Visualization of mitochondria and some other cytoplasmic structures in hematoxylin-eosin stained sections by fluorescence microscopy.
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Biomedical subjects
Publications and source records attributed to K Adachi.
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It has been suggested that various factors related to dilated cardiomyopathy (DCM) may concern its onset and/or progression. This study was performed to clarify whether these factors contribute different clinical and morphological characteristics. Subjects were 39 patients with DCM, consisting of 28 men and 11 women whose average age was 46.5 years. The subjects were divided into five groups; namely, the Familial, Myocarditic, Alcoholic, Hypertensive, and Unknown Groups. Clinical parameters including past history, blood pressure, chest radiographs, electrocardiograms, echocardiograms and left ventricular end-diastolic pressures (LVEDP) were evaluated. Morphology of right ventricular endomyocardial biopsy specimens was evaluated in terms of hypertrophy, disarrangement, fibrosis, degeneration, endocardial thickening, interstitial changes, and types of fibrosis. The results were as follows: The Familial Group was characterized by the onset at younger age, highly elevated LVEDP, a lack of myocardial hypertrophy, and proliferation of small vessels. The Myocarditic Group was characterized by the onset at young age, elevated LVEDP, severe fibrosis showing a plexiform pattern in more than half of the patients, cellular disarrangement, and cellular infiltration. The Alcoholic Group showed possible improvement clinically and fatty infiltration in half of the patients. The Hypertensive Group was characterized by high prevalence of a previous alcohol intake, high diastolic blood pressure on admission, clinical improvement, and myocardial hypertrophy with a mild degree of perivascular fibrosis. From these findings, it is thought that each factor related to DCM offers a somewhat different clinical and histological profiles and that these factors may play an important role in the onset and/or progression of DCM. Furthermore, it is highly suggestive that specific therapy against these factors or the removal of these factors is especially necessary for favorable long-term prognosis of DCM.
The influences of IAP on the residual pancreatic endocrine function and carbohydrate metabolism after extensive pancreatectomy in the rat were studied with oral glucose tolerance test (OGTT), arginine tolerance test (ATT), and measurement of hepatic glycogen, and hepatic glycolytic enzyme activity, and histological examination, etc. Wistar male rats weighing around 300 g were divided into the groups with IAP treatment and without it, and in the group with IAP treatment IAP 10 micrograms/kg was administered without anesthesia via the tail vein. In each group 60 and 90% pancreatectomies were performed in accordance with Scow's method, and the simple laparotomy group was used as control. Slight abnormality of glucose tolerance was shown in 60% pancreatectomy. The abnormality became worse with time in 90% pancreatectomy. Glucagon secretion was not damaged markedly even after extensive pancreatectomy. IAP stimulated IRI secretory response and improved glucose tolerance in 60% pancreatectomy group. IAP showed no effect in 90% pancreatectomy group. IAP did not stimulate IRG secretory response after pancreatectomy. Hepatic glycolytic enzyme activity was high in the group with IAP treatment. From the above observation, it has been suggested that IAP may be indicated for the abnormal carbohydrate metabolism after pancreatectomy, if pancreatectomy is not too extensive.
Asymmetrical hybrid hemoglobins formed in mixtures of Hb A and Hb S, Hb F and Hb S, Hb S and Hb York(beta 146 His----Pro), and Hb A and Hb York were separated by high performance liquid chromatography on cation and anion exchange columns under anaerobic conditions. The ratio of the hybrid hemoglobin to the total mixture was consistently lower than that theoretically expected and decreased with longer elution times. The hybrid tetramer appears to be unstable even under anaerobic conditions and dissociates into alpha beta dimers. The time course of dissociation of the hybrid hemoglobins was determined by varying the separation programs and thus separating the hybrid hemoglobin at different elution times. The rate of the dissociation of the hybrid hemoglobins studied follows first order kinetics. The lines representing the time course of dissociation of hybrid hemoglobins were extrapolated to time 0 to determine the fraction of the hybrid hemoglobin in the mixture prior to separation. The values obtained for equimolar mixtures of Hb A and Hb S and Hb York and Hb S or Hb A were in agreement with the expected theoretical value (50%). In contrast, the value obtained for hybrid hemoglobin FS was slightly less (about 40%). AY and SY hybrid hemoglobins dissociated into dimers at a considerably faster rate than did AS and FS hybrid hemoglobins, possibly because of the mutation at the beta 146-position in hybrid hemoglobins containing alpha beta Y dimers. This mutation hinders the formation of salt bridges that normally stabilize the "T" quaternary conformation. Since such hybrid hemoglobins have a partial "R" conformation even when deoxygenated, their rate of dissociation to dimers is expected to increase.
The effects of nicardipine on sodium-calcium exchange activity of cardiac sarcolemma-enriched vesicles isolated from the rat heart were examined. Sodium-loaded, sarcolemma-enriched vesicles, when exposed to a medium containing 40 microM CaCl2, exhibited about 5 nmoles Ca2+/mg protein of the maximal calcium uptake; the initial rate was 21 nmoles Ca2+/mg protein/min. The calcium uptake was dependent on the extravesicular concentration of calcium ion. Nicardipine at concentrations of 0.1 to 10 microM depressed the rate of calcium uptake activity by 60-90%. The isolated membrane vesicles preloaded with Ca2+ showed a calcium efflux activity, when exposed to a medium containing sodium ion. The rate of calcium efflux was 2.5 nmoles Ca2+/mg protein/min, when measured in a medium containing 6.5 mM NaCl. The efflux rate was facilitated with increased concentrations of sodium ion in the medium. About 75% of the preloaded calcium in the vesicles was released within 3 min of incubation. The rate of calcium efflux was stimulated in the presence of 0.1 to 10 microM nicardipine (2.5- to 4-fold increase). The present results suggest a possible action of nicardipine on the sodium-calcium exchange mechanism at cardiac sarcolemmal sites.
Asymmetrical cross-linked FS (alpha 2 gamma beta s) hybrid hemoglobin (Hb FS-fumarate) was prepared by reacting mixtures of hemoglobins F and S with double-headed aspirin, bis(3,5-dibromosalicyl) fumarate. When the molar ratio of hemoglobin to the cross-linking agent was 1 to 2 in a 1:1 FS mixture, the relative ratio of the products, cross-linked hemoglobins F (Hb F-fumarate), FS (HB FS-fumarate), and S (Hb S-fumarate), was 1.0:2.6:2.0, in contrast to a 1:2:1 ratio of cross-linked hemoglobins A, AS, and S in a 1:1 AS mixture. These results suggest that the fumaryl group reacts differently with Hb F, Hb FS and Hb S, and that the difference could be attributed to the difference in the structure in the vicinity of the EF6 Lys of non alpha-chains. The oxygen-binding properties of Hb F-fumarate, Hb FS-fumarate, and Hb S-fumarate were similar, except that the n-value of Hb F-fumarate was slightly lower than n-values of Hb S-fumarate and Hb FS-fumarate. Kinetic studies on aggregation showed that the addition of Hb FS-fumarate to unmodified Hb S did not affect the delay time prior to aggregation, but did increase the total turbidity. Electrophoretic and densitometric scanning analysis of the aggregate phase of this mixture showed the fraction of Hb FS-fumarate to be 19%. Hb F-fumarate's effect on the delay time is concentration-dependent; the greater the concentration of Hb F-fumarate, the longer the delay time. The turbidity after aggregation of the mixture of Hb S and Hb F-fumarate was much less than that of Hb S and Hb FS-fumarate. However, the fraction of Hb F-fumarate in the aggregate phase was 19%, which is similar to that of Hb FS-fumarate. These data suggest that Hb F and FS hybrid hemoglobin cannot participate in nuclei formation, but can participate in aggregation after sufficient amounts of nuclei are formed from Hb S, and that increased levels of Hb F do not have an inhibitory effect on the formation of nuclei but on the growth of aggregates.
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The effect of intraluminal bile on the well-known feedback regulatory mechanism of exocrine pancreatic secretion exerted by intraluminal trypsin was investigated in conscious rats with pancreatic, biliary and duodenal fistulae. The stimulated pancreatic enzyme secretion caused by diversion of bile-pancreatic juice from the intestine was apparently suppressed by intraduodenal reintroduction of pancreatic juice or bile-pancreatic juice, while it was slightly suppressed by intraduodenal reintroduction of bile. Although additional reintroduction of bile did not alter the already suppressed pancreatic enzyme secretion by the presence of pancreatic juice in the intestine, diversion of bile stimulated the suppressed pancreatic enzyme secretion by intraluminal bile-pancreatic juice. Infusion of sodium taurocholate into the duodenum with diversion of bile-pancreatic juice effectively inhibited pancreatic enzyme secretion. The inhibitory effect seemed to be dependent on the concentration of taurocholate infused into the duodenum. The results suggest that bile and bile acid have an important role in the feedback regulatory mechanism of pancreatic enzyme secretion, at least partly directly inhibiting the secretion.
The concentrations of immunoreactive thyrotropin-releasing hormone (ir-TRH) in the brain of patients with olivoponto-cerebellar atrophy (OPCA) were studied. Three patients with OPCA and 8 non-central nervous system degenerative diseases were subjects in this study. Ir-TRH concentration in the brain was measured by radioimmunoassay. Ir-TRH was present in all parts of the dissected brain tissues (hypothalamus, frontal lobe, cerebellar cortex, olivary n., dentate n. and caudate n.) of patients with OPCA and non-central nervous system degenerative diseases. Ir-TRH concentration in the brain of case 1 and 2 was lower in the cerebellar cortex and olivary n., in contrast, ir-TRH concentration in case 3 was higher in the dentate n. The regions and the severity of pathological changes were different in each case of OPCA and changes in ir-TRH concentration in the brain did not always correlate with the severity of pathological changes. These findings suggest that changes in ir-TRH concentration in the brain of patients with OPCA may differ in each case, and may play some pathophysiological role in OPCA.
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We have studied NK cell activity and numbers in the peripheral blood obtained from patients with Behcet's disease and from normal healthy controls. NK cell activity in the peripheral blood of patients in the clinically-active stage of Behcet's disease was significantly lower than that of patients in the inactive stage and normal controls. In contrast, it was observed that the actual number of NK cells was markedly increased in the peripheral blood of patients with active disease. The addition of alpha-interferon (INF-alpha) to these cells showed significant augmentation of NK cell activity. These results suggest that the patients with active Behcet's disease lack a factor which activates NK cells.
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An autopsy case of an advanced form of hypertrophic cardiomyopathy (HCM) showing marked fibrosis with intramural small arterial abnormalities is presented in this report. A 52-year-old woman, who had a positive family history of HCM, was admitted because of palpitations. The chest roentgenogram showed a mildly enlarged cardiac silhouette and the electrocardiogram revealed abnormal Q waves and R wave and T wave abnormalities. The echocardiogram revealed hypokinesis with thinning of the interventricular septum and the anterior wall of the left ventricle. Percutaneous right ventricular endomyocardial biopsies demonstrated moderate interstitial fibrosis with small arterial thickening. At necropsy, the anterior and posterior walls of the left ventricle and the interventricular septum were markedly thinned and showed a massive transmural fibrosis. Moreover, the intramural small arteries, 50-300 microns in diameter, showed marked intimal and medial hypertrophy with proliferation of elastic fibers and smooth muscle cells. From these findings, it is suggested that this was originally a case of HCM which progressed to a decompensated stage because of the abnormal intramural small arteries. The significance of small arterial lesions in HCM is discussed.
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