T-8 to L-1 spinal spinous process. Neurological examination revealed that the patient had mild consciousness clouding, total paraplegia in the legs, sensory disturbance of a partial degree at L-1 to L-3 and totally below L-3, brisk but equal tendon reflexes in the upper extremities, areflexia in the legs with positive bilateral Babinski signs and sphincter disturbance. Otherwise she was neurologically unremarkable. Acute inflammatory reactions were prominent among the laboratory findings on admission. A lumbar tap yielded purulent fluid with more than 170,000 cells/mm3, 5,000 mg/dl of protein, 44 mg/dl of glucose and culture of the fluid isolated Escherichia coli. T1-weighted sagittal MRI disclosed an ill defined mass which showed the same or locally higher with gadopentetate dimeglumine (Gd-DTPA) signal intensity as soft tissue, compressing the spinal cord anteriorly from T-7 to L-3. The lesion was noticed to have a more extensive rostral-caudal extent than was inferred from myelography and myelo-CT.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

Schizophrenia after prenatal exposure to 1957 A2 influenza epidemic.

The birth dates of schizophrenic inpatients in eight health regions in England and Wales were reviewed for any effect of the 1957 A2 influenza epidemic. 5 months after the peak infection prevalence, the number of births of individuals who later developed schizophrenia was 88% higher than the average number of such births in the corresponding periods of the 2 previous and the next 2 years. This finding is in accordance with a study from Helsinki and with clinical and neuropathological evidence of aberrant fetal brain development in the pathogenesis of schizophrenia.

Adult↗
PubMed1991

Production of basic fibroblast growth factor in cultured rat brain microglia.

The production of basic fibroblast growth factor (bFGF) in cultured rat brain microglia was investigated. Rat brain microglia were found to express mRNA of bFGF in analysis by polymerase chain reaction (PCR) technique. Basic FGF was also detected in microglial cell lysate by Western blot analysis. These results indicate that microglia produce bFGF and possibly contribute to the regulation of neuronal development and regeneration.

Animals↗
PubMed1991

Interleukin-6 improves the survival of mesencephalic catecholaminergic and septal cholinergic neurons from postnatal, two-week-old rats in cultures.

Interleukin-6 (human recombinant) supported the survival of cultured mesencephalic, catecholaminergic and septal cholinergic neurons from postnatal, two-week-old (P13-P15) rats. Significantly, more catecholaminergic neurons, stained by monoclonal anti-tyrosine hydroxylase antibody, were found in cultures supplemented with interleukin-6 at a concentration of 5 ng/ml than in cultures not treated with interleukin-6. The optimal dose used was 50 ng/ml. The survival effect of interleukin-6 on postnatal rat, tyrosine hydroxylase-positive neurons was observed both in cultures using serum-containing and serum-free medium. Contents of dopamine and noradrenaline in cultures with interleukin-6 were also larger than in control cultures. Interleukin-6 also increased the survival of cultured embryonic (E17) rat midbrain tyrosine hydroxylase-positive neurons. The effect on these neurons was, however, smaller, and the optimal dose of interleukin-6 was nearly 5 ng/ml. Interleukin-6 also supported the survival of cultured postnatal (P13) rat septal cholinergic neurons, visualized by acetylcholinesterase staining. The concomitant addition of mouse nerve growth factor (100 ng/ml) and interleukin-6 (50 ng/ml) had a synergetic effect on the survival of acetylcholinesterase-positive neurons in culture. Our data suggest that the survival of cultured tyrosine hydroxylase-positive, mesencephalic, and acetylcholinesterase-positive, septal neurons from postnatal two-week-old rats was supported by interleukin-6, just as there was a different dose dependency of interleukin-6 on the cultured postnatal neurons compared with embryonic neurons.

Animals↗
PubMed1991

Neuronal survival factor from bovine brain is identical to neuron-specific enolase.

Neuronal survival factors in the central nervous system were investigated by using a primary culture of embryonic rat neocortical neurons. Bovine hippocampus was homogenized, and the supernatant from high-speed centrifugation was used as the starting material. At the step of DE-52 ion-exchange chromatography, neuronal survival activity was recovered in two fractions, fraction 14 (F14) and fraction 23 (F23). Antisera to the crude F14 and F23 fractions were raised in rabbits. These two antisera completely inhibited the neurotrophic activity of both fractions. Western blotting analysis revealed that anti-F14 antiserum recognized mainly a 30-kDa protein in F14 and anti-F23 antiserum recognized mainly a 44-kDa protein in F23. After sodium dodecyl sulfate-polyacrylamide gel electrophoresis of F23, the 44-kDa protein was cut out from the gel and partial amino acid sequences of the protein fragments were determined. A GenBank data bank indicated that the amino acid sequence of the fragment was identical to that of neuron-specific enolase (NSE). In our assay system, commercially available NSE itself possessed neuronal survival activity for the cultured neocortical neurons. The effects of NSE and F23 were inhibited completely by anti-NSE polyclonal antibody. Furthermore, highly purified NSE supported the survival of cultured neurons in a dose-dependent manner, and the neurotrophic effect was inhibited by monoclonal antibody to the NSE. These results strongly suggest that NSE is one of the neuronal survival factors in the central nervous system.

Animals↗