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Biomedical subjects

T Yanagihara

Publications and source records attributed to T Yanagihara.

At least 271 records · Page 15Linked to original sources
PubMed1984

Immunohistochemical localization of creatine kinase BB-isoenzyme and tubulin in gerbil brain.

Cellular distribution of creatine kinase BB-isoenzyme and tubulin was investigated immunohistochemically with tissue sections from various areas of the gerbil brain. Both the reaction for creatine kinase BB-isoenzyme and tubulin visualized nerve cell bodies, dendrites and axons. While the reaction for tubulin was similar between nerve cell bodies and their dendrites, the reaction for creatine kinase BB-isoenzyme tended to be more intense in dendrites. While the reaction for tubulin could be seen in nerve cell bodies of different sizes, the reaction for creatine kinase BB-isoenzyme was more intense in larger neurons. Both the reaction for creatine kinase BB-isoenzyme and tubulin visualized astrocytic cytoplasm but only in the corpus callosum and in the white matter of limited areas. Visualization of dendrites to their peripheries with the reaction for creatine kinase BB-isoenzyme may indicate participation of this isoenzyme in maintainance of high energy-phosphates locally within dendrites. A combination of the immunohistochemical procedure for creatine kinase BB-isoenzyme and tubulin may be very useful for demonstration of various pathophysiological states of the central nervous system which affect dendrites.

Animals↗
PubMed1984

A progressive neurologic disorder with supranuclear vertical gaze paresis and distinctive bone marrow cells.

Nine patients with a progressive neurologic disorder that was characterized by mental deterioration, supranuclear vertical gaze paresis, and foam cells or sea-blue histiocytes in the bone marrow are described and compared with patients who were previously described as having " neurovisceral storage disease with vertical supranuclear ophthalmoplegia" and "dystonic lipidosis." The clinical manifestations of our patients and those described by others and the pathologic findings and profiles of lipid analysis reported by others are similar to those in patients with Niemann-Pick disease, type C. Sphingomyelinase activities in leukocytes and skin fibroblasts were normal in our patients and in more than half of the reported cases; these findings are also compatible with those in patients with Niemann-Pick disease, type C. Until the biochemical and genetic abnormalities of Niemann-Pick disease, type C are clearly defined, it is justifiable to classify the disorder under discussion as a subgroup of Niemann-Pick disease, type C because it seems to be a heterogeneous group. From the clinical point of view, the diagnosis is difficult to establish in the absence of abnormalities in the bone marrow in patients who are older than 20 years; repeat examinations of the bone marrow are necessary in such patients. Clinicians should be aware of this disorder not only in patients in the first and second decades of life, when this disorder usually becomes symptomatic, but also in patients in the fourth and fifth decades.

Adolescent↗
PubMed1984

[Immunohistochemical study of ischemic neuronal damage with antiserum to tubulin, a microtubular protein].

The limitation of conventional histological methods to demonstrate ischemic change of neurons in early phase has been a major drawback in histopathological and pathophysiological studies of cerebral ischemia. Cellular metabolism is disturbed immediately after cessation of the regional circulation and rapid alterations in macromolecular and ultrastructural integrity in neurons may take place before any evidence of histopathological changes could be detectable. To demonstrate ischemic change of neurons more sensitively on a histological level, we applied immunohistochemical method using antiserum to tubulin, a protein of microtubules. As this organelle has been implicated in several important cellular functions such as control of cell shape, intracytoplasmic transport of materials or synaptic transduction, immunohistochemical alterations in microtubules may indicate structural as well as functional damage of neurons. In order to study the ischemic change in neurons, the posterior communicating artery of a gerbil brain was occluded by the method previously reported by us, and the hippocampus, which is one of the most vulnerable structures of the brain to ischemia, was observed. Five or 30 minutes after occlusion, animals were sacrificed by decapitation. Brains were removed, cut coronary vessels and fixed in ethanol-acetic acid (95:5). Tubulin used for this study was extracted from normal gerbil brains and specific antiserum was raised in goats Peroxidase-antiperoxidase method was performed on paraffin sections. Immunohistochemical distribution of tubulin in a normal gerbil brain demonstrated by the present method was in good accordance with the reported electronmicroscopical distribution of microtubules.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Immunohistochemical localization of creatine kinase BB-isoenzyme in human brain: comparison with tubulin and astroprotein.

The distribution of creatine kinase BB-isoenzyme in the human central nervous system (CNS) was investigated immunohistochemically and the findings were compared with the distributions of tubulin and astroprotein. Creatine kinase BB-isoenzyme existed both in neurons and astrocytes, and was universally distributed within the CNS. Tubulin was visualized only in the neuronal elements, namely perikarya, dendrites and axons, while astroprotein was exclusively visualized in astrocytes. A combination of immunohistochemistry for structural and soluble proteins may be a useful tool for the investigation of pathophysiological conditions within the CNS.

Astrocytes↗
PubMed1983

Creatine kinase BB isoenzyme in CSF in neurologic diseases. Measurement by radioimmunoassay.

The concentration of creatine kinase BB isoenzyme (CK BB) was measured by radioimmunoassay in CSF from 306 patients with various neurologic disorders. Levels above 2.0 ng/mL were not found in patients without neurologic disease. Whereas mean CSF CK BB level was less than 2.0 ng/mL in groups of patients with systemic malignant neoplasms, latent syphilis, peripheral neuropathy, disk disease, polyradiculopathy, myelopathy, multiple sclerosis, neurodegenerative disease, encephalopathy, and hydrocephalus, it was elevated in groups of patients with convulsive disorder, CNS neoplasm, cerebrovascular disease, vasculitis, and meningoencephalitis.

Central Nervous System Diseases↗
PubMed1983

Regional cerebral ischemia by occlusion of the posterior communicating artery and the middle cerebral artery in gerbils.

The authors have created an experimental model of regional cerebral ischemia in gerbils that is reproducible and has a low mortality rate. In gerbils, either the posterior communicating artery (PCoA) or the middle cerebral artery (MCA) was occluded, and the distribution of cerebral ischemia from each surgical procedure was compared with that produced by occlusion of the common carotid artery (CCA). In contrast to the widespread cortical and subcortical infarctions seen after occlusion of the CCA, occlusion of the PCoA caused infarction that was restricted to the hippocampus, the piriform cortex, and the posterior part of the thalamus, and occlusion of the MCA resulted in infarction that was restricted to the central part of the cerebral hemisphere and the caudate nucleus and putamen. Intracranial occlusion of the PCoA or MCA in the gerbil resulted in lesions that were reproducible with low mortality rates over a long-term period. Occlusion of the PCoA, MCA, or CCA also produces a model that is suitable for investigation of the postischemic period. A combination of these three experimental models is useful for investigation of regional vulnerability and for the study of regional metabolic differences in cerebral ischemia.

Animals↗
PubMed1982

Ionic shift in cerebral ischemia.

Electrolyte and water contents were measured in gerbil brain after unilateral cerebral ischemia. Increase of Na+ and water, and decrease of K+ occurred after an ischemic period of 30 minutes. However, these abnormalities disappeared within 3 hours. When the ischemic period was extended to 3 hours, the abnormalities observed after ischemia for 30 minutes were again encountered, but more significant alterations occurred immediately after re-establishment of blood flow. In addition to more pronounced increase of Na+ and decrease of K+, Ca2+ became significantly elevated after recirculation for 15 minutes and progressively increased during recirculation for 3 hours. The steady rise of Ca2+ appears to be related to the irreversibility of cerebral ischemia.

Animals↗
PubMed1982

Alterations of nuclear thyroid hormone receptors in cerebral cortex in vivo.

Investigation was conducted under in vivo conditions in the adult male rat to determine the basic characteristics of the nuclear thyroid hormone receptors in the cerebral cortex. Equilibrium with cortical nuclei of an intravenous dose of triiodothyronine (T3) occurred 3 h after injection and showed a t1/2 of 1 h for dissociation. Saturation of receptors occurred at 0.5--06. ng/mg DNA. The endogenous level of binding in the normal rat was 0.07--0.1 ng/mg DNA, representing a 15% occupancy of total receptors at a serum concentration of 66 ng/dl. These characteristics were then examined under several pathophysiological conditions. In the hypothyroid rat, an apparent 37% increase in total binding sites occurred. Under either fasting conditions or insulin or glucagon administration declines in serum T3 were noted, and the endogenous binding also decreased in parallel. Only glucagon produced a significant reduction in total binding sites. Under the hypoxic condition produced by maintenance under a 7% oxygen atmosphere, a slight increase in apparent total binding sites was found with no change in endogenous binding level. Severe narcosis resulted in no effects on T3 binding parameters. These results demonstrate specific alterations of thyroid hormone receptors that may be important physiologically.

Animals↗
PubMed1981

Computed tomography and EEG in cerebrovascular disease.

In three patients with cerebrovascular diseases, the EEG showed active dysfunction of varied extent and severity in one cerebral hemisphere, but computed tomography showed no demonstrable abnormalities in the corresponding areas. These patients had occlusion or severe stenosis of one or both internal carotid arteries, either extracranially or intracranially. Both clinical symptoms and the EEG abnormalities resolved or improved after surgical anastomosis of the superficial temporal artery to the middle cerebral artery.

Adult↗
PubMed1980

Phosphorylation of chromatin proteins in cerebral anoxia and ischemia.

Phosphorylation of nuclear protein was investigated in cerebral anoxia up to 30 min with rabbit brain and in cerebral ischemia up to 6 h with gerbil brain in vitro. Isolated nuclei were incubated in the presence of [gamma-32P]ATP and were then fractionated into the NaCl-soluble, HCl-soluble, and phenol-soluble protein fraction. Each protein fraction was further separated by gel electrophoresis, and profiles of 32P incorporation were evaluated in these pathophysiological conditions. 32P incorporation of the acidic phenol-soluble nonhistone chromatin protein became significantly suppressed in cerebral anoxia after 15 min, and there were decreases of 32P incorporation in protein with high molecular weight and increase in protein with low molecular weight on gel electrophoresis. With gerbil brain nuclei, 32P incorporation into the NaCl-soluble and HCl-soluble fraction was increased without significant decrease in the phenol-soluble fraction after an ischemic period of 3 h. However, further separation of the phenol-soluble fraction demonstrated decrease of 32P incorporation in protein with high molecular weight and increase in protein with low molecular weight. At present, the significance of these findings, particularly in relation to chromatin template activity or irreversibility of these pathophysiological conditions, is not clear.

Adenosine Triphosphate↗
PubMed1979

Protein synthesis in rat brain in hypoxia, anoxia and hypoglycemia.

The effect of cerebral hypoxia on protein synthesis was investigated by exposing rats to 5% O2, and examining polypeptide synthesis and size distribution profiles of ribosomes. The findings were compared with the results from cerebral anoxia (decapitation) and hypoglycemia. In cerebral hypoxia there was suppression of polypeptide synthesis, though to a lesser extent than in cerebral anoxia, while no effect was detected in hypoglycemia. Among 4 different ribosomal fractions used for polypeptide synthesis, the microsome was the most sensitive for hypoxia and anoxia, and the polyribosome after short centrifugation was the least sensitive. The size distribution profiles of 3 different ribosomes revealed an increase in the size of the monomere-dimer complex and a decrease of the polysome peak both in cerebral hypoxia and anoxia. Comparison of the energy state and the extent of lactic acidosis in cerebral hypoxia, anoxia and hypoglycemia available in the literature and the functional and structural state of polyribosomes in the present investigation suggests that intracellular acidosis may be the main cause of the suppression of polypeptide synthesis and disaggregation of polyribosomes in hypoxia, and the depletion of energy reserve may be the main cause in anoxia-ischemia.

Animals↗