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Biomedical subjects

K Kogure

Publications and source records attributed to K Kogure.

At least 397 records · Page 22Linked to original sources
PubMed1986

[Brain edema initially develops in the periphery of focal cerebral ischemia].

Ischemia causes disturbances of the ionic equilibrium, i.e., Na+ and water influx and K+ efflux. When the ischemic tissue keeps contact with cerebral blood flow, brain tissue equilibrates with systemic circulation and consequently shifts of electrolytes and water are induced. Therefore, brain edema should initiate in the peripheral area of focal cerebral ischemia. To test this hypothesis, we performed the following experiments. Focal ischemia was induced by occlusion of the right common carotid artery in gerbils and by embolization with microspheres in rats. Water and electrolyte content was determined using punched out samples and regional K+ and Ca2+ distribution was visualized by histochemical K+ staining and 45Ca-autoradiography, respectively. Cerebral blood flow and glucose metabolism were evaluated by 14C-iodoantipyrine or 18F-fluoroantipyrine and 14C-deoxyglucose autoradiographies, respectively. Two hours of ischemia in gerbils with definite hemiparesis caused K+ depletion in the ischemic area, often most pronounced in the periphery of the lesion. Water content of cerebral cortex was 79.0 +/- 0.9, 82.0 +/- 1.0, 80.7 +/- 0.9 (%; mean +/- SD) for nonischemic, periphery and center of ischemia, respectively (significantly different with each other). Na+ content was increased and K+ content was decreased most prominently in the periphery of ischemia. Exogenous Ca2+ was also accumulated in the periphery. In the embolized stroke in rats, K+ depletion and Ca2+ accumulation obviously rimmed the ischemic focus. Furthermore the infarcted area was only part of the disturbed area of acute-phase glucose metabolism. Thus water and ionic disturbances were different between in the periphery and in the center of focal cerebral ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Autoradiographic visualization of adenosine A1 receptors in the gerbil hippocampus: changes in the receptor density after transient ischemia.

N6-cyclohexyl-[3H]adenosine [( 3H]CHA) was used for the in vitro visualization of the hippocampal adenosine A1 receptors in the gerbil. The strata radiatum and oriens of the hippocampus showed particularly high binding activity. Depletion of pyramidal cells and consequent severe decrease in [3H]CHA binding activity in the CA1 subfield were observed after transient ischemic insult. These results suggest that most adenosine receptors in the CA1 region are localized in association with pyramidal cells.

Adenosine↗
PubMed1985

Correlations between proton nuclear magnetic resonance imaging and retrospective histochemical images in experimental cerebral infarction.

Evaluation of ischemic brain injury in experimental cerebral infarction in gerbils and rats was performed by means of both proton nuclear magnetic resonance imaging ([1H]NMR-CT) and various histochemical analyses. In vivo nuclear magnetic resonance (NMR) imaging was carried out employing saturation recovery, inversion recovery, and spin echo pulse sequences. Spatial resolution of the images was excellent. The ischemic lesions were detected with a remarkable contrast in inversion recovery and spin echo images within a few hours after insult. Those changes in NMR images consistently corresponded with the various retrospective histochemical observations, especially with methods related to brain edema (K+ staining) rather than structural (enzymatic) studies. Calculated T1 and T2 relaxation times indicated the evolution of the edema state in the brain in situ. They correlated excellently with the retrospective water content measurement. As a result, detailed characterization of the edema state induced by cerebral ischemia was possible in vivo using [1H]NMR imaging.

Adenosine Triphosphatases↗
PubMed1985

Evaluation of sequential glucose metabolism in cerebral ischemia using a chrono-autoradiographic method.

A chrono-autoradiographic technique (sequential double label 2-deoxyglucose method) was performed to evaluate postischemic regional glucose metabolism. Using this method, two sequential autoradiograms, one immediately after the stroke and one 7-8 hr after the stroke, were obtained from the same brain slice. Comparison of the two images strongly suggested that the ischemic core and the regions adjacent to the core died, while the periphery recovered from the metabolic injury, and that postischemic metabolic abnormality itself didn't necessarily determine the fate of the ischemic tissue.

Animals↗
PubMed1985

[Weak chemiluminescence from infarcted rat brain and basic studies on the generation of chemiluminescence].

Chemiluminescence measurement in vivo system and its related studies on free radical reaction were reported. Weak chemiluminescence from rat brain surface subjected to ischemic cerebral stroke could be detected. It was observed just after embolization and lasted at least four hours. In order to investigate the mechanism of the generation of chemiluminescence and a side reaction of lipid peroxidation, several studies were made using 10% brain homogenate under oxygenated conditions at 37 degrees C. Brain homogenate showed increasing chemiluminescence that reached a plateau level a few hours later. Chemiluminescence, accompanying with thiobarbituric acid reactive substance (TBARS) formation, was based on free radical reaction with requirement of oxygen. Time course increase in TBARS formation, however, revealed some differences from that of integrated light intensity. Chemiluminescence spectrum in the visible region showed that excited indole chemicals (triplet states) generated in the present system emitted light during their return to ground state, but not singlet molecular oxygen. Suspension of acetone powder in Tris-HC1 buffer prepared from brain homogenate also disclosed chemiluminescence to some extent, whereas liposomes made of extracted brain lipid did not. These results probably indicate that proteins are essential for luminescence, but not lipid only, and involves the lipid-protein interaction in oxygenated brain homogenate. In the process of lipid-protein interaction, neither fatty acids composition nor protein molecules significantly altered, except for a newly-appeared high molecular weight protein. On the other hand, SH group was suggested to be quite vulnerable to free radical attack.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Ascorbate induced lipid peroxidation results in loss of receptor binding in tris, but not in phosphate, buffer. Implications for the involvement of metal ions.

Rat brain homogenate was incubated with various concentrations of ascorbate in a Tris-HC1 buffer. Thiobarbituric acid-reactive substances (TBARS) were measured and 3H-QNB (quinuclidinyl benzilate) binding was also assayed on the same homogenate. Good parallelism between TBARS formation and loss of 3H-QNB binding activity confirmed that loss of 3H-QNB binding resulted from ascorbate-induced lipid peroxidation. However, neither formation of TBARS nor loss of 3H-QNB binding occurred in phosphate buffer or in the Tris-HC1 system in the presence of metal-chelating reagents. This indicates that phosphate addition prevents the ascorbate effects due to complete chelation of intrinsic metal ions.

Animals↗
PubMed1984

Immunocytochemical localization of herpes simplex virus antigen in the trigeminal ganglia of experimentally infected mice.

The peroxidase anti-peroxidase (PAP) technique was used to study the distribution of herpes simplex virus (HSV) antigens in mouse ganglia during the acute infection and the transition into the latent infection. At 2 days after HSV inoculation by the corneal route, immunoperoxidase staining was present in occasional isolated neurons of the trigeminal ganglion and also in scattered satellite cells. By 4 days, more cells were stained with the infection centered in the medial portion of the ganglion. Inflammatory cells were present around PAP-labeled fragments from lysed cells. Stained satellite cells often with a hypertrophic appearance surrounded labeled or unlabeled neurons in a ring-like array. At 6 days after HSV inoculation, there was a decrease both in the number of cells stained and in the intensity of staining. By 8 days, HSV antigens could be detected by weak PAP staining only in neurons. Otherwise, these neurons appeared morphologically normal. No immunoperoxidase staining was present after the 8th day. These results are compatible with retrograde axoplasmic transport of HSV and cell to cell spread of virus in ganglia. Also the appearance of infected ganglion cells during the transition to latency suggests that neurons can be switched from an HSV-permissive to a non-permissive (latent) state.

Animals↗
PubMed1984

Functional significance of the corpus callosum based on the analysis of rhythmic capabilities in the split-brain patients.

We carried out our Systematic Rhythm Test for the Brain-Damaged Patients named "The Asian Rhythm Test" on our four patients with lesions of the corpus callosum, and analyzed their rhythmic capabilities--their performances in rhythm perception (auditory distinction) and in rhythm expression (rhythm-tapping)--in accordance with the neuropsychological model proposed in 1980 by us. All our partial split-brain patients showed the abnormal one-ear inferiority (superiority) and the one-hand inferiority under our testing conditions. The patients with lesions of the anterior corpus callosum showed the interhemispheric (the left-to-right) transfer-dysfunction of motor-programming information, while the patient with the lesion of the posterior corpus callosum showed the interhemispheric transfer-dysfunction of auditory information. The patients with lesions including the truncus showed the interhemispheric integration-loss in the process of rhythm perception and its expression. And moreover, we could see the specific auditory interruption between the ipsilateral and the contralateral systems in the patient with the lesion including the anterior commissure. Based on these our findings, the roles of the corpus callosum and the anterior commissure were discussed.

Adult↗
PubMed1983

alpha-Tocopherol and ubiquinones in rat brain subjected to decapitation ischemia.

Levels of alpha-tocopherol (alpha-Toc), reduced ubiquinones (QH2) and oxidized ubiquinones (Q) were assayed in rat forebrain subjected to decapitation ischemia. Post-decapitation levels of alpha-Toc decreased by 16% at 3 min and 20% at 15 min. Increases in Q9H2 (83%) and in Q10H2 (107%) were observed immediately following decapitation; thereafter their levels began to decrease and approached to the pre-ischemic values at 15 min. In contrast, Q9 and Q10 tended to increase continuously during ischemia. The data indicate that complete ischemia results in distinct changes in the cerebral content of lipid-soluble antioxidants. The decrease of alpha-Toc may make the brain prone to peroxidative attack when cerebral tissue is subsequently reoxygenated.

Animals↗
PubMed1983

Motor disabilities and effects of thyrotropin-releasing hormone on ataxia of spinocerebellar degeneration.

Fine aiming task was studied quantitatively in 20 patients with spinocerebellar degeneration (SCD) and 8 normal control subjects, utilizing a manual control system with random-step input signal. The transfer function of the system was an integral function and ability to perform a 'differentiating action' compensating for this integral function was analyzed. This 'differentiating action' was defective in all patients with SCD and was normal in all control subjects. A display of the dynamic characteristics of subjects on the plane defined by principal component analysis of the parameters showed definite delineation of the characteristics of patients from those of the controls. The intramuscular injection of thyrotropin-releasing hormone (TRH) resulted in an increase in amplitude of manipulation, a shortening of reaction time and consequently an improvement in motor disabilities in 65% of 20 patients with SCD.

Adolescent↗
PubMed1983

Electromyographic assessment of fatiguability and recovery of orbicularis oculi in myasthenia gravis.

Orbicularis oculi fatiguability following maximal voluntary contraction and its recovery after administration of Tensilon (edrophonium chloride) were studied in 13 patients with myasthenia gravis (MG) and 8 normal controls. The number of EMG pulses per sec (C) was calculated using an experimentally manufactured EMG pulse counting system and the mean amplitude of the motor unit potentials per sec (A) was measured using the action potential analysis module (Medelec APA-6 MK-1) during maximal voluntary contraction of the orbicularis oculi muscle. Fatiguability was estimated as percentage change of C, the pre-exercise value being taken as 100%. It was 74.4 +/- 18.2% (mean +/- S.D.) in patients and was significantly different from 110.8 +/- 8.4% found in the controls (p less than 0.01). Recovery following intravenous injection of Tensilon was estimated as percentage change in C and A, the values before Tensilon injection being taken as 100%. The change in EMG pulse per sec (C) was 360.0 +/- 90.0% in MG and 113.0 + 21.2% in controls (p less than 0.005). The mean amplitude of the motor unit potential per sec (A) increased by 180.0 +/- 95.0% in MG and 120.0 +/- 42.0% in controls (p less than 0.01). This technique is thought to be valuable to confirm the diagnosis of MG when routine electrophysiological tests fail to demonstrate abnormalities in neuromuscular transmission.

Adolescent↗