Biomedical subjects

T Matsubara

Publications and source records attributed to T Matsubara.

At least 343 records · Page 19Linked to original sources

PubMed1991

[Interleukin 6 activities and tumor necrosis factor-alpha levels in serum of patients with Kawasaki disease].

Interleukin 6 (IL-6) activities and tumor necrosis factor-alpha (TNF-alpha) levels in serum were determined in 25 patients with Kawasaki disease (KD), 9 with measles, 8 with anaphylactoid purpura (AP), and in healthy children. IL-6 activity in the sera was assayed by a colorimetric assay using a murine IL-6-dependent hybridoma clone, MH60. BSF-2. Serum levels of TNF-alpha were measured by a sandwich enzyme immunoassay. IL-6 activity in the sera of patients with KD and measles was seen to increase during the acute stage. However, IL-6 activity in the sera of AP patients did not increase during the active stage. IL-6 activity in the sera of KD patients correlated with serum CRP levels and the maximum platelet counts during the course of illness. Serum TNF-alpha levels in patients with KD and AP but not measles increased during the acute stage. Since the pathogenesis of KD is systemic vasculitis with severe inflammation and thrombocytosis, the combination of IL-6, which may be responsible for severe inflammation, and TNF-alpha, which may be responsible for severe vascular injury, does play an important role in acute KD.

Child, Preschool↗

PubMed1990

Possible interaction of alpha 1-adrenergic receptor with pertussis-toxin-sensitive guanine-nucleotide-binding regulatory proteins (G proteins) responsible for phospholipase C activation in rat liver plasma membranes.

Islet-activating protein (IAP; pertussis toxin) was employed to test the hypothesis that IAP-sensitive GTP-binding regulatory proteins (G proteins) are coupled with alpha 1-adrenergic receptor in rat liver plasma membranes. The high-affinity state of the binding of alpha 2-adrenergic agonist, which is known to be coupled with IAP-sensitive G protein, was abolished in IAP-treated plasma membranes. IAP treatment of plasma membranes could also diminish the high-affinity state of the alpha 1-adrenergic receptor for the agonist. Restoration of the high-affinity state of the alpha 1-adrenergic receptor for the agonist occurred on reconstitution of the bovine brain IAP-sensitive G proteins. The alpha 1-adrenergic receptor agonist stimulated inositol triphosphate (InsP3) production from [3H]inositol-labeled liver plasma membranes in a concentration-dependent manner. IAP treatment also decreased alpha 1-adrenergic-agonist-induced InsP3 production but not completely. From these results, we concluded that there is a possibility that both IAP-sensitive and IAP-insensitive G proteins were involved in alpha 1-adrenergic-receptor-stimulated phospholipase C activation in rat liver plasma membranes.

Adenosine Diphosphate Ribose↗

PubMed1990

Cromakalim, a vasodilator, differentially inhibits Ca2+ currents in NG108-15 neuroblastoma x glioma hybrid cells.

Extracellular perfusion with the antihypertensive agent cromakalim produced an inhibition of 22-66% in the low-threshold transient Ca2+ (T-like) current in NG108-15 hybrid cells. Cromakalim suppressed the high-threshold and long-lasting Ba2+ current (L-like Ca2+ current) by 29-73%, but had almost no effect on the high-threshold and inactivating Ba2+ current (N-like Ca2+ current). IC50 for T-like and L-like currents was the same at about 100 microM. The inhibitory effect developed relatively fast and was reversible. These results indicate that cromakalim can selectively inhibit the activity of inward Ca2+ currents.

Animals↗

PubMed1990

Possible role of coronary artery spasm in unexplained syncope.

Coronary spasm provocation by intracoronary methylergonovine was performed in 14 patients (8 men and 6 women, mean age 56 +/- 6 years) with syncope that remained unexplained despite neurologic and noninvasive cardiac evaluations. Electrophysiologic testing was also performed in 6 of 14 patients. No patient had structural heart disease or significant fixed stenosis of greater than or equal to 75% in the coronary arteries. Six patients had no history of chest pain even when they developed syncope. Serious arrhythmia was documented in 2 patients, cardiac standstill in 1 and complete atrioventricular block in the other. Coronary spasm was induced in 9 patients using the methylergonovine provocation test. Multivessel spasms were found in 3 patients. Coronary spasm was induced in the artery supplying the inferior wall in 7 of 9 patients with positive results. In 4 of 9 patients who had a positive result, there was no prior history of chest pain. In 1 patient, whose electrocardiogram was recorded during syncope, cardiac standstill was documented and cardiac standstill and syncope also occurred during the provocation test. Monomorphic ventricular tachycardia was not induced by the electrophysiologic study. These results suggest that coronary spasm is involved in unexplained syncope.

Cardiac Pacing, Artificial↗

PubMed1990

Determination of the presence of ceramide aminoethylphosphonate and ceramide N-methylaminoethylphosphonate in marine animals by fast atom bombardment mass spectrometry.

Phosphonosphingolipids from 15 kinds of shellfish were analyzed by fast atom bombardment mass spectrometry to determine the contents of ceramide aminoethylphosphonate (CAEPn) and ceramide N-methylaminoethylphosphonate (CMAEPn). Two pairs of ions, at m/z 126 and 140 in the positive ion mode and at m/z 124 and 138 in the negative ion mode, were used to distinguish between aminoethylphosphonic acid and N-methylaminoethylphosphonic acid in CAEPn and CMAEPn. Interestingly, mollusca in the early stage of evolution have both CAEPn and CMAEPn, while most in the middle stage have only CMAEPn and those in the highest stage have only CAEPn.

Aminoethylphosphonic Acid↗

PubMed1990

Mastoparan, a peptide toxin from wasp venom, stimulates glycogenolysis mediated by an increase of the cytosolic free Ca2+ concentration but not by an increase of cAMP in rat hepatocytes.

A wasp venom, mastoparan, rapidly increased the cytosolic free Ca2+ concentration [( Ca2+]i) and activated phosphorylase in rat hepatocytes in a concentration-dependent manner. Mastoparan could increase [Ca2+]i even in the absence of extracellular Ca2+, but a larger increase was observed in the presence of extracellular Ca2+. Thus, mastoparan mobilized Ca2+ from intracellular and extracellular Ca2+ stores. It also activated inositol triphosphate (IP3) accumulation, but did not stimulate cAMP production. From these results, we conclude that mastoparan activates rat hepatic glycogenolysis mediated by the accumulation of IP3, which causes an increase of [Ca2+]i but not that mediated by cAMP.

Adenylyl Cyclases↗

PubMed1990

Isolation and characterization of major urinary amino acid O-glycosides and a dipeptide O-glycoside from a new lysosomal storage disorder (Kanzaki disease). Excessive excretion of serine- and threonine-linked glycan in the patient urine.

Four major sialo compounds, termed GP-M1, GP-D1, GP-D2, and GP-D3 have been isolated from the urine of a novel glycoprotein storage disorder patient with angiokeratoma corporis diffusum which was discovered by Kanzaki et al. (Kanzaki, T., Yokota, M., Mizuno, N., Matsumoto, Y., and Hirabayashi, Y. (1989) Lancet April 22, 875-877). Based on the results of fast atom bombardment mass spectrometry, methylation analysis, and proton nuclear magnetic resonance spectroscopy, their chemical structures were concluded to be: (formula; see text) The yields of GP-M1, GP-D1, GP-D2, and GP-D3 were approximately 15, 6, 50, and 5 mg/liter of urine, respectively. The most major compound GP-D2, was further purified into single molecular species, threonine and serine type, by reversed phase high performance liquid chromatography. NMR analysis of the two purified compounds with single molecular species showed that the chemical shifts of anomeric protons of GalNAc were significantly different between threonine- and serine-linked GalNAc. Neither mannose-containing glycopeptides nor glycosphingolipids were excreted in the patient urine. From these results, this disease is thought to be caused by the deficiency of a lysosomal enzyme(s) acting on O-linked glycan chains.

Carbohydrate Metabolism, Inborn Errors↗

PubMed1990

Reduction of peripheral blood macrophages/monocytes in Kawasaki disease by intravenous gammaglobulin.

The effects of intravenous gammaglobulin (IVGG) on changes in the peripheral blood mononuclear cell subsets during acute Kawasaki disease (KD) were studied by a random selection trial of IVGG plus Aspirin (group G) compared to Aspirin alone (group A). Group G received IVGG with 200 mg/kg per day x 5 dose. The absolute counts of peripheral blood mononuclear cell subsets were assayed by a fluorescence-activated cell sorter using monoclonal antibodies of Leu series. Before therapy, patients in each treatment group had increased counts of CD14 + macrophage/monocytes compared to healthy childhood controls (P less than 0.01). After IVGG treatment group G underwent a greater decrease in their CD14 + macrophage/monocyte counts (P less than 0.01) than group A. The changes of CD3+ T cells. Leu 7+ NK/K cells and CD19+ B cells in the peripheral blood mononuclear cell subsets with treatment in group G, were similar to those in group A. These results suggest the possibility that IVGG therapy is effective in KD by modulating macrophages/monocytes.

Aged↗

PubMed1990

Evaluation of clonidine suppression and various provocation tests in the diagnosis of pheochromocytoma.

Recent investigations have shown that the widely used clonidine suppression test is sometimes fallible for the diagnosis of pheochromocytoma. A comparative assessment was made of the following suppression and provocation tests, the clonidine suppression test, and the glucagon, metoclopramide, and naloxone provocation tests. The assessment was performed in 6 patients with pheochromocytoma and in 19 patients without pheochromocytoma who were initially suspected of harboring a tumor. BP response did not predict the presence of pheochromocytoma in any test. Plasma norepinephrine (NE) concentrations determined at 120 and 180 min after oral 150 micrograms of clonidine gave false negative results in 2 of the 5 patients with pheochromocytoma tested. Both plasma NE and epinephrine (E) concentrations were measured before and sequentially after each provocative agent. Neither NE nor E responded to 1 mg of glucagon iv in 2 of the 4 patients with pheochromocytoma tested. Determination of the peak level, peak increment, and % peak increment of NE and E following 10 mg of naloxone iv did not distinguish the two groups. The % peak increments of both NE and E in all 4 patients with pheochromocytoma given 5 mg of metoclopramide iv exceeded the mean + 3 SD values of the patients without pheochromocytoma (25 + 28% for NE, and 25 + 42% for E). These results suggested that, when performed with judicious patient selection (ambiguous plasma or urinary catecholamine levels), the measurement of plasma catecholamines in response to metoclopramide can be a useful adjunctive tool in the diagnosis of pheochromocytoma.

Adrenal Gland Neoplasms↗

PubMed1990

Expression of Fc epsilon R2/CD23 on peripheral blood macrophages/monocytes in Kawasaki disease.

We analyzed the expression of Fc epsilon R2/CD23 on peripheral blood macrophages/monocytes in 12 patients with Kawasaki disease (KD) using a fluorescence-activated cell sorter. The absolute counts of CD14+ macrophages/monocytes and CD23+ macrophages/monocytes were high, and were positively correlated during the acute stage of KD. These results indicate that the increased number of macrophages/monocytes during acute KD have the Fc epsilon R2/CD23 antigen present on the surface of the cells, suggesting that peripheral blood macrophages/monocytes have been activated.

Acute Disease↗

PubMed1990

Serum levels of tumor necrosis factor, interleukin 2 receptor, and interferon-gamma in Kawasaki disease involved coronary-artery lesions.

We investigated 45 patients with Kawasaki disease (KD) and report the first simultaneous determination of tumor necrosis factor (TNF), interleukin 2 receptor (IL-2R) and interferon-gamma (IFN-gamma) in the serum during acute phase. Serum levels of TNF were measured by a sandwich enzyme-linked immunosorbent assay. Serum levels of soluble IL-2R and IFN-gamma were measured by a sandwich enzyme immunoassay and radioimmunoassay, respectively. Serum levels of TNF, IL-2R, and IFN-gamma were seen to increase during the acute phase of KD. In KD patients with coronary-artery lesions (CAL), the percentage of positive cases for TNF (greater than or equal to 10 U/ml), IL-2R (greater than or equal to 1056 U/ml), and IFN-gamma (greater than or equal to 0.3 U/ml) was higher than that in patients without CAL. Our results suggest that aggressive activation of immunocompetent cells develops in KD with CAL.

Child, Preschool↗

PubMed1990

Pituitary peptides other than ACTH may not be aldosterone secretagogue in primary aldosteronism.

In order to elucidate whether pituitary peptides other than ACTH which are derived from the proopiomelanocortin (POMC) are involved for aldosterone secretion in primary aldosteronism, we administered ovine corticotropin releasing factor (CRF), beta-endorphin and naloxone to seven patients with aldosterone producing adenoma. One hundred micrograms of CRF produced an augmented aldosterone response in patients with aldosteronism, while 500 micrograms of beta-endorphin infusion failed to cause any significant changes in neither normal subjects nor patients. An opioid antagonist, naloxone (10 mg, iv) produced no noticeable change in plasma aldosterone in normal subjects, while it caused a slight increase in patients with primary aldosteronism. Plasma cortisol increased to a similar degree in response to CRF and naloxone in normal subjects and patients. In three patients with isolated ACTH deficiency, neither aldosterone nor cortisol responded to these stimuli. The present results indicate that POMC-derived pituitary peptides other than ACTH are unlikely to participate in the aldosterone secretion in normal subjects or in patients with primary aldosteronism.

Adenoma↗

PubMed1990

On the mode of cardioprotection produced by a new bradycardic agent, FR 76830, during ischaemia and after reperfusion in the isolated perfused rat heart: a 31P-NMR study.

STUDY OBJECTIVE: The aim was to investigate the effects of a newly synthesised bradycardiac agent, FR 76830, on cardiac mechanical function and metabolism during ischaemia and reperfusion. DESIGN: FR 76830 and diltiazem were infused during 15 min before ischaemia. Hearts were then subjected to ischaemia (40 min) followed by reperfusion (40 min). High energy phosphate compounds and myocardial pH were assessed by 31P-NMR. The effects of bradycardia induced by FR 76830 before induction of ischaemia on the metabolic derangement resulting from ischaemia and on functional and metabolic recovery after reperfusion were examined in comparison with diltiazem. EXPERIMENTAL MATERIAL: Male Wistar rats (about 250 g) were used. MEASUREMENTS AND MAIN RESULTS: FR 76830 and diltiazem produced a dose dependent decrease in heart rate before ischaemia. However, the decrease in the double product (heart rate x left ventricular pressure) was observed only with diltiazem. Both FR 76830 and diltiazem attenuated the fall in myocardial pH during early ischaemia and improved the level of ATP during late ischaemia. Diltiazem also produced an improvement in myocardial acidosis during late ischaemia and in the level of ATP during early ischaemia. CONCLUSIONS: The importance of bradycardia in protection of the myocardial cells during early ischaemia and in preservation of ATP content during late ischaemia and after reperfusion was shown. However, to produce an improvement in myocardial pH during late ischaemia a decrease in the double product is needed.

Adenosine Triphosphate↗

PubMed1990

Neonate blood IgE levels on filter paper as indicators of atopic disease.

Measurements of IgE levels in the blood of neonates were investigated using filter paper for blood collection in mass screening of congenital metabolic disorders. Time-resolved fluoroimmunometric assay system for the measurement of filter paper blood IgE levels was also studied. In an analysis of the present results, IgE values of at least 0.015U/ml, the measurement limit, were considered as high. High IgE levels in filter paper blood were seen in 28 (7.2%) of the 389 cases. When the relation with serum IgE levels at 18 months of age was investigated in 134 of 389 subjects, high serum IgE levels were also found in about 86.7% of the subjects with high IgE levels in filter paper blood. In addition, when the relation between family history of atopic disease and presence of atopic disease in the first 18 months of age was investigated in 203 of the 389 subjects, about 90% of the subjects with a family history of atopic disease and high IgE levels in filter paper blood developed atopic disease. Since filter paper blood is routinely collected in Japan, IgE levels in this blood should be widely checked for the prediction of onset of atopic disease in infants.

Female↗

PubMed1990

Systemic and regional effects of endothelin in rabbits: effects of endothelin antibody.

1. The effects of porcine endothelin-1 (10(-12)-5 x 10(-10) mol/kg) on arterial blood pressure (BP) and the renal, mesenteric and carotid blood flow (BF), and the effects of endothelin-1 antibody were studied in rabbits. 2. Endothelin-1 caused a sustained increase in BP. The renal, mesenteric and carotid BF were decreased dose-dependently by endothelin-1. The approximate half-maximal effective values (ED50) were 5.5 x 10(-11), 8.6 x 10(-11) and 2.0 x 10(-10) mol/kg for renal, mesenteric and carotid BF respectively. Compared with carotid BF, the renal and mesenteric BF responses were significantly more sensitive to endothelin-1. 3. Combined administration of endothelin-1 and its antibody showed a significant inhibition of the BP and renal BF responses. However, endothelin-1 antibody alone did not change either BP, renal BF, mesenteric BF or carotid BF in vivo. 4. The present results demonstrate that endothelin is a potent vasoconstrictor in vivo. However, circulating endothelin may not contribute to the control of BF and BP. The role of endothelin as a local modulator of the vascular tone remains to be investigated.

Animals↗

PubMed1990

Mineralocorticoid and renal receptor binding activity of 21-deoxyaldosterone.

Since several aldosterone metabolites are known to be active, we have assessed the mineralocorticoid biological and renal receptor binding activities of the aldosterone metabolites, 21-deoxyaldosterone (21-deoxy-Aldo), 21-deoxytetrahydroaldosterone (21-deoxy-THAldo), and 3 alpha, 5 beta-tetrahydroaldosterone (THAldo). We synthesized these steroids by bioreduction of aldosterone with intestinal bacteria. Mineralocorticoid agonist activity of 21-deoxy-Aldo, 21-deoxy-THAldo and THAldo, determined by bioassay using adrenalectomized rats, was 1-5%, less than 0.01%, and 0.1-0.5% that of aldosterone, respectively. 21-Deoxy-Aldo showed no antagonist activity. The relative affinity in competing with [3H]aldosterone for binding to mineralocorticoid receptors in adrenalectomized rat kidney cytosols was 94%, less than 0.01%, and less than 0.01% that of aldosterone. The relative binding affinity for rat renal glucocorticoid receptors was 23%, less than 0.01%, and less than 0.01% that of dexamethasone, and for corticosteroid-binding globulin 17%, less than 0.01%, and less than 0.01% that of cortisol. These results show that the naturally occurring steroid, 21-deoxy-Aldo, possesses mineralocorticoid agonist activity which is equivalent to that of 11-deoxycorticosterone, and has substantial affinity for rat renal mineralocorticoid and glucocorticoid receptors. The results also implicate the pathophysiological role of 21-deoxy-Aldo as a potential mineralocorticoid in 21-hydroxylase deficiency, where urinary excretion of this steroid is invariably elevated.

Adrenalectomy↗

PubMed1990

Clinical characteristics and possible role of coronary artery spasm in syncope and/or aborted sudden death.

We investigated the clinical and pathophysiologic characteristics in patients with vasospastic angina who developed syncope and/or experienced aborted sudden death (SD). Vasospastic angina was diagnosed using the methylergonovine test. Syncope was found in 32 (10.4%) patients among 309 who were admitted to our institute in a one-year period. The most frequent cause of syncope was ventricular tachycardia which was found in 10 (31.2%) of the 32 patients. The next important cause of syncope was vasospastic angina which was found in 7 patients (21.8%). Among the 7 patients with vasospastic angina who experienced one or more syncopal episodes, there were 3 patients with aborted SD, 3 with syncope and one with shock. Cardiovascular collapse was observed in 4. Interior wall ischemia was found in 5 and anterior wall ischemia in 2 during the methylergonovine test. None of the 7 patients had significant coronary stenosis. Two patients had no prodromal symptom such as chest pain. Our results suggest that coronary artery spasm may be one of the most frequent cardiovascular diseases that causes syncope which is not always accompanied by a prodromal symptom. Therefore, coronary spasm should be distinguished in patients with unexplained syncope or aborted SD.

Coronary Angiography↗

PubMed1990

[Effect of cefaclor on guinea pig platelet aggregation in vitro].

Effects of cefaclor (3-chloro-7-D-(2-phenyl-glycinamido)-3-cephem-4-carboxylic acid) on PAF, ADP, collagen, endotoxin, and thrombin-induced platelet aggregation were examined in vitro with the use of guinea pig platelet-rich plasma and washed platelets. PAF, even at concentrations lower than its minimum effective concentration, enhanced ADP- or endotoxin-induced platelet aggregation and prolonged the time to attain the maximum aggregation. PAF also enhanced collagen-induced platelet aggregation and shortened the lag time. Cefaclor (CCL) inhibited the PAF, ADP or thrombin induced platelet aggregation and shortened their maximum aggregation times at higher concentrations such as 300 micrograms/ml or more. CCL also inhibited the collagen-induced platelet aggregation and prolonged the lag time, but showed no effect on endotoxin-induced platelet aggregation. The effect of CCL was almost the same as that of latamoxef (LMOX). CCL and LMOX, however, showed no effect on cellular Ca2+ increase produced by PAF, ADP, or thrombin, suggesting that the inhibitory effect of CCL and LMOX on platelet aggregation is caused by the inhibition of fibrinogen binding to the glycoprotein IIb/IIIa complex.

Adenosine Diphosphate↗