Biomedical subjects

S Takashima

Publications and source records attributed to S Takashima.

At least 19 recordsLinked to original sources

PubMed1997

Hypoxia-induced ABR change and heat shock protein expression in the pontine auditory pathway of young rabbits.

The auditory brainstem response (ABR) was compared with the immunohistochemical expression of heat shock protein (HSP-72) and microtubule-associated protein 2 (MAP-2) of the brainstem auditory pathway in young rabbits subjected to hypoxic stress. Severe hypoxia for 2 h produced significant prolongation and decreased amplitude of the later component of ABR. HSP-72 expression was distinctly increased in the cochlear nucleus, but there was less induction in the inferior colliculus under severe hypoxia. MAP-2 immunostaining of neuropiles in the inferior collicular nucleus was decreased slightly after severe-long hypoxia, but cytoplasmic staining did not change. The present ABR change, which was produced by brainstem hypoxia-ischemia and acidosis, may be due to the neural cytoarchitectural derangement and less induction of stress proteins in the upper brainstem.

Animals↗

PubMed1997

Increased cerebral choline-compounds in Duchenne muscular dystrophy.

We investigated the hypothesis that cell membrane function is abnormal in brains of subjects with Duchenne muscular dystrophy (DMD) using proton-nuclear magnetic resonance (NMR) spectroscopy of human brain extracts. The total amount of choline-containing compounds was significantly higher (about three times) than in normal controls and patients with other myopathies, while N-acetyl-L-aspartic acid and creatine were within the normal range. These findings indicate that abnormal cell membrane function may be correlated with the abnormal dystrophin or lack of dystrophin in the brain of patients with DMD.

Adolescent↗

PubMed1997

Induction of cyclo-oxygenase 2 in brains of patients with Down's syndrome and dementia of Alzheimer type: specific localization in affected neurones and axons.

Immunohistochemical and immunoblotting studies with an antibody against cyclo-oxygenase 2 (COX2) were performed in the cerebral cortex of patients with Down's syndrome (DS) and dementia of Alzheimer type (DAT). A high level of COX2 expression was observed in DAT and older DS patients, specifically localized in neurones with neurofibrillary tangles (NFT) and damaged axons. Furthermore, immunohistochemical study of patients with DS of varying age showed that the induction of COX2 correlated well with the appearance of NFT as well as with ageing. These findings demonstrated the induction of COX2 in DAT and DS, which may lead to the production of free radicals and may be causally related to neuronal degeneration.

Adolescent↗

PubMed1997

Depletion of cerebral D-serine in non-ketotic hyperglycinemia: possible involvement of glycine cleavage system in control of endogenous D-serine.

Tissue concentrations of D-serine and other chiral and non-chiral amino acids were measured post-mortem in the cerebral cortex of the neonatal or infantile individuals with (three cases) or without (seven cases) non-ketotic hyperglycinemia (NKH) using high performance liquid chromatography with fluorometric detection. In the cortical tissues of the NKH patients lacking activity of glycine cleavage system, there was a marked reduction and elevation of the contents of D-serine and glycine, respectively, compared to non-NKH controls. Systemic administration of an inhibitor of glycine cleavage system (GCS), cysteamine, mimicked the changes in the cortical concentrations of these amino acids in the 8-day-old rats. Augmentation of brain glycine levels by means of intraperitoneal injection of glycine itself resulted in an increase in cortical D-serine contents in the neonatal rats with normal activity of GCS. These findings provide the first evidence that GCS might be implicated in the biosynthesis or content regulation of endogenous D-serine in the mammalian brain.

Amino Acid Oxidoreductases↗

PubMed1997

Granulocyte colony stimulating factor-producing tongue carcinoma.

BACKGROUND: Leukocytosis without infection in patients with malignancies is known as the leukemoid reaction. The mechanisms involved in this phenomenon remain uncertain. METHODS: We describe the clinical, biochemical and immunohistochemical findings in a patient with recurrent tongue carcinoma accompanied by marked leukocytosis as high as 96200/ mm3. RESULTS: The serum granulocyte colony stimulating factor (G-CSF) concentration was increased to 204 (normal: < 30) pg/ml, which paralleled to the elevation of white blood cell (WBC) count and the tumor growth. The G-CSF content of the tumor tissue was also elevated (131 pg/mg protein) compared to that in control patients (6.63 +/- 2.63 pg/mg protein). Production of G-CSF from the tumor was evidenced by immunohistochemical staining with monoclonal antibody against human recombinant G-CSF. CONCLUSIONS: We suggest that the G-CSF production of the tumor participates in the mechanisms of the leukemoid reaction.

Aged↗

PubMed1997

Improved detection of cortical and subcortical tubers in tuberous sclerosis by fluid-attenuated inversion recovery MRI.

We carried out fluid-attenuated inversion recovery (FLAIR) pulse sequences with long repetition and echo times in seven children with tuberous sclerosis, and compared them with conventional spin-echo (SE) sequences. FLAIR images exhibited higher sensitivity than conventional SE images to cortical and subcortical tubers. The low signal intensity of cerebrospinal fluid on FLAIR images allowed more accurate delineation of the cortical and subcortical tubers. However, T1-weighted imaging was still superior for delineation of subependymal nodules.

Adolescent↗

PubMed1997

Ubiquitin-immunoreactive granular inclusions in neuronal migration disorders.

This report describes novel ubiquitin-immunoreactive inclusions in neurons in 3 out of 27 patients with neuronal migration disorders (NMDs). One patient was pathologically diagnosed as having cortical microdysgenesis, and the other two were consistent to have polymicrogyria. The inclusions were present in the perikaryon as compact granular structures, 0.5-2 microns in diameter. Since ubiquitin acts as a cellular scavenger and has a crucial role in selective protein degradation, the presence of ubiquitin-immunoreactive inclusions suggests that altered or abnormal proteins may accumulate in neurons in NMDs, although the nature of accumulated proteins remains unknown.

Adolescent↗

PubMed1997

Developmental changes of glutamate receptors in the rat cerebral cortex and hippocampus.

We studied the immunohistochemical localization of the glutamate receptors (GluR-1, -2, and -3,) in the developing rat cerebral cortex and hippocampus using antibodies to GluR1 and to an epitope common to GluR2 and GluR3 (GluR2/3) subunits. In the cerebral cortex, GluR1 immunoreactivity appeared in the neurons from postnatal day (PND) 0, increased with maturation, was highest at PND 10, decreased until PND 30, and thereafter remained at the same level as on PND 0. GluR2/3 immunoreactivity appeared earlier in scattered neurons on embryonal day (ED) 18, increased with maturation and reached a peak between PND 10 and PND 15, after which the immunoreactivity gradually decreased and reached a plateau at PND 30. For both GluR1 and GluR2/3, some of the pyramidal neurons showed intense staining. In the pyramidal layers of the hippocampus, GluR1 and GluR2/3 immunoreactivity was found in all the pyramidal neurons of the CA1-4 area from ED 20. In the dentate gyrus of the hippocampus, GluR1 and GluR2/3 immunoreactivity was found in the neurons of the granule cells after PND 0. Immunoreactivity in the neurons of the subiculum was found after PND 5 and that of the polymorphic cell layers was found after PND 15-20. Our results indicate that the development of glutamate receptor subunits in the rat cerebral cortex and hippocampus is expressed in different spatial patterns and distinct temporal patterns throughout development and is scheduled during the early postnatal period, when synaptic plasticity or synaptic connection occurs in these regions.

Animals↗

PubMed1997

Neuropathological findings in the cerebro-oculo-facio-skeletal (Pena-Shokeir II) syndrome.

An autopsy case is described of an infant with cerebro-oculo-facio-skeletal (COFS) (Pena-Shokeir II) syndrome who died of pneumonia at the age of 5 months, and the pathology of the CNS in this case and the cases in literature were reviewed. Neuropathological examination revealed a partial defect of the corpus callosum, lobulation of the caudate nucleus and putamen, polymicrogyria in the parietal lobes and neuronal heterotopia in the cerebral and cerebellar white matter. The migration disorders suggest that the onset starts in the early fetal period.

Agenesis of Corpus Callosum↗

PubMed1997

Neuronal maturation and N-acetyl-L-aspartic acid development in human fetal and child brains.

The developmental changes in N-acetyl-L-aspartic acid (NAA) were assessed in human fetal and child brains by means of high resolution proton magnetic resonance spectroscopy (MRS). NAA was detected in the cerebral cortex and white matter of fetuses of 16 weeks' gestation. NAA increased gradually from 24 weeks' gestation and remarkably from 40 weeks' gestation to 1 year of age. The developmental changes in tissue NAA in postnatal brains were found to be similar to those of NAA/Cr on clinical proton MRS. As the neuronal cell density in the cerebral cortex decreases with dendritic maturation, an increase in NAA with age may reflect the normal and abnormal development of axons, dendrites and synapses as well as neuronal soma.

Adolescent↗

PubMed1997

Peroxisomal bifunctional enzyme deficiency: serial neurophysiological examinations of a case.

We report on a case of 21-month-old girl with peroxisomal bifunctional enzyme deficiency, which was diagnosed by means of complementation analysis. Serial neurophysiological examinations were also carried out. The motor and sensory nerve conduction velocities of the median nerve showed lower borderline values at 3 months of age and were within range at 11 months of age. Later, those velocities gradually decreased. The electrically elicited blink reflex at 3 months of age showed the prolongation of latencies of R1, R2 and R2' and the interpeak latencies of R1-R2 and R1-R2'. Furthermore, R1, R2 and R2' showed prolonged latencies at 11 months of age and were absent at 15 months of age. The auditory brainstem response (ABR) showed, bilaterally, normal latency of wave I, prolonged interpeak latencies of waves I-V. At 11 months of age, waves III and IV-V of ABR were detected, but their amplitude was very low. At the age of 15 months ABR was absent. These results and the following report are valuable for understanding the pathogenesis of neurological symptoms.

3-Hydroxyacyl CoA Dehydrogenases↗

PubMed1997

Developmental and aging changes in the expression of amyloid precursor protein in Down syndrome brains.

We studied immunohistochemically the expression of beta-amyloid precursor protein (APP) in the frontal lobes of 18 Down syndrome (DS) patients (20 gestation weeks (GW) to 50 years) and 15 controls (17 GW to 50 years) using six purified antibodies against the secretory forms (N-terminal, N-Amy and Amy540), the Kunitz-type protease inhibitor (KPI) domain, residues 1-28 of beta protein (Affi28), and the carboxyl-terminal fragment (Ac) of APP. In the cortex of fetuses, neonates and infants, immunoreactivity for N-Amy and Ac was observed in both neurons and glial cells, and that for Affi28 in glial cells in the subpial layer in both DS patients and controls suggesting the functioning role of APP was a growth factor. This immunoreactivity disappeared in childhood and reappeared in adulthood in only DS patients. The earlier reappearance of those in DS patients from a young adult age than in normal controls may result from a gene dosage effect, since APP is encoded on chromosome 21. The N-Amy, Amy540, Affi28 and Ac immunoreactivity in glial cells in the developing white matter in the both DS patients and controls may be associated with myelination glia. Immunoreactivity for KPI was noted on the tunica media of the arteries from the neonatal period to adulthood in only DS patients. In senile plaques in DS patients, N-terminal and Affi28 immunoreactivity became detectable at the age of 32 years. N-terminal immunoreactivity in the senile plaques was noted along the periphery of the senile plaques, while that for Affi28 was around the amyloid core. Thus, each fragment of APP exhibited a different localization and time course of immunohistochemical expression. The results indicated that APP plays a role in neuronal development and that its earlier reappearance in adult DS patients is associated with the regeneration process related to aging.

Adolescent↗

PubMed1997

Differential development of the human cerebellar vermis: immunohistochemical and morphometrical evaluation.

Differential development of regions of the human cerebellar vermis was evaluated immunohistochemically and morphometrically between 18 weeks of gestation and 10 years of age. The density of Purkinje cells in the cerebellar vermis decreased rapidly until 38 weeks of gestation and slowly thereafter. At all stages of development, the density was higher in the posterior (lobules VI-IX) than the anterior vermis (lobules I-V). The area of cut sections of the anterior and posterior vermis in the mid-sagittal section increased rapidly before 40 weeks of gestation and gradually after birth, whereas growth was slower in the nodules. These developmental characteristics may be related to the selective susceptibility of cerebellar regions to environmental insults.

Cell Count↗

PubMed1997

Warthin's tumor of the parotid gland with extension into the parapharyngeal space.

A case of Warthin's tumor of the parotid gland which extensively extended into the parapharyngeal space is presented. The tumor border against the parotid gland was ill-defined but the border towards the parapharyngeal structures was clear. Solid portions of the tumor appeared hypointense relative to the gland on both unenhanced T1- and T2-weighted MR images without fat suppression, whereas cystic portions appeared hypointense on T2-weighted images and hyperintense on unenhanced T1-weighted images. Pathologic study showed that the ill-defined margin was caused by inflammation and cystic material consisted of highly proteinaceous material. We concluded that the atypical extension into the parapharyngeal space of the tumor was caused by its location in the deep lobe of the parotid gland and its bulky size.

Adenolymphoma↗

PubMed1997

Assessment of parotid masses: which MR pulse sequences are optimal?

The objective of this paper is to determine which MR pulse sequences are optimal for delineation of lesion and predicting pathologic nature of lesion with signal intensity. A prospective study was performed in 53 parotid masses (39 benign and 14 malignant lesions) in 53 patients. Signal intensity of lesion was visually assessed and lesion/parotid contrast-to-noise ratios were measured. On visual assessment, detection sensitivity was 100% for nonenhanced nonfat-suppressed T1-weighted images, 91% for nonfat-suppressed fast spin-echo (FSE) T2-weighted images, 83% for gadolinium-enhanced fat-suppressed T1-weighted images, and 75% for fat-suppressed FSE T2-weighted images. The highest contrast-to-noise ratios were obtained with nonenhanced T1-weighted images. Hypointensity of lesion relative to the parotid gland on nonfat-suppressed FSE T2-weighted images was seen in 11 of 14 malignancies, 12 of 15 Warthin tumors, and two of 18 pleomorphic adenomas. Cystic portion of hyperintensity on nonenhanced T1-weighted images was solely seen in benign tumors (n = 11). Thus, the highest accuracy (81%) (79% sensitivity and 82% specificity) for predicting malignancy was obtained with a criterion of hypointensity on nonfat-suppressed FSE T2-weighted images plus absence of cystic portion of hyperintensity on nonenhanced T1-weighted images. Nonenhanced T1-weighted images combined with nonfat-suppressed FSE T2-weighted images is optimal for delineation of lesion and prediction of pathologic nature of parotid masses.

Adolescent↗

PubMed1997

Expression of the LIS-1 gene product in brain anomalies with a migration disorder.

Miller-Dieker syndrome (MDS) is a prototype of brain malformations characterized by abnormal neuronal migration. To clarify the pathomechanisms underlying these anomalies, we performed immunohistochemical studies using specific antibodies against the protein product of LIS-1, the candidate gene responsible for the MDS phenotype. The LIS-1 protein was present abundantly and ubiquitously in normally developing brains. Loss of LIS-1 immunoreactivity was observed in brains with MDS, but not in brains with other malformations, such as isolated lissencephaly, holoprosencephaly, Fukuyama-type congenital muscular dystrophy, and Zellweger syndrome. These results suggest that the pathomechanism underlying abnormal neuronal migration in MDS may be specific to this particular type of malformation.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗

PubMed1997

Immunohistochemical expression of cell adhesion molecule L1 in hemimegalencephaly.

We demonstrated immunohistochemically an abnormal expression of the neural cell adhesion molecule L1 in 10 developing brains of children with hemimegalencephaly (HM) aged from 36 weeks gestation to 10 years of age, comparing them with 23 controls aged from 13 weeks of gestation to 14 years. There was dense L1 expression in focal regions of the molecular layer beneath leptomeningeal glioneuronal heterotopia, in areas of cerebral cortex with large neurons, and in the disorganized or neuronal heterotopic sites in the white matter in HM. L1 was also heterogeneously enhanced in the abnormal cortex after 1 year of age, suggesting that axonal growth was delayed. These changes persisted into the older age group in the abnormal areas of cortex in HM. The cell bodies of many enlarged neurons in HM were immunopositive for L1, whereas L1 was usually localized to the processes of normal neurons. The delayed L1 immunoreactivity and enlarged L1-immunopositive neurons may be closely related to the pathogenesis of unilateral megalencephaly with cortical dysplasia and heterotopia.

Adolescent↗

PubMed1997

Cu, Zn-superoxide dismutase reaction in neonatal pontosubicular neuron necrosis.

The immunohistochemical localization and changes in copper/zinc superoxide dismutase (Cu, Zn-SOD) were examined in 14 neonates with pontosubicular neuron necrosis (PSN), as compared with those in 15 controls in which the cytoplasm of neurons and glial cells showed SOD immunoreactivity. In the temporal lobes and hippocampus with PSN, Cu, Zn-SOD reactivity was negative in neurons at 0 and 1 days after birth, but was positive after 5 days of age in 8 of 10 cases. In the pons and cerebellum, SOD-positive neurons appeared soon after birth, but eosinophilic or karyorrhectic neurons were SOD negative. On the other hand, glial cells were positive after birth in all cases of PSN, and their reactivity was increased in the cases of reactive astrogliosis. Early loss of the scavenging system directed at free radicals may lead to neuronal damage, and the induction of Cu, Zn-SOD may act as a defense mechanism against damage of neurons in neonates with PSN. Therefore, oxygen-derived free radicals may be one of the pathogenetic factors of PSN with characteristics of apoptosis in neonates.

Case-Control Studies↗