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Biomedical subjects

M Matsuda

Publications and source records attributed to M Matsuda.

At least 1,009 records · Page 56Linked to original sources
PubMed1987

Effect of calcium antagonist and agonist on free fatty acid liberation in the ischemic brain of rats.

Using an experimental model of global ischemia of the brain in rats, we have shown that a Ca2+ antagonist nicardipine attenuates, and a Ca2+ agonist YC-170 accelerates, the liberation of free fatty acids in the ischemic whole brain. The effects of YC-170 were negated by the previous administration of an adequate dose of nicardipine. This is the first report on the action of a Ca2+ agonist on the metabolism of the brain, and the results seem to provide supportive evidence for the role of Ca2+ in ischemic injury of the brain.

Animals↗
PubMed1987

Ca2+ antagonist and protection of the brain against ischemia. Effects of nicardipine on free fatty acid liberation in the ischemic brain in rats.

Using a model of global cerebral ischemia in rats, we examined the effects of a dihydropyridine Ca2+ antagonist, nicardipine, on the liberation of free fatty acids (FFAs). After decapitation of the animals, FFAs showed a rapid progressive increase for a whole experimental period of up to 60 minutes without reaching a plateau. Nicardipine in a dosage of 1 mg/kg effectively attenuated the liberation of FFAs, particularly that of arachidonic acid which is known as the precursor of prostaglandins, thromboxanes, and leukotrienes. The FFAs of the brain have been known as one of the biochemical markers that indicate ischemic damage of the brain cell membrane. The results of the present study support a possible protective effect of Ca2+ antagonist against cerebral ischemia.

Animals↗
PubMed1987

Genetic characterization of JC virus Tokyo-1 strain, a variant oncogenic in rodents.

The genome DNA of JC virus Tokyo-1 strain [JCV(Tokyo-1)], a variant oncogenic in rodents, was molecularly cloned directly from the brain of a Japanese patient with progressive multifocal leukoencephalopathy and from tissue culture, and the restriction enzyme cleavage pattern and regulatory sequences were determined. The restriction pattern of the cloned JCV(Tokyo-1) DNA was different from those of JCVs previously reported in the United States and Germany. Also, the arrangement of the regulatory sequence was unique to this strain. Thus JCV(Tokyo-1) can be classified as a new subtype. The relationship between the restriction pattern and the regulatory sequence of JCV(Tokyo-1), and its characteristic oncogenicity, is discussed.

Animals↗
PubMed1987

Lysis of autologous tumor cells by peripheral blood lymphocytes treated with interleukin 2 in patients with renal cell carcinoma.

Peripheral blood lymphocytes derived from patients with renal cell carcinoma were stimulated with interleukin 2 and tested in a 4-hour 51chromium-release cytotoxicity assay against autologous cultured tumor and myeloid K562 cells. Of 23 patients autologous tumor lysis of more than 0 per cent was observed in 20 (range 5.3 to 82.8 per cent) and more than 10 per cent lysis was noted in 16. Since no significant correlation between the degree of cytotoxicity and the pathological findings of tumor stage, grade, cell type or lymphocyte infiltration in the tumor was found, it was impossible to predict from the pathological findings which tumor could be lysed by peripheral blood lymphocytes treated with interleukin 2. Comparison of natural killer cell activity against K562 of freshly prepared peripheral blood lymphocytes to that of interleukin 2-treated lymphocytes revealed significant augmentation from 23.6 +/- 9.7 to 65.2 +/- 29.1 per cent. From the kinetics study the lysis of autologous tumor cells was detectable on day 2 of interleukin 2 exposure and the peak activity was observed on day 5. A similar trend was noted in regard to K562 cell lysis. Measurements of peripheral blood lymphocyte subsets with monoclonal antibodies and argon ion laser flow cytometry resulted in a significant decrease of cells positive for OKT 4 (helper/inducer) and a significant increase of cells positive for OKT 8 (suppressor/cytotoxic) and Leu 7 (natural killer) by interleukin 2 treatment. A cold target cell inhibition test was performed in 2 patients with unlabeled autologous tumor and K562 cells as cold inhibitors. In 1 patient unlabeled K562 completely inhibited the tumor lysis but in 1 complete inhibition by autologous tumor and incomplete blockade by K562 were found. From this observation we concluded that peripheral blood lymphocytes treated with interleukin 2 lysed not only autologous tumor cells but also K562. Our results demonstrate that adoptive immunotherapy with peripheral blood lymphocytes activated by interleukin 2 in patients with renal cell carcinoma could be appropriate as a therapeutic procedure.

Adult↗
PubMed1987

Treatment of the West syndrome with high-dose pyridoxal phosphate.

Fifteen (12.7%) among 118 cases of the West syndrome were effectively treated by high-dose pyridoxal phosphate (PAL-P). 1) Clinical seizures were completely suppressed in 12 cases with PAL-P alone, and in 3 cases by an addition of PAL-P to the previously poorly-effective regimen. At the follow-up, 12 cases have continued to be free from seizures, while two cases relapsed into the Lennox-Gastaut syndrome, and one died. 2) Electroencephalographically hypsarhythmia disappeared by PAL-P in all 15 effective cases. 3) Effective daily dose of PAL-P was 30 to 400 mg. 4) Notably, PAL-P was effective even in the cases with obvious organic brain pathology, such as tuberous sclerosis, porencephaly, holoprosencephaly, postmeningitis, besides 5 idiopathic cases. 5) Efficacy of PAL-P was significantly higher in idiopathic cases than symptomatic cases; 35.7% vs 9.6%. 6) Response to PAL-P was not predictable by any laboratory data nor clinical features. 7) Prognosis of PAL-P responsive cases was favorable; as many as 6 cases developed normally among 14 cases followed-up. Treatment with a high-dose PAL-P should be tried in all cases of the West syndrome at first.

Administration, Oral↗
PubMed1987

A case of replantation of a completely amputated digit after 26 hours of warm ischemia.

A seven-year-old-boy received a digit replantation after 26 hours of warm ischemia and showed good recovery of motor and sensory functions. In the case reported, replantation was performed after a much longer ischemic time than had been considered an indication for the procedure in previous reports. Successful replantation and revascularization can thus be achieved, even in cases of extensive warm ischemia.

Amputation, Traumatic↗
PubMed1987

Digital replantations distal to the distal interphalangeal joint.

Microvascular replantations of digits distal to the distal interphalangeal (DIP) joint were reviewed in 33 digits of 29 patients. Twenty-five digits were completely amputated and eight were incompletely amputated. Ten of 33 replants failed and 23 digits survived. Even without venous reconstruction, good results were obtained in Zone I. Of eight completely amputated digits in Zone 1 in which venous reconstruction was not performed, seven digits survived. Of four completely amputated digits in Zone 2 without venous reconstruction, all became necrotic. In digits followed for six months or more after surgery, 11 of 13 replantations showed good functional recovery. Two digits that developed paresthesia after replantation were functionally useless. Seven digits without bilateral digital nerve reconstruction were reviewed six months or more after surgery. Sensory recovery was good in the digital phalanx; the factor impeding functional recovery was the development of paresthesia. Replanted digits distal to the DIP joint are thus satisfactory in both function and cosmesis, even if digital nerves have not been reconstructed. The replantation of such digits should be considered.

Amputation, Traumatic↗
PubMed1987

Fibrinogens Kawaguchi and Osaka: an amino acid substitution of A alpha arginine-16 to cysteine which forms an extra interchain disulfide bridge between the two A alpha chains.

Structural analyses of fibrinogens from patients with congenital dysfibrinogenemia, designated as fibrinogens Kawaguchi and Osaka, have been performed to identify the difference responsible for the lack of fibrinopeptide A release. For the structural studies, a new strategy was employed. Amino acid sequence analysis of one of the lysyl endopeptidase-peptides isolated from the abnormal fibrinogens indicated that in both fibrinogens, arginine-16 of the A alpha chain had been replaced by cysteine. To characterize the chemical nature of the sulfhydryl group of cysteine-16, a tryptic peptide containing cysteine-16 of the A alpha chain was prepared from intact fibrinogen Kawaguchi. The amino acid composition and the molecular weight determination of this aberrant peptide revealed that it was a dimeric NH2-terminal peptide corresponding to residues 1-19 derived from the abnormal A alpha chain. These results indicate that the half-cystine at position 16 in the abnormal A alpha chain forms an intramolecular disulfide bridge with the same residue in the other abnormal A alpha chain and that fibrinogen Kawaguchi is a homo dimer composed of two identical abnormal halves.

Amino Acid Sequence↗
PubMed1987

Developmental change in the amount of polysialosyl glycopeptides isolated from the rat brain.

Polysialosyl glycopeptides were coisolated with glycosaminoglycans by Pronase digestion of the whole brains of perinatal rats and could be separated from known glycosaminoglycans by two-dimensional electrophoresis on cellulose acetate film. The polysialosyl glycopeptides could not be obtained from fetal rat brain on day 13 of gestation, but began to be detected on day 14. The amount of polysialosyl glycopeptides was estimated from the dye concentration of the Alcian blue-stained spot in the electrophoretogram. The glycopeptide content increased almost linearly, on the basis of brain DNA, up to 10 days after birth. Thereafter, the content decreased rapidly, and hardly any polysialosyl glycopeptides could be isolated from the brain at approximately 30 days. This developmental change may be involved in morphogenesis and maturation of the brain. The polysialosyl glycopeptides could be isolated from the cerebellum, from the cerebrum, or from the brainstem of the neonatal rat. However, each region of the brain had a postnatal developmental change in glycopeptide content different from those of the other regions.

Animals↗
PubMed1987

Collagen and elastin fibers in human pulmonary alveolar mouths and ducts.

To provide a quantitative basis for the understanding of the mechanical properties of the lung tissue, the morphology of the pulmonary alveolar ducts was studied and the dimensions of the collagen and elastin fiber bundles in the alveolar mouths were measured. Statistical data are presented in this report. It was found that the probability frequency functions of the widths of both the collagen and elastin fibers are skewed to the right, but the fourth roots of the widths are normally distributed. Hence, knowing the mean and standard deviation of (width)1/4, the probability of finding fiber bundles of width D is known. On the other hand, we already know the analytic expressions of the strain energy per unit length of fibers of given width. With the probability distribution of width and an estimation of the length of alveolar mouths, the strain energy of the alveolar mouths can be computed. Then the contribution of the alveolar mouths to the stress in the lung parenchyma due to any strain can be obtained by a differentiation of the strain energy function with respect to that strain.

Autopsy↗
PubMed1987

Quantitative analysis of contraction band and coagulation necrosis after ischemia and reperfusion in the porcine heart.

To assess the importance of contraction band necrosis (CBN) in reperfusion, CBN, coagulation necrosis (CN), and infarct size, expressed as CBN + CN, were quantitatively analyzed in 25 porcine hearts without collateral circulation. The left anterior descending coronary artery was ligated for 20, 30, 60, and 120 min and then reperfused for 8 hr (groups 1 to 4, respectively). Five hearts were not reperfused (group 5). The areas of CBN and CN were traced at a magnification of X 100 under an inverted microscope and quantified with use of an image analyzer. There was no change in hemodynamics with either occlusion or reperfusion. Regional myocardial blood flow, measured by the generated hydrogen gas clearance method, decreased to almost zero after occlusion but recovered during reperfusion. Percent of risk area infarcted in groups 1 to 4 was 0 +/- 0%, 11 +/- 7%, 80 +/- 9%, and 96 +/- 2%, respectively, and the percent of risk area infarcted in group 4 was the same as that in hearts subjected to permanent occlusion (95 +/- 3%). The percent area of CBN was 100 +/- 0% in group 2, 68 +/- 11% in group 3, 2 +/- 1% in group 4, and 2 +/- 2% in group 5. In group 3, the inner third of the ischemic left ventricular wall showed CN and the middle and outer third CBN. These findings show that in pig hearts without collateral circulation, the transmural infarct, two-thirds of which is occupied by CBN, is evident even when reperfusion is achieved after 1 hr occlusion. Therefore, protection against CBN might reduce infarct size after reperfusion.

Animals↗
PubMed1987

Quantitative analysis of narrowings of intramyocardial small arteries in normal hearts, hypertensive hearts, and hearts with hypertrophic cardiomyopathy.

To clarify the pathophysiologic role of intramyocardial small artery (IMSA) diseases in hypertrophied hearts, narrowings of the IMSA were quantitatively evaluated in 39 autopsied hearts, 10 from patients with typical hypertrophic cardiomyopathy (HCM), four from patients with HCM showing features mimicking dilated cardiomyopathy (DCM-like HCM), 10 from patients with hypertension, and 15 from normal adults. The relations of narrowings of the IMSA to myocytic hypertrophy, myocardial fiber disarray, and fibrosis were also examined. The external caliber and the ratio of the luminal area to the total vascular area (percent luminal area, % lumen) were calculated by an image analyzer in 85 to 203 IMSAs from each patient. The external calibers of the IMSAs were similar among groups of hearts with HCM, hypertensive hearts, and normal hearts but were greater in those with DCM-like HCM. The mean % lumen of the IMSAs was similarly reduced in the hearts with HCM (29 +/- 5% in the ventricular septum and 31 +/- 5% in the left ventricular free wall) and in hypertensive hearts (30 +/- 8% and 31 +/- 7%) compared with that in normal hearts (40 +/- 5% and 38 +/- 5%) and was the lowest in the ventricular septum of hearts with DCM-like HCM (17 +/- 3%). The mean % lumen of the IMSA was inversely correlated with heart weight (r = -.59), the mean size of myocytes (r = -.66 in the ventricular septum, r = -.63 in the free wall), and percent fibrotic area in the septum (r = -.68). The mean % lumen values of the IMSAs in the tissues with and without disarray in the hearts with HCM were similar. Thus IMSA disease is of pathophysiologic importance in patients with HCM, DCM-like HCM in particular, or with hypertension.

Adult↗
PubMed1987

Quantitative analysis of infarct size, contraction band necrosis, and coagulation necrosis in human autopsied hearts with acute myocardial infarction after treatment with selective intracoronary thrombolysis.

To assess the importance of contraction band necrosis (CBN) in patients with acute myocardial infarction (AMI) treated with selective intracoronary thrombolysis, CBN, coagulation necrosis, and infarct size (expressed as CBN + coagulation necrosis) were analyzed quantitatively in 16 autopsied hearts. Intracoronary thrombolysis was performed from 2 to 6 hr after the onset of AMI, and the time from the onset of AMI to death was 7 to 168 hr. Cineangiography revealed no evidence of good collateral circulation in any of the patients. The 16 patients were classified into three groups: six patients with successful thrombolysis (100% to 99% stenosis, group I), five patients with unsuccessful thrombolysis (100% to 100%, group II), and five patients with 99% stenosis before thrombolysis (group III). Among the three groups, there were no significant differences in the time from the onset of AMI to thrombolysis, the time from the onset of AMI to death, the cause of death, or the degree of collateral circulation. The percentage of the risk area involved by the infarct in group I (82 +/- 6%) was similar to that in group II (80 +/- 11%). Infarct size was not reduced in group I because collateral circulation was not good and because the degree of recanalization after thrombolysis was 1%. However, the percentage of the infarct area with CBN was significantly higher in group I (20 +/- 9%) then in group II (3 +/- 3%). This finding shows that diffuse CBN occurred after reperfusion in patients with AMI treated with thrombolysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Limitation of coronary thrombolysis: experimental study of reperfusion after ischemia.

Contraction band necrosis (CBN), coagulation necrosis (CN) and infarct size, expressed as CBN + CN, were quantitatively analyzed in 15 pig hearts without collateral circulation. The left anterior descending coronary artery was ligated for 60 and 120 minutes and then reperfused for eight hours (group 1 and 2, respectively). Five hearts were not reperfused (group 3). There was no change in hemodynamics with either occlusion or reperfusion. Regional myocardial blood flow, measured by the generated hydrogen gas clearance method, decreased to almost zero after occlusion but recovered during reperfusion. Percent infarct area of the perfused area in group 1, 2 and 3 were 80 +/- 9, 96 +/- 2% and 95 +/- 3%, respectively. The percent area of CBN was 68 +/- 11% in group 1, 2 +/- 1% in group 2 and 2 +/- 2% in group 3. We conclude that in pig hearts without collateral circulation, the transmural infarct, two-thirds of which is occupied by CBN, is evident even in reperfusion following one-hour occlusion. Therefore, in patients with acute myocardial infarction, coronary thrombolysis should be performed within one hour after the onset of the infarction to reduce the infarct size.

Animals↗
PubMed1987

Idiopathic giant cell myocarditis accompanied by asymmetric septal hypertrophy.

We report a case of idiopathic giant cell myocarditis accompanied by asymmetric septal hypertrophy. A 64-year-old woman was admitted because of dyspnea. There was no past history of hypertension or heart disease and no family history of hypertrophic cardiomyopathy. Laboratory examinations revealed general inflammatory changes and mild elevation of serum CK and GOT. The clinical course was fulminant and the patient died of heart failure one day after admission. On autopsy, asymmetric septal hypertrophy was revealed and the pathohistological examination revealed panmyocarditis with mononuclear cell infiltration, interstitial edema, necrosis of myocytes, and giant cells. The inflammatory changes were most severe in the ventricular septum with asymmetric septal hypertrophy. The extent of myocardial fibers with disarray was within normal limits. Thus, the asymmetric septal hypertrophy appeared to be due to marked interstitial edema and inflammatory cell infiltration in the septum. This case suggests that myocardial inflammation and edema may cause thickening of the ventricular wall during the course of acute myocarditis.

Cardiomegaly↗
PubMed1987

Pathogenetic role of myocardial fiber disarray in the progression of cardiac fibrosis in normal hearts, hypertensive hearts and hearts with hypertrophic cardiomyopathy.

To define the pathogenetic role of myocardial fiber disarray in the progression of cardiac fibrosis, the percent area of fibrosis in tissue with disarray was compared with that in tissue without disarray. Thirty autopsied hearts, 10 from patients with hypertrophic cardiomyopathy, 10 from patients with hypertension and 10 from normal adults, were studied. The percent areas of fibrosis in tissues with and without disarray were significantly different (p less than 0.01) among hearts with hypertrophic cardiomyopathy (12.6 +/- 4.0 and 8.2 +/- 3.3%), hypertensive hearts (6.6 +/- 3.6 and 2.5 +/- 1.4%) and normal hearts (2.8 +/- 1.2 and 1.0 +/- 0.4%). The percent area of fibrosis in tissue with disarray was greater than in that without disarray in all 3 groups and the ratios of these percentages were similar in the 3 groups: 2.9 +/- 4.2 in hypertrophic cardiomyopathy 2.5 +/- 1.7 in hypertensive hearts and 2.5 +/- 1.8 in normal hearts. The conclusions are: 1) disarray promotes fibrosis to a similar degree, not only in hypertrophic cardiomyopathy, but also in hypertensive hearts and normal hearts; 2) the increased level of fibrosis in hearts with hypertrophic cardiomyopathy and in hypertensive hearts, together with widespread fibrosis in hearts with hypertrophic cardiomyopathy in particular cannot be explained by disarray alone.

Cardiomegaly↗
PubMed1987

Morphological features of hypertrophic cardiomyopathy with congestive heart failure and a small left ventricular cavity.

To clarify the morphologic basis of marked congestive heart failure in cases of hypertrophic cardiomyopathy with a small left ventricular cavity, the size of myocytes, the extent of myocardial fiber disarray and fibrosis were quantitatively evaluated in two autopsied cases. Compared with the control hypertrophic cardiomyopathy, both cases had larger myocytes and less fibrosis, and one of them had markedly extensive myocardial fiber disarray. Probably, the hypertrophy of the myocytes or myocardial fiber disarray or both rather than myocardial fibrosis are important in the pathogenesis of severe congestive heart failure in these cases.

Adult↗