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Biomedical subjects

M Arita

Publications and source records attributed to M Arita.

At least 109 records · Page 6Linked to original sources
PubMed1997

Friedreich-like ataxia with retinitis pigmentosa caused by the His101Gln mutation of the alpha-tocopherol transfer protein gene.

The alpha-tocopherol transfer protein (alpha-TTP) is a cytosolic liver protein that is presumed to function in the intracellular transport of alpha-tocopherol, the most biologically active form of vitamin E. We studied 4 unrelated patients with autosomal recessive Friedreich-like ataxia who had isolated vitamin E deficiency. A point mutation was identified in all of them at position 101 of the gene for alpha-TTP, where histidine (CAT) was replaced with glutamine (CAG). Three of the 4 patients developed retinitis pigmentosa subsequent to the onset of ataxia. Neurological symptoms included ataxia, dysarthria, hyporeflexia, and decreased proprioceptive and vibratory sensations. Electrophysiological and pathological examinations showed that the cardinal sites affected were the central axons of dorsal root ganglion cells and the retina, with minor involvement of the peripheral sensory nerve, optic nerve, and pyramidal tract. The vitamin E tolerance test performed showed that the absorption of vitamin E was normal but that its decrease from the serum was accelerated. Oral administration of vitamin E appeared to halt the progression of visual and neurological symptoms. We propose a new treatable syndrome of Friedreich-like ataxia and retinitis pigmentosa caused by a defect in the alpha-TTP gene.

Aged↗
PubMed1997

Effects of KT-362, a sarcolemmal and intracellular calcium antagonist, on calcium transients of cultured neonatal rat ventricular cells: a comparison with gallopamil and ryanodine.

We evaluated the effects of KT-362 (5-[3-([2-(3,4-dimethoxyphenyl)-ethyl]amino)-1-oxopropyl]-2,3,4,5, -tetrahydro-1,5-benzothiazepine fumarate), a putative intracellular calcium antagonist, on the intracellular free calcium concentration ([Ca2+]i) of cultured neonatal rat ventricular cells using microfluorometry of fura-2. The effects were compared with those of gallopamil (D-600), a sarcolemmal calcium channel antagonist, and ryanodine, a modulator of sarcoplasmic reticulum (SR) function. KT-362 decreased both systolic [Ca2+]i (sCa) and diastolic [Ca2+]i (dCa) in cell aggregates, in a concentration (1, 3, 10, and 30 microM) and stimulation frequency (0.2, 0.5, and 1.0 Hz) dependent manner. The time to peak of the Ca2+ transient was significantly prolonged by KT-362 at a concentration of 30 microM, while the half-life of the Ca2+ transient was prolonged at concentrations of > or = 10 microM. Gallopamil (1 microM) decreased both sCa and dCa in a frequency (0.2, 0.5, and 1.0 Hz) dependent fashion, as was the case for KT-362, but did not change the time course of Ca2+ transients. Ryanodine (10 microM) prolonged the time to peak and half-life of the Ca2+ transient, as was also the case for KT-362, while the effect of ryanodine on dCa differed from that of KT-362. Finally, the effect of KT-362 on Ca2+ transients could be mimicked by simultaneous application of gallopamil and ryanodine. These results suggest that KT-362 is a novel compound that exerts depressant effects on both sarcolemmal Ca2+ channels, and perhaps Ca2+ release channels of the sarcoplasmic reticulum, in cultured neonatal rat ventricular cells.

Analysis of Variance↗
PubMed1997

Rate-dependent prolongation of action potential duration in isolated rat ventricular myocytes.

Rate-dependent alterations of action potential duration (APD) in rat ventricular myocytes were investigated. Action potentials of the isolated myocytes were recorded with patch electrodes containing EGTA (11 mM), and showed a marked rate-dependent prolongation in the APD (0.2-5 Hz). This prolongation was significantly inhibited in the presence of 4-aminopyridine (4-AP), a blocker of the transient outward K+ current (Ito). Thus, the rate-dependent decrease in Ito may underlie the change in APD. In contrast, the action potentials recorded from rat ventricular papillary muscles with conventional microelectrodes did not show rate-dependent alterations in the APD, i.e., the APD remained practically unaltered at the frequency range of 0.2-5 Hz. These results suggest that the rate-dependent prolongation of APD (due to rate-dependent blockade of Ito) becomes evident when the intracellular Ca2+ was chelated by the internal application of EGTA via patch pipette. We speculate that the rate-dependent prolongation of APD (via decreases in Ito) is masked in the ventricular papillary muscles, probably due to rate-dependent decreases in the inward current (e.g., electrogenic Na(+)-Ca2+ exchange current) that is regulated by the intracellular calcium.

4-Aminopyridine↗
PubMed1997

Inflammatory fibroid polyp of the ileum with the appearance of a Borrmann type II lesion, caused by colostomy irrigation: report of a case.

Inflammatory fibroid polyps (IFPs) are rarely found in the gastrointestinal tract. The majority of IFPs are sessile-pedunculated or pedunculated polypoid lesions, whereas a polyp presenting like a Borrmann type II lesion is extremely unusual. This report describes the case of a 74-year-old man with a history of intussusception, in whom a preoperative diagnosis of a cecal tumor of the ileocecal valve was made. A laparotomy subsequently revealed a lesion similar to a Borrmann type II tumor located 15 cm above the ileocecal valve, but not at the valve. The lesion was diagnosed as an IFP which had been caused by repeated colostomy irrigation. The aim of the present report is to draw attention to this entity, which should be included in the differential diagnosis of intussusception and small bowel obstruction.

Aged↗
PubMed1997

Mechanical stretch increases intracellular calcium concentration in cultured ventricular cells from neonatal rats.

We investigated the effects of mechanical stretch on intracellular calcium concentration ([Ca2+]i) of cultured neonatal rat ventricular cells using microfluorometry with fura-2. Myocytes were cultured on laminin-coated silicon rubber and stretched by pulling the rubber with a manipulator. Myocytes were either mildly stretched (to less than 11.5% of control length), moderately so (to 115%-125% of control length), or extensively (to over 125% of the control length). "Quick stretches" (accomplished within 10s) of moderate to extensive intensities produced a large transient increase of [Ca2+]i in the early phase of stretch (30 s-2 min), followed by a small but sustained increase during the late phase of stretch (5-10 min). The initial transient increase in [Ca2+]i after the "quick stretch" was preserved in the presence of gallopamil (10(-7) M) or ryanodine (10(-5) M), but was absent in Ca(2+)-free medium or in the presence of gadolinium (10(-7) M). The late or steady state [Ca2+]i increase was observed in the presence of gadolinium, gallopamil, or ryanodine but was abolished in Ca(2+)-free medium. A steady-state increase in [Ca2+]i was also evoked by "slow stretch" in which cells were slowly pulled to the final length within 1-2 min. As the presence of external Ca2+ was indispensable, increased trans-sarcolemmal Ca2+ influx appears to be involved in both initial and steady-state increases in [Ca2+]i. The initial increase in [Ca2+]i after the "quick stretch" can be attributed to the activation of gadolinium-sensitive, stretch-activated channels.

Animals↗
PubMed1997

Anoxia-induced activation of ATP-sensitive K+ channels in guinea pig ventricular cells and its modulation by glycolysis.

OBJECTIVE: Exposure to anoxia has been reported to activate ATP-sensitive potassium (K+(ATP)) channels in isolated ventricular myocytes. We aimed to investigate the mechanisms underlying the anoxia-induced activation of K+(ATP) channels. METHODS: Guinea pig ventricular myocytes were isolated using collagenase digestion. Action potentials and membrane currents were recorded in the whole-cell mode of patch clamp. Exposure to anoxia was performed in a semi-closed airtight chamber, which prevented the diffusion of atmospheric oxygen into anoxic perfusate. RESULTS: Exposure to glucose-free anoxia shortened the action potential duration (APD) to less than 20% of control in 13 +/- 3 min. Subsequent reoxygenation rapidly and completely restored the APD. The time-independent large outward current which developed during anoxia was completely suppressed by reoxygenation or by the application of glibenclamide, a K+(ATP) channel blocker. The presence of extracellular glucose did not prevent APD shortening during anoxia, although it significantly decreased the rate of shortening. Reoxygenation-induced restoration of the APD was inhibited after a long-lasting anoxia. In addition, repeated exposures to anoxia/reoxygenation progressively impaired the recovery of APD during reoxygenation. CONCLUSIONS: Activation of K+(ATP) channels occurs during anoxia. The primary source of ATP that regulates the channel activity seems to be oxidative phosphorylation. ATP derived from anaerobic glycolysis (attained by the increase of extracellular glucose) was observed to partially suppress the channel activity only when oxidative phosphorylation was severely impaired during anoxia.

Action Potentials↗
PubMed1997

Transcranial magnetic stimulation-induced changes in EEG and responses recorded from the scalp of healthy humans.

We determined the changes and responses in the electroencephalogram (EEG) induced by transcranial magnetic stimulation (TMS) of the scalp of five healthy men. The center of a circular coil was positioned at the vertex, and 80 stimulations were administered clockwise with the maximum output of electric current. To reduce stimulus artifacts, we created a circuit that blocked the input for 150 ms after stimulation. EEGs were recorded from F3,4, C3,4, P3,4, and T3,4. The following results were obtained: (1) slowing of the EEG was observed immediately (150 m) after each stimulation. The incidence of changes ranged from 25-80%; their duration ranged from 200-600 ms. (2). Electroencephalographic responses in the averaged form appeared as gentle positive waves. In some subjects and leads, 1 to 3 negative peaks were fused. The methods used in the present study may be useful in evaluating the sensitivity to TMS of patients with stroke and other types of brain injury.

Adult↗
PubMed1997

The effect of glibenclamide on the production of interstitial adenosine by inhibiting ecto-5'-nucleotidase in rat hearts.

1. Adenosine exerts cardioprotective effects on the ischaemic myocardium. The production of adenosine in the ischaemic myocardium is attributed primarily to the enzymatic dephosphorylation of adenosine 5'-monophosphate (AMP) by 5'-nucleotidase. We determined the activity of 5'-nucleotidase in rat hearts. The objective of the study was to determine the effects of ATP-sensitive K+ (K[ATP]) channel antagonists (glibenclamide and 5-hydroxydecanoate) on the production of adenosine, by use of a flexibly mounted microdialysis technique. 2. Rats were anaesthetized and the microdialysis probe was implanted in the left ventricular myocardium, followed by perfusion with Tyrode solution. The baseline level of dialysate adenosine was 0.51 +/- 0.09 microM (n = 16). Introduction of AMP (100 microM) through the probe increased the dialysate adenosine markedly to 9.79 +/- 0.43 microM (n = 12, P < 0.001 vs baseline), and this increase was inhibited by the ecto-5'-nucleotidase inhibitor, alpha,beta-methyleneadenosine 5'-diphosphate (100 microM), to 0.76 +/- 0.12 microM (n = 8). Thus, the dialysate adenosine noted during the perfusion of AMP originated from dephosphorylation of AMP by ecto-5'-nucleotidase, and the dialysate level of adenosine attained reflects the ecto-5'-nucleotidase activity in the tissue in situ. 3. Glibenclamide (0.1-100 microM) decreased the adenosine concentration measured during the perfusion of AMP (100 microM) in a concentration-dependent manner (IC50 = 10.5 microM). In contrast, 5-hydroxydecanoate (10-100 microM) did not affect the concentrations of dialysate adenosine, measured in the presence of AMP (100 microM). These results suggest that glibenclamide inhibits the activity of endogenous ecto-5'-nucleotidase and decreases the concentration of adenosine in the interstitial space of rat ventricular muscles in situ.

5'-Nucleotidase↗
PubMed1997

Effects of locally administered argatroban on restenosis after balloon angioplasty: experimental and clinical study.

1. This study was undertaken to evaluate the preventive effects of locally administered argatroban, a competitive inhibitor of thrombin-induced platelet activation, on restenosis after balloon angioplasty. 2. A hydrogel-coated balloon catheter was immersed three times in argatroban/saline solution (1 mg/mL) for 60 s, inflated to a pressure of 606 kPa and left in the rabbit common carotid artery for 1 min. The same procedure was performed, without drug, as a control. The pharmacokinetics of delivered argatroban in the arterial wall were assessed using [14C]-argatroban. Platelet deposition 2 h after balloon injury was quantified by fluorescence studies using antiplatelet antibody. Vascular smooth muscle cell (VSMC) proliferation 3 days after balloon injury was assessed by immunohistochemical staining for proliferative cell nuclear antigen (PCNA). In a clinical study, we divided 50 elective patients into two groups: argatroban and control. 3. In the experimental study, the mean quantities of argatroban at 0, 2 and 6 h after deflation were 24.63, 0.49 and 0.11 nmol/g wet weight of artery, respectively. Argatroban was undetected 24 h after deflation. Two hours after deflation, argatroban-treated arteries showed less platelet adhesion than saline-treated controls. The mean number of PCNA-positive cells was 16.9 and 43.8% in the argatroban and control groups, respectively (P < 0.01). In the clinical study, the mean late gain loss was 8.2 and 27.3% in the argatroban and control groups, respectively (P < 0.05). The mean late restenosis rate was 11.1 and 41.4% in the argatroban and control groups, respectively (P < 0.05). 4. These data suggest that blood coagulation plays a significant role in VSMC proliferation after balloon injury and that locally administered argatroban using hydrogel-coated balloon catheter may prevent post-percutaneous transluminal coronary angioplasty restenosis.

Angioplasty, Balloon↗
PubMed1997

Demonstration of Purkinje potential during idiopathic left ventricular tachycardia: a marker for ablation site by transient entrainment.

During VT of QRS morphology with right bundle branch block and left axis deviation in a patient without obvious structural heart disease, entrainment by pacing from the right ventricular outflow tract and high right atrium was demonstrated. During entrainment of VT, a Purkinje potential preceding the QRS and recorded at the left ventricular mid-septum was activated by orthodromic impulses in the reentry circuit. The interval between the Purkinje potential and the earliest left ventricular activation was decrementally prolonged with shortening of pacing cycle length. Radiofrequency energy was applied to this site, resulting in successful elimination of VT. Therefore, the Purkinje potential represented activation by an orthodromic wavefront in the reentry circuit, while the orthodromically distal site to this potential showed an area of slow conduction with decremental property.

Adult↗
PubMed1997

Host range phenotype induced by mutations in the internal ribosomal entry site of poliovirus RNA.

Most poliovirus strains infect only primates. The host range (HR) of poliovirus is thought to be primarily determined by a cell surface molecule that functions as poliovirus receptor (PVR), since it has been shown that transgenic mice are made poliovirus sensitive by introducing the human PVR gene into the genome. The relative levels of neurovirulence of polioviruses tested in these transgenic mice were shown to correlate well with the levels tested in monkeys (H. Horie et al., J. Virol. 68:681-688, 1994). Mutants of the virulent Mahoney strain of poliovirus have been generated by disruption of nucleotides 128 to 134, at stem-loop II within the 5' noncoding region, and four of these mutants multiplicated well in human HeLa cells but poorly in mouse TgSVA cells that had been established from the kidney of the poliovirus-sensitive transgenic mouse. Neurovirulence tests using the two animal models revealed that these mutants were strongly attenuated only in tests with the mouse model and were therefore HR mutants. The virus infection cycle in TgSVA cells was restricted by an internal ribosomal entry site (IRES)-dependent initiation process of translation. Viral protein synthesis and the associated block of cellular protein synthesis were not observed in TgSVA cells infected with three of four HR mutants and was evident at only a low level in the remaining mutant. The mutant RNAs were functional in a cell-free protein synthesis system from HeLa cells but not in those from TgSVA and mouse neuroblastoma NS20Y cells. These results suggest that host factor(s) affecting IRES-dependent translation of poliovirus differ between human and mouse cells and that the mutant IRES constructs detect species differences in such host factor(s). The IRES could potentially be a host range determinant for poliovirus infection.

Animals↗
PubMed1997

Inactivation of human viruses by povidone-iodine in comparison with other antiseptics.

Inactivation of a range of viruses, such as adeno-, mumps, rota-, polio- (types 1 and 3), coxsackie-, rhino-, herpes simplex, rubella, measles, influenza and human immunodeficiency viruses, by povidone-iodine (PVP-I) and other commercially available antiseptics in Japan was studied in accordance with the standardized protocol in vitro. In these experiments, antiseptics such as PVP-I solution, PVP-I gargle, PVP-I cream, chlorhexidine gluconate, alkyldiaminoethyl-glycine hydrochloride, benzalkonium chloride (BAC) and benzethonium chloride (BEC) were used. PVP-I was effective against all the virus species tested. PVP-I drug products, which were examined in these experiments, inactivated all the viruses within a short period of time. Rubella, measles, mumps viruses and HIV were sensitive to all of the antiseptics, and rotavirus was inactivated by BAC and BEC, while adeno-, polio- and rhinoviruses did not respond to the other antiseptics. PVP-I had a wider virucidal spectrum, covering both enveloped and nonenveloped viruses, than the other commercially available antiseptics.

Adenoviridae↗
PubMed1997

Effects of locally administration of argatroban using a hydrogel-coated balloon catheter on intimal thickening induced by balloon injury.

The purpose of this study was to evaluate the inhibitory effects of locally delivered argatroban, a competitive inhibitor of thrombin-induced platelet activation, on intimal proliferation after balloon injury. A hydrogel-coated balloon catheter was immersed 3 times in an argatroban/saline solution (1, 0.1, or 0.01 mg/ml) for 60 s and inflated at 6 atm pressure for 1 min in the rabbit common carotid artery. Immersion in a saline solution without drug followed by the same procedure served as a control. Accumulation of argatroban in the vascular wall was confirmed by chemical determination using high-performance liquid chromatography (HPLC). The concentration of argatroban in the vessel wall immediately after deflation after balloon immersion in solutions of 1 and 0.1 mg/ml was 14.8 +/- 10.9 and 5.5 +/- 4.6 nmol/g wet weight of artery, respectively. Argatroban was not detected in arteries treated with a balloon that had been immersed in the 0.01 mg/ml argatroban/saline solution. Intima-media area ratios 20 days after balloon injury in the groups treated with 1 mg/ml (n = 8) and 0.1 mg/ml (n = 6) agratoban were significantly smaller than that in the groups treated with 0.01 mg/ml (n = 7) argatroban or saline (n = 8) (0.35 +/- 0.11, 0.50 +/- 0.17, 1.24 +/- 0.39, and 1.35 +/- 0.43, respectively; p < 0.001). These data suggest that locally administered argatroban dose-dependently inhibits intimal thickening in a rabbit model of carotid artery injury.

Angioplasty, Balloon, Coronary↗
PubMed1997

Identifying areas with vitamin A deficiency: the validity of a semiquantitative food frequency method.

OBJECTIVES: The prevalence of vitamin A deficiency has traditionally been assessed through xerophthalmia or biochemical surveys. The cost and complexity of implementing these methods limits the ability of nonresearch organizations to identify vitamin A deficiency. This study examined the validity of a simple, inexpensive food frequency method to identify areas with a high prevalence of vitamin A deficiency. METHODS: The validity of the method was tested in 15 communities, 5 each from the Philippines, Guatemala, and Tanzania. Serum retinol concentrations of less than 20 micrograms/dL defined vitamin A deficiency. RESULTS: Weighted measures of vitamin A intake six or fewer times per week and unweighted measures of consumption of animal sources of vitamin A four or fewer times per week correctly classified seven of eight communities as having a high prevalence of vitamin A deficiency (i.e., 15% or more preschool-aged children in the community had the deficiency) (sensitivity = 87.5%) and four of seven communities as having a low prevalence (specificity = 57.1%). CONCLUSIONS: This method correctly classified the vitamin A deficiency status of 73.3% of the communities but demonstrated a high false-positive rate (42.9%).

Child, Preschool↗
PubMed1997

[Management of permanent pacemaker implantation in elderly patients].

We evaluated the clinical characteristics of 297 consecutive patients who underwent permanent pacemaker implantation. Their mean age was 67 +/- 13 years; those at least 75 years old accounted for 30.9%. The underlying diseases were sick sinus syndrome in 36.7%, atrioventricular block in 58.9%, and atrial fibrillation with bradycardia in 4.4%. There was no association between age and either the voltage threshold or the R wave amplitude at the time of implantation. When pacemakers were exchanged, only patients aged 75 years or less had voltage thresholds that were higher and lead resistances that were lower than those measured at the time of initial implantation. No clear differences were observed in the R wave amplitude, regardless of age. With careful long-term management, permanent pacemaker implantation and follow-up clinical care can be safe, even in aged patients.

Aged↗
PubMed1997

[Lesion-related factors associated with restenosis after percutaneous transluminal coronary angioplasty in the absence of patient-related factors].

Restenosis after percutaneous transluminal coronary angioplasty (PTCA) is one of the biggest problems in the treatment of coronary artery disease. Although many studies have been performed on lesion-related factors, they are influenced by patient-related factors such as smoking, hyperlipidemia, and the presence of acute coronary syndrome. In this study, lesion-related factors were assessed in the absence of other factors by univariate and multivariate analysis. One hundred and nine lesions were reviewed in 37 consecutive patients with both restenotic lesion(s) and non-restenotic one(s) confirmed by coronary arteriography performed 4.4 +/- 2.2 months after PTCA. Angiographic findings before and immediately after angioplasty were compared between restenotic and non-restenotic lesions. The overall lesion-restenosis rate was 42%. Univariate analysis revealed that calcified lesions (p < 0.05), multiple irregularities (p < 0.01) before angioplasty, residual percentage stenosis (p < 0.05), and angiographical intraluminal haziness (p < 0.05) were related to restenosis. Intimal dissection after PTCA was not associated with restenosis. Multivariate analysis with multiple logistic regression revealed that multiple irregularities (t = 2.8) was the most predictive of restenosis before PTCA and residual percent stenosis (t = 2.6) after the procedure. Coronary lesions with calcification or multiple irregularities indicate high risk of restenosis after PTCA. Optimal dilatation of the lesions without intraluminal haziness regardless of intimal dissection is important to prevent restenosis.

Aged↗
PubMed1997

[Epidemiological research on incidence of atopic disease in infants and children in relation to their nutrition in infancy].

Incidence and relative risk of atopic disease (atopic dermatitis; AD, bronchial asthma; BA, allergic rhinitis; AR) in Japanese infants and children in relation to their nutrition in infancy was analyzed from the data of the epidemiological survey which was conducted for 10,000 mothers of infants and children in 1993. A total of 4,610 replies were received: 2,714 from mothers of infants (12 months old) and 1,896 from mothers of children (2 years old). The subjects were allocated to following 3 groups based on their nutrition during first 3 months after birth; the breast-fed group (BF), the formula-fed group (EF), the mixed-fed group (MF). Incidence of atopic disease in BF, FF and MF was 23.5%, 22.2% and 21.8%, respectively and no statistical difference could be found among these 3 groups. AD was developed 17.0%, 14.4% and 13.9%; BA was 4.4%, 8.5% and 5.2%; AR was 4.9%, 6.5% and 5.8% in BF, FF and MF, respectively. Incidence of AD was significantly different between BF and MF (p < 0.01). Incidence of BA was also significantly different between BF and FF (p < 0.01). Risk of onset of BA and AR in FF was higher (adjusted odds ratio 2.2, 95% confidence interval 1.5-3.2 and adjusted odds ratio 1.5, 95% confidence interval 1.0-2.2, respectively) than that of BF controlled by age and family history with Cochran-Mantel-Haenzel test. With multiple logistic regression analysis, relative risk of the onset of BA in FF at the age of one year was 2.1, 95% confidence interval 1.2-3.5 and at the age of two years old was 2.5, 95% confidence interval 1.4-4.4. These results suggest that the breast-fed have certain suppression effects on incidence of bronchial asthma in infants and children.

Asthma↗