Reverse passive haemagglutination test for identification and serotyping of polioviruses.
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Hemagglutination Tests↗
Biomedical subjects
M Arita
Publications and source records attributed to M Arita.
Crystallization and preliminary X-ray crystallographic analysis of Mirabilis antiviral protein.
Mirabilis antiviral protein is a single-chain ribosome-inactivating protein purified from the tuberous root of Mirabilis jalapa L. We obtained several forms of crystals of the protein by the hanging drop vapor diffusion method, but most of these crystals were not suitable for X-ray crystallography. After refining the growth conditions, crystals of crystallographic quality were grown in 20-microliters droplets of an equi-volume mixture of 1.5% (w/v) protein solution and a reservoir solution containing 49 to 50% (w/v) ammonium sulfate and 50 mM-ammonium citrate (pH 5.4) at room temperature. Addition of 2 mM-adenine sulfate reduced twinning and "crystal shower". The resulting trigonal crystals diffract beyond 2.5 A resolution using a rotating anode X-ray generator. The space group was determined to be P3(1)21 or P3(2)21 (a = b = 103.9.A, c = 134.6 A, alpha = beta = 90 degrees, gamma = 120 degrees) based on their precession photography of h0l and hk0 zones. There seems to be three monomers in an asymmetric unit for VM = 2.51 A3/Da.
Antiviral Agents↗
Inhibitory effects of palmitoylcarnitine and lysophosphatidylcholine on the sodium current of cardiac ventricular cells.
We investigated the effects of ischemia-related amphipathic compounds, palmitoylcarnitine (PamCar, 0.5-50 microM) and lysophosphatidylcholine (lysoPtdCho, 5-50 microM) on sodium current (INa) of guinea-pig ventricular myocytes. The cells were perfused with low-Na+ (60 mM) Tyrode's solution, and Ca2+ and K+ currents were blocked by external Co2+ (3 mM) and internal Cs+ (140 mM), respectively. INa was elicited by depolarizing voltage steps from a holding potential of -100 mV at a temperature of 33 degrees C. PamCar (5 microM) decreased the peak INa (attained at -20 mV or -30 mV) from 6.1 +/- 2.1 nA to 3.9 +/- 1.4 nA (n = 11), or by 36.1% within 2 min, and shifted the curve of steady-state INa inactivation by 5.4 mV in the positive direction (from -76.3 +/- 4.6 mV, control to -70.9 +/- 4.0 mV, in PamCar, n = 4). Partial restoration of the amplitude and the shift of the steady-state inactivation curve of INa was attained after washout of PamCar. In contrast, lysoPtdCho at concentrations over 10 microM irreversibly depressed the INa within 0.5-3 min and the reduction of INa was followed by cell contracture or cell death (n = 9). The survival time, defined as a period from the start of lysoPtdCho application to the time of the last successful recording of the INa (before evolution of sudden changes in the holding current), depended on the concentrations of lysoPtdCho. Both PamCar and lysoPtdCho retarded the time course of activation and inactivation of INa.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
A comparative study of once-a-day morning and once-a-day bedtime administration of 40 mg famotidine in treating duodenal ulcers.
A randomized controlled study comparing once-a-day morning and once-a-day bedtime administration of 40 mg famotidine in treating duodenal ulcers was carried out in 99 Japanese patients. Endoscopic examinations were performed at the baseline and repeated at 3-week intervals until healing was confirmed. Eighty-two patients fulfilled the evaluation criteria (38 in the morning group and 44 in the bedtime group). In 13 of these patients the antisecretory effects of these regimens were also assessed by 24 h intragastric pH monitoring. The healing rates were 66% after 3 weeks and 95% after 6 weeks in the morning group, and 57% after 3 weeks and 80% after 6 weeks in the bedtime group. The differences were insignificant between the two groups, but there was a higher healing rate tendency after 6 weeks in the morning group (0.05 less than P less than 0.10). Regarding pain subsidence, there were no significant differences between the two groups. Both treatments were significantly superior to the control group in increasing 24 h intragastric pH. The morning regimen was significantly superior to the bedtime regimen in suppression of daytime acidity. On the contrary, the bedtime regimen was significantly superior to the morning regimen in suppression of nocturnal acidity. These findings suggest that suppression of nocturnal acidity is important but not essential to promote duodenal ulcer healing and suppression of daytime acidity is equally important. Thus, once-a-day morning administration of 40 mg famotidine seems to be at least as effective as once-a-day bedtime administration of 40 mg famotidine in treating duodenal ulcers.
Adult↗
Acute toxicity of ozone against morphology of gill and erythrocytes of Japanese charr (Salvelinus leucomaenis).
1. Acute toxicity of ozone exposure to Japanese charr (Salvelinus leucomaenis) was studied histopathologically, and hematologically on gill tissue and red blood cells (RBC) under different ozone concentrations (0-0.7 ppm). 2. Exposure of ozone above 0.7 ppm led to characteristic symptoms and all died of choking in 30 min. 3. Many swollen RBC were seen under the scanning electron microscope. 4. RBC congestion was serious in the gill where degeneration of lamellar epithelium was observed. However, injury to chloride cells was not clear.
Animals↗
Blockade of 2,4-dinitrophenol induced ATP sensitive potassium current in guinea pig ventricular myocytes by class I antiarrhythmic drugs.
OBJECTIVE: The aim was to assess the effects of various antiarrhythmic drugs on 2,4-dinitrophenol (DNP) induced outward current (IDNP), presumably the ATP sensitive K+ current (IK,ATP) of isolated cardiac cells and to discuss mechanisms involved in the hypoglycaemia which occurs in patients on these drugs. METHODS: The quasi-steady state current-voltage relationship from the isolated guinea pig ventricular cells was measured using whole cell voltage clamp techniques with a ramp pulse programme. The effects of seven different antiarrhythmic drugs on IDNP were examined. Action potentials were elicited at a rate of 0.2 Hz by an intracellular current injection. RESULTS: DNP (50 mumol.litre-1) increased the quasi-steady state outward current at potentials positive to about -60 mV. This current (IDNP) was completely inhibited by the subsequent application of glibenclamide (1 mumol.litre-1), thereby suggesting that the IDNP is probably IK,ATP. Cibenzoline (10 mumol.litre-1, class Ia), disopyramide (30 mumol.litre-1, class Ia), and procainamide (100 mumol.litre-1, class Ia) significantly inhibited the IDNP by 95.5(SD 11.3)%, 77.8(21.2)%, and 76.4(23.9)% respectively. Flecainide (class 1c) inhibited the IDNP by 66.9(23.9)% at 10 mumol.litre-1 but not at 2 mumol.litre-1. Mexiletine (30 mumol.litre-1, class Ib), pilsicainide (50 mumol.litre-1, class Ic), and E4031 (10 mumol.litre-1, class III) at concentrations as high as approximately fivefold the clinically effective blood levels, did not suppress IDNP. Except for 10 mumol.litre-1 flecainide, all the concentrations listed above which blocked IDNP were within twofold of the clinical blood concentrations documented to be effective for suppression of arrhythmias. Cibenzoline, disopyramide, and procainamide, but not flecainide, belong to class Ia antiarrhythmic drugs. All these class Ia antiarrhythmic drugs "shortened" the action potential duration of guinea pig ventricular cells, an opposite change to that noted for multicellular preparations, eg, guinea pig papillary muscles. CONCLUSIONS: Class Ia antiarrhythmic drugs (cibenzoline, disopyramide, and procainamide) inhibit IDNP (presumably IK,ATP) in guinea pig ventricular cells within a range of therapeutic concentrations. This inhibitory effect of IK,ATP can probably explain the hypoglycaemia which occurs in some patients receiving these drugs, and the prolongation of the action potential duration alleged to occur in "superfused" papillary muscles.
2,4-Dinitrophenol↗
Changes in cardiovascular mass, left ventricular pumping ability and aortic distensibility after calcium antagonists in Wistar-Kyoto and spontaneously hypertensive rats.
OBJECTIVES: To determine the effects of different dihydropyridine calcium antagonists on cardiovascular mass and function in normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). METHODS: The rats were treated daily for 3 weeks with nitrendipine (20 mg/kg), nifedipine (30 mg/kg), nisoldipine (6 mg/kg) or their vehicles. At the conclusion of that period left ventricular pumping ability and aortic distensibility were determined, and the aortic, cardiac and left and right ventricular masses. RESULTS: Each drug reduced arterial pressure in both rat strains; each decreased left ventricular mass in SHR but not in WKY rats. All three agents increased right ventricular mass in WKY rats; only nisoldipine did so in SHR. Each compound improved left ventricular pumping ability in WKY rats, maintaining function even when pressure was abruptly increased to pretreatment levels. In contrast, although all three calcium antagonists improved cardiac performance in SHR at the pharmacologically reduced pressures, pumping ability was not maintained when pressure was increased to pretreatment levels in nisoldipine-treated SHR. All three agents improved aortic distensibility in both strains, but only in SHR was reduced aortic mass demonstrated. CONCLUSIONS: These data not only continue to demonstrate a functional/structural dissociation associated with antihypertensive therapy, but also suggest subtle functional and structural effects that differ even within the same class of calcium antagonists.
Animals↗
Effects of vagal stimulation on cesium-induced early afterdepolarizations and ventricular arrhythmias in rabbits.
BACKGROUND: Previous evidence has shown that increased sympathetic tone enhances the cesium chloride (Cs)-induced early afterdepolarizations (EADs) and ventricular tachycardias (VTs). METHODS AND RESULTS: We assessed the effects of vagal stimulation on Cs-induced EADs and ventricular arrhythmias in the rabbit heart. Monophasic action potentials (MAPs) of the left ventricular endocardium were recorded simultaneously with surface ECG. Two protocols were used: 1) While in their intrinsic sinus rhythm, 11 rabbits were given three intravenous Cs injections (1 mM/kg) 20 minutes apart, and the effects of vagal stimulation on the ventricular arrhythmias thus induced were examined. 2) Under constant atrial pacing (cycle length, 250 msec), EAD amplitude was measured after Cs injection (1 mM/kg) without (five rabbits, control group) or with (four rabbits, vagal stimulation group) vagal stimulation. We observed the following. 1) Cs produced EADs and VTs of polymorphic (PVT) and monomorphic (MVT) types. During PVT, the take-off potential of repetitive premature action potentials in MAP recordings was about the same as the peak level of EADs, and during MVT, the take-off potential was the level of full repolarization. Vagal stimulation suppressed PVT but not MVT. Vagal stimulation after spontaneous termination of MVT restarted MVT of the same morphology at a rate much slower than the preceding sinus rate. 2) EAD amplitude was significantly smaller in the vagal stimulation group than in the control group. CONCLUSIONS: The results suggest that PVT originated from triggering by EADs, whereas MVT was of different origin, and that vagal stimulation suppressed PVT by decreasing the amplitude of EADs.
Action Potentials↗
[Characteristics of drug-refractory sustained ventricular tachycardia].
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Aged↗
Cooperative modulation of voltage-dependent sodium channels by brevetoxin and classical neurotoxins in cultured bovine adrenal medullary cells.
The effects of Ptychodiscus brevis toxin (PbTx-3) on 22Na influx, 45Ca influx and catecholamine secretion were examined in cultured bovine adrenal medullary cells and compared with the effects of classical neurotoxins. PbTx-3 alone had no effects, but greatly enhanced veratridine (30 microM)-induced Na influx, Ca influx and secretion, with a EC50 of 30, 25 and 23 nM, respectively. PbTx-3 (1 microM) reduced EC50 values of veratridine approximately 3-fold and increased the maximal responses caused by saturating concentration (300 microM) of veratridine approximately 1.3 fold. alpha- and beta-Scorpion venom shifted the concentration-response curves of veratridine to the left without altering maximal responses. PbTx-3 in combination with either alpha- or beta-scorpion venom showed only additive effects on Na influx, but augmented veratridine (30 microM)-induced Na influx to a greater extent than PbTx-3, alpha- or beta-scorpion venom alone. Na influx due to these toxins was abolished by 1 microM saxitoxin. Our results suggest that Na channels in adrenal medullary cells have neurotoxin receptors for brevetoxin that allosterically stimulate Na influx initiated by veratridine, leading to increased Ca influx and catecholamine secretion. Allosteric interactions do not exist between brevetoxin and alpha-scorpion venom, or between brevetoxin and beta-scorpion venom, but once Na channels are gated by veratridine, these toxins cooperatively augment Na influx.
Adrenal Medulla↗
[Beta-adrenergic modulation of cardiac Na+ current].
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Action Potentials↗
[A case of hypersensitivity pneumonitis presenting with copious sputum and marked obstructive impairment of lung function].
A 44-year-old male was hospitalized due to dyspnea and persistent cough with copious sputum (about 100 ml/day). Chest radiograph on admission showed hyperinflation and fine nodular shadows throughout both lungs, as well as a tram line appearance in the right lower lung field which suggested thickening of bronchial walls. Pulmonary function tests demonstrated moderate to severe reduction of %VC, FEV1.0 and PaO2. Fiberoptic bronchoscopy revealed inflammatory change in the walls of proximal bronchi. Although his dyspnea resolved rapidly, productive cough and impaired lung function were persistent and improved very slowly over the one-month-period following admission. After resolution, similar symptoms were provoked again 5 to 6 hours after returning to his home, suggesting the recurrence of hypersensitivity pneumonitis. Open lung biopsy was performed for the differential diagnosis of hypersensitivity, diffuse panbronchiolitis, and bronchial asthma, because neither transbronchial lung biopsy nor broncho-alveolar lavage was diagnostic. Histopathology of the open lung biopsy specimens revealed marked desquamation of bronchiolar epithelium in addition to bronchiolo-alveolitis with epithelial granulomas, consistent with hypersensitivity pneumonitis. Copious sputum is a very uncommon clinical feature in hypersensitivity pneumonitis. We consider that the large volume of airway fluid was caused by epithelial ulceration of bronchioles and catarrhal bronchitis associated with hypersensitivity pneumonitis.
Adult↗
A comparative study of once-a-day morning and once-a-day bedtime administration of 40 mg famotidine in treating gastric ulcers.
A randomized controlled study comparing once-a-day morning and once-a-day bedtime administration of 40 mg famotidine in treating gastric ulcers was carried out in 179 Japanese patients. Endoscopic examinations were performed at the baseline and repeated at 4-wk intervals until healing was confirmed. One hundred and sixty-four patients fulfilled the evaluation criteria (81 in the morning group and 83 in the bedtime group). The healing rates were 50.7% after 4 wk and 88.9% after 8 wk in the morning group and 46.5% after 4 wk and 74.7% after 8 wk in the bedtime group. The difference was statistically significant after 8 wk. Significant reductions from baseline for overall pain, beginning during the first 3 days, were likewise found in the two treatment groups. However, the pain severity in hunger state 1 wk after treatment was significantly higher in the bedtime group than in the morning group. Thus, once-a-day morning administration of 40 mg famotidine seems to be superior to once-a-day bedtime administration of 40 mg famotidine in treating gastric ulcers.
Adult↗
Species differences in the distribution and coexistence ratio of serotonin and substance P in the monkey, cat, rat and chick spinal cord.
Serotoninergic raphe-spinal motor neuron projections exhibit wide species differences in both innervation pattern and coexistence of serotonin and substance P. The coexistence ratios vary widely ranging from more than 80% (rat) to less than 1% (chick). Serotonin and substance P positive fibers are also unevenly distributed in the ventral horn of different species: dense clusters of serotonin and substance P positive fibers were preferentially located in the motor neuron pools of extensor muscles of the hip joint (chick) as well as antigravity muscles of the forelimb (cat and rat).
Animals↗
Trimetazidine inhibits Na+,K(+)-ATPase activity, and overdrive hyperpolarization in guinea-pig ventricular muscles.
The effect of trimetazidine on Na+,K(+)-ATPase activity or the Na+,K+ pump was studied in guinea pig ventricular muscles with the use of biochemical and electrophysiological methods. The effect of trimetazidine on enzyme activity was compared with that in the liver, jejunum and kidney obtained from the same species. Na+,K(+)-ATPase activity in the heart and liver was significantly and concentration dependently decreased by trimetazidine (above 1.5 x 10(-5) M). Even the highest concentration (1.5 x 10(-4) M) of trimetazidine failed to decrease the Na+,K(+)-ATPase activity in the jejunum and kidney. The membrane potential was recorded in the ventricular muscle with a microelectrode. The hyperpolarization which followed 1-min overdrive stimulation (3.3 Hz) was decreased by trimetazidine (1.5 x 10(-4) M), but the depolarization during the stimulation was not affected by this drug. Ouabain, a potent Na+,K+ pump inhibitor, markedly decreased the overdrive hyperpolarization and increased the depolarization during the stimulation (10(-7), 5 x 10(-7), 10(-6) M). Therefore, the effect of trimetazidine and ouabain on the Na+,K+ pump-mediated alteration in the resting potential is different, suggesting that trimetazidine has additional direct membrane effects, e.g. a decrease in K+ conductance. In conclusion, trimetazidine inhibits Na+,K(+)-ATPase activity and thus the Na+,K+ pump in the ventricular muscles but with an inhibitory effect about 300 times less than that of ouabain. Trimetazidine inhibited the Na+,K(+)-ATPase in the liver as well, but not that in jejunum and kidney.
Animals↗
Acetylcholine reverses isoproterenol-induced depression of Vmax in residual Na channel-dependent action potentials of guinea-pig cardiac muscles.
We examined effects of acetylcholine (ACh) on isoproterenol (ISP)-induced changes of the upstroke velocity of the action potential (Vmax) in isolated 13.5 mM K(+)-depolarized atrial muscles from guinea-pigs, using conventional glass microelectrode techniques. In some experiments, ventricular muscles were also used, for purposes of comparison. ISP (0.1 microM) decreased the fast component of Vmax (Vmax,fast) and increased the slow component of Vmax (Vmax, slow) of the atrial muscle, as has been noted in ventricular muscle. ACh (0.1 microM) reversed or antagonized these effects of ISP. However, in the presence of atropine (0.1 microM), the antagonism disappeared. In the presence of the Ca2+ channel blocker, D600 (1 microM), the depressant effect of ISP on the Vmax,fast was augmented while ACh exerted a much less restorative effect on the ISP-induced, depressed Vmax,fast. Similar findings were obtained in low (0.36 and 0.072 mM) Ca2+ media. To investigate the possible involvement of GTP-binding protein (Gi) on these ACh effects, we performed similar experiments using atrial muscles obtained from guinea pigs pre-treated with pertussis toxin (150 micrograms/kg) for 48 h. In these preparations, the depressant effect of ISP on the Vmax,fast remained unaffected, while the reversing effect of ACh on the ISP-induced depression of Vmax,fast either specifically diminished or disappeared. These results show that ACh antagonizes the ISP-induced Vmax changes via stimulation of muscarinic ACh receptors and that this effect is presumably mediated by Gi and modified by intracellular Ca2+. Clinical implications are discussed.
Acetylcholine↗
Heart rate-dependent alteration of the frequency and coupling interval of ventricular arrhythmias as measured by 24-hour ECG monitoring.
Twenty-four hour ECG recordings of 132 patients with frequent (greater than 1000/day) ventricular premature contractions (VPCs) were analyzed using a computerized system, designed to evaluate the relationships between 1) the VPC frequency and heart rate (HR) (VPC-HR relation), 2) the coupling interval (CI) of VPCs and HR (CI-HR relation), and 3) the incidence of ventricular tachycardia (VT) and HR (VT-HR relation). The patterns of the VPC-HR relation included: 1) an increase in VPCs with increasing HR (positive correlation, 43 patients), 2) an increase in VPCs at low HR range and a decrease at high HR range, with increasing HR (bidirectional correlation, 74 patients), 3) a decrease in VPCs with increasing HR (negative correlation, 7 patients) and 4) constant VPCs over all HRs (flat correlation, 8 patients). Patients were divided into 2 broad categories according to whether they had a positive correlation (P group, 43 patients) or the other correlations (non-positive or NP group, 89 patients). Of 132 patients, the CI-HR relation was negative in 129 (98%) and positive in only 3 (2%). Patients with frequent VTs (10 or more events over 24h) were significantly more frequent in the P (9 patients, 21%) than in the NP group (7 patients, 8%, p less than 0.05). However, mean HR, mean CI, total VPC counts and the slope of CI-HR relation were not significantly different between the groups. The VT-HR relation observed in 16 patients with frequent VTs were positive in 9 of the P group and in 2 of the NP group and non-positive in 5 of the NP group.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
[Effects of calcium antagonist, angiotensin-converting enzyme inhibitors and beta-blocker on hemodynamic and sympathetic nerve responses to exercise in essential hypertension].
To investigate the effects of antihypertensive drugs on hemodynamic and sympathetic nerve responses to exercise, graded ergometer exercise tests were performed before and after two-week administration of nifedipine, captopril and metoprolol in 18 patients with essential hypertension. The arterial pressure, heart rates (HR), and left ventricular functions as obtained by echocardiography, and the plasma norepinephrine (PNE) levels, were evaluated at rest and during submaximal exercise before and after two-week treatment with nifedipine (40 mg/day, 5 cases), captopril (37.5-75 mg/day, 6 cases) and metoprolol (60 mg/day, 7 cases). These 3 drugs significantly reduced systolic (SBP) and diastolic (DBP) blood pressures but caused no significant changes in resting PNE levels. Nifedipine produced no significant changes in HR and cardiac output (CO) at rest, but augmented the increase in HR (delta HR) and SBP (delta SBP) during submaximal exercise. The increase in PNE (delta PNE) was also augmented by nifedipine. Captopril reduced left ventricular end-diastolic volume and CO without changes in HR and fractional shortening (FS) at rest; whereas, it did not affect delta HR, delta CO, delta SBP or delta PNE during exercise. Metoprolol reduced HR and CO at rest, and also resulted in a decrease in delta FS and delta CO during submaximal exercise. delta SBP was unchanged and delta PNE was increased by treatment with metoprolol. These results indicate that, in hypertensive subjects, the effects on the hemodynamic and sympathetic nerve responses to exercise are different among these 3 antihypertensive drugs despite their identical effects on blood pressure.
Adrenergic beta-Antagonists↗