Biomedical subjects

Y Hashizume

Publications and source records attributed to Y Hashizume.

At least 73 records · Page 4Linked to original sources

PubMed1998

[Patho-MR imaging study in the putaminal margin in multiple system atrophy].

The slit hyperintensity of the lateral margin of the putamen in T2 weighted MRI is a characteristic finding in those patients with multiple system atrophy (MSA) involving extrapyramidal system. In spite of some speculations such as demyelination, gliosis, iron deposition or increased extracellular fluid, the nature of the abnormal signal intensity has still been remained uncertain. In this paper, we report the coincidental findings of pathology and magnetic resonance imaging of the putaminal margin in a case of MSA. The patient was sixty three years old woman with nine years history of intreatable parkinsonism, mild ataxia and dysautonomia. At six months prior to her death, 0.5T MRI showed the pontocerebellar system atrophy, slit hyperintensity in the bilateral outer margin and left inner margin of the putamen in T2 weighted image as well as linear hypointensity in T1 weighted image. The neuropathological examinations showed severe degeneration in the olivopontocerebellar and striatonigral systems, and glial cytoplasmic inclusion in widespread regions in the brain. The putamen showed severe degeneration with rarefaction. The intertissue space was observed at the outer putaminal margin in both sides and inner margin in left side, which seemed to be caused by severe shrinkage and rarefaction of the putamen. Thus, slit hyperintensity in the putaminal margin in MSA was disclosed to represent widened intertissue space.

Female↗

PubMed1998

[An autopsied case of multiple system atrophy with remarkable cerebral atrophy].

In this paper, we report the pathological findings of a multiple system atrophy (MSA) patient with remarkable frontal lobe atrophy. The patient was a 65-year-old woman with a 13-year history of untreatable parkinsonism, dysautonomia and progressive motor aphasia. The cranial imaging study disclosed progressive atrophy of the frontal lobe, striatum and pontocerebellar system. She died of pneumonia. The brain weight was 810 g, and there was remarkable atrophy of the cerebrum predominantly in the frontal lobe, striatum, pons and cerebellum. The microscopic examination revealed a preserved cortical structure with laminar gliosis in the sixth layer of the precentral and superior frontal gyri of the frontal lobe, and postcentral gyrus and inferior parietal lobule of the parietal lobe. The cortices of these regions also revealed to be in a spongy state in the second layer, and mild cell loss was seen in the fifth and six layers. The frontal lobe white matter showed a slight pallor, a mild loss of myelinated fiber and axon, and mild gliosis. Glial cytoplasmic inclusions (GCIs) were abundantly observed in the deep layer of the cortex in the regions mentioned above, and were more abundant in the white matter of the frontal and parietal lobes, callosal body, and internal, external and extreme capsules. There were severe degenerations in the olivopontocerebellar and striatonigral systems, and GCIs in widespread regions of the brain. We could not detect any Pick bodies, Lewy bodies, ballooned neurons, senile plaques, or any significant amounts of neurofibrillary tangles. There were no vascular changes. Thus, this was a verified MSA patient with progressive aphasia and remarkable frontal lobe atrophy. We indicate a possible involvement of the cerebral lobes in MSA.

Aged↗

PubMed1998

Salient factors that influence the meaning of family caregiving for frail elderly parents in Japan from a historical perspective.

This paper is a literature review of factors that influence family-centered caregiving for frail elderly parents in modern Japan from a historical perspective and in the context of an aging society. The meaning of family caregiving in Japan is affected by many sociocultural and historical factors and is changing together with societal changes and developments. These factors include: (a) Japanese cultural background and its current changes, (b) the value of dependence and how it affects the caregiving process, (c) the nonmutable nature of frailty, (d) the value of privacy and the stigma associated with long-term institutionalization, and (e) the devaluation of unhealthiness. Implications for clinical nursing practice are addressed.

Attitude to Health↗

PubMed1997

Relationship between brainstem MRI and pathological findings in progressive supranuclear palsy--study in autopsy cases.

The relationship between the features of MRI in brainstem and pathological findings was investigated in eight autopsy cases with progressive supranuclear palsy (PSP). Features of T1-weighted images at midbrain level were atrophy of tegmentum and tectum, and dilatation of aqueduct. Histologically, these findings were consistent with atrophy of periaqueductal gray matter, quadrigeminal plate, and tegmentum. In these lesions, we detected neuronal loss, decrease in density of myelinated fibers, gliosis, rarefaction of tissues, and tau-positive structures such as neurofibrillary tangles (NFTs), glial fibrillary tangles (GFTs) and neuropil threads. At pons level, atrophy of tegmentum, atrophy of pontine base, and dilatation of prepontine cistern were found. Tau-positive structures were observed not only in tegmentum but also in pontine base. The density of the tau-positive structure was closely related to the severity of atrophy. Features of T2-weighted images were high intensity in the periaqueductal lesion and tegmentum in pons. In these lesions, severe histological findings were detected. The MRI features in brainstem were closely related to the histological findings as PSP.

Aged↗

PubMed1997

A neutral N-methyltransferase activity in the striatum determines the level of an endogenous MPP+-like neurotoxin, 1,2-dimethyl-6,7-dihydroxyisoquinolinium ion, in the substantia nigra of human brains.

An endogenous MPTP-like dopaminergic neurotoxin, N-methyl(R)salsolinol, increases in the parkinsonian cerebrospinal fluid and accumulates in the human nigro-striatum. An N-methyltransferase specific for (R)salsolinol was found in human brain with optimal pH at 7.0 and 8.5. The correlation of the enzyme activity with the level of N-methyl(R)salsolinol and its oxidation product, 1,2-dimethyl-6,7-dihydroxyisoquinolinium ion was examined in the brain regions. Neutral N-methyltransferase activity in the striatum was found to correlate with the level of the endogenous MPP+-like isoquinolinium ion in the substantia nigra (P < 0.001). Considering that this neutral N-methyltransferase activity increases in parkinsonian lymphocytes, the enzyme may be an endogenous factor in the pathogenesis of Parkinson's disease.

Caudate Nucleus↗

PubMed1997

Alteration of the kinetics of type I procollagen synthesis in human osteosarcoma cells by 1,25-dihydroxyvitamin D3.

The kinetics of type I procollagen synthesis in a human osteosarcoma cell line, MG 63, were investigated after treatment with 1,25-dihydroxyvitamin D3 (1,25-(OH)2 D3), a hormonal inducer of phenotypic differentiation. Pulse label and chase experiments demonstrated greatly enhanced production and more rapid reduction of intracellular procollagen molecules in the 1,25-(OH)2 D3-treated cells as compared to the nontreated case. After a chase for 1 h, labeled procollagen was reduced by nine-tenths in 1,25-(OH)2 D3-treated cells, while half of the radioactivity still remained in nontreated cells. The expression rate of type I collagen, which was examined by pulse label experiment, was elevated in association with an increase in the mRNA coding for the type I collagen alpha 1 chain by 1,25-(OH)2 D3 treatment. However, the amount of intracellular procollagen present after 4 h continuous labeling was almost the same, independent of the 1,25-(OH)2 D3 treatment. Thus, we conclude that strage of the molecule was not affected. The results therefore suggest an increase in both the synthesis and secretion of type I collagen. The 1,25-(OH)2 D3 treatment was also found to induce the alpha subunit of prolyl 4-hydroxylase and to be associated with an elevated level of hydroxyproline in the procollagen. Moreover, gelatinase B-resistant procollagen molecules, indicative of intracellular procollagen molecules in the stable triple helical form, were detected only in the 1,25-(OH)2 D3-treated cells. These data suggest more efficient proline hydroxylation is involved in rapid secretion of procollagen after hormone administration. The present evidence points to posttranslational control of procollagen synthesis.

Animals↗

PubMed1997

A dopaminergic neurotoxin, 1(R), 2(N)-dimethyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, N-methyl(R)salsolinol, and its oxidation product, 1,2(N)-dimethyl-6,7-dihydroxyisoquinolinium ion, accumulate in the nigro-striatal system of the human brain.

N-Methyl(R)salsolinol was found to be an endogenous dopaminergic neurotoxin inducing parkinsonism in rodents and to increase in the cerebrospinal fluid of parkinsonian patients. The amounts of N-methyl(R)salsolinol and related compounds in the human brain regions were quantitatively analyzed. Only the (R)-enantiomer of salsolinol derivatives were detected, which suggests their enzymatic synthesis in situ. In the nigro-striatal system, the concentration of N-methyl(+)salsolinol was higher than in the frontal cortex, and its oxidized catechol isoquinolinium ion was detected only in the substantia nigra significantly. The accumulation of these neurotoxins in the nigro-striatal region might account for selective cell death of dopamine neurons in the substantia nigra of Parkinson's disease.

Chromatography, High Pressure Liquid↗

PubMed1997

N-methyl-(R)salsolinol as a dopaminergic neurotoxin: from an animal model to an early marker of Parkinson's disease.

A dopamine-derived 1(R), 2(N)-dimethyl-6,7-dihydroxy-1,2,3,4-tetrahydrosioquinoline [N-methyl-(R)salsolinol] was found to occur enantioselectively in human brain. This isoquinoline induced parkinsonism in rat after injection in the striatum, and the behavioral, biochemical and pathological changes were very similar to those in Parkinson's disease. N-Methyl-(R)salsolinol depleted dopamine neurons in the rat substantia nigra without necrotic tissue reaction, which may be due to the apoptotic death process, as proved by its induction of DNA damage in dopaminergic neuroblastoma SH-SY5Y cells. N-Methyl-(R)salsolinol was found to increase significantly in the cerebrospinal fluid of parkinsonian patients. All these results suggest that N-methyl-(R)salsolinol may be an endogenous neurotoxin to cause Parkinson's disease and the enzymes involved in its biosynthesis and catabolism may be endogenous factors in the pathogenesis of this disease.

Animals↗

PubMed1997

Activation of cardiac muscarinic receptor and ischemic preconditioning effects in in situ rat heart.

Activation of cardiac muscarinic receptors by vagal stimulation decreases cardiac work, which may have a protective effect against ischemic injury. To determine whether cardiac muscarinic receptors contribute to the mechanisms of preconditioning effects, we examined the effect of carbachol on ischemia/reperfusion damage and the effect of vagotomy on cardioprotection induced by ischemic preconditioning. Rats were subjected to 30 min of left coronary artery occlusion followed by 30-min reperfusion in situ. Pre-conditioning was induced by three cycles of 2-min coronary artery occlusion and, subsequently by 5 min of reperfusion. The incidence of ischemic arrhythmias, such as ventricular tachycardia (VT) and ventricular fibrillation (VF), and the development of myocardial infarction were markedly reduced by the preconditioning. Carbachol infusion (4 micrograms/kg per min) delayed the occurrence of VT and VF during ischemia and reduced the infarct size. Compared with non-ischemic left ventricle, the cyclic guanosine monophosphate (GMP) content in the ischemic region of the left ventricle was decreased by ischemia/reperfusion, whereas the cyclic adenosine monophosphate (AMP) content of this region was increased. These changes were reversed by preconditioning. Similar changes in cyclic GMP and AMP content in the ischemic region were seen in rats undergoing carbachol treatment. These results suggest the possible contribution of muscarinic receptor stimulation to preconditioning. Vagotomy prior to preconditioning diminished the antiarrhythmic effects, whereas it did not block the anti-infarct effect afforded by pre-conditioning. Vagotomy abolished the preconditioning effect on the tissue cyclic GMP, but it did not attenuate the decrease in tissue cyclic AMP. The results suggest that muscarinic stimulation exerts preconditioning-mimetic protective effects in ischemic/reperfused hearts, but that a contribution of reflective vagal activity to the mechanism for preconditioning is unlikely.

Animals↗

PubMed1997

The lateral corticospinal tract and spinal ventral horn in X-linked recessive spinal and bulbar muscular atrophy: a quantitative study.

A quantitative study was performed on spinal cord lesions in seven patients with X-linked recessive spinal and bulbar muscular atrophy. The myelinated fiber density of the lateral corticospinal tracts at the T7 cord level was well preserved for both large and small myelinated fibers. On the other hand, neurons in the L4 ventral horn were markedly depleted; marked loss was noted of the large alpha and medium-sized gamma motor neurons located in the lateral and medial nuclei as well as the small neurons in the intermediate zones of the ventral horn. These results suggest that myelinated fiber density and fiber-size distribution in the corticospinal tract are well preserved and that neuronal loss in the ventral horns is not restricted to alpha and gamma motoneurons but also involves small interneurons.

Aged↗

PubMed1997

Experimental chronic compression on the spinal cord of the rabbit by ectopic bone formation in the ligamentum flavum with bone morphogenetic protein.

This study was conducted to induce chronic spinal cord compression myelopathy in rabbits. The L5 lumbar lamina was cut partially in 70 rabbits, and bone morphogenetic protein (BMP) was implanted on the ligamentum flavum in 35 of them. In the BMP group, new bone formed on the dorsal side of the spinal canal and flattened the spinal cord in an anteroposterior direction. No pathological changes were detected in the intramedullary tissues by light microscopic examination. In rabbits it is possible to induce compression of the cord by using BMP, although sufficient cord compression to induce myelopathy was not achieved.

Animals↗

PubMed1997

Differential localization of the gamma 3 and gamma 12 subunits of G proteins in the mammalian brain.

The localization of two forms of the gamma subunit of G proteins, gamma 3 and gamma 12, was examined in the mammalian brain. Concentrations of these two gamma subunits increased markedly, as did those of glial fibrillary acidic protein, during postnatal development in the rat cerebral cortex. In aged human brains, by contrast, the concentration of gamma 3 tended to decrease with age, whereas that of gamma 12 in the temporal cortex increased slightly. An immunohistochemical study of human brains revealed that gamma 3 was abundant in the neuropil, whereas gamma 12 was localized in glial cells. In the hippocampal formation of aged human brains, levels of gamma 12-positive cells, as well as levels of glial fibrillary acidic protein- and vimentin-positive astrocytes, increased, in particular in the CA1 subfield and the prosubiculum, in which there was a decrease in the number of pyramidal cells. The appearance of gamma 12-positive cells associated with the loss of pyramidal cells was also observed in the hippocampus of rats that had been treated with kainic acid. These results indicate that gamma 12 is strongly expressed in reactive astrocytes. In a study of cultured neural cells, we found that gamma 12 was predominant in glioma cells, such as C6 and GA-1 cells, in contrast with the specific localization of gamma 3 in PC12 pheochromocytoma cells, which are neuron-like cells. Taken together, the results indicate that gamma 3 and gamma 12 are selectively expressed in neuronal and glial cells, respectively, and that concentrations of gamma 3 and gamma 12 in the brain are related to the numbers and/or extent of maturation of these cells.

Age Factors↗

PubMed1997

An endogenous dopaminergic neurotoxin, N-methyl-(R)-salsolinol, induces DNA damage in human dopaminergic neuroblastoma SH-SY5Y cells.

Recently, an endogenous neurotoxin, 1(R),2(N)-dimethyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline [N-methyl-(R)-salsolinol], was found to elicit parkinsonism in rats with selective depletion of dopamine neurons in the substantia nigra without necrotic tissue reaction. The mechanism of the cell death was examined by detection of DNA damage using a single-cell gel electrophoresis (comet) assay in human dopaminergic neuroblastoma SH-SY5Y cells. Only N-methylsalsolinol was found to induce DNA damage, whereas other catechol isoquinolines, such as (R)-salsolinol, (S)-salsolinol, and 1,2-dimethyl-6,7-dihydroxyisoquinolinium ion, did not. The (R)-enantiomer of N-methylsalsolinol damaged DNA much more profoundly than the (S)-enantiomer. Cycloheximide protected the cells from DNA damage, suggesting that an apoptotic process may account for the DNA damage. Morphological changes indicating apoptotic cell death were also confirmed. Antioxidants and deprenyl reduced DNA damage, indicating that the damage was initiated by oxidative stress and that neuroprotection by deprenyl may be partially ascribed to its prevention of DNA damage. Apoptosis induced by neurotoxins may be a mechanism underlying the cell death of dopamine neurons in the substantia nigra of Parkinson's disease.

Antioxidants↗

PubMed1997

Fluctuations of rectal and tympanic temperatures with changes of ambient temperature during night sleep.

Many studies have demonstrated a decline in core temperature during slow wave sleep (SWS) in animals and humans. However, there are few studies that have investigated core temperature fluctuation during rapid eye movement sleep (REM) at different ambient temperatures. This study examined the effects on core temperature of continuous hot or cold exposure during sleep. Ten male subjects were exposed to hot and cold stress from 00 h to 1:00 h, when SWS is most predominant, and from 5:00 h to 7:00 h, when REM is predominant. Rectal temperature (Tr) and tympanic temperature (Tt) were monitored for 3 days, and polysomnographies (PSG) were recorded from 23:00 h to 7:00 h. The experiments lasted 3 weeks for each subject, over 2 consecutive nights each week (including an adaptation night and an experimental night). On the experimental night, subjects were exposed to hot (29 degrees C) or cold (21 degrees C) ambience. The core temperature fluctuation under the hot or cold ambience were compared with under the thermoneutral ambience. Under hot ambience, Tr declined significantly in the first 2 hours of sleep, but Tt did not change. In the last 2 hours, both Tr and Tt were significantly elevated. Under cold ambience, both Tr and Tt declined significantly in the first 2 hours. However, in the last 2 hours, neither Tr not Tt showed any change. The result that Tr and Tt rose in hot ambience during the last 2 hours when REM is predominant suggests that body temperature during REM is influenced by ambient temperature.

Adult↗

PubMed1997

[Clinical and diagnostic characteristics of Legionella pneumonia].

We have characterized clinical and diagnostic features in 18 cases of Legionella pneumonia. Age average of patients was 62.0 years old (male:female = 14:4) and underlying diseases were observed in 12 patients. Legionella pneumonia were diagnosed in 3, 5, 8 and 9 cases by culture, serum antibody measurement, urinary antigen detection and PCR, respectively. Sixteen cases were caused by L. pneumophila, while the other 2 cases were L. bozemanii pneumonia and L. pneumophila or L. dumoffii pneumonia. Chest X-rays of those patients showed multiple pneumonia shadows in 14 cases, alveolar shadows in 10 cases, pleural effusion in 5 cases. Blood-gas analysis on admission indicated hypoxemia in all cases with abnormal A-a DO2. Laboratory findings showed abnormal data in WBC, CRP, LDH, CPK and liver function tests (ex. GOT, GPT) in most cases. Serum antibody testing showed positive by 5 weeks after onset of pneumonia, but 10 cases of Legionella pneumonia diagnosed by other techniques were judged to be negative. In urinary antigen detection test, 6 and 2 cases showed positive 1 and 4 weeks after onset of pneumonia, respectively. Macrolide antibiotics were administered in all cases during the episode, but delay of macrolide administration was observed in 3 of 4 cases of dead outcome. Serum antibody measurement, urinary antigen detection and PCR, in addition to culture to bacteria, may be required for exact diagnosis of Legionella infection.

Adult↗

PubMed1997

Upper motor neuron lesions in stroke patients do not induce anterograde transneuronal degeneration in spinal anterior horn cells.

BACKGROUND AND PURPOSE: To determine whether upper motor neuron lesions in stroke can cause transneuronal degeneration of lower motor neurons, we assessed spinal anterior horn cells in patients dying with poststroke hemiplegia. METHODS: Subjects were four stroke patients with severe left hemiplegia and four age-matched control subjects who died of nonneurological disease. After histological processing and staining, cytoarchitectonic assessment was made of all neurons in the ventral horns of the 4th lumbar segment of the spinal cord according to cell diameter and topography. RESULTS: In the four stroke patients, no differences were seen in anterior horn cell populations or diameter and size distribution patterns between affected and unaffected sides or between these patients and the control subjects. CONCLUSIONS: The present quantitative analysis provides no evidence of anterograde transneuronal degeneration of lower motor neurons after upper motor neuron damage in stroke patients.

Adult↗

PubMed1997

Axonal pathology in Japanese Guillain-Barré syndrome: a study of 15 autopsied cases.

We assessed the frequency and extent of axonal involvement in the ventral spinal roots in 15 Japanese autopsied patients with Guillain-Barré syndrome (GBS). Teased-fiber preparation revealed that five had predominantly axonal pathology with minimal segmental demyelination, seven had predominantly segmental demyelination with minimal axonal changes, two patients showed a mixture of both conditions, and one patient did not show any particular pathologic changes. We confirmed axon loss by immunohistochemical analysis of high-molecular-weight neurofilament protein. Macrophage invasion was a prominent feature in nerves with predominantly axonal changes. Two patients with severe axonal involvement and prolonged clinical courses exhibited motor neuron loss with astrogliosis in the ventral horns. These results suggest that autopsy-verified axonal involvement is more frequent among Japanese GBS patients than in Caucasian populations but less frequent than that reported from northern China.

Adult↗

PubMed1997

[Automatic movements of extremities induced in primary massive brain lesion with apneic coma].

In three cases of primary massive brain lesion with apneic coma, various automatic movements of the extremities were elicited by physical or sensory stimulation. In each case, these movements appeared after a period of cessation of spontaneous respiration followed by flaccid tetraplegia. Brainstem reflexes were absent throughout in all cases. The movements were induced mainly by ventroflexion of the neck, and each case showed movements as described below: in the first case, the patient flexed her elbows and raised both arms slowly, a typical Lazarus sign; in the second case, the patient raised both arms and showed myoclonic movements; and the third case showed abduction of both legs and extension in the upper extremities. Pathology in the first case showed ischemic changes in the entire brain and brainstem. Although ischemic change was also found in the anterior horn cells and white matter of the spinal cord of C1-C4 and of T4 and below, the spinal cord of C5-T3 was relatively well-preserved. These movements appear to have essentially originated in spinal neurons; however, it is assumed that they must have recovered from spinal shock which occurred due to upper level transection. These movements were induced by ventroflexion of the neck, so mechanical extension of the spinal roots, mechanical compression of the spinal cord, and various modalities of the sensation afferent might have some relation to these movements. As tonic neck reflex might also be a cause of these, movements, association with the lower medulla could not be ruled out completely. These movements appeared nearing or after brain death. Although in each case of brain death the spinal cord may have been affected by specific conditions, such as impaired circulation of whole central nervous sysytem, it might have been transversed at upper level, which then causes spinal automatism. These movements might appear even in the state of brainstem death. In each case, the distribution and severity of hypoxic changes in the spinal cord may have resulted in variations in the type and characteristics of these movements.

Aged↗