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Biomedical subjects

K Kogure

Publications and source records attributed to K Kogure.

At least 325 records · Page 18Linked to original sources
PubMed1990

Cognitive impairment in Parkinson's disease assessed by visuomotor performance system and P300 potential.

Motor impairment, clinically defined as bradykinesia has been considered as resulting only from motor system problems. Combined analysis of cognitive function and dynamic characteristics was studied in 20 patients with Parkinson's disease by a simple aiming task on visuomotor performance system. The dynamic characteristics in a Parkinson's disease patient was evaluated by two parameters: decreased amplitude of the voluntary movement (= low gain constant) and delayed initiation of voluntary movement (= long reaction time). The visual event-related potential elicited in a target detection paradigm (P300 component) was recorded in 12 patients with Parkinson's disease. P300 latency was significantly prolonged in the patient group than in the normal control group (p less than 0.05). P300 has been shown to be intimately related to the cognitive process in the human brain and might well serve as a tool to monitor and evaluate the cognitive state in a clinical situation. The main cause of cognitive involvement in Parkinson's disease may include coexisting dementia and defective motivation. This type of cognitive disturbance may also serve partly as a cause of bradykinesia.

Adult↗
PubMed1990

Effects of co-dergocrine mesylate (Hydergine) in multi-infarct dementia as evaluated by positron emission tomography.

Three female patients aged from 74 to 79 with multi-infarct dementia were studied using positron emission tomography (PET) to assess the effect of co-dergocrine mesylate (Hydergine) on cerebral glucose metabolism. The cerebral glucose utilization (CMRGlc) of each patient was evaluated by PET scan using 2-deoxy-[18F]-2-fluoro-D-glucose (FDG). Following the first PET study, 0.04 mg/kg of co-dergocrine mesylate was injected intravenously with 250 ml saline solution, and then the second PET study was performed. The CMRGlc was determined from the images of the PET scan and the radioactivity of 18F in the plasma. After the administration of co-dergocrine mesylate, the value of CMRGlc increased significantly in the cerebral cortex (p less than 0.01 and p less than 0.05) and basal ganglia (p less than 0.05) compared with values before the administration, but no significant increase was found in the centrum semiovale. These results suggest that co-dergocrine mesylate stimulates glucose metabolism of neurons in the human brain.

Aged↗
PubMed1990

The pathological differences of rejection in the heart allografts which are transplanted alone or with synchronous skin grafts in rats.

The morphological patterns of rejection of the heart allografts which were combinedly transplanted with skin grafts was examined to determine whether it was different from that of the heart grafts transplanted alone. The results showed that there were distinct differences in the pathology of the rejection between the two groups because in the single heart grafts mononuclear cells concentrated in almost all layers of myocardium but in the combinedly transplanted heart grafts not only concentration of them but also severe hemorrhage and edema were observed in it, and it suggests that skin graft has effects on rejection process of heart grafts. As we used an outbred strain of rats some survived heart grafts were observed and their pathology was characteristic in the interstitial accumulation of hypertrophic mast cells, most of which were degranulating.

Animals↗
PubMed1990

Uncoupling of blood flow and glucose metabolism in the neighboring postischemic edematous brain area.

Postischemic events cause exacerbation of brain injury, not only in the postischemic area but also in the area originally free from the ischemic insult. The present study was performed in rats. After the animals were anesthetized with a mixture of 70% N2O, 0.5% halothane, a focal ischemia was induced by occlusion of the right MCA by means of a silicone rubber cylinder introduced from the internal carotid artery. Three hours after the MCA occlusion, the embolus was pulling out from the artery by an attached nylon surgical thread. Three hours after the recanalization, animals were decapitated to acquire water content of the brain, local CBF, or local CMRgl. After recirculation, water content markedly increased in the MCA area whereas the CBF returned near normal. However, the CMRgl decreased below half of the normal value. In the neighboring, originally nonischemic area, water content remained within the normal limit although the CBF markedly decreased and the CMRgl increased. Deductions from these data were as follows: (a) If the brain tissue cannot recover from the ischemic-induced injury, restored blood flow may exacerbate the brain edema; and (b) the edematous brain tissue affects the neighboring area with lowering blood flow and rising glucose consumption.

Animals↗
PubMed1990

[Simultaneous in situ detection of JC virus antigens and RNA in progressive multifocal leukoencephalopathy (PML) by immunocytochemistry and in situ hybridization].

We detected simultaneously JC virus (JCV) antigen and RNA in the frozen brain tissue from a patient with PML using immunocytochemistry and in situ hybridization. Histologically, the majority of JCV antigen positive cells were mainly located at the margin of demyelinated lesions. By simultaneous in situ detection of JCV antigen and RNA, the percentage of both JCV antigen and RNA positive cells in total number cells were 20 in the periplaque region and 2.3 in the central region of plaque respectively. On the contrary, only JCV RNA positive cells were detected 3.6% in the periplaque region and 4.6% in the central region of plaque, while there was not found any positive cells in apparently normal white matter. Moreover, JCV antigen in both antigen and RNA positive cells found in the periplaques was stained homogeneous and filled the whole swollen nucleus, whereas most of both antigen and RNA positive cells appeared in the center of plaques showed small amounts of antigen in the nucleus. From the results, it seems likely that most of the cells displaying only RNA detected in the periplaque were oligodendrocytes in the early stages of productive infection prior to viral protein synthesis. However, a small number of cells displaying only RNA in the center of plaques were likely to be oligodendrocytes and seemed to be in the nonproductive stages of a JCV infection, limited expression of viral protein, influenced by the host immune response including the infiltration of macrophages and humoral immunity.

Antigens, Viral↗
PubMed1990

[The detection and quantitative analysis of viral antigens, infiltrating mononuclear cells, IFN-gamma, LT and IL-6 bearing cells in the frozen brain tissue sections from a patient with herpes simplex encephalitis by immunocytochemistry].

To identify viral antigens, the types of infiltrating mononuclear cells and cytokine bearing cells, the frozen brain tissue sections form a patient with herpes simplex encephalitis who died on 12th hospital days, were examined by immunocytochemistry methods and combined immunocytochemistry and in situ hybridization. The avidin-biotin peroxidase complex (ABC) techniques were applied for the detection of antigens. All monoclonal antibodies to Leu series and polyclonal antisera to lymphotoxin (LT), interleukin-6 (IL-6) and interferon-gamma (IFN-gamma) were purchased form Becton Dickinson Co., and Genzyme Co., (USA) respectively. A large number of neurons and glial cells staining positively HSV-1 antigens were found in the gray matter. Moreover, although a moderate number of HLA-DR (Ia) positive cells were found in the parenchyma, there were few cells displaying positively for Leu-3a, Leu-2a and Leu-7 respectively. To evaluate the number of positive cells appeared in the brain tissues, Leu stain for 4, 2a, 3a, 7, 12 and HLA-DR demonstrated 1.6%, 0.4%, 0.9%, 0.7% and 10% respectively. In addition, numerous number of IFN-gamma positive cells were detected around the lesion and randomly distributed thoroughly the lesion. IL-6 positive cells and LT positive cells were also similar in distribution to IFN-gamma positive cells. Moreover, in simultaneous detection of HLA-DR and HSV-1 mRNA by the combined immunocytochemistry and in situ hybridization, there were seen glial cells staining positively for HLA-DR (Ia) and several cells with mRNA.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigens, Viral↗
PubMed1990

Prevention of hippocampus neuronal damage in ischemic gerbils by a novel lipid peroxidation inhibitor (quinazoline derivative).

We investigated the effect of a novel quinazoline derivative (KB-5666), a lipid peroxidation inhibitor, on ischemic neuronal damage using Mongolian gerbils. The animals were sacrificed 7 or 30 days after 5 min of forebrain ischemia induced by bilateral common carotid artery occlusion. Morphologic changes, a microtubule-associated protein 2 (MAP2) immunohistochemical study and quantitative autoradiographic study using [3H]phorbol 12, 13-dibutyrate ([3H]PDBu) were evaluated in the hippocampus after ischemia. KB-5666 (3-50 mg/kg, i.v.) showed protective effects against neuronal death of the CA1 subfield 5 min before ischemia, immediately or 1 hr after ischemia, but not 4 hr after ischemia. KB-5666 (i.p.) also showed protective effects in a dose-dependent manner immediately after ischemia. Furthermore, KB-5666 dose-dependently prevented a marked decrease in microtubule-associated protein 2 immunoreactivity in the dendritic fields of the CA1 pyramidal cells after ischemia. The [3H]PDBu binding activity in the stratum oriens and the stratum lacunosum-moleculare of the CA1 subfield was reduced by 19 and 30%, respectively, 7 days after ischemia. [3H]PDBu binding sites were unchanged in the stratum oriens in the CA3 subfield. By contrast, in the molecular layer of the dentate gyrus, the [3H]PDBu binding activity increased by 15%. KB-5666 (i.v.) prevented a decrease in the [3H]PDBu binding activity in the stratum oriens and stratum lacunosum-moleculare of the CA1 subfield and an increase in the molecular layer of the dentate gyrus. These histologic, immunohistochemical and receptor-autoradiographic data indicate that KB-5666 protects the brain from both cellular and functional consequences of ischemia.

Animals↗
PubMed1990

[Exo-focal neuronal death in the rat brain].

We describe delayed neuronal damage in ipsilateral remote areas outside the ischemic area of rat brain after transient focal ischemia. The distribution of the neuronal damage was determined by using the 45Ca autoradiographic technique and the histological method, and we investigated the mechanism involved by measuring local cerebral glucose metabolism. Wistar rats were used throughout the experiments. Under 2% halothane anesthesia with a mixture of 70% N2O and 30% O2, the right middle cerebral artery (MCA) was embolized by insertion from the internal carotid artery of a nylon surgical thread with a cylindrical coating of silicone on the distal portion. Animals were divided into 4 groups based on duration of ischemia. After 15, 30, 60 and 90 min of MCA occlusion, recirculation was achieved by removal of the embolus. Immediately after recirculation and then after 24 hr, 3 days, 1 week and 2 weeks of recirculation, 300 microCi 45CaCl2 in aqueous solution (0.3 ml) was administered intravenously; 6 hr later, animals were decapitated to obtain autoradiograms. Histological examination was carried out according to the same protocol. In the 15-min MCA occlusion group, neither 45Ca accumulation nor histological change was observed. In the 30-min MCA occlusion group, 45Ca accumulation extended from the lateral margin to the lateral segment of the caudate-putamen and the cerebral cortex supplied by the occluded MCA depending on the duration of recirculation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

[Multi-focal delayed neuronal damage after transient regional ischemia--mechanism of vascular dementia].

We describe multi-focal delayed neuronal death of rat brain after transient regional ischemia induced by embolization of the right middle cerebral artery (MCA). After sixty minutes of MCA occlusion, recirculation was achieved by removal of the embolus. Chronological changes in the distribution of the neuronal damage were determined by using the 45Ca autoradiographic technique and the histological examination. Sixty minutes after MCA occlusion, 45Ca accumulation extended to the lateral segment of the caudate putamen and the cerebral cortex supplied by the occluded MCA. Moreover, three days after ischemic insult, 45Ca had accumulated in the ipsilateral thalamus and substantia nigra. Histological examination revealed that the neurons in both area suffered damage and were selectively reduced in number. Both areas lie outside the ischemic area, but have transsynaptic connections with the ischemic focus. We suggest that the postischemic delayed neuronal death in exo-focal remote areas may be caused by a transsynaptic process associated with the infarcted areas and that these delayed multi-focal brain damage may exacerbate clinical symptoms in the chronic stage of stroke.

Animals↗
PubMed1990

Imaging of water distribution in the rat brain by activation autoradiography.

Regional water distribution in the rat brain was obtained autoradiographically by activation analysis. The autoradiogram obtained for the normal rat brain showed high accumulation of water in the areas of sensory-motor cortex, hippocampus, thalamus, and amygdaloid cortex, whereas corpus callosum and internal capsule showed low water contents as expected. The estimated values of water content were 78.6 +/- 4.9 weight % for gray matter, and 73.5 +/- 4.9 weight % for white matter, respectively. The mean values of the water content were consistent with those obtained by a conventional drying-weighing method.

Animals↗
PubMed1989

Increase in choline acetyltransferase activity in septum of rats after transient forebrain ischemia: a possible role of factors released in the hippocampus.

Choline acetyltransferase (ChAT) activity increased in rat septum 2 weeks after a transient forebrain ischemia. Extracts were prepared from hippocampus in which CA1 pyramidal neurons had been selectively destroyed by the ischemic insult. ChAT activity in septal neuronal cultures treated with these extracts for 6 days was significantly higher than that in control cultures.

Animals↗
PubMed1989

A serotonin S2 antagonist, naftidrofuryl, exhibited a protective effect on ischemic neuronal damage in the gerbil.

The effect of a serotonin S2 antagonist, naftidrofuryl, on ischemic neuronal damage was examined in the gerbil. Naftidrofuryl was injected i.p. 5 min prior to a single 5-min forebrain ischemia or immediately after each of three 2-min forebrain ischemic insults at 60-min intervals. In both groups the number of intact hippocampal CA1 neurons were significantly higher than in the saline-treated group. These results indicate that serotonin S2 antagonists have a protective effect against ischemic neuronal damage.

Animals↗
PubMed1989

Neuronal damage in the rat hippocampus in a new model of repeated reversible transient cerebral ischemia.

The influence of the interval of the repeated reversible transient cerebral ischemia on the neuronal damage in the hippocampal CA1 sector was investigated in the rats using a 4-vessel occlusion (4-VO) model. A single 3-min 4-VO did not produce any significant neuronal damage in the hippocampal CA1 sector, whereas the rats subjected to three 3-min 4-VO at 1-h intervals revealed a very severe neuronal damage which was much more severe than that in the rats subjected to a single 9-min 4-VO. In contrast, the rats subjected to three 3-min 4-VO at 6-h intervals revealed only a mild neuronal damage. The degree of the neuronal damage in the rats subjected to three 3-min 4-VO at 5-min intervals was similar to that in the rats subjected to a single 9-min 4-VO. The present study indicates that even such a brief, non-lethal ischemia as 3-min 4-VO can produce a severe neuronal damage if it occurs repeatedly at 1-h intervals.

Animals↗
PubMed1989

Mapping second messenger systems in the rat hippocampus after transient forebrain ischemia: in vitro [3H]forskolin and [3H]inositol 1,4,5-trisphosphate binding.

Autoradiographic imaging demonstrated predominant and reciprocal localization of forskolin and inositol 1,4,5-trisphosphate (IP3) binding sites in synaptic areas in the hippocampus. We produced selective damage to the CA1 pyramidal cells in the rat hippocampus by means of transient forebrain ischemia and analyzed the alteration of the intracellular signal transduction using quantitative autoradiography of these second messenger systems. The dendritic fields (stratum oriens, radiatum and lacunosummoleculare) in the CA1 showed 20% decrease in [3H]IP3 binding activity 3 h after ischemia, when no morphological abnormalities were obvious. Thereafter, grain density in these layers decreased and half of the binding sites were lost 2 days after ischemia. By contrast, the stratum pyramidale of the CA1 showed no significant change until 2 days after recirculation. Seven days after ischemia, when CA1 pyramidal cells were depleted, all layers in the CA1 subfield lost 85% of [3H]IP3 binding sites. In the CA3 subfield, only a small and transient alteration in the [3H]IP3 binding was noticed during recirculation. Postischemic reduction of [3H]forskolin binding sites was obvious in the CA1 only 1 h after ischemia followed by loss of 50% of binding activity 7 days after recirculation. These results suggest that forskolin and IP3 binding sites are predominantly distributed on the pyramidal cells in the CA1 subfield and that marked alteration of intracellular signal transduction precedes the delayed CA1 pyramidal cell death.

Animals↗
PubMed1989

Postischemic changes of calcium and endogenous antagonist in the rat hippocampus studied by proton-induced X-ray emission analysis.

Proton-induced X-ray emission analysis (PIXE) was applied to determine ischemia-induced changes in the content of calcium, iron, nickel and zinc in the rat hippocampus. After 30 min or 2 h reperfusion following 20 min of ischemia, the nickel content decreased and the zinc content increased. The calcium content was increased 50% after 30 min but was normal after 2 h reperfusion.

Animals↗