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Biomedical subjects

A Terashi

Publications and source records attributed to A Terashi.

At least 73 records · Page 4Linked to original sources
PubMed1996

[Regional cerebral blood flow and periventricular hyperintensity in silent cerebral infarction--comparison with multi-infarct dementia].

In order to investigate relationship between regional cerebral blood flow (rCBF) and the white matter lesions on MRI in silent cerebral infarction, we quantitatively measured rCBF by 123I-IMP autoradiography method (IMP ARG method) and single photon emission tomography (SPECT) in 36 patients with silent cerebral infarction (SCI group), 22 patients with multi-infarct dementia (MID group), and 16 control subjects without periventricular hyperintensity (PVH) and lacunar infarction on MRI (CL group). Regions of interest (ROIs) on rCBF images were set in the frontal (F), temporal (T), parietal (P), occipital (O) cortex, and the cerebral white matter (W). The severity of PVH on MRI T2-weighted image was divided into four grades (grade 0-3). Our results: 1) Though the frequency of hypertension was significantly higher in SCI group and MID group compared with CL group, no significant difference was seen in the mean age among these three groups. 2) rCBF in the white matter and cerebral cortices except the occipital cortex in SCI group was significantly low compared with CL group (gamma CBFSCI/gamma CBFCL: W 0.87, F 0.87, P 0.88, O 0.92). 3) rCBF in the white matter and cerebral cortices, especially in the white matter and frontal cortex, in MID group was significantly low compared with SCI group (gamma CBFMID/gamma CBFCL: W 0.69, F 0.71, T 0.74, P 0.75, O 0.81). 4) The mean grade of PVH in MID group was significantly higher that that in SCI group (SCI 1.1 vs MID 2.5). 5) The severity of PVH was significantly correlated with each rCBF in the white matter and cerebral cortices, especially in the white matter and frontal cortex. Our findings suggest that the quantitative measurement of rCBF by IMP ARG method is useful for the follow-up study in the patients with silent cerebral infarction as well as the evaluation of the severity of PVH on MRI.

Aged↗
PubMed1996

[Two siblings with familial schizencephaly--report of a family and review in relation to clinical features and neuroradiological findings].

We examined 2 siblings with schizencephaly. A 23-year-old female (Case-1) had a mild left hemiparesis, and her 25-year-old brother (Case-2) presented a quadriplegia. Both cases achieved a borderline intellectual level and both had seizure disorders. The magnetic resonance imaging (MRI) of Case-1 revealed thickened gray matter around the fused schizencephalic clefts in the bilateral frontal lobes, mild ventricular enlargement and absence of the septum pellucidum. And, the MRI result of Case-2 disclosed similar but more severe abnormalities. The positron emission tomography (PET) using 18F-Fluoro-2-deoxy-D-glucose of Case-1 demonstrated focal hypermetabolic activity in the ectopic gray matter with the absence of epileptic discharges on the electroencephalogram on the day of PET study. And the single photon emission computed tomography (SPECT) using 123I-N-isopropyl-p-iodoamphetamine of Case-1 delineated focal hyperperfusion in the same lesions. The PET and SPECT findings are unique, since previous reports have indicated focal hypoperfusion and hypometabolism in abnormal gray matter. Familial schizencephaly is a very rare malformation, and this is the first report of that in Japan. Further evaluation in similar cases is needed to determine the pathophysiology of this anomaly.

Adult↗
PubMed1996

[Acute effects of human recombinant erythropoietin on cardiovascular dynamics and vasoactive substances].

Treatment with human recombinant erythropoietin (r-EPO) can dramatically improve renal anemia, whereas it has been reported that such improved anemia may involve or worsen hypertension. When we administered a single dose of r-EPO at 9,000 units to 16 patients with end-stage renal failure requiring examination with a right cardiac catheter immediately before the introduction of dialysis, we measured cardiovascular dynamics and various vasoactive substances. The mean blood concentration of EPO was 3,035 units/ml 15 minutes after administration. As compared with the value of 107.6 +/- 3.2 mmHg obtained before administration, the mean arterial blood pressure significantly increased following the administration of r-EPO to 111.5 +/- 3.8 mmHg after 5 minutes, 112.4 +/- 4.2 mmHg after 10 minutes, 113.7 +/- 4.3 mmHg after 20 minutes, and 113.6 +/- 4.3 mmHg after 30 minutes (p < 0.05). The mean pulmonary arterial blood pressure tended to increase to 17.9 +/- 1.8 mmHg after 10 minutes from the level of 16.3 +/- 1.8 mmHg before administration (p = 0.096). The pulmonary vascular resistance index (PVRI) was 165.0 +/- 18.0 mmHg before administration and significantly increased to 193.2 +/- 19.0 and 199.0 +/- 16.6 dyn.S.cm-5.m2 after 10 and 30 minutes, respectively (p < 0.01, p < 0.05). The systemic vascular resistance index (SVRI) also significantly increased to 2,587 +/- 195 dyn.S.cm-5.m2 after 30 minutes from the level of 2,454 +/- 207 dyn.S.cm-5.m2 before administration (p < 0.05). Changes in SVRI showed a bimodal pattern, as with changes in PVRI. Angiotensin-II concentration significantly decreased to 13.7 +/- 4.4 pg/ml after 15 minutes from the level of 15.7 +/- 3.2 pg/ml before administration (p < 0.05). There were no significant changes in endothelin, prostaglandin, or adrenaline concentration after the administration of r-EPO. From these results, it was revealed that pulmonary intra-arterial administration of r-EPO has the acute effect of increasing pulmonary vascular resistance, thereby pointing to a direct effect of r-EPO in pulmonary vasoconstriction. Although no changes in vasoactive substances were observed in the present investigation, further studies with more sensitive measuring methods may be necessary.

Angiotensin II↗
PubMed1995

Preferential dependence of autoantibody production in murine lupus on CD86 costimulatory molecule.

Blockade of the interactions between CD28/CTLA-4 and their ligands, CD80 (B7, B7.1)/CD86 (B70, B7.2), seems an attractive means to induce antigen-specific peripheral tolerance in organ transplantation and autoimmune disease. Recently, diversities between CD80 and CD86 in expression, regulation, and function have been reported in certain cell populations and murine experimental disease models. To investigate the possible differential role of CD80 and CD86 in the development of lupus, we treated lupus-prone NZB/W F1 mice with specific monoclonal antibodies (mAb) against CD80, CD86, or both. The treatment with a combination of anti-CD80 and CD86 mAb before the onset of lupus completely prevented autoantibody production and nephritis, and prolonged survival. Interestingly, we found that anti-CD86 mAb alone, but not anti-CD80 mAb, efficiently inhibited autoantibody production. Subclass study on IgG anti-double-stranded (ds) DNA antibody revealed that the treatment with anti-CD86 mAb almost completely inhibited both IgG1 and IgG2b, but not IgG2a production. The incomplete reduction of IgG2a anti-dsDNA antibody by anti-CD86 mAb was compensated by the addition of anti-CD80 mAb. A significant reduction of mRNA for interleukin (IL)-2, interferon-gamma, IL-4 and IL-6 was observed in mice treated with a combination of anti-CD80 and CD86 mAb or anti-CD86 mAb alone. Treatment with both mAb after the onset of lupus resulted in a significantly prolonged survival with reduction of autoantibody production. These results suggest that CD86 plays a more critical role in autoantibody production, and CD86, but not CD80, contributes to Th2-mediated Ig production. However, the blockade of both CD80 and CD86 are required for preventing the development and progression of lupus.

Animals↗
PubMed1995

Paired helical filaments and straight tubules in astrocytes: an electron microscopic study in dementia of the Alzheimer type.

Ultrastructural investigation of the hippocampal CA1 and CA4 of nine autopsy-proven cases of dementia of the Alzheimer type (duration of disease: 3-16 years; age: 76-92 years) revealed paired helical filaments (PHFs) and straight tubules (STs) in astrocytes of three advanced cases of long duration (> 13 years). The PHFs and STs were indistinguishable from those seen in neurons. The abnormal glial fibrils were confined to the astrocytic processes that were associated with small vessels or, more frequently, with ghost tangles. In both locations the astrocytic PHFs and STs were located in the cytoplasm without limiting membranes, and were thicker than the straight filaments that composed ghost tangles. These findings, combined with the presence of regular constrictions of astrocytic PHFs, suggest that abnormal astrocytic fibers are produced by the glial cells, not engulfed by them. In addition, the presence of these abnormal glial filaments in only advanced, long-duration cases of dementia of the Alzheimer type suggests that disease duration has a significant effect upon the formation of these astrocytic profiles.

Aged↗
PubMed1995

Platelet activation is not involved in acceleration of the coagulation system in acute cardioembolic stroke with nonvalvular atrial fibrillation.

BACKGROUND AND PURPOSE: It is generally accepted that the coagulation system is activated in ischemic stroke and that platelet activation is involved in the pathogenesis of this disease. However, little is known about how and to what extent platelet activity participates in coagulation system enhancement. We evaluated the hemostatic condition, especially with regard to platelet function and the coagulation system, within 3 days of onset of acute stroke. The study participants were limited to elderly patients with cardioembolic stroke due to nonvalvular atrial fibrillation. METHODS: Seventeen elderly patients with acute cardioembolic stroke due to nonvalvular atrial fibrillation were investigated. Within 3 days of stroke onset, beta-thromboglobulin (BTG), platelet factor 4 (PF4), thrombin-antithrombin III complex (TAT), and D-dimer from arterial blood were carefully evaluated in these patients. Blood samples from 19 healthy age- and sex-matched control subjects were also examined. RESULTS: The two studied markers of platelet activity did not change in the patients or the control subjects, and the between-group differences between the stroke and control groups were not statistically significant (BTG, 43.8 versus 31.9 ng/mL; PF4, 9.06 versus 5.78 ng/mL; respectively). In contrast, the two studied coagulation-system indicators were markedly elevated in the patients compared with the control subjects (TAT, 13.8 versus 3.5 ng/mL, P < .01; D-dimer, 366.3 versus 147.2 ng/mL, P < .01; respectively). CONCLUSIONS: Platelet function was not enhanced in the acute stage of cardioembolic stroke with nonvalvular atrial fibrillation. This result indicates that enhancement of the coagulation system in cardioembolic stroke is not the result of platelet hyperfunction, ie, "platelet-fibrin" thrombi, but rather of "stasis-related" thrombi formation.

Aged↗
PubMed1995

Temporal thresholds of reperfusion in the middle cerebral artery occlusion model in rats.

In this study, the middle cerebral artery (MCA) of adult male Sprague-Dawley rats was occluded by the modified Koizumi method to determine the temporal thresholds of reperfusion for the treatment of cerebral embolism. Regional cerebral blood flow (rCBF) and pathological findings were measured at 1 and 2 h of ischemia and after 24 h and 7 days of reperfusion following 1 or 2 h of ischemia. rCBF was decreased the most (less than 10% of control CBF) in the parietal cortex (Pcor) and the lateral caudoputamen (Lcp) at both 1 and 2 h of ischemia. There was no significant difference in rCBF in these areas between the 2 ischemic groups. The 2 h ischemia group clearly showed infarction in the area perfused by the middle cerebral artery (including the Pcor and Lcp) after 24 h and 7 days of reperfusion, while the 1 h ischemia group showed only slight infarction. These findings suggest that temporal thresholds of reperfusion in this model exist between 1 and 2 h of ischemia, and that rCBF levels during ischemia and the duration of ischemia are the most important factors in producing brain infarction.

Animals↗
PubMed1995

Effects of an HMG-CoA reductase inhibitor on cytokine production by human monocytes/macrophages.

It has been reported that the HMG-CoA reductase inhibitor simvastatin does not always effectively lower plasma LDL. This drug acts to monocytes/macrophages directly and inhibits cholesterol ester accumulation in these cells. However cytokine production in macrophages when simvastatin was administrated has not been described. In this study, we examined whether simvastatin affects cytokine production in human monocyte-derived macrophages. Simvastatin at doses ranging from 10(-9) to 10(-5) M did not affect the synthesis of proinflammatory cytokines (IL-1 beta, IL-6, IL-8) from human peripheral mononuclear cells. In addition, any changes in cytokine-induced cytokine production (IL-1-induced IL-8 synthesis) were not detected after the addition of simvastatin. The present results suggest that simvastatin suppresses foam cell formation in monocyte/macrophage, without affecting the immunological or inflammatory functions of these cells.

Cells, Cultured↗
PubMed1995

[Difference in MRI findings and risk factors between multiple infarction without dementia and multi-infarct dementia].

MRI findings and risk factors for vascular dementia were evaluated with multi-variate analysis in 96 multi-infarct patients without dementia and 40 multi-infarct patients with dementia (MID). Only subjects with small infarcts in the territory of the perforator artery or deep white matter were studied. The diagnosis of MID was diagnosed according to DMS-III criteria and Hachinski's ischemia score. Location and area of patchy high-intensity areas including small infarcts, the degree of periventricular high intensity (PVH), and the degree of brain atrophy were examined with MR images. Independent variables were: history of hypertension, diabetes mellitus, other complications; systolic and diastolic blood pressure, atherosclerotic index, hematocrit, history of smoking, level of education, and activities of daily life (ADL). Hayashi's quantification method II was used to analyze the data. The most significant correlation was found between history of hypertension and dementia (partial correlation coefficient: 0.39). Significant correlations were also found between ADL and dementia (0.32), between thalamic infarction and dementia (0.31), and between PVH and dementia (0.27). Age, brain atrophy index, and history of diabetes mellitus contributed little to dementia. The contribution to dementia did not differ significantly between right and left patchy high-intensity areas on MR images. Location of infarcts, except for bilateral thalamic infarcts and large PVH, contributed little to dementia. Thus it would be difficult to base a prediction of the prevalence of vascular dementia on MRI findings. However, both hypertension and ADL contribute to vascular dementia and both are treatable, which may be significant for the prevention of dementia.

Aged↗
PubMed1995

[Regional cerebral blood flow in status epileptics measured by single photon emission computed tomography (SPECT)].

Status epileptics (SE) due to a cerebral vascular accident can cause a change for the worse in the quality of life of patients. We have performed single photon emission computed tomography (SPECT) with 99mTc-hexamethylpropylene amineoxim (HM-PAO) to evaluate regional cerebral blood flow (rCBF) in SE caused by a cerebral vascular accident. In addition, we have discussed the neurophysiology of SE based on the SPECT findings. A total of sixteen patients (5 males and 11 females, average age; 78.2 years old) with SE who were suffering from prolonged consciousness disturbance were investigated. When SPECT was performed in the ictal state, there was a remarkable increase in Radio Isotope (RI) uptake at the focus which correlated well with EEG findings. However, in other cortical regions, basal ganglia and thalamus, there was a relatively demonstrated decrease in RI uptake compared with that of the focus. Additionally in the interictal state, we found a decrease in RI uptake in the epileptic foci and normal recovery of the RI uptake level in other cerebral regions. We speculate that these characteristic patterns of cerebral blood flow distribution shown by SPECT scans in the ictal state reflect the state of consciousness disturbance due to SE. In general, in the elderly, it is difficult to make a differential diagnosis between prolonged consciousness disturbance due to nonconvulsive SE and other diseases such as cardiovascular, dehydration, metabolic disorder, etc. Nevertheless, nonconvulsive SE causes diffuse cell loss and irreversible brain damage. Therefore the elderly who have suffered from prolonged consciousness disturbance due to SE need an exact diagnosis and immediate medical treatment. When we diagnose a nonconvulsive SE, the characteristic findings of SPECT scans in the ictal state are very clear and useful. In conclusion, SPECT is a very simple and non-invasive method that demonstrates abnormalities of brain function exactly. Therefore, we should perform not only EEG but also SPECT scans when making a diagnosis of SE.

Aged↗
PubMed1995

[Relationship between cognitive function and regional CBF in hereditary spinocerebellar degeneration--comparison between Joseph disease and OPCA of Menzel type].

Regional cerebral blood flow (rCBF) was measured using positron emission tomography (PET) in patients with Machado-Joseph disease (Joseph disease), hereditary OPCA of Menzel type (Menzel type), and in normal control subjects in order to investigate relationship between cognitive function and rCBF in 2 subgroups of hereditary spinocerebellar degeneration (SCD). Though absolute rCBF in the cerebellar hemisphere and pons was significantly low in each of 2 subgroups of SCD compared to the control group, no difference was seen between 2 subgroups of SCD in these regions. In addition, absolute rCBF in the cerebral cortices did not show significant difference among all groups. However, when the rCBF data was normalized to the occipital cortex for relative rCBF, in the patient group with Menzel type, relative rCBF in the thalamus was significantly low value compared to the control group and relative rCBF in the frontal, temporal, and parietal cortex, especially in the frontal, was significantly low value compared to the patient group with Joseph disease. Moreover, clinically cognitive impairments were seen in patients of Menzel type, but not in patients of Joseph disease. These findings suggest that the measurement of rCBF by PET is useful for the understanding of the pathophysiology of hereditary SCD subgroups as well as for the differential diagnosis of these diseases.

Adult↗
PubMed1995

[Changes in regional cerebral blood flow in nondominant hemisphere during speech task in aphasics.: a PET activation study].

To investigate the patients with language disorder and to detect the activated areas in language processing, we measured the changes in the regional cerebral blood flow (CBF) during speech task (¿counting¿ task) using O-15 water PET activation technique in six normal subjects (age 58.3 +/- 8.1), mean +/- SD), ten fluent aphasics (age 60.3 +/- 12.5) and six nonfluent aphasics (age 50.5 +/- 8.3). In ¿counting¿ task, the subjects were instructed to count the number aloud from 1 to 10 and repeat the sequence over and over in the native language (Japanese) at the rate of one number per 2.5 sec. The data were analyzed with stereotactic intersubject averaging analysis for the normal subjects. Apart from it, the regions of interest (ROI) analysis (a circular ROI of 12 mm diameter) was performed in the language-related areas: posteroinferofrontal areas (PIF), posterosuperotemporal area (PST), and Rolandic areas (related to the mouth and lips) were significantly activated bilaterally in the ¿counting¿ task. PIF were activated with a dominance in the left side. In the resting state, rCBF in the left PIF and left PST were activated with a dominance in the left side. In the resting state, rCBF in the left PIF and left PST was reduced in both fluent and nonfluent aphasics. In nonfluent aphasics, the magnitude of activation in the right PIF by ¿counting¿ task was significantly greater than normal subjects and patients with fluent aphasia (ANOVA). It suggests the importance of the right PIF in the simple language processing in the nonfluent aphasia. In the sixteen aphasic patients, the increase in rCBF in the right PST during the ¿counting¿ task was negatively correlated with the score of comprehension (WAB) in the Spearman ranked correlation (p < 0.05). It suggests that, while the activity of the right PST is minimal for the ¿counting¿ in normal subjects, it plays an important and compensatory role in aphasic patients.

Adult↗
PubMed1995

[Regional cerebral glucose metabolism associated with ataxic gait--an FDG-PET activation study in patients with olivopontocerebellar atrophy].

We studied changes in regional cerebral glucose metabolism during bipedal gait in 7 patients with olivopontocerebellar atrophy (OPCA) and 7 control subjects without neurological disease. All OPCA patients in this study were able to walk on the treadmill without a support or handrails. We used 18F-2-fluoro-2-deoxy-D-glucose (18F-FDG) and positron emission tomography (PET) to evaluate glucose metabolism under two different conditions; 30 minutes' treadmill walking, and supine resting. The two sets of PET images were three-dimensionally registered to the magnetic resonance image (MRI) in each subject. Then, the PET images were normalized by the global value. Regions of interest (ROIs) were drawn on the cerebellar vermis, cerebellar hemispheres, pons, and thalamus, and FDG uptake was obtained to calculate the activation ratio (= [FDG uptake under walking]/[FDG uptake under resting]) for each region. We used unpaired t-test for statistical analysis to compare the OPCA patients and the normal control subjects. Normalized resting FDG uptake had no significant difference between control subjects and OPCA patients in any region. Activation ratio of OPCA patients was significantly decreased in the cerebellar vermis compared with the control subjects. In the control subjects, FDG uptake had little difference between resting and walking in the cerebellar hemisphere, pons and thalamus. On the other hand, the FDG uptake of OPCA patients was moderately increased by walking in these regions. In the cerebellar vermis, in spite of no significant difference between the normals and the patients during resting, the activation ratio in OPCA patients was significantly decreased. We speculate that the reduction of activation ratio in the cerebellar vermis reflects the dysfunction caused by degeneration. The result suggests that the PET activation study can demonstrate cerebellar dysfunction in the early phase of OPCA, in which other neuro-imaging methods cannot detect the tissue atrophy, hypometabolism or hypoperfusion in the resting state. In the cerebellar hemisphere, pons and thalamus, the activation ratio was nearly equal to one in control subjects, while it was larger in OPCA patients. We speculate that the instability during the ataxic gait increases the inputs from the vestibular, somatosensory and visual systems to these regions and outputs from these regions to the other neural systems. In conclusion, PET activation study is a useful and noninvasive technique for investigating the brain function associated with human gait.

Adult↗
PubMed1995

[Cerebello-cerebral functional relationship in spinocerebellar degeneration using positron emission tomography].

In order to investigate the laterality of cerebellar ataxia and its influence for the cerebral cortex in spinocerebellar degeneration (SCD), regional cerebral blood flow (r CBF) was measured using positron emission tomography (PET) in 10 patients with sporadic olivopontocerebellar atrophy (sOPCA), 7 patients with hereditary SCD (h SCD), and 10 age matched control subjects. The laterality of cerebellar ataxia was evaluated by the total score of the difference between left and right limbs of three limb-coordination tests. The lateralities of rCBF were calculated by asymmetry indices (AIs) of each region of interest in the cerebellum, thalamus, caudate, putamen, cerebral cortices. The laterality of cerebellar ataxia was significantly correlated with AI in the cerebellum in patients with sOPCA. Furthermore, significant negative correlations were observed between AI in the cerebellum and each AI in the thalamus, frontal cortex in patients with sOPCA. However, no correlations were observed between AI in the cerebellum and the other AIs in controls and patients with h SCD. Duration of illness in patients with sOPCA with laterality is shorter than that in patients without laterality. These results suggest that the existence of crossed cerebello-cerebral diaschisis (CCCD) resulting from transneuronal deactivation through cerebello-thalamo-cerebral pathway in patients with the early stage of sOPCA with laterality.

Adult↗
PubMed1994

Effect of a new calcium antagonist (SM-6586) on experimental cerebral ischemia.

SM-6586 (SM) is a new derivative of dihydropyridine with potent calcium blocking activity and inhibitory activity of the Na+/H+ and Na+/Ca++ exchange transport. The effect of SM on survival rate, brain edema and metabolites was evaluated using two different models in spontaneously hypertensive rat (SHR). Global ischemia was induced by bilateral common carotid artery ligation (BLCL) and focal ischemia was induced by middle cerebral artery occlusion. The survival rate after BLCL was higher in the SM-treated group. The brain water content was lower, the ATP level was higher and lactate level was lower in the SM-treated group compared to the control group. In focal ischemia models, the SM-treated group showed a reduction of T1 relaxation time. The brain water content was significantly decreased in the SM-treated group. These results indicate that SM was effective in ameliorating the ischemic insult in global and focal cerebral ischemia models.

Animals↗
PubMed1994

Comparison of the effects of glycerol, mannitol, and urea on ischemic hippocampal damage in gerbils.

The effects of glycerol and mannitol, as well as urea, on delayed neuronal death (DND) in the gerbil hippocampus were investigated. 20% solution of glycerol, mannitol and urea were prepared, and 6.5 ml/kg of each agent, or saline, was administered to male Mongolian gerbils intraperitoneally 30 min before ischemia. The animals were subjected to transient forebrain ischemia for 5 min. Seven days after the ischemic insult, the brains were fixed and stained for histopathological analysis. The number of normal neurons (neuronal density, ND) in a 1 mm linear length of hippocampal CA1 region was counted. ND of sham-operated group (n = 6) was 275.3 +/- 16.7 (mean +/- SD). ND in the saline-treated group (n = 6) was 14.8 +/- 5.0. ND of groups treated with glycerol (n = 6), mannitol (n = 6) and urea (n = 4) was 68.2 +/- 56.7 (p < 0.01), 52.8 +/- 54.4 (p < 0.01) and 12.0 +/- 2.5 (NS), respectively. The present study demonstrates that glycerol and mannitol have some protective effects against DND in the gerbil hippocampus, whereas urea has no effect.

Animals↗