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S Komori

Publications and source records attributed to S Komori.

At least 91 records · Page 5Linked to original sources
PubMed1997

Characterization of fertilization-blocking monoclonal antibody 1G12 with human sperm-immobilizing activity.

A mouse hybridoma (1G12) producing sperm-immobilizing MoAb to human sperm was established and characterized in order to study the antigens relevant to sperm immobilization by antibodies. MoAb 1G12 had strong sperm-immobilizing and agglutinating activities and also showed a fertilization-blocking activity on in vitro fertilization tests. The antibody absorption experiments showed that MoAb 1G12 reacted not only to ejaculated sperm but also human seminal plasma, suggesting that the corresponding antigen might be a sperm coating antigen. The MoAb also reacted with peripheral blood lymphocytes. In histochemical studies, the epithelia of corpus epididymis were most strongly stained. Ejaculated sperm were stained with a granular pattern for their entire surface by immunofluorescence. MoAb 1G12 recognized polymorphic glycoproteins of 15-25 kD in the ejaculated sperm extract in Western blot analysis. After deglycosilation of the sperm extract, only a single staining band of under 15 kD was detected by MoAb 1G12. This suggests that the antigen epitope recognized by MoAb 1G12 might be a peptide of the core portion of the glycoprotein. MoAb 1G12 might be a useful tool for studying the mechanism of egg-sperm interaction, and also be applied to identifying the corresponding antigen by using gene technology.

Absorption↗
PubMed1997

DNA analysis of the androgen receptor gene in two cases with complete androgen insensitivity syndrome.

OBJECTIVE: Androgen insensitivity syndrome is an X-linked disorder of sexual differentiation resulting from abnormalities of the androgen receptor gene. In this study, we analyzed the androgen receptor gene in 2 cases with complete androgen insensitivity syndrome (CAIS). METHODS: DNAs were isolated from patients with CAIS, and the androgen receptor gene was amplified by a polymerase chain reaction. Sequence analysis of the androgen receptor gene was performed. RESULTS: In Patient 1, one substitutional mutation [glutamine (CAA) to arginine (CGA) at position 194] was identified in exon A, and the premature termination of the androgen receptor gene was also demonstrated due to the deletion of one nucleotide at the codon in exon C (position 597). In Patient 2, one substitutional mutation [arginine (CGC) to cysteine (TGC) at position 855] in exon G was identified. This position was located in the hormone-binding domain and appeared to be a hot spot of mutations because the mutations at the same position have been reported before in several unrelated cases. CONCLUSION: The results of this study suggest that these abnormalities might be related to the pathogenesis of complete androgen insensitivity syndrome.

Adult↗
PubMed1997

Administration-time-dependent effects of diltiazem on the 24-hour blood pressure profile of essential hypertension patients.

The aim of this study was to identify differences in the patterns of efficacy and duration of effect by diltiazem given in different dosage forms and schedules. Blood pressure (BP) and heart rate (HR) were monitored before and after treatment by ambulatory blood pressure monitoring for 48 h every 30 min. Patients were divided for treatment assignment into 4 groups -nocturnal BP dippers and nondippers. In dipper hypertension, diltiazem-retard at 08:00 (n = 7) had the most marked antihypertensive effects during nighttime rest (SBP; 136 +/- 14/118 +/- 9 mmHg, p < 0.01 before vs. after treatment). Diltiazem-retard at 19:00 (n = 6) exerted greatest effect during daytime activity (152 +/- 7/139 +/- 6, p < 0.01) with inhibition of the morning BP rise. Diltiazem (t.i.d., n = 5) had the best effect during daytime activity (151 +/- 16/136 +/- 9, p < 0.05). However, in nondipper hypertensive patients, diltiazem (t.i.d., n = 8) had the most pronounced antihypertensive effects during nightly rest (144 +/- 12/127 +/- 12, p < 0.05). Evening medication with diltiazem retard appears to be more efficacious than the other dosage schedules.

Adult↗
PubMed1997

[Circadian variation of blood pressure and heart rate in normotensive pre- and postmenopausal women].

The aim of this study was to assess the effect of menopause on circadian profile of blood pressure (BP) and heart rate (HR) in the normotensive pre- and postmenopausal women. Systolic BP (SBP), diagnostic BP (DBP) and HR were monitored every 30 min for 48 hrs using noninvasive ambulatory BP monitoring in 24 premenopausal and 40 postmenopausal women. Mean 48-hours, daytime (awake), and nighttime (sleeping) SBP, DBP and HR values were analyzed by reviewing the patients' diaries, and the nocturnal reduction rate (NRR) of SBP, DBP and HR were calculated according to the following formula. NRR (%9 = [(daytime mean-nighttime mean)/daytime mean] x 100. The study subjects were then divided into two groups according to the presence (dipper) or absence (nondipper) of a significant reduction in nocturnal BP (> 10%). Mean SBP, DBP and HR measured over 48 hours were similar between the premenopausal and the postmenopausal group. The NRR of DBP and HR in the postmenopausal group were significantly smaller than those in the premenopausal group (17.1 +/- 6.0% vs. 13.5 +/- 7.0%, 241.1 +/- 6.0% vs. 19.8 +/- 9.0%: p < 0.05). There tended to be higher prevalence of nondipper in the postmenopausal (37%) than in the premenopausal group (29%).

Adult↗
PubMed1997

What time is the "biologic zero hour" of circadian variability?

Most ambulatory blood pressure monitoring (ABPM) studies have used a mechanical clock as the reference time, but there is no biologic background for assuming that midnight by the mechanical clock is zero hour by the biologic clock. The aim of this study was to determine the biologic zero hour as the zero reference time by evaluating the circadian rhythm of blood pressure, heart rate, and activity. Twenty healthy medical students (18 men, 2 women, mean age 26 years old) were recruited and blood pressure, heart rate, and physical activity were monitored simultaneously by an ABPM device every 30 min for 48 h. Four concepts of zero time were selected in this study and analyzed regarding biologic zero hour: 24:00 by the mechanical clock (clock time); the time of awakening, based on a diary (diary time); the time of a sudden increment in physical activity in the morning (activity time); and the middle of the total sleeping time, based on the diary (midsleeping time). The awakening time is a better individual index than the mechanical clock, and the midsleeping time as the zero reference point is better than the awakening time. We assessed the reproducibility of the data regarding the circadian troughs between the first and second day. The reproducibility of the day-to-day variation of the blood pressure and heart rate was poor. The reproducibility of physical activity was fairly good, but the magnitude of activity was small. A 48-h monitoring profile is superior to a 24-h monitoring period.

Adult↗
PubMed1996

Modulation of peristalsis by neurotensin in isolated guinea-pig intestinal segments.

Neurotensin (1-100 nM) produced an inhibitory effect and an excitatory effect on the peristaltic activity elicited by intraluminal distension using the Trendelenburg method or the intraluminal perfusion method in isolated segments of guinea-pig small intestine. The relative contribution of these effects to the overall effect varied from one region to another of the small intestine. In the Trendelenburg preparation, the excitatory effect was found to be accompanied by a decrease in the threshold intraluminal pressure required to trigger a peristaltic reflex. A substantial difference between the jejunum and the ileum was noted in that neurotensin-induced stimulation of peristaltic activity was observed in a smaller number of the segments in the jejunum than in the ileum. A nonpeptide neurotensin receptor antagonist, SR 48692, 2-[(1-(7-chloro-4-quinolinyl)-5-(2,6-dimethoxyphenyl) pyrazol-3-yl)carbonylamino]tricyclo(3.3.1.1.(3.7))decan++ +-2-carboxylic acid (90 nM), abolished both the inhibitory and excitatory effects. Apamin (10 nM) abolished the inhibitory effect. From these results, neurotensin appears to exert both excitatory and inhibitory actions, via its receptors sensitive to SR 48692, on peristaltic activity in guinea-pig small intestine. The excitatory action varies with an increasing gradient toward the terminal end of the small intestine, and the inhibitory action involves apamin-sensitive mechanism.

Animals↗
PubMed1996

Carbachol-induced [Ca2+]i oscillations in single smooth muscle cells of guinea-pig ileum.

1. Changes in cytosolic Ca2+ concentration ([Ca2+]i) produced by carbachol (CCh) were measured in single smooth muscle cells of guinea-pig ileum using a Ca(2+)-sensitive fluorescent dye, fura-2, to clarify the underlying mechanisms of muscarinic [Ca2+]i oscillations. 2. Half of the cells, when exposed to 0.2 microM CCh, exhibited repeated changes in [Ca2+]i giving a serrated appearance. The oscillatory changes in [Ca2+]i were very similar to those evoked by increasing extracellular K(+) concentration ([K+]o) to 30 mM, which were abolished by removal of extracellular Ca2+, nifedipine and La3+, but remained unchanged after depletion of internal Ca2+ stores with cyclopiazonic acid, thapsigargin and ryanodine. 3. Every individual [Ca2+]i oscillation was just like a [Ca2+]i increase generated spontaneously in about 8% of cells or triggered by an action potential evoked by a current pulse in current-clamped cells. 4. In the remaining half of the cells exposed to 0.2 microM CCh, slower [Ca2+]i oscillations were elicited and every individual [Ca2+]i oscillation was always preceded by the fast brief increase in [Ca2+]i. 5. [Ca2+]i oscillations elicited by 2 microM CCh were temporally and functionally distinct from those induced by high [K+]o. They were more or less regular in the periodicity and pattern, comprised pacemaker potential-like [Ca2+]i increases or sinusoidal types of [Ca2+]i increases, and could be elicited even in 100 mM K+(o). 6. Removal of extracellular Ca2+ or application of nifedipine, methoxyverapamil (D600), diltiazem or La3+ during CCh (2 micro M)-induced [Ca2+]i oscillations caused them to disappear. In cells i which internal Ca2+ stores were depleted, 2 microM CCh did not evoke [Ca2+]i oscillations but occasionally induced single or repeated generation of the increase in [Ca2+]i with a serrated appearance. 7. The results indicate that CCh can induce two types of [Ca2+]i oscillation in guinea-pig ileal smooth muscle cells; one arises from Ca2+ influx associated with action potential discharges and the other from periodic release of Ca2+ from internal stores. The latter [Ca2+]i oscillation requires extracellular Ca2+ to sustain it.

Animals↗
PubMed1996

Prenatally detected hepatic hamartoma: another cause of non-immune hydrops.

Although various conditions associated with non-immune hydrops have been reported, primary hepatic tumours are rare. As a mesenchymal hamartoma of the liver is a rare benign tumour, it has not been listed as a cause of hydrops. In this report we describe a case in which a large cystic mass in the fetal liver associated with non-immune hydrops was prenatally detected with sonography and magnetic resonance imaging, and histopathologically confirmed as a mesenchymal hamartoma of the liver.

Adult↗
PubMed1996

IK independent class III actions of MS-551 compared with sematilide and dofetilide during reperfusion in anaesthetized rats.

1. The antiarrhythmic and haemodynamic effects of three class III antiarrhythmic drugs, MS-551, sematilide and dofetilide, were examined in the coronary artery, ligation-reperfusion model of pentobarbitone-anaesthetized rats, a species deficient in functional cardiac IK. MS-551 is a non-selective potassium channel blocker, while both sematilide and dofetilide are selective delayed rectifier potassium (K) channel (IK) blockers. 2. Before coronary ligation, 3 and 10 mg kg-1 MS-551 decreased the heart rate by 6% (P < 0.01) and 12% (P < 0.01), and increased mean arterial pressure (MAP) by 14% (P < 0.05) and 33% (P < 0.01), respectively. Sematilide at 10 and 30 mg kg-1 also decreased the heart rate by 4% (P < 0.01) and 9% (P < 0.01), respectively, and the higher dose of 30 mg kg-1 decreased MAP by 29% (P < 0.01). Dofetilide, 1 mg kg-1, decreased the heart rate (P < 0.01), but had no significant effect on MAP. 3. The QT interval was increased by 10% (P < 0.01) and 31% (P < 0.01), when 3 and 10 mg kg-1 MS-551 were given. Sematilide and dofetilide had no effect on the QT interval. 4. Immediately after reperfusion, lethal ventricular fibrillation (VF) was induced in 80% of the saline group. MS-551 at 3 and 10 mg kg-1, reduced the incidence of lethal VF to 50% and 20% (P < 0.05). Neither dofetilide 1 mg kg-1 nor sematilide (10 and 30 mg kg-1) decreased the incidence of lethal VF (70%, 80% and 50%, respectively). None of the three drugs had any effect on the occurrence of reperfusion-induced VT or the total incidence of VF. However, 10 mg kg-1 MS-551 delayed the onset of reperfusion-induced VF (27 +/- 5 s compared with 12 +/- 2 s of the control group, P < 0.05). 5. In conclusion, in rats which are deficient in cardiac IK MS-551 prolonged the QT interval and reduced the incidence of sustained VF after reperfusion. Blockade of channels other than IK might participate in the defibrillatory effect of MS-551. Sematilide and dofetilide, which are selective IK blockers, did not increase the QT interval nor did they show antiarrhythmic effects Mechanisms other than K channel block may be involved in the different effects of the three drugs on blood pressure.

Animals↗
PubMed1996

Some evidence against the involvement of arachidonic acid in muscarinic suppression of voltage-gated calcium channel current in guinea-pig ileal smooth muscle cells.

1. To see if arachidonic acid (AA) plays a role in the sustained suppression of voltage-gated calcium channel currents produced by muscarinic receptor stimulation by carbachol (CCh), the effects of AA on membrane currents were examined in whole-cell voltage-clamped smooth muscle cells of the guinea-pig ileum. 2. In cells bathed in Ba2+ PSS and dialysed with Cs(+)-based low EGTA (0.05 mM) pipette solution, and in which Ba2+ current (IBa) flowing through voltage-gated calcium channels was evoked repeatedly by stepping to 0 mV from the holding potential of -60 mV, AA (1-30 microM), applied extracellularly, gradually suppressed IBa in a concentration-dependent manner. The IBa suppression was observed even with 20 mM EGTA in the pipette. 3. AA (3 microM) and CCh (10 microM) shifted the voltage-dependent inactivation curve of IBa in the negative potential direction, but the effect of AA differed from that of CCh in that an accompanying appreciable decrease in the slope was observed. 4. The sustained suppression of IBa induced by CCh (10 microM) remained almost unaltered after pretreatment with 4-bromophenacyl bromide (10 microM), an inhibitor of phospholipase A2, or a combination of indomethacin (10 microM), an inhibitor of the cyclo-oxygenase pathway, and nordihydroguaiaretic acid (10 microM), an inhibitor of the lipoxygenase pathway. 5. In cells bathed in Ca2+ PSS and dialysed with K(+)-based pCa 6.5 pipette solution, voltage-dependent Ca2+ current (ICa) and K+ current (IK) were recorded simultaneously. AA (3 microM) suppressed IK as well as ICa, whereas CCh (10 microM) suppressed ICa but not IK. 6. We conclude from these results that AA or its metabolite is unlikely to be involved in the sustained suppression of voltage-gated calcium channel current induced by muscarinic receptor stimulation in guinea-pig ileal smooth muscle cells.

Animals↗
PubMed1996

Modulation of carbachol-induced [Ca2+]i oscillations by Ca2+ influx in single intestinal smooth muscle cells.

1. Oscillations of cytosolic Ca2+ concentration ([Ca2+]i) evoked by carbachol (CCh; 2 microM), a muscarinic agonist, were detected as oscillatory changes of muscarinic receptor-coupled cationic current (Icat) in guinea-pig ileal smooth muscle cells by the whole cell patch-clamp technique. 2. Reduction of extracellular Ca2+ from 2 mM to 0.2 or 0.05 mM, during CCh-induced Icat oscillations, caused them to disappear or to decrease markedly in frequency. A return to 2 mM Ca2+ concentration restored the initial Icat oscillations. 3. Application of nifedipine (1-3 microM) or D600 (2-5 microM) to block the voltage-gated Ca2+ channel (VGCC) decreased the frequency of the ongoing Icat oscillations in the cells held at -20 mV, but it was without effect in cells held at -60 mV. 4. Displacement of the holding potential of -20 mV to -60 mV to deactivate VGCC produced a decrease, an increase or no noticeable change in the frequency of the Icat oscillations in different cells. Displacement to 20 mV to inactivate VGCC invariably produced a decrease in the frequency. In nifedipine-treated cells, the Icat oscillations varied in frequency voltage-dependently in a reverse and linear way within the range -80 to 40 mV. 5. Application of thapsigargin (1 or 2 microM), an inhibitor of Ca(2+)-ATPase in the membrane of internal Ca2+ stores, caused CCh-induced Icat oscillations to disappear with a progressing phase during which their amplitude, but not frequency, declined. 6. The results suggest that membrane Ca2+ entry has a crucial role to play in regulation of the frequency of CCh-induced [Ca2+]i oscillations in addition to persistence of their generation, and that the effect is brought about by a potential mechanism independent of Ca2+ store replenishment. They also provide evidence that two types of Ca2+ permeant channels, VGCC and an as yet unidentified channel, are involved in the Ca2+ entry responsible for modulation of [Ca2+]i oscillations.

Animals↗
PubMed1996

Inhibitory effect of CV4151, a thromboxane A2 synthetase inhibitor, on ventricular arrhythmias induced by coronary artery occlusion in rats.

The purpose of this study was to determine whether thromboxane A2 (TXA2) is involved in the development of ventricular arrhythmias produced by coronary artery occlusion. Ventricular arrhythmias were induced by coronary artery occlusion in 66 male Sprague-Dawley rats. Rats were separated into 4 groups, and saline (n = 19) or CV4151 (a TXA2 synthetase inhibitor)(10 mg/kg, n = 14; 30 mg/kg, n = 15; or 100 mg/kg, n = 18) was injected intravenously 5 min before coronary artery occlusion. The antiarrhythmic effect of CV4151 was assessed in terms of the number of ventricular premature complexes (VPCs), the combined duration of ventricular tachycardia (VT) and ventricular fibrillation (Vf), the incidence of Vf, and the mortality rate within 30 min after occlusion. The total number of VPCs was as follows; control: 1789 +/- 330 beats: 10 mg/kg group: 1289 +/- 302 beats: 30 mg/kg group: 1008 +/- 229 beats: 100 mg/kg group: 986 +/- 275 beats, with no significant differences between groups. The incidence of Vf was significantly reduced in the 30 mg/kg and 100 mg/kg groups, as was the combined duration of VT and Vf and the mortality rate. Our results indicate that the TXA2 synthetase inhibitor CV4151 reduces the incidence of lethal arrhythmias induced by coronary artery occlusion in rats.

Animals↗
PubMed1996

Pharmacological characterization of adrenoceptors mediating contractile and relaxant responses to noradrenaline in the longitudinal muscle of guinea-pig ileum.

Mechanical responses to noradrenaline (NA) were recorded in longitudinal muscle strips from the terminal and intermediate regions (3-10 cm and 30-40 cm from the ileo-caecal junction, respectively) of the guinea-pig ileum. NA(0.16-1,600 microM) produced a concentration-dependent contraction in the terminal ileum with the EC50 value of 11.9 +/- 4.3 microM (n = 5). In the intermediate ileum, NA produced relaxation at concentrations ranging from 0.016 microM to 1.6 microM. Responses to NA at 16 microM varied among preparations: no noticeable change in tension, a moderate relaxation and a small contraction. At higher concentrations, NA produced contractile responses and their peak tension increased in a concentration-dependent manner. The contractile effect of NA in the terminal ileum remained unaltered after treatment with propranolol (1.4 microM) or yohimbine (1.1 microM), or a combination of these drugs. In the intermediate ileum, the relaxant effect of NA was markedly reduced or abolished by propranolol (1.4 microM). Yohimbine (1.1 microM) had little effect on NA-induced relaxation. The contractile effect of NA in both the terminal ileum and intermediate ileum was inhibited by prazosin (1.1 microM), so that the contractions were converted to relaxation or markedly reduced. Propranolol abolished the relaxant response induced by NA at 0.16 microM, but did not inhibit those induced by NA at 1.6 microM. Methoxamine (0.16-1,600 microM) produced a concentration-dependent contraction in both the terminal ileum and the intermediate ileum. The EC50 was 93.5 +/- 28.5 microM (n = 8) in the terminal ileum and 83.3 +/- 27.7 microM (n = 10) in the intermediate ileum. There was no significant difference between the values. The results showed that NA is capable of producing contraction or relaxation in the longitudinal muscle layer of the terminal and intermediate regions of the guinea-pig ileum. The contraction, which is mediated by alpha 1-adrenoceptors, predominates in the terminal ileum, but relaxation, which is mediated by beta-adrenoceptors and uncharacterized adrenoceptors, predominates in the intermediate ileum.

Animals↗
PubMed1995

Inhibitory effect of muscarinic receptor activation on Ca2+ channel current in smooth muscle cells of guinea-pig ileum.

1. The effect of muscarinic receptor stimulation on voltage-gated calcium channel currents was examined in whole-cell voltage-clamped smooth muscle cells of the guinea-pig ileum. 2. In cells voltage clamped at -60 mV and in which calcium channel currents (ICa) were elicited repeatedly by depolarizing pulses (25 ms duration, 0.25 Hz frequency) to 0 mV, carbachol (CCh, 10 microM) induced an inward current (ICCh) and were suppressed ICa, in a biphasic manner; an initial transient component was followed by a more sustained one. 3. A calcium channel current (IBa), when Ba2+ was used as a charge carrier, was also suppressed by CCh in a biphasic manner, as with ICa. The sustained phase of the IBa suppression was significantly smaller than that of the ICa suppression, suggesting that Ca2+ entry exerts a potentiating effect on the current suppression. 4. CCh had little or no effect on calcium channel currents (ICa and IBa) in cells dialysed with a pipette solution containing EGTA (20 mM). 5. Inclusion of GDP-beta-S (1 mM) in the pipette solution abolished ICCh and the suppression of IBa. With GTP-gamma-S (10 microM) in the pipette, the sustained phase of the IBa suppression remained almost unchanged even after removal of CCh. 6. Pretreatment with 2 micrograms ml-1 pertussis toxin (PTX), which abolished ICCh, did not change noticeably the initial transient and sustained phases of IBa suppression. 7. Neomycin (100 microM) or heparin (5 mg ml-1) in the pipette each abolished the initial transient component of ICCh as well as the initial transient phase of IBa suppression. 8. The biphasic effect of CCh on IBa was observed in the presence of either staurosporine (1 microM) or 1-(5-isoquinolinesulphonyl)-2-methylpiperazine (100 microM). Phorbol 12-myristate 13-acetate and phorbol 12,13-dibutyrate (up to 10 microM) had no inhibitory effect on ICa and IBa. 9. The results suggest that stimulation of the muscarinic receptor causes a biphasic suppression of the voltage-gated calcium channel currents through a PTX-insensitive G protein in guinea-pig ileal smooth muscle cells. The initial transient phase may be brought about by the release of Ca2+ from internal storage sites, and the sustained phase by a Ca(2+)-dependent mechanism which is independent of the phosphatidylinositol pathway.

Animals↗