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Biomedical subjects

N Takeda

Publications and source records attributed to N Takeda.

At least 469 records · Page 26Linked to original sources
PubMed1989

A temperature-sensitive defect of enterovirus 70 is located at the uridylylation of the genome-linked protein VPg in vitro.

The temperature-sensitive phenotype of enterovirus 70 (EV70) was examined by use of an in-vitro RNA replication system derived from a membrane fraction (crude replication complex, CRC) of EV70-infected HeLa cells. This system was capable of synthesizing the nucleotidyl proteins VPg-pU and VPg-pUpU. Formation of these nucleotidyl proteins was completely abolished when the in-vitro reaction was performed at the nonpermissive temperature for virus replication. Considering our previous observation that the defective stage of the temperature-sensitive growth of EV70 resides in the initiation step of RNA transcription in vivo, it is most likely that the lack of uridylylation of VPg at the restricted temperature in vitro is directly involved in the temperature-sensitive defect of virus growth in vivo.

Amino Acid Sequence↗
PubMed1989

Neuroendocrine markers in central nervous system neuronal tumors (gangliocytoma and ganglioglioma).

We studied five cases of central nervous system neuronal tumor, one gangliocytoma and four gangliogliomas, both ultrastructurally and immunohistochemically, using antibodies to neuroendocrine markers including tyrosine hydroxylase (TH), serotonin (5HT), somatostatin (SOM), met-enkephalin (MEK), leu-enkephalin (LEK), substance P (SP), gastrin, vasopressin, oxytocin, vasoactive intestinal polypeptide, adrenocorticotropic hormone and calcitonin. In all cases, the presence of dense-core vesicles (60-250 nm) in the neuronal elements was the characteristic ultrastructural finding. Synapses were observed in two cases. Immunohistochemically, variable numbers of neuronal cells showed positive staining for SOM in five cases, TH, MEK and LEK in three cases, and 5HT and SP in one case each. The others were negative. Positive immunoreactivity for multiple markers was shown in all cases. SOM, TH, 5HT and SP were present in the small- to medium-sized cells, while MEK and LEK were almost exclusively confined to the large cells. Our study clearly indicated that these tumors contained neuronal cells which were not homogeneous with regard to neuroendocrine markers.

Biomarkers↗
PubMed1989

Contralateral trigeminal neuralgia as a false localizing sign in calcified chronic subdural hematoma: a case report.

A case of trigeminal neuralgia caused by a contralateral calcified chronic subdural hematoma is reported. Preoperative magnetic resonance imaging revealed rotational displacement of the pons caused by huge chronic subdural hematoma. The neuralgia was completely alleviated after removal of the hematoma. The clinical and radiological features are described, and the possible mechanism of the neuralgia is briefly discussed.

Calcinosis↗
PubMed1989

Effects of ethyl alcohol and heavy-water administration on vestibulo-ocular reflex in rabbits.

The effects of ethyl alcohol and heavy water on the long-time constant (T1) of the vestibulo-ocular reflex, an index of the dynamics of the cupula-endolymph system of the semicircular canal, were investigated in rabbits. Ethyl alcohol with a specific gravity of 0.793 caused two types of direction-changing positional nystagmus. In the early period after its administration, geotropic type positional nystagmus was induced. In this period, ethyl alcohol reduced T1. In the later period after its administration, apogeotropic type positional nystagmus was induced. In this period, T1 was again prolonged. Heavy water with a specific gravity of 1.10 caused apogeotropic type positional nystagmus and prolonged T1. These findings demonstrated that ethyl alcohol and heavy water directly affect the cupula-endolymph system, suggesting that the semicircular canal was responsible for the positional nystagmus.

Animals↗
PubMed1989

Symptomatic Rathke's cleft cyst simulating arachnoid cyst--case report.

A case of symptomatic Rathke's cleft cyst simulating an arachnoid cyst is presented. Although computed tomography and magnetic resonance imaging showed that the cyst content was identical to cerebrospinal fluid, there was faint contrast enhancement in part of the wall. Histological observation suggested that the somewhat vascular connective tissue associated with nests of pituitary cells might have contributed to the enhancement. This type of Rathke's cleft cyst requires further clinical and neuroradiological studies.

Arachnoid↗
PubMed1989

[Diffuse axonal injury manifested as corpus callosum damage on magnetic resonance imaging. Case report].

A 26-year-old male was injured in a motorcycle accident and arrived unconscious at a local general hospital. Lack of improvement despite intensive care prompted his referral to the neurosurgical department, approximately 10 hours after the accident. On neurological examination his Glasgow Coma Scale score was 8, and mild right hemiparesis and right radial nerve palsy were noted. There was no skull fracture. Computed tomography disclosed intraventricular hemorrhage and small hemorrhagic foci in the prepontine area and the border between the gray and white matter. No hemorrhage was demonstrated in the corpus callosum. Magnetic resonance imaging (MRI) was performed 3 weeks after admission with a 0.5-tesla resistive Vista magnetic resonance scanner. The inversion recovery technique was used, with a repetition time (TR) of 2100 msec, an inversion time of 500 msec, and an echo time (TE) of 40 msec, for T1-weighted images. The spin-echo technique was used, with a TR of 2000 msec and a TE of 80 msec, for T2-weighted images. In the body and splenium of the corpus callosum, T1-weighted images showed a spotty area of low signal intensity with an irregular margin; this area was of high signal intensity on T2-weighted images. On repeat MRI performed 4 months after injury, T1-weighted images showed, in the same region, granular low signal intensity, while T2-weighted images showed high signal intensity. The MRI findings in the subacute and chronic stages of diffuse axonal injury are discussed.

Adult↗
PubMed1989

Localization and origins of calcitonin gene-related peptide containing fibres in the vestibular end-organs of the rat.

The distribution, origin and fine structure of nerve terminals immunoreactive to calcitonin gene-related peptide (CGRP) were investigated in the vestibular end-organs of the rat by means of immunocytochemistry. Dense plexus of CGRP-like immunoreactive (CGRPI) fibres were observed just beneath the sensory epithelial layers of the ampullary crista of the semicircular canal, and utricular and saccular maculae of the otolith organ. Some CGRPI fibres left the plexus to enter the sensory epithelial layer. Parasagittal transection of the brain just medial to the cochlear nucleus revealed the presence of a few CGPRI fibres in the vestibular end-organs ipsilaterally, indicating that these fibres originate in the central nervous system. A combination of retrograde tracing and immunocytochemistry was then used to identify the origins of CGRPI fibres found in the vestibular end-organs. After injection of fast blue dye (FB) into the vestibular cistern, CGRPI neurons in the area dorsolateral to the genu of the facial nerve were labelled by FB bilaterally. The present ultrastructural study has revealed that most of the CGRPI fibres in the vestibular end-organs form direct contacts with afferent nerve terminals which surround type I vestibular sensory cells.

Acoustic Maculae↗
PubMed1989

DNA synthesis, blood flow, and glucose utilization in experimental rat brain tumors.

The relationships between distribution of deoxyribonucleic acid (DNA)-synthesizing cells (S-phase cells) and blood flow and glucose utilization were investigated in rat brain tumors using an autoradiographic technique and immunoperoxidase staining for bromodeoxyuridine (BUdR). Two strains of rat brain tumor were used: strain A and B, both induced by the Rous sarcoma virus. Strain A was biologically more malignant than strain B. The blood flow was unevenly distributed in the tumor, compared with the contralateral cortex, the average blood flow in the tumor was about 50% in strain A and 60% in strain B. The distribution of blood flow did not correlate with the distribution of S-phase cells or with the distribution of vessels in the tumor in either strain A or B. The average glucose utilization in strain A was about 250% and in strain B about 170% of that of the contralateral cortex. The high glucose utilization area correlated well with the distribution of BUdR-positive nuclei in strain B. These findings suggest that the biological malignancy of a tumor correlates with glucose utilization rather than with blood flow, and that malignant brain tumors show a marked increase in glucose utilization for nucleic acid synthesis.

Animals↗
PubMed1989

[A study of aphasia caused by putaminal hemorrhage].

Aphasia was evaluated in 21 right-handed patients (39-74 years old) with putaminal hemorrhage, and compared with that caused by thalamic hemorrhage. The patients were divided into three groups by the volume of the hematoma: small hematoma (I, n = 6), middle hematoma (II, n = 8) and large hematoma (III, n = 7) groups in computed tomographic findings. Aphasia examination was performed 8-37 days (mean 21 days) after the onset. In group I, aphasia was not seen or just transient, if any. In group II, aphasia was mainly a mixed type, and the prognosis was excellent in many patients. In group III there were expressive type at anterior lesion, receptive type at posterior lesion and global aphasia at anterior-posterior lesion, and the prognosis was not good. It is suggested that the putamen itself does not participate in language behavior, and that aphasia caused by putaminal hemorrhage is due to destruction of the surrounding tissue of the putamen. The type of aphasia and prognosis are varied by the site of a lesion and a hematoma volume. It is also suggested that the thalamus is related to language behavior in a circle of thalamus-cortical language area-thalamus. Aphasia caused by putaminal or thalamic hemorrhage was observed to be different from classical cortical aphasia. But there was no significant difference between aphasia caused by putaminal lesions and that by thalamic lesions.

Adult↗
PubMed1989

A pedigree of cervical stenosis, brachydactyly, syndactyly, and hyperopia.

Cervical myelopathy due to developmental cervical canal stenosis occurred in a 13-year-old boy. The patient's father and aunt also had an abnormally small cervical canal, although both were asymptomatic. The patient and his family had many congenital anomalies including hereditary brachydactyly, syndactyly, and hyperopia. The association of these anomalies seems not to have been previously reported in the literature.

Abnormalities, Multiple↗
PubMed1989

[T cell receptor delta chain gene rearrangement in acute unclassified leukemia].

A 31 year-old male who was treated with radiation under the diagnosis of malignant lymphoma was admitted to our hospital because of systemic erythema and tumor of bilateral upper arms in October, 1987. Leucocyte count of peripheral blood showed 4,400/microliters with 36% leukemic cells and bone marrow was hypercellular with 85.6% leukemic cells. Leukemic cells were negative for peroxidase reaction and lineage specific monoclonal antibodies such as CD3, CD4, CD8, CD10, CD19 and CD20. T cell receptor (TCR) delta gene was rearranged but TCR beta, TCR gamma and immunoglobulin (Ig) genes were in germline configuration. He was treated with combination regimen of doxorubicin, vindesine, prednisolone and L-asparaginase, and complete remission was obtained. These observations suggest that TCR delta gene rearrangement is useful for determination of clonality in cases without rearrangements of the other TCR and Ig genes.

Acute Disease↗
PubMed1989

[Objective assessment of senile changes in visual function by visually evoked cortical potentials].

The P100 peak latency of pattern visually evoked cortical potentials (P-VECP) was found to increase and amplitude decrease in the elderly depending on stimulus conditions. Using either of these as a criterion, changes of visual function with aging were quantitatively assessed both in humans and animals. Contrast threshold was found to increase at higher spatial frequency ranges and the luminance threshold increased more than 0.8 log unit. Also, the contrast threshold increased due to a smaller pupillary area and there was progressive decrease of the temporal frequency curves with age for lower frequency ranges of less than 10 rev/sec. In addition, a sensitivity decrease for the upper visual field was detected plus blue-yellow defects and a decrease in the amplitude of accommodation. In order to exclude the effect of senile changes of the crystalline lens, the luminance threshold, the accommodation power and color sense were investigated in pseudo-phakic eyes with a posterior chamber lens. No significant differences were found between phakic and pseudo-phakic eyes. Accordingly, it was suggested that reduced transparency and yellowish changes of the crystalline lens do not essentially contribute to the loss of function in the elderly found in the present study, but the neuronal pathway was responsible. As a clinical model of senescence, cases of juvenile parkinsonism were investigated, during L-dopa treatment and after ceasing it. The deficiency of the neural-transmitter of the higher visual pathway was indicated in the elderly, also. Animal experiments on neuronal dysfunction in rats and mice suggested no aging effects in ERGs, whereas VECP peak latency for higher temporal frequencies increased with age. The assumption that the elderly changes occur at the neuronal level was supported by a loss of optic nerve fibers in mice with age. The numbers of optic nerve fibers measured were 48,115, 50,875 in the 3-month-old and 6-month-old groups, respectively, and decreased to 43,175 in the 30-month-old group. Though our results indicated the senescence of visual function at the neuronal level, it was not as much as shown by other sensory organs. It was therefore presumed that there might be a certain feed-back system from the brain to the retina.

Adolescent↗
PubMed1989

[Triploid clone observed at blastic crisis in chronic myelogenous leukemia with complex Ph1 translocation (9; 22; 12)].

A 56-year-old female, who was diagnosed as CML in 1983 and had been well controlled with busulfan, was admitted to our hospital because of fever and iliac bone pain. Peripheral blood showed leukocytosis (WBC 70,000/microliters and bone marrow was normocellular with 53% leukemic cells, suggesting that she was in the blastic crisis. Chromosomal analysis of bone marrow cells at that time revealed t (9; 22; 12) and some additional abnormalities. The number of chromosomes ranged from 44 to 131 and the mode of chromosome number was 65. She was treated with combination regimen consisting of vincristine, 6-mercaptopurine and prednisolone and right iliac tumor was irradiated. Three months after admission, she died of DIC and pulmonary insufficiency due to leukemic infiltration.

Blast Crisis↗
PubMed1989

[Double minute chromosomes (DMs) in a case of acute myelomonocytic leukemia].

A 71-year old male was admitted to our hospital because of general malaise and fever. Peripheral blood showed Hb 8.1 g/dl, platelet 7.0 X 10(4)/microliters, and WBC 18.100/microliters with 64% leukemic cells. Bone marrow showed normocellularity with 73.4% leukemic cells. They were positive for peroxidase and alpha-naphthyl butyrate esterase stainings. Serum and urine lysozyme levels were elevated. He was diagnosed as having acute myelomonocytic leukemia (M 4 in FAB classification). Chromosome analysis of bone marrow cells showed 45, XY, -17, t (9; 17) (q22; p13) and double minute chromosomes (DMs) were observed in the 50 cells analyzed. A complete remission (CR) was obtained by DCMP regimen, but he relapsed as acute monocytic leukemia (M 5 b in FAB classification) and died 5 months after diagnosis. DMs appear to be rare in acute leukemia and the clinical and etiologic implications of DMs are discussed.

Aged↗
PubMed1989

Cerebral glioblastoma with cerebrospinal fluid dissemination: a clinicopathological study of 14 cases examined by complete autopsy.

During the last 17 years, complete autopsies were performed on 51 patients who died of cerebral glioblastoma, and 14 were found to have dissemination by cerebrospinal fluid (CSF). In these 14 cases of glioma, the extent of intraparenchymal invasion by the primary tumor and the degree of seeding were studied in connection with histological findings and immunohistochemical staining for glial fibrillary acidic protein (GFAP) as the most reliable marker of astrocytic differentiation. From the findings obtained, the cases were divided into two groups. In one group, consisting of 7 gliomas, autopsy revealed intense seeding, despite only slight invasion by the primary tumor. Among these 7 extensively disseminated gliomas, 4 expressed almost no GFAP, 2 contained only a few GFAP-positive cells, and only 1 displayed an immunohistochemically high degree of astrocytic differentiation. Clinically, 6 of the 7 affected patients developed symptoms attributable to CSF seeding. In the other group consisting of the remaining 7 gliomas, only slight dissemination was seen, despite extensive infiltration of the primary tumor. Each of these 7 gliomas contained many GFAP-positive cells. None of the affected patients developed symptomatic seeding. This study shows the existence of two clinicopathologically distinct groups of disseminated cerebral glioblastomas and suggests that, regardless of morphological features, glioblastomas showing immunohistochemically poor astrocytic differentiation tend to shed tumor cells more vigorously but are less invasive at the primary site than those with many GFAP-positive cells. It is also suggested that, as a consequence, the former glioma type produces symptomatic seeding more frequently than the latter type.

Adult↗
PubMed1989

[Progressive mental deterioration after radiotherapy in adult patients with brain tumors].

We report a study on changes of mental function in twenty five adult patients with cerebral low-grade gliomas after radiotherapy. None of them had shown mental deterioration before radiotherapy nor tumor recurrence after radiotherapy. Radiation was given at a dose of 48 to 78 Gy (mean: 54.2 Gy). Patients were assigned for mental functional levels according to Karnofsky performance scale (KPS) after radiotherapy. Ten patients (40%) were normal. Seven patients (28%) showed moderate disabilities and 8 (32%) severe disabilities. The median interval time from radiotherapy to the onset of mental deterioration was 2.5 years in the moderate group and 1.6 years in the severe group. CT findings in severe group demonstrated severe brain atrophy and diffuse low density in the white matter after radiotherapy. The risk factors responsible for progressive mental deterioration after radiotherapy may be radiation site and size (whole frontal lobe), total dose (over 60 Gy) and patients age at the time of radiotherapy (over 60 yrs).

Adult↗