Search PubMed⌕ Search

Biomedical subjects

H Kido

Publications and source records attributed to H Kido.

At least 163 records · Page 9Linked to original sources
PubMed1992

Anti-glycoprotein IIb/IIIa autoantibodies are reversibly internalized into platelets in idiopathic (autoimmune) thrombocytopenic purpura.

We used flow cytometry to investigate the binding of platelet-binding IgG (PBIgG) to unfixed platelets in idiopathic thrombocytopenic purpura (ITP), including that of anti-glycoprotein (GP) IIb/IIIa antibodies. Anti-GPIIb/IIIa antibodies were detected in 13/64 ITP patients using antigen-capture ELISA and immunoblotting. When unfixed platelets were incubated with ITP plasma, the PBIgG level was significantly higher than after incubation with normal plasma. When 1 microM ADP was added to unfixed platelets, which were incubated with ITP plasma and washed, the PBIgG level increased additively. GMP-140 is a constituent of platelet alpha-granules, and a monoclonal antibody directed against this protein showed weak binding to platelets after 1 microM ADP stimulation. The increase of PBIgG produced by ADP was significantly greater when ITP plasma positive for anti-GPIIb/IIIa antibody was used compared with that obtained using antibody-negative ITP plasma. This increase of PBIgG was markedly inhibited by the removal of extracellular calcium with EDTA or the dissociation of the GPIIb/IIIa complex by EDTA treatment at 37 degrees C. These results suggest that anti-GPIIb/IIIa autoantibodies are internalized by unfixed ITP platelets and stored somewhere other than the alpha-granules. This stored antibody pool can be reversibly redistributed on the platelet surface by weak stimulants such as ADP and a functional GPIIb/IIIa complex appears to be necessary for this to occur.

Adolescent↗
PubMed1992

Biomodulators of glucocorticoid: amplifiers and suppressors of glucocorticoid action.

We have found several compounds that specifically modulate the action of glucocorticoid in vivo and in vitro without themselves having any glucocorticoid-like action and have proposed the concept of "Glucocorticoid Action Biomodulators". These biomodulators consist of "Glucocorticoid Sensitivity Amplifier" (GSA), "Glucocorticoid Potency Amplifiers" (GPAs), and suppressors of glucocorticoid action. GSA increased the incorporation of glucocorticoid into the liver and its binding to cytosol receptor without changing the total receptor concentration in liver cytosol and the equilibrium constant of the glucocorticoid binding reaction. GPAs, potent activators of protein kinase C, markedly enhanced the glucocorticoid action and the glucocorticoid action was inhibited by the inhibitors of protein kinase C. H-7, an inhibitor of protein kinase C, inhibited the translocation of glucocorticoid-receptor complex into nuclei without affecting the extent of phosphorylation of glucocorticoid receptor. These findings suggest that GPA(s) and the suppressors modulate some protein(s) which regulates the translocation of glucocorticoid receptor into nuclei.

Animals↗
PubMed1992

[Analysis of adhesive proteins on the surface of platelets from the patients with lung cancer: studies in histological type and clinical stage].

Flow cytometry was used to detect platelet-associated fibrinogen (PA-Fbg), platelet-associated fibronectin (PA-FN) and platelet-associated thrombospondin (PA-TSP) on the surface membrane of platelets and plasma (P)-TSP in 30 patients with lung cancer (16 case of adenocarcinoma and 14 of squamous cell carcinoma). ELISA was used to analyze beta-TG and PF4. In the lung cancer group, beta-TG and PF4 were higher than those of a normal control group. PA-Fbg values were correlated with beta-TG and PF4 values. Each adhesive protein had a higher value in the patient than in the normal control group, and the degree of the increase was related to the progression of clinical disease stage. In the squamous cell carcinoma group, the P-TSP value was significantly elevated. Platelet size increased as the clinical stage of the disease progressed. These results suggest the following: 1. An increase in PA-Fbg can indicate the presence of activated platelets. 2. In patients with lung cancer, activated platelets appear in the blood, and their numbers increase as the clinical stage of the disease progresses. 3. Differences in histologic type led to differences in binding adhesive protein.

Adenocarcinoma↗
PubMed1991

Anti-aldosteronergic effect of torasemide.

The diuretic actions of torasemide and furosemide were studied in normotensive rats and in deoxycorticosterone acetate (DOCA)-saline-loaded hypertensive rats. Torasemide (0.3-3 mg/kg) and furosemide (3-30 mg/kg) had a dose-dependent and significant diuretic action in normotensive rats. Potassium retention was only observed in the case of torasemide. Torasemide also had a dose-dependent and significant diuretic action in DOCA-saline-loaded hypertensive rats, whereas furosemide did not. Higher doses of torasemide (10 mg/kg) and furosemide (100 mg/kg) increased both plasma renin activity and aldosterone concentration in normotensive rats in a similar manner. In vivo aldosterone receptor binding was determined to test the possible anti-aldosteronergic effect of torasemide. Torasemide inhibited the binding of aldosterone to its receptor in the cytoplasmic fraction of rat kidney in a dose-dependent manner, while furosemide produced no effect. These results suggest strongly that an anti-aldosteronergic action of torasemide contributes to producing less kaliuresis.

Administration, Oral↗
PubMed1991

Purification and characterization of N-acyl-D-glutamate deacylase from Alcaligenes xylosoxydans subsp. xylosoxydans A-6.

The purification and properties of N-acyl-D-glutamate deacylase from the cell extracts of Alcaligenes xylosoxydans subsp. xylosoxydans A-6 were studied. The two active fractions (peaks I and II) were obtained by a Mono Q column chromatography. The predominant enzyme (peak I) has been purified, 1960-fold to homogeneity and characterized. The enzyme was a monomer with a molecular weight of 59,000. The optimum pH and the isoelectric point were 8.0 and 5.5, respectively. The enzyme catalyzed the hydrolysis of N-acyl derivatives of D-glutamate. The Kms for N-acetyl, N-butyryl and N-propionyl derivatives of D-glutamate were 0.129, 0.066 and 0.01 mM, respectively.

Alcaligenes↗
PubMed1991

A membrane-bound metallo-endopeptidase from rat kidney hydrolyzing parathyroid hormone. Purification and characterization.

A metallo-endopeptidase, which appears to be an integral membrane protein of rat kidney, was purified to homogeneity by a series of standard chromatographic procedures. This enzyme significantly hydrolyzed human parathyroid hormone [hPTH(1-84)] and a synthetic substrate Suc-Leu-Leu-Val-Tyr-Mec (Suc = succinyl, Mec = 4-methyl-coumarinyl-7-amide). The purified enzyme had apparent molecular masses of 250 kDa on gel filtration, and 88 kDa and 245 kDa on sodium dodecyl sulfate/polyacrylamide gel electrophoresis under reducing and non-reducing conditions, respectively. Its pH optimum for activity was 8.0-8.5 and its isoelectric point was pH 4.9. Its activity was inhibited by EDTA, EGTA and o-phenanthroline, but not by phosphoramidon. The metal-depleted enzyme was reactivated by the addition of metal ions. The enzyme was also inhibited by chymostatin and eglin C, and by thiol compounds. Of the synthetic substrates examined, the enzyme hydrolyzed only Suc-Leu-Leu-Val-Tyr-Mec, one of the synthetic substrates for alpha-chymotrypsin. It did not hydrolyze synthetic substrates with less than four amino acid residues with tyrosine in the P1 position. The enzyme hydrolyzed hPTH and reduced hen egg lysozyme but did not hydrolyze azocasein or [3H]methyl-casein. NH2-terminal amino acid sequence analyses of the degradation products of hPTH(1-84) and reduced hen egg lysozyme by the purified enzyme revealed that the enzyme preferentially cleaved these peptides at peptide bonds flanked by hydrophilic amino acid residues. Amino acid analyses showed that the main degradation products of PTH were hPTH(17-29), hPTH(30-38) and hPTH(74-84). The ability of the enzyme to hydrolyze peptide bonds flanked by hydrophilic amino acid residues and its inability to degrade azocasein distinguish it from several other kidney endopeptidases reported, such as endopeptidase 24.11 and meprin.

Amino Acid Sequence↗
PubMed1991

Tryptase TL2 in the membrane of human T4+ lymphocytes is a novel binding protein of the V3 domain of HIV-1 envelope glycoprotein gp 120.

A novel membrane-bound serine esterase in cultured human T4+ lymphocytes, recently purified and named tryptase TL2, binds specifically to the external envelope protein gp 120 of HIV-1, interacting with its V3 domain. This binding was selectively blocked by inhibitors of tryptase TL2 with a GPCR sequence in their reactive site, synthetic peptides corresponding with the sequences of the V3 domains of various HIV-1 strains with the GPGR sequence, and antibody against tryptase TL2, or neutralizing antibody against the V3 domain of HTLV-IIIB. These findings suggest that tryptase TL2 is a binding protein of the V3 domain of HIV-1 envelope glycoprotein.

Amino Acid Sequence↗
PubMed1991

Phosphoramidon inhibits the conversion of intracisternally administered big endothelin-1 to endothelin-1.

It is suggested that endothelin-1 (ET-1), a potent vasoconstrictor peptide, is involved in the pathogenesis of cerebral vasospasm following subarachnoid hemorrhage (SAH). We examined the effects of intracisternal administration of big ET-1 on the cerebral arteries in the absence or presence of pretreatment with phosphoramidon, an inhibitor of ET converting enzyme, in anesthetized dogs. After intracisternal administration of big ET-1 (10 micrograms/dog), the caliber of the basilar artery on the angiogram was decreased to about 59% of the control. This was accompanied by a marked increase in immunoreactive ET in the cerebrospinal fluid. Systemic arterial pressure was markedly elevated following big ET-1 injection. All changes induced by big ET-1 were effectively prevented with phosphoramidon. These data suggest that intracisternally administered big ET-1 is converted to ET-1 and that the generated ET-1 produces cerebral vasospasm and hypertension. A phosphoramidon-sensitive metalloproteinase appears to contribute to this conversion.

Animals↗
PubMed1991

Microparticle generation during in vitro platelet activation by anti-CD9 murine monoclonal antibodies.

We used flow cytometry and two anti-CD9 murine monoclonal antibodies (NNKY1-19, MALL13) to investigate the glycoprotein composition and the potential functions of microparticles (MP) released by platelets exposed to these antibodies in vitro. NNKY1-19 produced aggregation with characteristics similar to those noted in previous reports. The action of MALL13 on platelets in platelet-rich plasma (PRP), however, differs from that of other anti-CD9 antibodies. The normal fluctuation in the MALL13-induced change in optical density disappeared when complement was present. MALL13-induced effect for platelet in PRP was not inhibited by preincubation with monoclonal anti-GPIIb/IIIa antibody, but was inhibited in washed platelets (WP). Furthermore, following MALL13 stimulation in PRP platelets, the amount of buffer LDH markedly increased and electron microscopy findings showed vacuoles appearing inside the platelets. These results suggest that MALL13 has at least two effects on platelets that differ for PRP platelets and WP. The number of MP released was increased by the addition of anti-CD9 antibodies. MP surfaces were found to be rich in CD9 protein. MALL13 stimulation lead to a significant increase in the binding of C1q and C3 to platelets and caused the production of MP to occur more rapidly than it did the exposure of fibrinogen binding sites in the presence of complement. The analysis of the relationship of MP to anti-CD9 monoclonal antibody may be useful in the investigation of the relationship between platelet function and coagulation regulation.

Antibodies, Monoclonal↗
PubMed1991

Antiplatelet autoantibody-related microparticles in patients with idiopathic (autoimmune) thrombocytopenic purpura.

We used flow cytometry to detect antiplatelet antibody-related microparticles (MP) in 56 patients with idiopathic thrombocytopenic purpura (ITP). We measured MP in platelets following various types of stimulation in two experimental systems. In one system washed platelets were incubated with normal serum which included the complement system, and in the other, washed platelets were incubated with Tyrode's buffer. There were no differences between the two measurement systems in the degree of increase in MP using various agonists. An increase in MP using ITP plasma was found in 12 out of 56 patients. In particular, four patients showed a significant increase in MP in washed platelets (WP) plus serum. Furthermore, the increase in platelet-associated IgM (PAIgM) was significant in these patients. There was also a definite positive correlation between PAIgM and the percentage of MP of WP plus serum. On the other hand, no specificity for MP formation with anti-GPIIb/IIIa or anti-GPIb autoantibodies was observed. IgM antibody-related MP appear to exist in some patients with ITP.

Adolescent↗
PubMed1991

Phosphoramidon prevents cerebral vasospasm following subarachnoid hemorrhage in dogs: the relationship to endothelin-1 levels in the cerebrospinal fluid.

There is increasing evidence that the conversion of big endothelin-1 (big ET-1) to endothelin-1 (ET-1) is specifically inhibited by the metalloproteinase inhibitor phosphoramidon. We investigated the effect of phosphoramidon on delayed cerebral vasospasm from subarachnoid hemorrhage (SAH) using a two-hemorrhage canine model. The magnitude of the vasospasm and the drug effect were determined angiographically. On SAH Day 7, diameter of the basilar artery decreased to about 55% of the control value obtained before SAH (on Day 0). Immunoreactive ET (IR-ET) in the cerebrospinal fluid (CSF) significantly increased after SAH (on Day 7). The intracisternal pretreatment of phosphoramidon potently suppressed the decrease in diameter of the basilar artery after SAH, i.e., observed decrease was only about 20%, compared with the value before SAH. In the phosphoramidon group, IR-ET in CSF markedly increased (on SAH Day 2), but the increased levels of IR-ET significantly declined on SAH Day 7. These results clearly indicate that phosphoramidon effectively prevents delayed cerebral vasospasm. Whether the prevention is due to the inhibition of conversion of big ET-1 to ET-1 is now under study.

Animals↗
PubMed1991

H-7 reduces the nuclear binding of [3H]dexamethasone in rat liver slices but does not affect the phosphorylation of glucocorticoid receptor.

The effect of 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7), an inhibitor of protein kinase C, on the nuclear binding of [3H]dexamethasone and on the phosphorylation of glucocorticoid receptor was studied in rat liver slices to ascertain the role of protein kinase C in the expression of glucocorticoid action. H-7 reduces the nuclear binding of [3H]dexamethasone in rat liver slices. It does not affect the extent of phosphorylation of glucocorticoid receptor both in the absence or in the presence of glucocorticoid. These findings indicate that protein kinase C may be involved in the nuclear binding of glucocorticoid receptor but does not directly influence the receptor phosphorylation.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1991

New monoclonal anti-human Fc gamma receptor II antibodies induce platelet aggregation.

We developed two new monoclonal antibodies, designated NNKY3-2 and NNKY4-7, that recognized a 40-kD platelet protein. They appeared to be monoclonal anti-Fc gamma receptor II (Fc gamma RII) antibodies from the results of flow cytometric binding inhibition studies using another monoclonal anti-Fc gamma RII antibody (2E1). The addition of NNKY3-2 or NNKY4-7 to platelet-rich plasma (PRP) led to a typical aggregation pattern preceded by a lag phase, but their addition to washed platelets did not induce aggregation. The aggregation of PRP by these antibodies was inhibited by prostaglandin E1 (PGE1) or staurosporine (protein kinase C inhibitor), whereas it was only slightly affected by a monoclonal anti-GPIIb/IIIa antibody or Arg-Gly-Asp-Ser. Furthermore, these antibodies induced the aggregation of washed platelets plus normal serum, but not that of washed platelets plus heat-treated serum (destruction of complement activity). These results suggest that NNKY3-2 or NNKY4-7-induced aggregation involves an unusual pathway independent of fibrinogen, and that the important factor is the participation of complement. NNKY3-2 and NNKY4-7 may be useful to study the relationship between autoantibodies, the Fc receptor, and complement in idiopathic thrombocytopenic purpura.

Adenosine Diphosphate↗
PubMed1991

Effects of clomipramine on the concentrations of catecholamines, indoleamines and their metabolites in 11 rat brain regions.

The effects of clomipramine (CMP) treatment on the brain concentrations of catecholamines, indoleamines and their metabolites were evaluated in 11 rat brain regions. An acute CMP treatment (15 mg/kg) reduced only the 5-hydroxyindole-3-acetic acid (5HIAA) concentrations in all regions. A long-term CMP treatment (14 days, 10 mg/kg/day) decreased the concentrations of dopamine (DA), 5-hydroxytryptamine and 5HIAA in the mesencephalon, and increased the DA concentrations in the hippocampus. In comparison with the values for the long-term treated rats, an acute injection of CMP (15 mg/kg) after a long-term treatment increased the norepinephrine concentrations in the hypothalamus and amygdala, and the concentrations of DA, 3,4-dihydroxyphenylacetic acid and homovanillic acid in the basal ganglia. On the other hand, it failed to decrease the 5HIAA concentrations in the basal ganglia, frontal cortex, hypothalamus, cerebellum, pons + medulla oblongata, and mesencephalon.

Animals↗
PubMed1991

Usefulness of the newly proposed International Classification of Epilepsies, Epileptic Syndromes, and Related Seizure Disorders (1989): a trial on adult patients in a neuropsychiatric clinic.

The utility of the "International Classification of Epilepsies, Epileptic Syndromes, and Related Seizure Disorders," proposed by ILAE in 1989, was investigated in a neuropsychiatric clinic with a patient population numbering 300. Two hundred and three patients (67.7%) had localization-related epilepsies (LRE), including one idiopathic case. Sixty-six patients (22%) had generalized epilepsies, 50 idiopathic, 2 Lennox-Gastaut syndrome, and 14 symptomatic. Thirty-one patients (10.3%) with generalized tonic-clonic seizures occurring only during sleep had the epilepsies undetermined whether they are focal or generalized. In the symptomatic LRE cases, 34 cases could not be classified, and 7 of the cases with frontal lobe epilepsies were difficult to subtype. Eleven of the symptomatic LRE cases had some independent seizures, multiple foci in surface EEGs and were intractable. These cases may be defined as "multifocal epilepsies."

Adult↗
PubMed1991

A case of epilepsy characterized by spike-wave stupor followed for long period.

A 34-year-old housewife with nonconvulsive status epilepticus was followed up for 20 years since the initial fit. She maintained some contact with reality during the stupor and recalled the episode to some extent, while the EEG showed continuous spike-wave complexes. During the clinical course, the main type of seizures was spike-wave stupor, of which the maximum frequency was several times a week in the hospital and the duration was many minutes to several hours, and also secondarily generalized convulsive seizures occurred approximately once a month. The lasting control of spike-wave stupor was not achieved in spite of the various medications for the long follow-up period. The ictal EEGs of spike-wave stupor always showed the frontal origin. The meaning of the term "nonconvulsive status epilepticus" in this case was briefly discussed.

Adult↗
PubMed1991

Analysis of idiopathic thrombocytopenic purpura patients with antiglycoprotein IIb/IIIa or Ib autoantibodies.

We analyzed the immunological characteristics of patients with idiopathic thrombocytopenic purpura (ITP) and antiglycoprotein (GP) IIb/IIIa or GPIb autoantibodies. Among 101 ITP patients, 32 had anti-GPIIb/IIIa and 19 had anti-GPIb autoantibodies. Thrombocytopenia was more severe in patients with anti-GPIb autoantibodies than in patients without these autoantibodies, whereas ITP patients with anti-GPIIb/IIIa autoantibodies did not develop severe thrombocytopenia. Patients with anti-GPIb autoantibodies showed significant increases of platelet-associated IgM and platelet-associated C3 in comparison with patients without the autoantibodies, despite there being no significant difference in the platelet-associated IgG levels. The lymphocyte subsets and the blastogenic response in patients with anti-GPIb autoantibodies were also significantly different from those in the patients without these autoantibodies. Furthermore, severe purpura and a poor response to prednisolone were far more common in the patients with anti-GPIb autoantibodies. Activation of the complement system and/or functional abnormalities of lymphocytes thus appear to be involved in the development of thrombocytopenia in ITP patients with anti-GPIb autoantibodies, and such antibodies may be associated with a particularly severe form of ITP.

Autoantibodies↗