Search PubMed⌕ Search

Biomedical subjects

E Ohama

Publications and source records attributed to E Ohama.

At least 127 records · Page 7Linked to original sources
PubMed1987

Effects of pentobarbital and ketamine on brain injury-induced anti-ischemic activity.

Survival rates following incomplete brain ischemia induced during pentobarbital anesthesia were significantly higher in mice with a minor brain injury, inflicted one week before, than in those given a sham operation. Improvement of the survival rates in mice with brain injury, however, became insignificant when brain ischemia was imposed during ketamine anesthesia, suggesting that the actions of certain factors or protective mechanisms against brain ischemia, developed by brain injury, are antagonized by ketamine and/or potentiated by barbiturate anesthesia.

Anesthesia↗
PubMed1987

Pineal neoplasms and third-ventricular teratomas in Niigata (Japan) and Western Australia. A comparative study of their incidence and clinicopathological features.

It is claimed that Japan has the highest incidence of pineal neoplasms in the world. To test this hypothesis, we reviewed all pineal neoplasms and third-ventricular teratomas that were diagnosed histopathologically and treated neurosurgically over 10 years (1975-1984) in Niigata City, Japan (12 patients) and in Perth, Western Australia (9 patients). The age-standardized incidence rates per million person-years were 0.61 for Niigata and 0.70 for Western Australia; thus, the contention that Japan has the highest incidence in the world of pineal neoplasms is not confirmed.

Adolescent↗
PubMed1987

Involvement of choroid plexus in mitochondrial encephalomyopathy (MELAS).

Morphological study of the choroid plexuses of two patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) revealed an enormously increased number of mitochondria with structural abnormalities in almost all of the choroidal epithelial cells. The majority of the cells also showed loss of microvilli and collapsed or attenuated apical cytoplasmic processes with increased electron density and lysosome-like dense bodies. The blood vessels of the choroid plexus showed the features of mitochondrial angiopathy previously described in the pial arteries of the same patients. These findings are interpreted as the morphological expression of a primary biochemical defect of the mitochondrial function in the choroid plexus, and as the probable explanation for increased CSF lactate and pyruvate levels in this disease.

Adolescent↗
PubMed1987

Mitochondrial angiopathy in cerebral blood vessels of mitochondrial encephalomyopathy.

We studied cerebral blood vessels of two autopsied patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). All the main cerebral arteries in the proximal portion at the brain base and more distal portion at the cortical surface, as well as within the brain parenchyma were examined by electron microscopy. There was a striking increase in number of mitochondria in the smooth muscle and endothelial cells, which were most prominent in the pial arterioles and small arteries up to 250 micron in diameter and less frequent and severe in the larger pial arteries and intracerebral arterioles and small arteries. These vascular changes have not hitherto been described in MELAS, or in other disorders affecting blood vessels of the brain and other organs. It is suggested that the vascular changes are caused by primary mitochondrial dysfunction in the vascular smooth muscle and endothelial cells of the brain and that they constitute the pathogenic base of the brain lesions and their unusual distribution pattern in MELAS.

Adolescent↗
PubMed1987

An autopsy case of a syndrome with muscular atrophy, decreased subcutaneous fat, skin eruption and hyper gamma-globulinemia: peculiar vascular changes and muscle fiber degeneration.

This is the first autopsy case report of a syndrome with autosomal recessive inheritance, muscular atrophy, contracture, skin eruption, hyper gamma-globulinemia, decreased subcutaneous fat, mental retardation and abnormal ECG findings. Skeletal muscles showed severe, discrete, multifocal muscular fibrosis which replaced several primary fasciculi. The tongue, heart and extraocular muscles showed identical but less severe findings. In the involved muscle fasciculi, veins and venules as well as arteries and arterioles showed medial hyperplasia and luminal constriction. Degeneration of endothelial cells of arterioles and narrowing of the lumen of terminal arterioles by the debris were observed. The peripheral nerves in the muscles were relatively well preserved. The correlation and pathogenesis of these findings are discussed.

Central Nervous System↗
PubMed1987

A mitochondrial encephalomyopathy with cardiomyopathy. A case revealing a defect of complex I in the respiratory chain.

We describe a 16-year-old Japanese girl with a mitochondrial encephalomyopathy who presented with progressive dementia, limb weakness and atrophy, episodic vomiting, generalized convulsions, myoclonic seizures, and hypertrophic cardiomyopathy. CT scan revealed transient focal low density areas in her occipital and parietal lobes, and cerebellar atrophy. The clinical features were consistent with mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS). Microscopically, most of muscle fibers in the skeletal muscles and heart were occupied by markedly increased mitochondria. Polarographic studies on mitochondria isolated from postmortem heart muscle showed severe impairment of oxidation of NADH-linked substrates in contrast to normal succinate oxidation. The rotenone-sensitive NADH-coenzyme Q reductase activity was markedly decreased in heart, skeletal muscle and liver mitochondria. The biochemical investigations have led to the identification of a defect of complex I in the respiratory chain. Reported cases of a defect of complex I have revealed pure myopathy, encephalopathy or encephalomyopathy. The reason for a varied clinical expression of a single defect remains to be clarified.

Adolescent↗
PubMed1987

[An autopsy case of myoclonus epilepsy associated with ragged-red fibers (Fukuhara disease)].

In 1980, Fukuhara et al. have reported two patients with "myoclonus epilepsy associated with ragged-red fibers" (MERRF), which is at present accepted as a distinctive clinical entity among the mitochondrial encephalomyopathies. We describe here postmortem findings of the case whose clinical findings were reported in detail by Fukuhara et al. (1980) as Case 1. The neuropathological findings were summarized as follows: 1) degeneration of dentate nucleus, red nucleus, globus pallidus, subthalamic nucleus and pontine tegmentum, 2) degeneration of the Clarke's column, spinocerebellar tract, posterior column and corticospinal tract, as well as of the posterior spinal nerve root and sural nerve, and 3) degeneration of substantia nigra, locus ceruleus, cerebellar cortex and inferior olivary nucleus. The lesions were degenerative in nature, and their distribution was different from those of dentato-rubropallidoluysian atrophy, Joseph's disease or Friedreich's ataxia. It was concluded that MERRF is a single disease entity also from pathological point of view.

Adult↗
PubMed1986

Joseph's disease: clinical and pathological studies in a Japanese family.

Joseph's disease is a hereditary ataxia found among descendants of Portuguese from the Azores Islands. We describe the clinical and pathological features of 4 members of a Japanese family who were diagnosed as having Joseph's disease. The illness began with cerebellar ataxia between the ages of 18 and 45 years. Nystagmus, dysarthria, and pyramidal signs were early manifestations. External ophthalmoplegia, dystonia and/or athetotic movements, and muscular atrophy appeared in the late stages. Neuropathological findings in one patient revealed degeneration of the dentatorubral and pallidoluysian systems, substantia nigra, pontocerebellar system, Clarke's column and spinocerebellar tracts, and anterior horn cells, as well as the cranial nuclei in the brainstem. Neurons in the inferior olivary nuclei, Purkinje's and granule cells, the cerebral cortex, thalamus, and striatum were spared. Involvement of the dentatorubral and pallidoluysian systems seems to be a characteristic feature of this disease in Japan.

Adolescent↗
PubMed1986

Distribution of serotonin-containing cell bodies in the brainstem of the human fetus determined with immunohistochemistry using antiserotonin serum.

The distribution of serotonin (5HT) neurons was investigated in the brainstem of 8 human fetuses ranging in age from 15 to 27 weeks of gestation. We conducted the peroxidase-antiperoxidase (PAP) immunohistochemical technique using antiserotonin serum to detect the cell bodies of 5HT-containing neurons. Positively stained 5HT neurons were clearly demonstrated in the brainstem of all fetuses examined. They varied in shape, showing round to oval cell bodies with unipolar, bipolar, or multipolar processes. A large number of 5HT neurons were located in the midline raphe nuclei. In addition, numerous 5HT neurons were observed widely in the other tegmental areas. The nuclei containing 5HT neurons were listed according to the terminology by Olszewski and Baxter for human brainstem, and an atlas was given. The distribution of 5HT neurons in the raphe nuclei of human fetuses was essentially similar to those of many mammals already reported. However, the lateral extension of 5HT neurons to the other tegmental areas beyond the midline raphe nuclei was much greater in human fetuses compared to other mammals.

Brain Stem↗
PubMed1986

[Topography of the catecholamine neurons in the brain stem of the human fetus: an immunohistochemical study using antibodies to tyrosine hydroxylase].

Immunohistochemistry using antibodies to tyrosine hydroxylase (TH), a rate-limiting enzyme which catalyzes the initial step in the catecholamine synthesizing pathway, has been widely accepted as one of the methods for identification of catecholamine neurons in the nervous system. In the present study, we performed immunohistochemical examination to elucidate the distribution of catecholamine neurons in brain stem of human fetuses. The brain stems were obtained from 8 human fetuses (CRL: 120-275 mm, GA: 15-27 wks) 1-3 h after death following therapeutic or spontaneous abortion. They were immediately fixed with 4% paraformaldehyde in 0.1 M phosphate buffer, pH 7.4, dehydrated with graded ethanol, and embedded in paraffin. Serial 6 microns sections were cut from 7 different levels of the brain stem of each fetus. These sections were stained by peroxidase-antiperoxidase (PAP) technique using TH antisera. The TH antisera used were raised in rabbits by injecting purified TH from bovine adrenal medulla. The preparation and the specificity of TH antisera were described in detail elsewhere (Nakashima et al, 1983). Catecholamine neurons were clearly demonstrated in the brain stem of all fetuses. They could be recognized as catecholamine cell groups in the same manner as is done in experimental mammals. Among these cell groups, the catecholamine neurons showed distinct cytological features in shape and size. The distribution of catecholamine positive neurons in the brain stem was almost the same in the 8 human fetuses, and an atlas was given with anatomical explanation under the terminology of Olszewski and Baxter (1982) for the human brain stem. In the mesencephalon, a large number of catecholamine neurons lay in the nucleus substantiae nigrae, pars compacta, the nucleus paranigralis, the middle of the ventral tegmentum and the tractus tegmentalis centralis, and fewer catecholamine neurons were scattered in the other tegmental area. In addition, a group of small catecholamine neurons was located in the griseum centrale mesencephali near the aqueduct. In the pons, catecholamine neurons occurred mainly in the nucleus locus coeruleus and the nucleus subcoeruleus. A band of TH-positive neurons extended from the nucleus locus coeruleus to the dorsolateral tegmentum, and further to the roof of the fourth ventricle. Occasional catecholamine neurons were present in the area medial to the upper portion of the nucleus locus coeruleus. More caudally, a small number of catecholamine neurons were scattered in the area medial to the nervus facialis and adjacent to the nucleus facialis and the nucleus olivaris superior.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic Fibers↗
PubMed1984

[Topography of the serotonin neurons in the brain stem of human fetus: an immunohistochemical study].

The distribution of serotonin neurons in the central nervous system (CNS) has been intensively examined in mammals, such as rats, cats and monkeys. However, the details of serotonin neuron system have been remained uncertain in human CNS, although two fluorescence histochemical studies were reported in human fetus. In this study, we performed immunohistochemical examination on the distribution of serotonin neurons in the brain stem of human fetuses. The brain stems from five human fetuses (CRL: 120-275 mm, GA: 15-27 wks) were fixed with 4% paraformaldehyde, dehydrated with graded ethanol, and embedded in paraffin. Serial sections, 6 micron in thickness, were cut from seven different levels of the brain stem of each fetus. The initial several sections were used for usual histological observations. The following serial ones were stained by peroxidase-antiperoxidase (PAP) technique using anti-serotonin sera. The anti-serotonin sera used were raised in rabbits by the methods of Ranadive and Sehon (1967), Grota and Brown (1974), and Steinbusch et al (1978). Before the use, the specificity of the antisera was confirmed by the immunohistochemical examination of the CNS of rat embryos and adults. Positively stained serotonin neurons were clearly demonstrated in the brain stems of all cases examined (Figs. 1A-1H). They were small to medium in size, 10 X 20 micron to 20 X 40 micron, and varied in shape, showing round to oval cell somata with unipolar, bipolar and multipolar processes. The distribution of serotonin neurons in the brain stems was almost the same among five human fetuses (Figs. 2A-2K). A large number of serotonin neurons were located in the midline raphe nuclei. In addition, numerous serotonin neurons were observed widely in the other tegmental area. The nuclei containing serotonin neurons were listed in Table 2 according to the terminology by Olszewski and Baxter (1982). The distribution of the serotonin neurons in the raphe nuclei of human fetuses was fundamentally similar to those of many mammals reported previously. However, the lateral extension of serotonin neurons to the other tegmental area beyond the midline raphe nuclei in human fetuses was much greater than in any other mammals. This distribution pattern of serotonin neurons was considered to be peculiar to human fetus. Since the histological architecture of the brain stems of five fetuses examined was very similar to that of human adults, the distribution of serotonin neurons demonstrated here may also represent that of human adults.

Brain Mapping↗
PubMed1983

Revised pathophysiology on BBB damage: the edema as an ingeniously provided condition for cell motility and lesion repair.

Probably, the most important evidence concerning the breakdown of the BBB is a large inflow of hematogenous fluid into the extravascular spaces. Thus all parenchymal cell elements represent freely floating cells in this fluid medium called the edema fluid. These essential morphological alterations, such as extremely expanded extracellular space and freely floating cells within the fluid, were also observed in the developing normal fetal brain. Many neuroblasts were vigorously migrating in the fetal brain, as were the macrophages and reactive astrocytes in the edema fluid. Obviously, hematogenous cells and reactive astrocytes in the edematous lesion take part in its repair. Many astrocytes, GFAP positive, in the 3 or 4 day-old lesions, revealed mitosis. And in vitro, when we immersed these astrocytes in the protein and glucose rich medium, they demonstrated a remarkably changed morphology and were moved into the M and G1 phases, thus gaining the ability of cell motility. This was also true in the edema fluid. Brain edema is definitely a serious "pathological" condition. But it is also conceivable from a different biological aspect that as a result of BBB "opening", free extracellular space essential for cell motility and a source of their energy is ingeniously provided for these cells, and thus the lesion can be effectively repaired. The biological significance of the edema fluid was emphasized and stereotaxic morphology and cinematography, supporting the above evidence, have also been presented.

Animals↗
PubMed1976

Parkinson's disease: distribution of Lewy bodies and monoamine neuron system.

A systematic study of the central and peripheral nervous systems in 3 cases of Parkinson's disease has demonstrated that Lewy bodies are present in 27 nuclei. Of these 20 nuclei (12 pigmented and 8 unpigmented) are involved in 2 or all 3 cases. It is noticed that the distribution of Lewy bodies in Parkinson's disease described here corresponds surprisingly well to that of monoamine (dopamine, noradrenaline and serotonin) cell bodies demonstrated in rats by the histochemical fluorescence method. This correlation is similar to that of Alzheimer's neurofibillary changes in postencephalitic Parkinsonism as described by Ishii. Inasmuch as these viewpoints are also in agreement with preciously reported biochemical data on Parkinsonism, it is suggested that Parkinsonism (idiopathic and postencephalitic) should represent a system degeneration of monoamine neuron systems.

Biogenic Amines↗