Biomedical subjects

Y Katsumi

Publications and source records attributed to Y Katsumi.

At least 19 recordsLinked to original sources

PubMed2000

Glucose metabolism in the rat frontal cortex recovered without the recovery of choline acetyltransferase activity after lesioning of the nucleus basalis magnocellularis.

We measured the cerebral metabolic rate of glucose (CMRglc) by using positron emission tomography (PET) with [18F]fluorodeoxyglucose (FDG) and the choline acetyltransferase (ChAT) activity at 3 days and 3 months after destruction of the nucleus basalis magnocellularis (NBM). Although the frontal ChAT activity remained 20% lower than that of controls even at 3 months post-lesioning, the frontal CMRglc, which was reduced by 40% at 3 days, returned to normal at 3 months, namely CMRglc recovered with time without the recovery of ChAT activity with time. Since glucose metabolism reflects mainly presynaptic neuronal activity, we speculate that presynaptic rearrangement may have some relation to the recovery of CMRglc.

Animals↗

PubMed1999

The effect of sequential lesioning in the basal forebrain on cerebral cortical glucose metabolism in rats. An animal positron emission tomography study.

We studied the effect of the cortical projection from the basal forebrain on the cerebral cortical metabolism using positron emission tomography (PET) with [(18)F] fluorodeoxyglucose. Unilateral damage of the nucleus basalis magnocellularis (NBM) did not cause a permanent reduction of cortical metabolism: recovery was observed 4 weeks after the operation. Destruction of the contralateral side after recovery from unilateral damage produced persistent bilateral suppression of glucose metabolism, with partial recovery. We speculate that recovery from the unilateral NBM lesions is partly ascribable to the cholinergic projection from the contralateral NBM, and partly due to non-cholinergic systems, and conclude that bilateral damage might be responsible for persistent cortical glucose metabolism suppression.

Animals↗

PubMed1999

Cerebral glucose metabolism in unilateral entorhinal cortex-lesioned rats: an animal PET study.

To evaluate the effect of entorhinal cortical lesion on cerebral cortical function, we studied cerebral glucose utilization (CMRGlc) using a high resolution PET scanner after quinolinic acid lesion of the unilateral entorhinal cortex in rats. [18F]Fluorodeoxyglucose PET was performed at 4 days and 4 weeks after surgery, and CMRGlc in the bilateral frontal, parietal and temporal regions were analyzed. At 4 days, the entorhinal lesion induced a 12-15% decrease in CMRGlc of frontal, parietal and temporal regions ipsilateral to the lesion. The hypometabolism continued at 4 weeks in the temporal region. These findings suggest that entorhinal lesion induces cerebral cortical hypometabolism, which implies a pathogenetic role of entorhinal area on the cortical hypometabolism in Alzheimer's disease.

Analysis of Variance↗

PubMed1999

Morphologic limitations of posterior decompression by midsagittal splitting method for myelopathy caused by ossification of the posterior longitudinal ligament in the cervical spine.

STUDY DESIGN: This is a retrospective study of the morphologic limitations of posterior decompression for ossification of the posterior longitudinal ligament in the cervical spine. OBJECTIVES: To determine the morphologic limitations of the posterior approach in the management of ossification of the posterior longitudinal ligament. SUMMARY OF BACKGROUND DATA: Thirty-eight patients who underwent laminoplasty by midsagittal splitting for ossification of the posterior longitudinal ligament were reviewed. Fifteen patients were included in the noncontact group, in which the spinal cord was free of the ossified lesion after posterior decompression. Twenty-three patients were included in the contact group, in which the spinal cord was not free of the ossified lesion even after posterior decompression. METHODS: The preoperative sagittal alignment of the cervical spine and preoperative maximal thickness of ossification were compared between the two groups. In addition, the morphologic limitations of posterior decompression for ossification of the posterior longitudinal ligament were investigated. RESULTS: The following factors were found to contribute significantly to contact between the spinal cord and ossification of the posterior longitudinal ligament after posterior decompression: 1) lordosis of less than 10 degrees or kyphosis in the preoperative sagittal alignment, and 2) preoperative maximal thickness of ossification of more than 7 mm. CONCLUSIONS: Patients who exhibit significant risk factors for continued contact of the spinal cord should be morphologically considered for anterior decompression.

Adult↗

PubMed1999

Enhanced lateral premotor activity during paradoxical gait in Parkinson's disease.

Parkinson's disease (PD) patients often show marked improvement of hypokinetic gait when exposed to special stimuli. To investigate physiological mechanisms underlying this "paradoxical gait" induced by visual cues in PD patients, we examined regional cerebral blood flow changes during gait on a treadmill guided by two different visual cues, the lines oriented transversely to the direction of walk (TL) and the lines parallel to it (PL). Ten PD patients and 10 age-matched controls received injections of 99mTc-hexamethylpropyleneamine oxime twice, once during each walking condition. Brain perfusion images were obtained by single-photon emission computed tomography. When affected by TL, PD patients showed marked improvement of gait parameters, mainly reduction of cadence. In regional cerebral blood flow analysis, when TL was compared with PL, both groups had common activation in the posterior parietal cortex and cerebellar hemispheres. Especially in the right lateral premotor cortex, PD patients showed enhanced activation induced by TL to a significantly greater degree than the controls. The present study indicates that the network dedicated to visuomotor control, particularly the lateral premotor cortex, plays an important role in the development of the paradoxical gait induced by special visual stimuli in PD patients.

Aged↗

PubMed1999

Transient neural activity in the medial superior frontal gyrus and precuneus time locked with attention shift between object features.

To investigate the contribution of the superior frontal gyrus and precuneus to the cognitive process of attention set shift, we examined the correlation between change in neural activity in these areas and the timing of attention set shift using event-related functional magnetic resonance imaging. Seven subjects underwent a card-sorting task in which they matched a test card to one of two target cards according to color or shape. The subjects had to determine the correct category based only on feedback and shift the sorting principle when the feedback changed from "correct" to "incorrect." Transient increase of neural activity time locked with attention shift phases was detected in the medial superior frontal gyrus (the rostral part of the supplementary motor area) and precuneus. During the control task, in which the feedback and the motor responses were preserved without any attention shift, this type of change in neural activity was not observed. Our findings indicate that increase in neural activity in these brain areas may be closely related to attention set shift between object features and suggest that these areas may play a role in the shifting of cognitive sets.

Adult↗

PubMed1999

Mechanisms underlying gait disturbance in Parkinson's disease: a single photon emission computed tomography study.

Single photon emission computed tomography was used to evaluate regional cerebral blood flow changes during gait on a treadmill in 10 patients with Parkinson's disease and 10 age-matched controls. The subjects were injected with [99mTc]hexamethyl-propyleneamine oxime twice: while walking on the treadmill, which moved at a steady speed, and while lying on a bed with their eyes open. On the treadmill, all subjects walked at the same speed with their preferred stride length. The patients showed typical hypokinetic gait with higher cadence and smaller stride length than the controls. In the controls, a gait-induced increase in brain activity was observed in the medial and lateral premotor areas, primary sensorimotor areas, anterior cingulate contex, superior parietal cortex, visual cortex, dorsal brainstem, basal ganglia and cerebellum. The Parkinson's disease patients revealed relative underactivation in the left medial frontal area, right precuneus and left cerebellar hemisphere, whereas they showed relative overactivity in the left temporal cortex, right insula, left cingulate cortex and cerebellar vermis. This is the first experimental study showing that the dorsal brainstem, which corresponds to the brainstem locomotor region in experimental animals, is active during human bipedal gait. The reduced brain activity in the medial frontal motor areas is a basic abnormality in motor performance in Parkinson's disease. The underactivity in the left cerebellar hemisphere, in contrast to the overactivity in the vermis, could be associated with a loss of lateral gravity shift in parkinsonian gait.

Aged↗

PubMed1999

Selective cerebral hematocrit decrease in the centrum semiovale after carotid artery occlusion: a PET study.

The centrum semiovale may be susceptible to hypoperfusion as a result of carotid artery occlusion. Recent studies suggest that the cerebral hematocrit decreases with diminished cerebral perfusion pressure. To investigate whether the effect of carotid artery occlusion on the hematocrit in the centrum semiovale is different from that in the cerebral cortex, seven patients with unilateral carotid artery occlusion were studied with positron emission tomography. The distributions of the red blood cell and plasma volumes were assessed using carbon monoxide labeled with oxygen 15 and human serum albumin-dithiosemicarbazone tracers labeled with copper 62, respectively. The CBF and CMRO2 were also measured with the (15)O steady-state technique. The calculated values for the hematocrit in the centrum semiovale ipsilateral to the arterial occlusion were significantly decreased compared with those in any of the other regions examined (the overlying cortical region and the contralateral cortex and centrum semiovale). This decrease in hematocrit, which resulted from a more pronounced increase in plasma volume than in red blood cell volume, was associated with a decrease in CBF and an increase in the oxygen extraction fraction. Hemodynamic disturbance caused by carotid artery occlusion may induce selective decrease of hematocrit limited to the centrum semiovale.

Aged↗

PubMed1998

Issues in measuring glucose metabolism of rat brain using PET: the effect of harderian glands on the frontal lobe.

We estimated the effect of the Harderian gland (an orbital gland of land vertebrates) on the measurement of cerebral metabolic rate of glucose (CMRGIc) of the rat brain using positron emission tomography (PET) for animal use. The Harderian gland had the high accumulation of 18-F labeled deoxyglucose (FDG) after intravenous injection. By placing the large regions of interest (ROI) (twice the full width at half maximum in diameter), the CMRGIc in the frontal region was slightly higher compared with the CMRGIc after Harderian gland resection, but the parietal and occipital regions and the cerebellum had the similar level of CMRGIc before and after Harderian gland resection. Therefore the Harderian gland has a slight effect on the frontal lobe CMRGIc, but such overestimation can be within the permissible range for PET study of rat brains.

Animals↗

PubMed1998

Neural activity during attention shifts between object features.

To investigate the neural mechanisms involved in shifting attention we used positron emission tomography to examine regional cerebral blood flow (rCBF) during a task that demands shifting attention between color and shape. Significant activation was observed in the right dorsal prefrontal cortex and parieto-occipital cortex at all frequencies of attention shifts. The frequency of shifts between categories correlated significantly with rCBF in the rostral part of the supplementary motor area and the left precuneus, whereas the number of successive correct responses correlated with rCBF in the orbitofrontal cortex and the caudate nucleus. This study suggests that several prefrontal regions may participate in the processes of shifting attention in different ways.

Adult↗

PubMed1998

Atrophy of the corpus callosum, cortical hypometabolism, and cognitive impairment in corticobasal degeneration.

OBJECTIVE: To investigate whether atrophy of the corpus callosum is associated with cognitive impairment and cerebral cortical hypometabolism in corticobasal degeneration. DESIGN: Prospective clinicoradiological correlation with magnetic resonance imaging and positron emission tomography. SETTING: A university hospital. PATIENTS: Eight right-handed patients with clinically diagnosed corticobasal degeneration (mean+/-SD age, 64+/-8 years). MAIN OUTCOME MEASURES: Midsagittal corpus callosum area-skull area ratio (on T1-weighted magnetic resonance images), the sum of the scaled scores of the 6 subtests on the Wechsler Adult Intelligence Scale-Revised (Digit Span, Arithmetic, Picture Arrangement, Object Assembly, Block Design, and Digit Symbol), and cerebral metabolic rate of glucose (measured with positron emission tomography by using fludeoxyglucose F 18 as a tracer). RESULTS: Compared with 36 age-matched right-handed control subjects, the patients had significantly decreased callosal area-skull area ratio. The reduction in this ratio was greatest in the middle half of the corpus callosum. The atrophy of the corpus callosum was accompanied by a decreased mean cortical glucose metabolic rate with hemispheric asymmetry and a decrease in the sum of the scaled subtest scores of the Wechsler Adult Intelligence Scale-Revised. CONCLUSIONS: Atrophy of the corpus callosum with middle predominance is present in corticobasal degeneration, and this atrophy is associated with cognitive impairment and cerebral cortical hypometabolism with hemispheric asymmetry. Atrophy of the corpus callosum might reflect the severity of the disconnection between cortical regions, and this may be an important factor in the development of cerebral cortical dysfunction in corticobasal degeneration.

Aged↗

PubMed1998

Cerebral hematocrit decreases with hemodynamic compromise in carotid artery occlusion: a PET study.

BACKGROUND AND PURPOSE: This study investigated whether in patients with internal carotid artery occlusion the regional cerebral hematocrit correlates with cerebral hemodynamics or metabolic state and, if so, how the regional cerebral hematocrit changes in the hemodynamically compromised region. METHODS: We used positron emission tomography to study seven patients with unilateral internal carotid artery occlusion and no cortical infarction in the chronic stage. The distributions of red blood cell and plasma volumes were assessed using oxygen-15-labeled carbon monoxide and copper-62-labeled human serum albumin-dithiosemicarbazone tracers, respectively. The calculated hematocrit value was compared with the hemodynamic and metabolic parameters measured with the oxygen-15 steady-state technique. RESULTS: In the cerebral cortex, the value of the cerebral hematocrit varied but was correlated with the hemodynamic and metabolic status. Stepwise regression analysis revealed that the large vessel hematocrit, the cerebral metabolic rate of oxygen, and the cerebral blood flow or the oxygen extraction fraction accounted for a significant proportion of variance of the cerebral hematocrit. The oxygen extraction fraction and the cerebral metabolic rate of oxygen negatively correlated with the cerebral hematocrit, whereas the cerebral blood flow correlated positively: patients with reduced blood supply relative to metabolic demand (decreased blood flow with increased oxygen extraction fraction) showed low hematocrit values. CONCLUSIONS: In carotid artery occlusion in the chronic stage, regional cerebral hematocrit may vary according to cerebral hemodynamics and metabolic status. Regional cerebral hematocrit may decrease with hemodynamic compromise unless oxygen metabolism concomitantly decreases.

Aged↗

PubMed1997

Atrophy of the corpus callosum, cognitive impairment, and cortical hypometabolism in progressive supranuclear palsy.

Recent studies disclosed neurofibrillary degeneration in layer 3 of the association cortex in patients with progressive supranuclear palsy. This lesion may be associated with corpus callosum atrophy and may impair the function of cortical regions indispensable for complex cognitive activity. To investigate whether corpus callosum atrophy is associated with cognitive impairment and cerebral cortical hypometabolism, we studied 10 patients with progressive supranuclear palsy using magnetic resonance imaging and positron emission tomography with fluorodeoxyglucose as a tracer. Compared with 23 age-matched control subjects, the patients had significantly decreased callosal area-skull area ratios, with anterior predominance of the degree of atrophy. The corpus callosum atrophy was accompanied by a decreased mean cortical glucose metabolic rate, predominantly in the frontal region of the cortex, and poor performance on the picture arrangement subtest of the Wechsler Adult Intelligence Scale and the verbal fluency task. We conclude that corpus callosum atrophy with anterior predominance is present in progressive supranuclear palsy, and that this atrophy is associated with cognitive impairment and cerebral cortical hypometabolism, especially in the frontal cortical region. Corpus callosum atrophy may reflect the pathological changes in the cerebral cortex, accentuated in the frontal region, that contribute to the development of frontal lobe dysfunction in this disease.

Aged↗

PubMed1997

Age-related changes in cerebral blood flow activation during a Card Sorting Test.

To determine the age-related changes in the neural processing involved in the Modified Card Sorting Test (MCST), we measured cerebral blood flow (CBF) during performance of the MCST and of the number-matching task in young and elderly subjects using positron emission tomography. Compared with that during the number-matching task, CBF during the MCST was increased in the left dorsolateral prefrontal cortex (DLPFC), left inferior parietal lobule, and left striate and prestriate cortices in both age groups. However, CBF activation in these areas was significantly lower in the elderly subjects than the young subjects. Furthermore, CBF activation was reduced in the left DLPFC, right parahippocampal gyrus, and prestriate cortex in proportion to the increase in the number of perseverative errors with aging. These results suggest that the impaired MCST performance in elderly subjects may be due, in part, to dysfunction of the network involving certain cortical areas such as the prefrontal and parahippocampal cortices, although the essential neural circuits for MCST performance were still preserved even in the elderly subjects.

Adult↗

PubMed1996

Cerebral oxygen and glucose metabolism in glycogen storage disease with normal acid maltase: case report.

A 26-year-old male with cardiomyopathy, cervical muscle weakness and mental retardation was diagnosed as having glycogen storage disease with normal acid maltase on the basis of his clinical, pathological and biochemical findings. Positron emission tomography showed that cerebral oxygen metabolism was normal, while cerebral glucose metabolism was decreased in the cerebral cortexes. The decrease of the glucose metabolic rate may reflect an abnormality of cerebral glucose metabolism in this disorder and may be related to mental retardation, which is one of the characteristic symptoms.

Adult↗

PubMed1996

Atrophy of the corpus callosum associated with cognitive impairment and widespread cortical hypometabolism in carotid artery occlusive disease.

OBJECTIVE: To investigate whether atrophy of the corpus callosum is associated with cognitive impairment and widespread cerebral cortical hypometabolism in carotid artery occlusive disease. PATIENTS: Twelve patients with unilateral internal carotid artery occlusive disease (1 with severe stenosis and 11 with occlusion) and no cortical infarction in the chronic stage (mean +/- SD age, 64 +/- 5 years). MAIN OUTCOME MEASURES: Midsagittal corpus callosum area-skull area ratio (on T1-weighted magnetic resonance images), the sum of the scaled scores of the 6 subtests on the Wechsler Adult Intelligence Scale-Revised (Digit Span, Arithmetic, Picture Arrangement, Object Assembly, Block Design, and Digit Symbol), and cerebral metabolic rate of oxygen (measured with position emission tomography by using the oxygen 15 steady-state technique). RESULTS: The degree of cognitive impairment varied but was strongly correlated with the severity of callosal atrophy (r = 0.92, P < .001). Patients with callosal atrophy and cognitive decline also showed decreased oxygen consumption in the bilateral cerebral cortices. Stepwise regression analysis revealed that the severity of white matter lesions, especially in the centrum semiovale, and that of cortical atrophy in the hemisphere with arterial disease were 2 important factors for callosal atrophy. CONCLUSIONS: Callosal atrophy is associated with cognitive impairment and widespread cerebral cortical hypometabolism in carotid artery occlusive disease without cortical infarction. Callosal atrophy might reflect the severity of the disconnection between cortical regions, and this may be an important factor in the development of cognitive impairment with widespread cortical hypometabolism in carotid artery occlusive disease without large cortical lesions.

Aged↗

PubMed1995

A serine protease zymogen in insect plasma. Purification and activation by microbial cell wall components.

A protease zymogen present in the plasma fraction of the hemolymph of silkworm, Bombyx mori, was purified to homogeneity as judged by SDS/PAGE and IEF/PAGE. An activating system for the zymogen was also isolated from the plasma fraction and was shown to be triggered by zymosan (yeast cell wall polysaccharide containing beta-1,3-glucan) or peptidoglycan. Using this system, the purified zymogen was activated and the active enzyme was purified to homogeneity. The physiological function of the zymogen or its active form is not yet known, but the active form was shown to have narrower substrate specificity than trypsin. Among 33 peptide derivatives examined, Boc-Gln-Arg-Arg-NH-Mec and Boc-Val-Pro-Arg-NH-Mec (Boc = tert-butoxycarbonyl, NH-Mec = 4-methylcoumaryl-7-amide) were the best and the second best substrates, respectively. The purified zymogen was determined to be a 39-kDa protein consisting of a single polypeptide. The active form of the zymogen was labeled with [3H]diisopropylfluorophosphate and was completely inactivated by (p-amidinophenyl)methanesulfonyl fluoride. The molecular mass of the [3H]-labeled enzyme was determined to be 38 kDa in SDS/PAGE under reducing conditions. These results indicate that the 39-kDa protein purified in the present study is a zymogen of a serine-type protease and that the activation of the zymogen occurs by limited proteolysis.

Amino Acid Sequence↗

PubMed1995

Sarcolemmal indentation in cardiomyopathy with mental retardation and vacuolar myopathy.

Muscle biopsies from three patients with cardiomyopathy, mental retardation and increased serum creatine kinase levels revealed scattered fibers with tiny intracytoplasmic vacuoles containing basophilic and acid phosphatase-positive material and slightly increased amounts of PAS-positive granules. These findings are consistent with those seen in the so-called lysosomal glycogen storage disease with normal acid maltase. In addition to the vacuoles, there were occasional folds or indentations in the sarcolemma which were connected to the membrane enclosing the vacuoles. These membranes were well demonstrated histochemically by the nonspecific esterase and acetylcholinesterase stains. On electron microscopy, most of the vacuoles were bounded by membranes with basal lamina. The vacuolar membrane stained positively with antibodies raised to dystrophin, dystrophin-associated glycoproteins, laminin and type 4 collagen, and it was identical to the sarcolemma and its basal lamina. Therefore, the membrane abnormality which causes sarcolemmal folding is probably critical to understanding the pathomechanism of this disease.

Adolescent↗