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S Komatsumoto

Publications and source records attributed to S Komatsumoto.

At least 19 recordsLinked to original sources
PubMed2000

[A case of codon 232 mutation-induced Creutzfeldt-Jakob disease visualized by the MRI-FLAIR images with atypical clinical symptoms].

A 50-year-old man was admitted to our hospital because of disorientation and nocturnal restlessness. The patient presented chronically progressive dementia. No myoclonus or periodic synchronous discharge (PSD) was found over time, with abnormal evidence in MRI-FLAIR (fluid-attenuated inversion recovery) images alone. Brain biopsy and prion protein gene analysis led to the final diagnosis of Creutzfeldt-Jakob disease (CJD) induced by the point mutation at codon 232 (Met to Arg). To date the cases of M232R mutation-induced CJD have been reported to present clinical symptoms and pathological evidences similar to sporadic CJD cases, and differential diagnosis between the types has been believed to be difficult. Our case suggests that some types of CJD induced by point mutation at codon 232 cannot be easily inferred from clinical findings.

Brain↗
PubMed1999

Encephalopathy in scleromyxedema.

The authors monitored CSF findings for over 5 months in a patient with a fatal case of scleromyxedema and two episodes of encephalopathy. During both encephalopathy episodes, CSF protein and immunoglobulin G (IgG) levels were elevated without an increased IgG index or IgG synthesis rate. A CSF-dominant increase in the concentration of interleukin-6 (IL-6) also was noted during encephalopathy. These findings suggest a disruption of the blood-brain barrier and that IL-6 may play some role in mediating the encephalopathy. OFF

Brain Diseases↗
PubMed1998

Imprint cytology of large B-cell lymphoma with high content of epithelioid cells. A report of two cases.

An association of epithelioid cell reaction in follicular center cell lymphomas seems to be a rare phenomenon. The cytological features of this type of B-cell lymphoma from two patients are presented. In both cases, immunohistochemistry applied to paraffin sections revealed reactivity of tumor cells for CD10, 20 and 79a. The first patient, a 77-year-old male, presented with bilateral inguinal bulky masses. The second patient, a 76-year-old female, revealed left supraclavicular bulky masses. Imprint cytological specimens of these two cases showed large lymphoid cells interspersed with epithelioid histiocytes, which were present in small aggregated clusters or in isolated forms. Most tumor cells showed centroblastic morphology, whereas the minority of them looked like immunoblasts. Occasionally, a monotonous proliferation of these large atypical blastic cells was also detected. On the other hand, in some parts of the imprint specimens, numerous epithelioid cells obscured the underlining tumor cells. Reactive cells other than epithelioid cells were not prominent. These cytologic features closely resembled the histologic patterns of this rare follicular center cell lymphoma. Careful examination of the cytological specimens is needed to detect the monotonous proliferation of tumor cells to establish the diagnosis of malignant lymphoma.

Aged↗
PubMed1997

Systemic lupus erythematosus (SLE) lymphadenopathy presenting with histopathologic features of Castleman' disease: a clinicopathologic study of five cases.

Lymph node enlargement is common in active systemic lupus erythematosus (SLE), a disease characterized by well defined clinical criteria. Although numerous reports have described the characteristic histology of SLE lymphadenopathy to include necrotizing lesions and hematoxylin bodies, no detailed description has examined the histopathologic features that are similar to Castleman's disease (CD) in SLE patients. In this report, we describe the clinicopathologic findings of CD-like peripheral lymphadenopathy, which was identified in five (26%) of 19 SLE patients. These five patients were all female with an age range of 24 to 44 years, and four of them presented with multicentric lymphadenopathy. They also had systemic symptoms and abnormal laboratory findings, indicating active disease, although two patients had not fulfilled the diagnostic criteria of SLE at the initial disease. The size of the enlarged lymph nodes seldom exceeded 2.0 cm in diameter, and biopsies revealed histopathologic features similar to CD, of intermediate type in three patients and hyaline vascular type in two according to the classification of Flendrig [7]. Immunohistochemical studies demonstrated polyclonal plasma cell populations in all five cases. Epstein-Barr virus genomes were detected in the small lymphocytes of two of the three cases examined by in situ hybridization studies. Recently, the histopathologic findings of CD have been associated with a disrupted immune response, and the present data suggest that SLE should be listed as one of the diseases showing the histopathologic features similar to CD.

Adult↗
PubMed1996

Correlation of in vivo nitric oxide and cGMP with glutamate/glutamine metabolism in the rat striatum.

We have examined how the suppression of endogenous production of nitric oxide (NO) in the striatal tissue affects release of glutamate (GLU) and glutamine (GLN) in pentobarbital-anesthetized male Sprague-Dawley rats. For the quantitative measurement of tissue NO production and amino acid release, an in vivo assay system for extracellular nitrite (NO2-) and amino acids was employed using an in vivo microdialysis technique. An NO synthase inhibitor (NG-nitro-L-arginine methyl ester, L-NAME) in concentrations ranging between 4-40 mM was perfused into the rat striatum using the assay system. Tissue NO production was found to be inversely proportional to the L-NAME concentration. L-NAME likewise decreased striatal levels of GLU and GLN. Furthermore, tissue NO production showed a positive correlation with GLU (R = 0.62, P < 0.02) and GLN (R = 0.86, P < 0.001) concentrations. Exogenous application of NO and cGMP by intrastriatal perfusion with 0.1-2.5 mM hydroxylamine and 0.4-10 mM 8-bromo-cGMP, respectively, increased striatal GLU release in a dose-related manner. Hydroxylamine reduced GLN release, and 8-bromo-cGMP showed a tendency to decrease GLN. In conclusion, striatal GLU/GLN metabolism is a function of the tissue concentration of NO. Normal endogenous concentration of NO causes GLU to be released at a consistent basal level, and enhanced tissue NO production facilitates GLU release via pathways including cGMP formation. We hypothesize that NO may suppress GLN formation by astrocytes.

Animals↗
PubMed1996

[Changes in the level of thrombomodulin with aging].

Thrombomodulin (TM) is a thrombin receptor on endothelial cells. When endothelial cells are damaged TM is degraded and released into the blood. We examined whether levels of TM in plasma reflect endothelial damage related to aging. We measured the TM level in samples of plasma from 93 healthy men aged from 22 to 81 years. None had hypertension, obesity, diabetes mellitus, or cardiovascular disease. The relationship between the level of TM (Y) and age (X) could be approximated by Y = 0.176X + 10.379, the correlation was significant (r = 0.647, p < 0.01). Basal levels of TM in subjects from 20 to 60 years old showed a gradual increase, that was not statistically significant. Basal concentrations of TM were significantly higher in the older subjects than in the younger subjects. The high levels of TM in the older subjects might reflect endothelial damage. In conclusion, a high TM level in plasma may be a sign of endothelial damage related to aging.

Adult↗
PubMed1996

[Multiple cerebral infarction after treatment with cisplatin].

A 46-year-old woman with a tumor the uterine cervix who experienced cerebrovascular accident as a complication of cisplatin-based chemotherapy is presented. Five days after the eleventh cycle of cisplatin 75 mg, intravenously, she had an acute onset of mild memory disturbance and right-sided weakness. On neurological examination, pyramidal sign was discovered on the right side. MRI of the brain showed multiple infarction on the left basal ganglia. There was no evidence of coagulopathy, vascular, or endocardial disease that may have led to a cerebrovascular accident. Similar characteristics in patients previously reported suggest that thrombosis secondary to vascular endothelial injury induced by cisplatin therapy may be responsible for cerebrovascular complications.

Basal Ganglia↗
PubMed1995

Clinicopathological observations in middle cerebral artery occlusion in the cat.

This study was designed to investigate the relationships among neurological deficits, changes in the electroencephalogram (EEG) and morphological damage over a one week period following temporary occlusion (2 h) of the middle cerebral artery (MCA) in the cat. The animals were grouped into mild, moderate, and severe stroke based on the EEG alterations produced 30 min after the MCA occlusion. All three grades of stroke showed a precipitous fall in mean EEG amplitude followed by a recovery during a 4 h recirculation period. Over the subsequent 7 days there was a gradual secondary depression in the EEG amplitude. Post-operatively, a secondary fall in EEG amplitude in the contralateral hemisphere was also noted in all stroke groups corresponding to the clinical phenomenon of 'diaschisis'. The overall neurological score differed significantly among the severe, moderate, and mild stroke groups. The neurological deficits on the 7th day were highly correlated with the degree of morphological damage. Additionally, the reduction of EEG was also well correlated with the pathological data. This stroke model in the cat has provided important data concerning the restitution of brain function following chronic focal ischaemia.

Animals↗
PubMed1995

[Changes in the level of endothelin-1 with aging].

Endothelin-1 (ET-1) is a potent and long-lasting vasoconstrictor peptide. In order to clarify the changes in the level of ET-1 with aging, we measured the ET-1 level in plasma by radioimmunoassay and used 74 healthy subjects including 61 males and 13 females, aged from 30 to 69, who were admitted in the health check center of Ashikaga Red Cross Hospital. None of them had risk factors related to hypertension, obesity, diabetes mellitus or cardiovascular disease. In the male group, the relationship between the level of ET-1 (Y) and age (X) was obtained as follows: Y = 0.08857 X +0.06363. The correlation between them was significant (gamma = 0.65894, p < 0.05). In the female group also, the increased level of ET-1 (Y) with age (X) showed an excellent linear relationship (Y = 0.163091 X -4.23, gamma = 0.762, p < 0.002). These studies demonstrated that the level of ET-1 increased in relation to aging and the increased ET-1 production with aging may be consistent with deterioration of endothelial function.

Adult↗
PubMed1995

[Lower level of endothelin-1 in migraine with aura].

Endothelin-1 (ET-1) exerts powerful vasoconstrictive and blood pressure elevating properties through endothelial cells. However, no systematic examination of ET-1 in migraine has ever been attempted. The present investigation was focused on evaluating the level of ET-1 in patients with migraine with aura. Studies on ET-1 were made in 17 patients with migraine with aura (age, 23.4 +/- 9.1 years old, mean +/- SD) according to the Classification of Headache of the Ad Hoc Committee. All patients had been free of migraine attacks for at least 7 days prior to the examination. Twenty-eight age-matched healthy volunteers (age, 23.0 +/- 12.3 years old) were similarly used as a control group. None of them revealed evidence of any other disease, such as hypertension, obesity, or heart disease. Informed consent was obtained from each subject. We measured the immunoreactive ET-1 in plasma by radioimmunoassay. The plasma level of ET-1 in migraine was 2.53 +/- 1.06 pg/ml. On the other hand, the level of ET-1 in the controls was 4.24 +/- 0.80 pg/ml. The ET-1 level in migraine was significantly lower than that in the controls (p < 0.002). We also measured the level of ET-1 in the cerebrospinal fluid (CSF). There was no significant difference between migraine (23.2 +/- 3.10 pg/ml) and the control group (20.85 +/- 3.20 pg/ml). In conclusion, the lower plasma level of ET-1 observed in the patients with migraine is consistent with the pathogenesis of migraine, further supporting the hypothesis that a lower ET-1 may be closely related to marked vasodilatation following constriction partly due to a deficiency of ET-1 for maintaining vasoconstriction.

Adolescent↗
PubMed1995

Effect of thyrotropin-releasing hormone (TRH) on cerebral blood flow in spinocerebellar degeneration and cerebrovascular disease.

The effect of TRH on cerebral blood flow in patients with spinocerebellar degeneration and cerebrovascular disease was investigated. Cerebral blood flow was measured by the 133Xenon arterial injection method before, and 30 min after, the intravenous administration of 1000 micrograms of TRH. TRH had no effect on mean arterial blood pressure in either group. In the spinocerebellar degeneration group, cerebral blood flow increased slightly after the injection of TRH, from 52.7 +/- 10.5 to 56.7 +/- 16.0 ml/100 g brain/min. In two patients with spinocerebellar degeneration, whose autonomic function was normal and whose brainstem structure appeared normal in the CT scan, cerebral blood flow increased from 54.8 to 66.4 ml (21.2%), and from 68.6 to 79.9 ml (16.5%), respectively. In the patients with cerebrovascular disease, cerebral blood flow did not change (49.7 +/- 10.8 ml before and 49.4 +/- 12.6 ml after TRH). Cerebral blood flow reportedly increases following an intravenous injection of TRH in animals, supposedly due to the activation of intrinsic cerebral vasodilative fibers situated in the submesencephalic brainstem region. Our results are consistent with this hypothesis and with the clinical finding that TRH especially improves ataxia in spinocerebellar degeneration where there is no pyramidal involvement or disorder of deep sensation.

Autonomic Nervous System↗
PubMed1994

A novel in vivo assay system for consecutive measurement of brain nitric oxide production combined with the microdialysis technique.

A novel spectrophotometric nitrite (NO2-)/nitrate (NO3-) assay system for a small quantity (5 microliter) of dialysate sample obtained by in vivo brain microdialysis was developed based on the diazotization reaction. The system has the advantage of in vivo consecutive measurement, high precision, good reproducibility, technical simplicity, relatively short resolution time (2.5-20 min), and wide availability. The NO3- level in the rat striatum was found to be 3 times higher than the NO2- level. A nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine methyl ester, reduced striatal NO2-/citrulline formation in a dose-related manner and increased arginine, indicating that the tissue NO2- level detected by this assay system adequately reflects the striatal NO synthase activity.

Amino Acid Oxidoreductases↗
PubMed1994

Modification of striatal arginine and citrulline metabolism by nitric oxide synthase inhibitors.

The effects of NG-substituted L-arginine (ARG) analogues on striatal ARG and citrulline (CIT) levels were investigated using in vivo microdialysis technique. A microdialysis probe was implanted into the striatum of anaesthesized Sprague-Dawley rats. Direct intrastriatal perfusion with 1 mM NG-nitro-L-arginine methyl ester (n = 8) increased striatal ARG release and decreased CIT release, suggesting suppressed NO synthase activity in the tissue. On the other hand, 1 mM NG-monomethyl-L-arginine (L-NMMA) (n = 6) evoked a persistent increase in both ARG and CIT. Considering that 4-320 microM L-ARG (n = 8) failed to increase CIT formation, CIT seems to be synthesized in the striatal tissue from L-NMMA by the enzyme that has been demonstrated in the kidney and aortic endothelium (NG,NG-dimethylarginine dimethyl-aminohydrolase).

Amino Acid Oxidoreductases↗
PubMed1994

Presynaptic glutamate receptors facilitate release of norepinephrine and 5-hydroxytryptamine as well as dopamine in the normal and ischemic striatum.

We investigated the effects of selective glutamate (Glu) agonists on the release of monoamine neurotransmitters and their implication in the enhanced monoamine release in cerebral ischemia. In the striatum of anesthetized Sprague-Dawley rats, in vivo microdialysis was performed and the release of excitatory amino acids (Glu and aspartate (Asp)) and monoamines (dopamine (DA), norepinephrine (NE) and 5-hydroxytryptamine (5-HT)) was measured by high-performance liquid chromatography with an electrochemical detector. (1) Forebrain ischemia by 4-vessel occlusion generated significant correlations between the Glu and Asp levels and the DA, NE and 5-HT levels (r = 0.922-0.967, P < 0.01, n = 6). (2) L-Glu and its selective agonists (N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) and kainate (KA)) evoked a simultaneous release of striatal DA, NE and 5-HT in a dose-dependent manner (P < 0.01, ANOVA, n = 8). The maximal monoamine release evoked by the Glu agonists showed different magnitudes in the order of DA >> NE > 5-HT (118-, 16- and 9-fold from the baseline levels by 62.5 mM L-Glu, respectively). Each Glu agonist exerted a different magnitude of transmitter release and the order of agonist efficacy was different among NE, 5-HT and DA release: AMPA = KA > L-Glu = NMDA for DA release, AMPA > L-Glu = NMDA = KA for NE release, and L-Glu = NMDA = KA = AMPA for 5-HT release.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Presynaptic ionotropic glutamate receptors modulate in vivo release and metabolism of striatal dopamine, noradrenaline, and 5-hydroxytryptamine: involvement of both NMDA and AMPA/kainate subtypes.

In order to explore further the presynaptic modulation of monoamine release by glutamatergic nerve fibers, we investigated the effects of selective agonists for ionotropic glutamate (GLU) receptors on striatal release of dopamine (DA), noradrenaline (NA) and 5-hydroxytryptamine (5-HT). In the striatum of anesthetized Sprague-Dawley rats, in vivo microdialysis was performed to measure the release of monoamines and metabolities, and also to administer GLU agonists locally in the tissue. L-GLU and its selective agonists (N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) and kainate (KA)) evoked simultaneous release of striatal DA, NA and 5-HT in a dose-dependent manner. Pretreatment with MK-801 (5 mg/kg i.p.), a noncompetitive NMDA receptor antagonist, selectively suppressed NMDA-evoked monoamine release. The rank order of GLU agonist efficacy in releasing monoamines was different among DA, NA, and 5-HTergic terminals: AMPA = KA > NMDA for DA release, AMPA > NMDA = KA for NA release, and NMDA = AMPA = KA for 5-HT release. In conclusion, presynaptic ionotropic GLU receptors exist extensively on monoaminergic terminals including not only catecholaminergic (DA and NA) but also indoleaminergic (5-HT) terminals in the rat striatum. Their subtypes include both NMDA subtype and AMPA/KA subtype, and show a differential distribution among these three monoaminergic terminals and a differential contribution to facilitating monoamine release.

Animals↗
PubMed1994

[Epidemiological analysis of deaths occurring while taking a bath].

An epidemiological analysis of deaths occurring while taking a bath was carried out in Tochigi Prefecture. Data concerning the numbers of deaths were obtained from the Tochigi Central Police Office. Long-term assessments from 1978 to 1992 were completed for a total number of 1,348 persons (793 men and 555 women). The annual number of deaths during taking a bath increased gradually from 43 in 1978 to 140 in 1992. Death occurred 1.43 times more frequently in males than in females. The number during summer was only one eighth that of the winter peak. In addition, the increase in mortality was proportional to age. The mortality figures per 100,000 were, 10 for 40-49 age group, 31 for 50-59, 79 for 60-69, 251 for 70-79 and 469 for those 80 and over. It is concluded that the number of deaths occurring while taking a bath has increased gradually in those 80 or over.

Adolescent↗
PubMed1993

Rheumatoid arthritis and B cell lymphoma with pathological changes of reactive histiocytosis.

A 67 year old woman with rheumatoid arthritis was admitted to hospital in acute renal failure. Her clinical features included increasing dyspnoea and oedema, and a computed tomogram of the abdomen showed a large mass in the retroperitoneum. Twenty six days later, she died, and a post mortem examination was carried out. The histological changes of the mass indicated B cell lymphoma of diffuse large cell type, with a reactive proliferation of erythrophagocytosing histiocytes. Immunocytochemical studies showed that the histiocytes were positive for CD-68 and lysozyme, but negative for S-100 protein. Such neoplastic B cell proliferation accompanied by activation of benign looking histiocytes with erythrophagocytosis is very rare.

Aged↗