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Biomedical subjects

M Endoh

Publications and source records attributed to M Endoh.

At least 253 records · Page 14Linked to original sources
PubMed1991

Homozygous C3 deficiency associated with IgA nephropathy.

A 23-year-old male patient with homozygous C3 deficiency who developed asymptomatic proteinuria and hematuria was reported. Renal biopsy disclosed typical IgA nephropathy with deposition of early- and late-complement components except for C3 deposition. C9 and membrane attack complex were detected in the glomeruli despite the absence of C3. It was suggested that there might be some unknown complement activation mechanism which does not require C3 component.

Adult↗
PubMed1991

Myocardial alpha 1-adrenoceptors mediate positive inotropic effect and changes in phosphatidylinositol metabolism. Species differences in receptor distribution and the intracellular coupling process in mammalian ventricular myocardium.

Species-dependent variations of myocardial alpha 1-adrenoceptor-mediated positive inotropic effects of epinephrine were assessed in relation to characteristics of alpha 1-receptor bindings and acceleration of phosphatidylinositol metabolism in the isolated rat, rabbit, and dog ventricular myocardium. Epinephrine in the presence of the beta-adrenoceptor antagonist bupranolol (10(-6) M) elicited a positive inotropic effect through activation of alpha 1-adrenoceptors in rat and rabbit, whereas in dog ventricular myocardium, bupranolol abolished the positive inotropic effect of epinephrine. [3H]Prazosin bound to membrane fractions derived from rat, rabbit, and dog ventricular muscle with high affinities in a saturable and reversible manner. In dog, Bmax and Kd values of alpha 1-adrenoceptor binding sites were identical to those in rabbit ventricular muscle. The Bmax value of alpha 1-adrenoceptors in rat ventricle was the highest, amounting to two to four times those in rabbit and dog. Epinephrine displacement curves for the specific binding of [3H]prazosin in the membrane fraction of these species showed high and low affinity sites with slope factors significantly less than unity, which were shifted to single low affinity sites with slope factors close to unity by addition of 5'-guanylylimidodiphosphate. Accumulation of [3H]inositol 1-phosphate [( 3H]IP1) in ventricular slices prelabeled with [3H]myo-inositol was increased by epinephrine in a time- and concentration-dependent manner in rat ventricular slices. [3H]IP1 accumulation likewise was facilitated by alpha 1-adrenoceptor stimulation in rabbit ventricular slices, whereas the extent of [3H]IP1 accumulation was much less than that in rat. In dog ventricular slices, [3H]IP1 was not accumulated by epinephrine. In rabbit papillary muscle, the time course of increase in contractile force induced by alpha-adrenoceptors coincided with the prolongation of the action potential duration with a similar time course, which is in strong contrast to previous findings in rat that the contractile response was dissociated from the electrophysiological response to alpha-adrenoceptor stimulation. The present results indicate that a wide range of variation of alpha 1-adrenoceptor-mediated regulation of myocardial contractility may be ascribed to different contributions of facilitatory as well as inhibitory regulatory processes that lead to intracellular Ca2+ mobilization subsequent to myocardial alpha 1-adrenoceptor activation among mammalian species.

Action Potentials↗
PubMed1991

Physiological and pathophysiological modulation of calcium signaling in myocardial cells.

The relationship between changes in intracellular Ca2+ transients and isometric contractions has been assessed in intact cardiac muscle preparations, superficial cells of which have been microinjected with the Ca(2+)-sensitive bioluminescent protein aequorin. Regulation of myocardial contractility by physiological and pathophysiological intervention is achieved by either (1) modulation of intracellular Ca2+ mobilization, or (2) modulation of Ca2+ sensitivity of myofibrils, or both. Regulation of contractility by changes in heart rate a well established frequency-force relationship that plays an important role in the cardiac pumping function in situ is mainly achieved by mechanism (1), other mechanisms becoming involved depending on the range of frequency of stimulation. The length-dependent regulation of contractility (length-tension relationship in vitro or Frank-Starling's law, or ventricular function curve in situ) is achieved essentially by mechanism (2). Catecholamines promote mechanism (1) through activation of beta- and/or alpha-adrenoceptors, alpha-adrenoceptor stimulation being much less effective than beta-stimulation in this respect. beta-Adrenoceptor stimulation decreases, while alpha-stimulation may increase the Ca(2+)-sensitivity of contractile proteins. Subsequent to exposure of muscle preparations to Ca2+ free solution, a prominent and reversible dissociation of force of contraction from Ca2+ transients was produced when the [Ca2+]0 was gradually returned to the level of the normal Krebs-Henseleit solution [( Ca2+]0 = 2.5 mM). The aequorin-injected multicellular intact myocardial cell preparation provides an excellent experimental paradigm through which to address the physiological, pharmacological and pathophysiological modulation of E-C coupling in mammalian cardiac muscle. The subcellular mechanism involved, especially in the pathophysiological modulation of Ca2+ signaling process in myocardial cells, awaits further study.

Animals↗
PubMed1991

Eosinophilic peritonitis responding to treatment with glycyrrhizin.

A 63-year-old man with diabetes mellitus for 15 years was admitted to our hospital in 1990 because of end-stage renal failure. Five days after beginning continuous ambulatory peritoneal dialysis (CAPD) he developed an eosinophilic peritonitis (EP). With protein loss in the dialysate and a decreased serum albumin level, the patient developed ankle edema. The patient was treated with glycyrrhizin, and his EP resolved. It is suggested that an allergic background may play an important role in the development of EP in patients on CAPD.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1991

No increase in antibodies to six food antigens in Japanese patients with IgA nephropathy.

It has been postulated that mucosa-related antigens are involved in the development of IgA nephropathy. The aim of this study was to elucidate whether food antigens have any relation to IgA nephropathy in Japan. Sera from 15 patients with IgA nephropathy and 15 healthy controls were examined using an enzyme linked immunosorbent assay (ELISA). IgG, IgA, and IgM antibody titers were measured against six food-derived antigens, i.e. rice, soy bean paste, soy sauce, egg yolk, egg white and gluten, all of which are frequently found in the ordinary Japanese diet. No significant differences between patients and controls were found. It was concluded that food antigens appear to have little, if any, relation to IgA nephropathy.

Egg Proteins↗
PubMed1991

[A case of post-traumatic medial longitudinal fasciculus syndrome].

Medial longitudinal fasciculus (MLF) syndrome recognized 2 days after a head injury is described. The patient was a 48-year-old man who had fallen from a ladder about 3m high. On his admission, scalp contusion on the left occipital area was noticed. Neurological examination revealed no neurological abnormalities except slightly disturbed consciousness. Plain skull X-ray films demonstrated a lineal skull fracture of the left occipital bone. Computed tomographic (CT) scans showed a slight subarachnoid hemorrhage within the bilateral sylvian fissures, but no parenchymal contusion in the brain stem was observed. On the 2nd day, when the patient regained full consciousness, impairment of adduction of the right eye and a fine nystagmus of the left eye on left lateral gaze were recognized. Convergence was intact. Right side MLF syndrome was diagnosed. This syndrome gradually disappeared followed by the initial improvement of adduction of the right eye, and the patient had completely recovered about 20 days after the head injury. Three major mechanisms leading to MLF syndrome caused by head injury are reported in the literature. They are: (1) primary brain stem injury, (2) secondary brainstem injury by trans-tentorial herniation, and (3) circulatory disturbance of perforating branches of the vertebro-basilar artery due to shearing force. In our case, the slightly disturbed consciousness at the time of the head injury indicates that this syndrome was not brought on by primary or secondary brain stem injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain Injuries↗
PubMed1991

Rheumatoid factors in patients with minimal change nephrotic syndrome.

Several immunological aberrations, especially T-cell abnormalities, have been shown to be involved in the development of the minimal change nephrotic syndrome (MCNS) although the responsible factors have not been identified. We studied rheumatoid factors (RF), thought to be a consequence of polyclonal B-cell hyperactivation, in sera from patients with MCNS using a sensitive fluorescence immunoassay (FIA). Significant increases of IgG and IgM RFs and marginal increase of IgA RF were observed during the nephrotic stages. Some patients still showed high titers of IgM RF in the early remission phases. The levels of RFs were normalized during complete remission. It was suggested that polyclonal B cell activation might be involved in the development of this disorder along with T cell abnormalities.

Adult↗
PubMed1991

Inotropic effects of endothelin on mammalian ventricular contractility.

Endothelin-1 elicited a concentration-dependent positive inotropic effect on the isolated rabbit, guinea pig, and rat, but not on the dog ventricular myocardium. The duration of isometric contractions was prolonged by endothelin-1 in a concentration-dependent manner, mainly by prolongation of relaxation time. Phorbol 12,13-dibutyrate (PDBu) (a tumor-promoting phorbol ester) inhibited the positive inotropic effect of endothelin-1, as well as myocardial alpha 1-adrenoceptor stimulation at low concentrations (10(-9) mol/l and above) without (10(-8) mol/l) or less (10(-7) mol/l) affecting the basal force of contraction, and the positive inotropic effect of beta-adrenoceptor stimulation. The present findings indicate that endothelin elicits a positive inotropic effect on mammalian ventricular myocardium, the characteristics of which are very similar to those of myocardial alpha-adrenoceptor stimulation.

Animals↗
PubMed1991

Preparation of specific antisera against antigens from pharyngeal cells in patients with IgA nephropathy.

Rabbit antisera were produced against antigens obtained from pharyngeal cells of patients with IgA nephropathy (IgAN). Extracts of pharyngeal cells from patients with IgAN were frozen and thawed, and the supernatants were cocultured with fibroblasts (Vero and Hel cells). Pieces of renal biopsy specimens of the same patients were sectioned and centrifuged. The supernatants which contained IgA were incubated with the fibroblasts, and were stained with FITC-labeled anti human IgA antisera. Two positive (A and B) and one control Vero cell lines were destroyed and centrifuged. The precipitates were injected into rabbits, and rabbit antisera (A, B and control) were produced. Renal tissues from patients with IgAN and proliferative glomerulonephritis without IgA deposition (PGN) were stained with the FITC-labeled antisera. Positive stainings with FITC-labeled antiserum A was observed in 87% and that with FITC-labeled antiserum B in 55% of the patients with IgAN. No positive staining was detected with FITC-labeled control antiserum. There was also no positive staining with these antisera in renal tissues with PGN. The immunological specificity of the antisera was evaluated. It was found that these antisera did not react with complements components or immunoglobulins. The above findings suggested that some antigens from pharyngeal cells were deposited in the glomeruli from IgAN patients.

Animals↗
PubMed1990

Differential effects of Ro 20-1724 and isobutylmethylxanthine on the basal force of contraction and beta-adrenoceptor-mediated response in the rat ventricular myocardium.

Effects of Ro 20-1724, a selective inhibitor of soluble cGMP-insensitive type IV phosphodiesterase, on the force and cAMP levels were compared with those of 3-isobutyl-1-methylaxanthine, a non-selective inhibitor, in the rat ventricular myocardium. Ro 20-1724 scarcely affected the basal force of contraction and cAMP levels, whereas it enhanced the positive intropic effect and cAMP accumulation induced by isoproterenol more effectively than 3-isobutyl-1-methylxanthine. These results imply that inhibition of the soluble cGMP-insensitive type IV PDE by Ro 20-1724 may be crucially involved in the regulation of myocardial contractility through the interaction with cAMP generation in the rat ventricular myocardium.

1-Methyl-3-isobutylxanthine↗
PubMed1990

The preferential inhibition of alpha 1- over beta-adrenoceptor-mediated positive inotropic effect by organic calcium antagonists in the rabbit papillary muscle.

Experiments were carried out to elucidate the mechanism that the positive inotropic effect mediated by alpha 1-adrenoceptors is more susceptible to organic calcium antagonists than the beta-adrenoceptor-mediated effect. Verapamil and diltiazem displaced the specific binding of [3H]prazosin to the membrane fraction derived from the rabbit ventricular myocardium, verapamil being about 70 times more potent than diltiazem. Nifedipine did not displace the binding. While these compounds suppressed the positive inotropic effect mediated via alpha 1-adrenoceptors in a concentration-dependent manner, there was no correlation between the potency of the compounds to displace the [3H]prazosin binding and to inhibit the alpha-mediated positive inotropic effect. The relative potency of three calcium antagonists to decrease the basal force of contraction and the alpha 1-mediated effect (of the same extent as compared to basal force of contraction) was consistent to each other. The positive inotropic effect mediated by beta-adrenoceptors was inhibited much less, and was enhanced by low concentrations of organic calcium antagonists. The differential action of calcium antagonists on the alpha- and beta-mediated positive inotropic effect was mimicked by lowering the extracellular calcium concentration to 1/2, 1/4 and 1/8 of that in normal Krebs-Henseleit solution (2.5 mmol/l). These results indicate that the alpha 1-adrenoceptor blocking activity does not play an essential role for the preferential inhibition of alpha-mediated positive inotropic effect by organic calcium antagonists. Difference in the subcellular mechanism involved in mobilization of intracellular Ca2+ subsequent to alpha 1- and beta-adrenoceptor activation may be responsible for the differential inhibitory action of calcium antagonists in the rabbit heart.

Animals↗
PubMed1990

Effects of a new 1,3-thiazole derivative ZSY-39 on force of contraction and cyclic AMP content in canine ventricular muscle.

A newly synthesized 1,3-thiazole derivative ZSY-39 increased the force of contraction in a concentration-dependent manner in association with elevation of tissue cyclic AMP levels in the isolated canine ventricular trabeculae electrically driven at 0.5 Hz at 37 degrees C. ZSY-39 shortened the duration of isometric contractions mainly by abbreviation of the relaxation time. The maximal response to and EC50 of ZSY-39 were 0.7 (isoproterenol = 1.0) and 4.6 x 10(-5) M. Bupranolol (3 x 10(-7) M) did not affect the positive inotropic effect of ZSY-39. The time course of increases in the force of contraction induced by ZSY-39 (10(-4) M) coincided with that of cyclic AMP accumulation. The concentration-response curve for the increase in the force of contraction produced by ZSY-39 was superimposable on that of the elevation of cyclic AMP levels. Carbachol (3 x 10(-6) M) shifted the concentration-response curve for the increase in force by ZSY-39 to the right and downward, and decreased the accumulation of cyclic AMP induced by ZSY-39 (10(-4) M). ZSY-39 (10(-5) M) enhanced significantly the positive inotropic effect of isoproterenol. The relationship between the force of contraction and cyclic AMP levels after the administration of ZSY-39 was not modified by the addition of carbachol or isoproterenol. These findings indicate that cyclic AMP plays an important role in the positive inotropic effect of ZSY-39 on canine ventricular muscle.

Animals↗
PubMed1990

Development of a cell culture assay for Bordetella parapertussis heat-labile toxin.

A cell culture assay for heat-labile toxin isolated from Bordetella parapertussis has been developed. In this assay, the ability of heat-labile toxin to induce contraction of vascular smooth muscle cells is measured. The method allows for detection of as little as 0.6 ng/ml of the toxin. The results obtained from this in vitro assay correlated well with those obtained with in vivo assays indicating that the cell culture assay may be a useful alternative to animal assays.

Animals↗
PubMed1990

Phorbol-12,13-dibutyrate antagonizes the alpha 1-adrenoceptor-mediated positive inotropic effect in the rabbit ventricular myocardium.

The phorbol ester phorbol-12,13-dibutyrate (PDBu) elicited a slight but significant positive inotropic effect (PIE) (10-100 nM) in the presence of a beta-adrenoceptor antagonist (+/-)-bupranolol (300 nM). PDBu (10-1000 nM) inhibited the alpha 1-adrenoceptor mediated PIE in a concentration-dependent manner, while beta-adrenoceptor-mediated PIE was not decreased by PDBu up to 300 nM. Thus, PDBu exerted a differential effect on alpha- and beta-adrenoceptor-mediated PIE, and was much more effective than 12-O-tetradecanoylphorbol-13-acetate (TPA) in antagonizing the alpha-adrenoceptor-mediated PIE. These findings imply that (1) certain subcellular process of myocardial alpha-adrenoceptor stimulation may be specifically antagonized by an activation of protein kinase C induced by PDBu or TPA; (2) there may be species difference in the response to activation of protein kinase C, which results in differential modulation of myocardial alpha 1-adrenoceptor-mediated regulation of contractility among different mammalian species.

Adrenergic alpha-Antagonists↗
PubMed1990

Rheumatoid factors and glomerulonephritis.

It is presently unknown whether rheumatoid factors have a pathogenic role in the development of various types of glomerulonephritis with immune deposits. Three isotypes of rheumatoid factors (RFs), which are autoantibodies to IgG, were measured using the solid-phase fluorescence immunoassay in sera from patients with diffuse proliferative lupus nephritis (DPLN), membranous lupus nephritis (MLN), IgA nephropathy (IgAN) and idiopathic membranous nephropathy (MN). RF activity of immunoglobulins deposited in the glomeruli from these patients was also studied by examining the binding of the FITC-conjugated human IgG and Fc portion of IgG to the glomeruli of renal biopsy specimens. IgG, IgA and IgM RFs were significantly increased in sera from patients with DPLN, and the increase was significantly lower in patients with MLN, IgAN and MN. Human IgG bound to immunoglobulin on the glomeruli only in DPLN, but not in MLN, IgAN or MN. The Fc portion of IgG was demonstrated to be involved in this reaction. It was suggested that RFs and IgG may play a major role in immune deposits on the glomeruli in DPLN and may be involved in the development of DPLN; however, this is not likely in MLN, IgAN or MN.

Antigen-Antibody Complex↗
PubMed1990

Inhibition of heat-labile toxin from Bordetella parapertussis by fatty acids.

The ability of heat-labile toxin (HLT) from Bordetella parapertussis to induce skin lesions in guinea pigs was found to be inhibited by lipids isolated from skin layers of adult mice, which are refractory to the lesion-inducing activity of HLT. These lipids were identified as linoleic and oleic acids. Other long-chain unsaturated fatty acids were also found to inhibit HLT; however, fatty alcohols, neutral lipids, phospholipids, cholesterol, prostaglandin, and leukotriene had no measurable effects on HLT action. The data presented in this report indicate that the ability of HLT to induce skin lesions in animals may depend, at least in part, on the free fatty acid content of the skin layer.

Animals↗
PubMed1990

Effects of exogenous agents on the action of Bordetella parapertussis heat-labile toxin on guinea pig skin.

Injection of sonic extracts of Bordetella parapertussis into the shaved backs of guinea pigs produced hemorrhagic necrosis, which previously has been attributed to the action of heat-labile toxin. As heat-labile toxin was purified from this crude mixture, its ability to induce hemorrhagic lesions decreased significantly. However, ischemic lesions were apparent after injection of the purified toxin. These lesions, while not hemorrhagic in nature, were marked by erythema surrounded by a region in which the ischemia was apparent. Exogenous agents were found to alter the nature of the skin lesion induced by heat-labile toxin. The lipid A portion of endotoxin in combination with heat-labile toxin caused hemorrhagic lesions surrounded by a ring of ischemia, whereas bovine serum albumin increased the area of erythema. While the nature of lesions induced by heat-labile toxin was affected by exogenous agents, the diameter of ischemia produced by the toxin was found to be independent of the presence of these agents and was linear with toxin dose. These results indicate that induction of hemorrhagic necrosis may not be a reliable indicator of heat-labile toxin activity. Instead, measurement of the ischemic lesion produced by heat-labile toxin may be a useful assay for the toxin.

Animals↗