Two-dimensional echocardiographic demonstration of flail pulmonic valve due to infective endocarditis.
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Biomedical subjects
Publications and source records attributed to K Matsui.
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The possibility of preservation and restoration of antigenicity of some antigens in paraffin-embedded tissue was evaluated by direct immunofluorescent technique on deparaffinized sections. Fixation with 96% ethanol-1% acetic acid, 10% neutral buffered formalin and p-formaldehyde was useful for the preservation of tissue antigens and immune deposits, whose antigenicity could be easily restored by trypsin digestion. Neutral buffered formalin was also a satisfactory fixative in immunofluorescent staining on lymphocyte/plasma cell-bound immunoglobulins. Fixation with alcohol-Bouin's fluid showed contrast results; feasible for staining of cell-bound immunoglobulins, but poor for that of glomerular immune deposits. After papain digestion, BSA and lysozyme, antigens of immune complexes, were easily detected in experimental chronic serum sickness glomerulonephritis. Pepsin was more efficient than trypsin in restoring the antigenicity of renal tissue antigens such as fibronectin and polyantigenic basement membrane, but the brush border antigen of the proximal renal tubules was frail to the pepsin digestion. In general, the enzymatic digestion time necessary for the restoration of antigenicity was in parallel with fixation time. Results obtained have shown that deparaffinized sections could be used as satisfactory substrate for immunohistochemistry when proper fixation and efficient proteolytic enzymatic pretreatments were performed.
Using the two-stage coronary ligation method, first described by Harris, (1950), anti-arrhythmic effects (AAE) of (-)-carnitine chloride (LCC) and acetyl (-)-carnitine chloride (ALCC) were studied in conscious unrestrained dogs in comparison with those of disopyramide (D). Two-stage ligation of the coronary artery resulted in a significant decrease in the myocardial free carnitine content. Intravenous administration of LCC (300 mg kg-1) and D (5 mg kg-1) suppressed the ventricular arrhythmia induced by coronary ligation after 24 hours. ALCC (300 mg kg-1) was found to be less potent. An improvement of the mitochondrial function (respiratory control index (RCI) and oxidative phosphorylation rate (OPR) ) was noted with LCC and ALCC and there was a linear correlation between AAE expressed as reduction of arrhythmic ratio and improvement in the OPR, whereas there was no improvement in mitochondrial function after D. Plasma carnitine concentration was increased after administration of LCC, attaining the value of around 8 mM at 10 min after 300 mg kg-1. At 60 min, the plasma carnitine concentration was still about half as high as at 10 min. After ALCC, both acetyl carnitine and free carnitine were found in the plasma. The concentration of the former was decreased after attaining a peak value of around 0.2 mM at 10 min, while the plasma concentration of free carnitine was gradually increased. The anti-arrhythmic effects of LCC and ALCC were ascribed to the improvement of mitochondrial oxidative phosphorylation, while effects other than the improvement of the mitochondrial activity were suggested as mechanisms of anti-arrhythmic effects of D.
Infusion of oxytocin into one vertebral artery of anesthetized dogs did not alter plasma vasopressin concentration, blood pressure or heart rate. However, there was a significant (p less than 0.01) increase in plasma renin activity (PRA; delta = 7.6 +/- 2.3 ng/ml X h). A 35% hemorrhage caused blood pressure to fall by 9.4 +/- 4.0 mm Hg (p less than 0.01) and PRA to rise by 8.8 +/- 2.7 ng/ml X h (p less than 0.05). In 8 dogs that were subjected to a similar hemorrhage and that also received an intravertebral infusion of oxytocin, blood pressure was maintained and PRA increased by 14 +/- 4.3 ng/ml X h (p less than 0.05). Heart rate and plasma vasopressin responses were similar in both hemorrhage groups. The results indicate that oxytocin prevented the fall in blood pressure associated with a hemorrhage, possibly by increasing renin release.
The cardiovascular and vasopressin-releasing effects of vertebral artery, carotid artery and intravenous (i.v.) infusions of lysine vasopressin (150 microU/kg X min) were studied in anesthetized dogs. Vertebral and carotid artery infusions of lysine vasopressin led to similar decreases in cardiac output as i.v. infusions. Heart rate, however, decreased to a greater extent with vertebral and carotid artery infusions of lysine vasopressin than i.v. infusions. There were no changes in either mean arterial blood pressure or the plasma vasopressin concentration. The results indicate that peripheral vasopressin: has a central effect to reduce heart rate; has a peripheral effect on the heart to reduce cardiac output, and probably does not feed back to inhibit its own release.
In order to investigate the role of central alpha 1- and alpha 2-adrenoceptors in the control of vasopressin (ADH) release and the cardiovascular system, norepinephrine (NE) (1.4 microgram/kg), methoxamine (1.4 microgram/kg), yohimbine (60 micrograms/kg), and prazosin (40 micrograms/kg) were administered via the cerebral ventricles in urethane-chloralose-anesthetized dogs after morphine sedation (n = 42). In the control study 0.9% saline was administered. NE resulted in a significant fall in blood pressure, heart rate, and ADH release. Methoxamine tended to activate the cardiovascular system, but did not affect the release of ADH significantly. Prazosin decreased blood pressure significantly with a significant rise in heart rate and ADH release. Pretreatment with prazosin did not block significantly the effect of NE on blood pressure, heart rate, and ADH release. Yohimbine did not affect the cardiovascular system and ADH release significantly. Pretreatment with yohimbine completely blocked the effect of NE on ADH release, and brought about a slight rise in blood pressure and heart rate. In none of the experiments could changes in ADH release be attributed to changes in plasma osmolality. These results indicate that central alpha 1-adrenoceptors might act to activate the cardiovascular system, but have no effects on ADH release in anesthetized dogs. On the other hand, central alpha 2-adrenoceptors might act to reduce ADH release and to depress the cardiovascular system.
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In order to investigate the role of ADH and the renal handling of sodium and water in patients with idiopathic edema, 21 patients were subjected to acute oral water load tests. Although a normal water diuresis was observed in al patients in supine posture, it was markedly impaired in upright posture with significant decreases in sodium, free water, and osmolar clearances. In particular, two patients exhibited the continuous production of concentrated urine after the water load in upright posture. The fractional reabsorption of sodium at the proximal tubules was significantly increased in upright posture, while the glomerular filtration rate did not change significantly. The constricting of both legs with elastic bandages tended to improve the water diuresis in upright posture, suggesting that the pooling of blood into the lower legs might be contributing to the formation of idiopathic edema. The patients showed normal osmoregulation of ADH release in supine, but not in upright posture: the suppression of ADH release in upright posture was only transient or incomplete despite a sufficient fall in plasma osmolality following the water load. Thus, both an increase in renal sodium reabsorption and the insufficient suppression of ADH release in upright posture might contribute to the retention of body fluid in patients with idiopathic edema.
Using tumour cell lines derived from human bone tumours, specific binding sites for epidermal growth factor (EGF), a potent growth stimulator in many tissues, and its effect on synthesis of prostaglandin (PG) E2, a potent bone-resorbing factor, by cultured osteosarcoma cell line were studied. Three tumour cell lines, one osteosarcoma (HOSO) and two giant cell tumours of the bone (G-1 and G-2), all possessed specific binding sites for 125I-labelled EGF: the apparent dissociation constant was approximately 4-10 X 10(-10) M and the maximal binding capacity was 50 000-80 000 sites/cell. EGF had no mitogenic effect in these cell lines. However, these cell lines did not have specific binding sites for 125I-labelled parathyroid hormone (PTH) or calcitonin. HOSO line produced and secreted PGE2 into medium, while no significant amount of PGE2 was demonstrated in G-1 or G-2 line. EGF significantly stimulated PGE2 production in HOSO line in a dose-dependent manner (0.5-50 ng/ml); its stimulatory effect was completely abolished by indomethacin, an inhibitor of PG biosynthesis. Exogenous PGE1 significantly stimulated cyclic AMP formation in HOSO line, whereas PGF2 alpha, PTH, calcitonin, or EGF had no effect. None of these calcium-regulating hormones affected cyclic AMP generation in either G-1 or G-2 line. These data indicate that human bone tumour cells have specific EGF receptors unrelated to cell growth, and suggest that EGF may be involved in bone resorption through a PGE2-mediated process in human osseous tissues.
Mouse monozygotic twins were produced by bisection of the compacted morulae and transfer of the pairs of half-embryos after culture in vitro. The compacted morulae (about 16 cells) were microsurgically bisected, using a fine glass needle attached to a micromanipulator, without any supporting micro-instruments, after pretreatment for zona-softening and decompaction. About 80% of the morulae were bisected without visible cell damage. After 20 h in culture, the half-embryos were classified morphologically as eu-blastocysts, pseudo-blastocysts, or trophectodermal vesicles or non-integrated forms. After culture of 131 pairs of bisected morulae, 75 (57.3%) pairs of eu-blastocysts, 20 (15.3%) pairs comprising a eu-blastocyst and pseudo-blastocyst, and 9 (6.9%) pairs of pseudo-blastocysts, were obtained. The pseudo-blastocysts were considered to be derived from half-morulae in which some blastomeres were destroyed or dissociated as a result of micromanipulation. From 30 pairs of eu-blastocysts transferred to 21 recipients, 5 twin fetuses on Day 17 (18 pairs/9 recipients) and 3 twin male young (12 pairs/12 recipients) were obtained. Survival rate of the twin-embryo pairs was 27.8% at autopsy and 25.0% at term. None of the 20 pairs of pseudo-blastocysts transferred to 10 recipients gave rise to normal conceptuses.
Antiataxic mechanisms were investigated in Rolling mouse Nagoya (RMN). The present study was to elucidate the influence of dopaminergic (pimozide, apomorphine) and cholinergic (atropine, physostigmine) drugs on the antiataxic effect of TRH. The degree of ataxic gait and spontaneous motor activities in RMN were measured by the open field method and ANIMEX-II Pretreatment with pimozide and apomorphine had no influence on the antiataxic effects of TRH, while pretreatment with physostigmine suppressed these effects and in contrast, with atropine, increased then. The increase of spontaneous motor activities after TRH injection was antagonized by pretreatment with pimozide and physostigmine, but accentuated by pretreatment with atropine. These results may indicate that the antiataxic effects of TRH are, at least partially, mediated by the cholinergic mechanism.
Valiolamine, a new aminocyclitol has been isolated from the fermentation broth of Streptomyces hygroscopicus subsp. limoneus and its structure has been determined to be (1(OH),2,4,5/1,3)-5-amino-1-C-(hydroxymethyl)-1,2,3,4-cyclohexanetetr ol. Valiolamine has more potent alpha-glucosidase inhibitory activity against porcine intestinal sucrase, maltase and isomaltase than valienamine, validamine and hydroxyvalidamine which were reported as building blocks of validamycins and microbial oligosaccharide alpha-glucosidase inhibitors. In addition, valienamine, validamine and hydroxyvalidamine have been isolated from the fermentation broth.
The enzymatic cleavage of C-N linkage in the degradation of validamycin A by Flavobacterium saccharophilum was examined using N-p-nitrophenyl derivatives of validamine and valienamine as synthetic model substrates for validoxylamine A. Incubation of N-p-nitrophenylvalidamine with the membrane fraction from the organism led to formation of N-p-nitrophenyl-3-ketovalidamine, and succeeding cleavage of C-N linkage. As the products of the cleavage step, one was identified as p-nitroaniline and another keto compound could not be purified enough because of its instability. However, on the basis of its hydrogenation products, the structure of the keto compound could be established as 5D-(5/6)-5-C-(hydroxy-methyl)-2,6-dihydroxy-2-cyclohexen-1-one. The same experiment was carried out with N-p-nitrophenylvalienamine. In this case, N-p-nitrophenyl-3-ketovalienamine could be isolated as an intermediate but the desired keto compound from the cleavage step could not be isolated because of its instability. The participation of two enzymes, that is, a dehydrogenase and a C-N lyase on the cleavage of C-N linkage was assured, and moreover, the analysis of its products, together with those of the previous studies allow us to propose a degradation pathway of validamycin A by Flavobacterium saccharophilum.
Ceftriaxone (Ro 13-9904, CTRX), a newly developed third-generation cephem antibiotic, reportedly has an antibacterial spectrum of wide-range and shows a much greater activity than cefazolin especially against Gram-negative bacteria and satisfactory effectiveness against anaerobes. In the gyneco-obstetric infections, the relation between the level in the intrapelvic organs and MIC is an important subject in many respects. The levels in the blood and each tissue determined in 54 cases, as presented in Fig. 2, show that a high concentration can be maintained for a long time. In particular the half-life time in the uterine artery and cubital vein was 8.2 hours and 7.8 hours, respectively, which was longer than that of any other existing antibiotics. This fact suggests that CTRX exhibits sufficient efficacy when administered intravenously even in a small dosage of 1 g in the present study. The clinical efficacy was good or above in all the 7 cases treated. There was neither clinical adverse reaction nor laboratory test abnormality found during and after the administration in any of the 54 cases in the fundamental study and 7 cases in the clinical study. It is suggested from the above-mentioned results that CTRX is an unprecedentedly useful antibiotic with an antibacterial spectrum of wide-range.
Pleural effusion is a common complication in patients with malignant neoplasm. A randomized controlled study of intrapleural instillation of Adriamycin (control group, 30 patients) and Adriamycin Nocardia rubra cell wall skeleton (N-CWS group, 26 patients) with tube thoracostomy was performed in 55 patients with malignant pleural effusion due to primary lung cancer. The response rates for control of pleural effusion were 73.4% in the N-CWS group and 46.1% in the N-CWS group. These results suggest that intrapleural instillation using a combination of anti-cancer agent and immunopotentiator is an effective treatment for malignant pleurisy. Cardiac tamponade secondary to cancer is a life-threatening complication requiring immediate treatment. Twenty-four patients with malignant pericardial effusion were treated by intrapericardial instillation of anti-cancer drugs, such as Carbazilquinone, Mitomycin-C or ACNU, with pericardial drainage. The range of survival time from the instillation of anti-cancer drug was 3-365 days (average days). In only 4 patients, reaccumulation of pericardial effusion was recognized. There were no serious complications with this procedure. It was considered that local instillation of anti-cancer agents with pericardial drainage was a useful therapeutic modality for malignant pericarditis.
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