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Biomedical subjects

T Emori

Publications and source records attributed to T Emori.

At least 37 records · Page 2Linked to original sources
PubMed1995

Clinical and electrophysiological characteristics of sustained ventricular tachycardia occurring 3 to 21 days after acute myocardial infarction.

Patients with sustained ventricular tachycardia (VT) in the post-infarction period, especially more than 48 h after acute myocardial infarction (AMI), have a high mortality. However, clinical characteristics of these patients are unknown, since previous studies have not clarified the relationship between sustained VT and acute myocardial damage. To clarify the prognostic factors in patients with sustained VT in the early post-infarction period, we retrospectively surveyed 961 consecutive patients with AMI. Eleven patients (9 men and 2 women, aged 54 to 80 years) who had no previous myocardial infarction had at least one documented episode of sustained VT between 3 and 21 days after AMI. Late potentials were detected in 7 of 7 patients who underwent signal-averaged electrocardiography within 2 days after the first occurrence of VT. Entrainment was seen in 2 patients. The 5 patients who died in hospital had the following clinical characteristics: 1) cardiogenic shock, 2) extensive infarction, 3) a short interval from AMI to the onset of VT (mean +/- SD: 4 +/- 2 days), and 4) recurrent and refractory VT. In contrast, the 6 patients who survived had the following clinical characteristics: 1) no cardiogenic shock, 2) a relatively late occurrence of VT (mean = SD: 14 +/- 7 days), 3) few episodes of VT, and 4) no recurrence of VT during the follow-up period of 12 to 58 months. The occurrence of sustained VT within 3 weeks after AMI was influenced by the general condition of the patient, and the prognosis was mainly related to cardiac function.

Aged↗
PubMed1995

Quantification of antiribosomal P0 protein antibodies by ELISA with recombinant P0 fusion protein and their association with central nervous system disease in systemic lupus erythematosus.

OBJECTIVE: Using solid phase ELISA with recombinant P0 fusion protein as the antigen for detecting antiribosomal P0 protein antibody, we analyzed the association of this antibody and anticardiolipin antibody (aCL) with central nervous system (CNS) disease in patients with active systemic lupus erythematosus (SLE). METHODS: Sera from 70 randomly selected Japanese patients with active SLE were assayed for IgG and IgM antiribosomal P0 protein antibody titers and IgG aCL. RESULTS: IgG and IgM antiribosomal P0 protein antibodies were present in 29 and 12 (41.4 and 17.1%) of the 70 patients, respectively. The incidence of CNS disease, excluding lupus psychosis, was significantly higher in patients with IgG and IgM antiribosomal P0 protein antibodies than in those who lacked them (IgG antiribosomal P0 protein antibody 11/29 vs 3/41; IgM antiribosomal P0 protein antibody 7/12 vs 7/58). In addition, both IgG and IgM antiribosomal P0 protein antibody titers were significantly higher in patients with CNS disease, excluding lupus psychosis, than those without. No significant association was observed between antiribosomal P0 protein antibodies and lupus psychosis. No significant association was observed between IgG aCL and CNS disease. Serial studies of antiribosomal P0 protein antibodies and aCL in patients with transverse myelopathy also showed that IgG and IgM antiribosomal P0 protein antibodies, but not IgG aCL, were associated with CNS disease, excluding lupus psychosis. CONCLUSION: These data suggest a strong association of IgG and IgM antiribosomal P0 protein antibodies with CNS disease, excluding lupus psychosis, in SLE.

Adolescent↗
PubMed1995

Conversion of GC-->AT recognition and elucidation of AT recognition mechanism in zinc finger transcription factor by permutational approach.

Zinc finger-DNA recognition has been investigated through GC-->AT conversion of recognition sequence 5'-GGG-GCG-GGG-3' of transcription factor Sp1 containing three zinc fingers. Three critical amino acid residues of the finger 2 in Sp1 were replaced with the corresponding residues of the finger 4 in CF2-II. The finger 2 of the hybrid protein is expected to recognize 5'-ATA-3' sequence. Indeed, the designed protein Sp1QTQ2 specifically bound to ATA and ATAN probes. The present study demonstrates that one zinc finger recognizes total sequence of the target DNA site rather than triplet base sequence.

Amino Acid Sequence↗
PubMed1994

Effects of TNF-alpha on hemodynamic changes and circulating endothelium-derived vasoactive factors in dogs.

To elucidate the relation of tumor necrosis factor-alpha (TNF-alpha)-induced hemodynamic change to endothelium-derived vasoactive factors, we simultaneously measured hemodynamic parameters and circulating endothelin (ET)-1, ET-3, nitrite/nitrate (NOx), and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) in anesthetized dogs following administration of TNF-alpha with or without NG-nitro-L-arginine (L-NNA), a nitric oxide (NO) synthase inhibitor, and indomethacin, a cyclooxygenase inhibitor. Natural human TNF-alpha (10 micrograms/kg, n = 5) with or without L-NNA (1 mg/kg, n = 5) or indomethacin (2 mg/kg, n = 5) was administered intravenously as a bolus, while administration of vehicle served as control (n = 5). After administration of TNF-alpha, mean arterial pressure and cardiac index significantly decreased, whereas systemic (SVRI) and pulmonary (PVRI) vascular resistance index increased. Plasma levels of ET-1, ET-3, NOx, and 6-keto-PGF1 alpha significantly (P < 0.01) increased at 1 h. L-NNA or indomethacin blocked TNF-alpha-induced hypotension and remarkably increased SVRI but did not affect decreased cardiac index. Our data suggest that endogenous ET-1 may partly contribute to TNF-alpha-induced increases in SVRI and PVRI, against which ET-3, NO, and prostacyclin may function as compensatory vasodilators.

6-Ketoprostaglandin F1 alpha↗
PubMed1993

Cellular mechanism of endothelin-induced nitric oxide synthesis by cultured bovine endothelial cells.

Endothelins (ETs) cause initial and transient vasodilation via an endothelium-dependent mechanism. We studied the cellular mechanism by which ETs stimulate synthesis and release of endothelium-derived relaxing factor (EDRF)/nitric oxide (NO) in cultured bovine endothelial cells (EC). ET-1 and ET-3 rapidly (within 1 min) and dose-dependently (10(-10) to 10(-7) M) stimulated production of nitrate/nitrite (NOx) in bovine EC; ET-3 was more potent than ET-1 at generating endothelial NOx. The ET-3-stimulated NOx production was completely abolished by a NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA), the effect of which was reversed by coadministration of excess L-arginine. NOx production stimulated by ET-3 was blocked by an intracellular Ca2+ chelator but not by an extracellular Ca2+ chelator. A selective calmodulin inhibitor W-7 dose-dependently inhibited the ET-3-stimulated NOx production, whereas a nonselective calmodulin inhibitor W-5 failed to affect NOx production. These data suggest that ETs stimulate receptor-mediated EDRF/NO synthesis via a Ca2+/calmodulin-dependent pathway in vascular endothelial cells.

Animals↗
PubMed1993

Monophasic action potentials in a patient with multiform ventricular tachycardia without QT prolongation.

A 41 year old woman had multiform ventricular tachycardia without QT prolongation. Monophasic action potentials were recorded from the right ventricle during the attacks of multiform ventricular tachycardia and effective refractory periods were examined at the same sites. There was no abnormal hump to suggest early afterdepolarisation in the monophasic action potentials, but there was dispersion of the effective refractory period in the right ventricle (80 ms). Stimulation from the right ventricular apex, where the effective refractory period was shortest, reproducibly induced multiform ventricular tachycardia. Two weeks after admission, when her condition was stable, multiform ventricular tachycardia could not be induced and the dispersion of the effective refractory period in the right ventricle was 20 ms.

Action Potentials↗
PubMed1993

Heparin has an inhibitory effect on endothelin-1 synthesis and release by endothelial cells.

We studied the inhibitory effects of heparin on basal and agonist-induced endothelin-1 biosynthesis and release from cultured bovine endothelial cells. Heparin dose-dependently and similarly inhibited endothelin-1 release, inositol trisphosphate production, and intracellular free Ca2+ levels stimulated by thrombin. Hirudin fragment had an inhibitory effect on thrombin-induced endothelin-1 release, whereas anti-thrombomodulin antibody had no effect. Heparin completely blocked phorbol ester-induced endothelin-1 release, whereas it had a partial inhibitory effect on endothelin-1 release stimulated by angiotensin and vasopressin. Northern blot analysis using complementary DNA for bovine preproendothelin-1 as a probe revealed that heparin reduced not only the basal but also the stimulated expression of preproendothelin-1 messenger RNA by thrombin and phorbol ester. These data suggest that heparin, in addition to its antithrombin effect, has an inhibitory effect on the biosynthesis and release of endothelin-1, possibly by inhibiting protein kinase C-dependent pathway.

Animals↗
PubMed1993

Endothelin receptor subtype B mediates synthesis of nitric oxide by cultured bovine endothelial cells.

Endothelins (ET) produce endothelium-dependent vasodilation through nitric oxide (NO) synthesis. The present study was designed to elucidate the cellular mechanism by which ET induces synthesis and release of endothelium-derived NO by cultured bovine endothelial cells (EC). Binding studies revealed that bovine EC membrane had the binding sites of a novel agonist (BQ3020) for non-isopeptide-selective receptor subtype (ETB). Affinity labeling studies showed a major labeled band with the apparent molecular mass of 50 kD. Northern blot analysis demonstrated the expression of mRNA for ETB receptor. BQ3020 rapidly and dose dependently induced formation of inositol-1,4,5-triphosphate and increased intracellular Ca2+ concentrations in fura-2-loaded cells. Concomitantly, BQ3020 dose dependently stimulated production of both nitrate/nitrite (NOx) and cyclic GMP; a highly significant correlation existed between NOx and cGMP production. The stimulatory effect on NOx and cGMP production by ETB agonist was inhibited by NO synthase inhibitor monomethyl-L-arginine; this effect was reversed by coaddition of L-arginine, but not D-arginine. NOx and cGMP production stimulated by BQ3020 was inhibited by pretreatment with pertussis toxin. ETB agonist-induced NOx production was blocked by a calmodulin inhibitor and an intracellular Ca2+ chelator, but not by an extracellular Ca2+ chelator or a Ca2+ channel blocker. These data suggest that endothelins stimulate ETB receptor-mediated phosphoinositide breakdown via pertussis toxin-sensitive G-protein(s), which triggers release of intracellular Ca2+, thereby activating Ca2+/calmodulin-dependent NO synthase in EC.

Amino Acid Oxidoreductases↗
PubMed1993

Cellular mechanism of natriuretic peptides-induced inhibition of endothelin-1 biosynthesis in rat endothelial cells.

We studied the cellular mechanism by which natriuretic peptides inhibit the synthesis and release of endothelin-1 (ET-1) in cultured rat aortic endothelial cells (EC). Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) showed dose-dependent and equipotent effects on displacement of [125I]ANP binding and generation of cGMP production in rat EC, whereas C-type natriuretic peptide and biologically inactive ANP analog had lesser effects. ANP and BNP as well as 8-bromo-cGMP had potent inhibitory effects on immunoreactive ET-1 release, the transient increase in the intracellular Ca2+ concentration, and the formation of inositol 1,4,5-trisphosphate stimulated by thrombin in rat EC. A cGMP-dependent protein kinase inhibitor (KT5823), but not a cAMP-dependent protein kinase inhibitor (KT5720), completely abolished the inhibitory effect of ANP on thrombin-induced immunoreactive Et-1 release. Northern blot analysis using cDNA for rat prepro-ET-1 as a probe showed that ANP and 8-bromo-cGMP, but not C-type natriuretic peptide, inhibited thrombin-induced prepro-ET-1 mRNA expression, whose effect was abolished by KT5823. These data suggest that ANP and BNP inhibit the thrombin-induced synthesis and release of ET-1 in cultured rat aortic EC by blocking phosphoinositide breakdown, possibly via natriuretic peptides type A receptor-mediated cGMP-dependent mechanism.

Animals↗
PubMed1993

Multiple coronary artery dissections diagnosed in vivo in a pregnant woman.

A 27-year-old, 37-weeks' primigravida survived an acute myocardial infarction. Coronary angiography 25 days after infarction demonstrated multiple dissections in the left coronary artery. She had no vascular risk factors or connective tissue disease. This is a rare case of spontaneous, multiple coronary artery dissections that were diagnosed by coronary angiography.

Adult↗
PubMed1992

Cellular mechanism of thrombin on endothelin-1 biosynthesis and release in bovine endothelial cell.

We have studied the cellular mechanism responsible for induction of preproendothelin (preproET)-1 mRNA and release of ET-1 by thrombin in cultured bovine endothelial cells (ECs). Thrombin induced an immediate and dose-dependent formation of inositol-1,4,5-trisphosphate (IP3) with a concomitant increase in intracellular Ca2+ concentration ([Ca2+]i). The thrombin-induced ET-1 release was abolished either by a phospholipase C inhibitor, a protein kinase C (PKC) inhibitor, or an intracellular Ca(2+)-chelator, whereas a Ca(2+)-channel antagonist was ineffective. A selective thrombin inhibitor (argatroban) decreased IP3 formation and the increase in [Ca2+]i and ET-1 release stimulated by thrombin. Northern blot analysis revealed that thrombin-induced expression of preproET-1 mRNA was inhibited completely by a PKC inhibitor and partially by argatroban. These data suggest that thrombin is involved in the mechanism of preproET-1 mRNA expression and subsequent ET-1 release, possibly through activation PKC and mobilization of intracellular Ca2+ resulting from the receptor-mediated phosphoinositide breakdown in ECs.

Animals↗
PubMed1992

Concomitant expression of receptor subtype and isopeptide of endothelin by human adrenal gland.

We studied whether specific receptors for endothelin (ET) isopeptide exist in human aldosterone-producing adenoma and normal adrenal cortex, and whether ET isopeptides are produced by human adrenal gland. Competitive binding studies using [125I]ET-1 as a radioligand revealed the presence of a single class of high-affinity binding sites for ET-1 with the apparent KD of 70 +/- 31 pM and Bmax of 226 +/- 139 fmol/mg protein in adenoma membranes almost comparable to those in adjacent normal cortex. The apparent Ki for ET-2 and ET-3 were 89 +/- 33 pM and 82 +/- 16 pM, respectively. Northern blot analysis of poly(A)+ RNA of adenoma and adjacent normal cortex using cDNAs for ET receptor subtype (ETA, ETB) and ET isopeptide (ET-1, ET-3) as probes revealed that ETA and ETB receptors as well as ET isopeptides (preproET-1, preproET-3) are concomitantly expressed in both tissues. Our data demonstrate for the first time that ET receptor subtype (ETA and ETB) and ET isopeptide (ET-1 and ET-3) are concomitantly expressed by human adrenal cortex, suggesting the potential role of ETs as a local mediator in human adrenal gland.

Adenoma↗
PubMed1992

Induction of TU abnormalities in patients with torsades de pointes.

1. TU abnormalities could be induced by the specific interventions in the majority of the patients with TDP in chronic stage: isoproterenol in congenital long QT patients, disopyramide in Ia-related TDP patients, and slow heart rate in bradycardia-related TDP patients. 2. Humps in MAP could be recorded in all patients with congenital long QT syndrome by isoproterenol, in half of the patients with Ia-related TDP by disopyramide, but in none of the control patients by these agents. 3. The results suggested that TU abnormalities and the occurrence of hump in MAP were hypersensitive reactions. 4. The results also suggested that specific intervention was not enough for the appearance of marked TU abnormalities in some TDP patients, especially in Ia-related TDP patients. Additional aggravating factors were probably required for marked TU abnormalities and the occurrence of TDP in these patients.

Action Potentials↗
PubMed1992

Effects of three distinct natriuretic peptides on receptor binding and guanylate cyclase activities in rat glioma cells.

Receptor binding and cyclic GMP generation by three distinct natriuretic peptides (ANP, BNP, CNP) were studied in a cultured rat glioma cell line (C6). Binding studies revealed the presence of high-affinity binding sites for three natriuretic peptides with almost comparable affinities. In contrast, CNP and BNP were almost equipotent in stimulating intracellular cyclic GMP generation over the low concentration range, but CNP caused further elevation in the high concentration range, whereas ANP was minimally effective. Our data suggest that the glioma cells possess receptors more responsive to CNP than ANP and BNP despite no apparent correlation between receptor binding affinities and cyclic GMP responses.

Animals↗
PubMed1992

Recovery functions of common peroneal, posterior tibial and sural nerve somatosensory evoked potentials.

We studied recovery functions of the somatosensory evoked potentials (SEPs) of common peroneal (CPN), posterior tibial (PTN) and sural nerves (SN) using a paired conditioning-test paradigm. The interstimulus interval (ISI) of paired stimuli ranged from 2 to 400 msec. In all SEPs with ISIs of 12-20 msec, the amplitude recovery was close to or beyond 100% of the control response, though their latencies and wave forms were not the same as the control. Further increases of the ISI resulted in significant depression of SEP (late phase suppression), most markedly in CPN, and less prominently in SN-SEP. With a longer than 50 msec ISI there was progressive recovery of SEP, but full recovery differed depending on the nerve stimulated; 400 msec ISI was required for CPN-, 250 msec for PTN- and 100 msec for SN-SEP. The peroneal nerve block by local anesthetic injected just distal to the stimulus electrodes abolished the late phase SEP suppression observed before the nerve block. These findings suggest that the late phase SEP suppression is attributable to the "secondary" afferents as a result of activation of peripheral receptors (muscle, joint and/or cutaneous) by the efferent volley initiated from the stimulus point. The greater and longer duration of peripheral receptor activation in CPN than in PTN or SN stimulation could explain the more pronounced and the longer duration of late phase suppression in CPN-SEP.

Adult↗
PubMed1992

L-arginine infusion induces hypotension and diuresis/natriuresis with concomitant increased urinary excretion of nitrite/nitrate and cyclic GMP in humans.

1. The vascular endothelium produces endothelium-derived relaxing factor (EDRF) or nitric oxide (NO), which exerts vasodilation through cyclic guanosine monophosphate (cGMP) as a second messenger. To determine whether EDRF has any vasodilating and natriuretic action in man, the present study examined the effects of L-arginine (L-Arg), a substrate for NO, on the responses of mean blood pressure (MBP) and heart rate (HR); plasma concentrations of cGMP, atrial natriuretic factor (ANF) and nitrite/nitrate (NOx); urinary excretion of sodium, cGMP and NOx; and urinary flow in eight normal male subjects. These parameters were compared with those following saline infusion in the same subjects. Clearance of para-aminohippuric acid (PAH) and inulin was studied in five normal subjects. 2. Infusion of L-Arg (30 g) caused a significant fall in MBP (-8 mmHg) with a concomitant rise in HR (10 beats/min), while saline infusion had no effects on these parameters. 3. Neither L-Arg nor saline infusion caused appreciable changes in plasma concentrations of ANF or NOx. Plasma cGMP concentrations increased significantly during (1.7-fold) and after (1.9-fold) L-Arg infusion, but only slightly (1.3-fold) during saline infusion. 4. Urine flow increased more remarkably following L-Arg infusion than that following saline infusion. Remarkable increases in urinary excretion of sodium and fractional excretion of sodium were observed after L-Arg infusion compared with those after saline infusion. Natriuresis was associated with enhanced urinary excretion of cGMP and Nox. Urinary Nox excretion showed positive correlations with urinary flow (r = 0.69, P less than 0.001) and with urinary cGMP excretion (r = 0.60, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Induction of endothelin-1 gene by angiotensin and vasopressin in endothelial cells.

To elucidate the cellular mechanism of endothelin-1 biosynthesis induced by angiotensin and vasopressin, we first cloned and sequenced full-length bovine preproendothelin-1 complementary DNA (cDNA) from a cultured bovine carotid artery endothelial cell cDNA library. The predicted bovine preproendothelin-1 consists of 202 amino acid residues and has a high percentage of homology to human, porcine, and rat preproendothelin-1 (70%, 81%, and 77%, respectively). Big endothelin-1, an intermediate form, consists of 39 residues differing only at position Val28 from porcine (Ile28) and His27 from rat (Arg27). The predicted 21-residue mature endothelin-1 is identical to human, porcine, rat, canine, and mouse endothelin-1. Northern blot analysis with the cloned cDNA as a probe demonstrated that a single 2.3-kb preproendothelin-1 messenger RNA (mRNA) is expressed not only in endothelial cells, but also in various bovine tissues, including lung, brain, heart, intestine, kidney, ovary, and urinary bladder. Angiotensin II and arginine vasopressin immediately and dose-dependently induced expression of preproendothelin-1 mRNA, whose effects were abolished by specific receptor antagonists. These findings suggest that stimulation of endothelin-1 secretion from endothelial cells by both agonists may be principally due to induction of preproendothelin-1 mRNA.

Amino Acid Sequence↗