Biomedical subjects

S Sada

Publications and source records attributed to S Sada.

10 recordsLinked to original sources

PubMed2001

Optimisation of shape kernel and threshold in image-processing motion analysers.

The aim of the work is to optimise the image processing of a motion analyser. This is to improve accuracy, which is crucial for neurophysiological and rehabilitation applications. A new motion analyser, ELITE-S2, for installation on the International Space Station is described, with the focus on image processing. Important improvements are expected in the hardware of ELITE-S2 compared with ELITE and previous versions (ELITE-S and Kinelite). The core algorithm for marker recognition was based on the current ELITE version, using the cross-correlation technique. This technique was based on the matching of the expected marker shape, the so-called kernel, with image features. Optimisation of the kernel parameters was achieved using a genetic algorithm, taking into account noise rejection and accuracy. Optimisation was achieved by performing tests on six highly precise grids (with marker diameters ranging from 1.5 to 4 mm), representing all allowed marker image sizes, and on a noise image. The results of comparing the optimised kernels and the current ELITE version showed a great improvement in marker recognition accuracy, while noise rejection characteristics were preserved. An average increase in marker co-ordinate accuracy of +22% was achieved, corresponding to a mean accuracy of 0.11 pixel in comparison with 0.14 pixel, measured over all grids. An improvement of +37%, corresponding to an improvement from 0.22 pixel to 0.14 pixel, was observed over the grid with the biggest markers.

Algorithms↗

PubMed1996

[A Japanese family with probably autosomal dominant adult-onset leukodystrophy].

We report here a family with leukodystrophy clinical features of which are characterized as adult onset, probably autosomal dominant inheritance, hyperreflexia, cerebellar ataxia, autonomic dysfunction and no peripheral nerve involvement. T2-weighted brain MRI revealed diffuse high signal areas in the cerebral white matter. The disorder in our subjects can be distinguished from most leukodystrophies in terms of genetic inheritance, clinical manifestations and laboratory data. Our family is quite similar to the kindred which Eldridge et al. described in 1984 as "hereditary adult-onset leukodystrophy simulating chronic progressive multiple sclerosis". Our family is the third report of this type of leukodystrophy and the first among non-Irish/Scottish family.

Age of Onset↗

PubMed1986

Recovery of the slow action potential is hastened by the calcium slow channel agonist, Bay-K-8644.

Effects of the positive inotropic drug, Bay-K-8644, were studied on the slow action potential (AP) parameters and diastolic recovery of Vmax in K+ (22 mM)-depolarized rabbit papillary muscles. Bay-K-8644 (10(-6) M) increased the amplitude, maximum rate of rise (Vmax) and duration of the slow APs. Diastolic recovery of Vmax, examined by a paired-pulse protocol, was approximated by a single exponential function, both in control and in drug-treated muscles. The time constant of the recovery for drug-treated preparations was 171 +/- 20 ms (n = 9), and was significantly smaller than that for control: 414 +/- 45 ms (n = 12) (P less than 0.001). The diastolic intervals which allow 90% recovery of Vmax (T90%) were: 752 +/- 106 ms (n = 12) for control and 364 +/- 53 ms (n = 9) in the presence of drug, the latter being significantly shorter (P less than 0.01). The extent of the reductions in Vmax, at driving frequencies higher than 0.5 Hz, was minimal in the presence of the drug compared to the control. It was concluded that Bay-K-8644 not only enhanced the slow inward current, but also accelerated the reactivation process of the slow inward current and Ca2+ slow channel.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1986

Effects of bucumolol, nadolol and nifenalol on maximum upstroke velocity of action potential in guinea pig papillary muscles.

The effects of bucumolol (BUC), nadolol (NAD) and nifenalol (NIF) on contractile forces and on action potentials (APs) were investigated in isolated guinea pig atrial and papillary muscles, respectively. Log 1/ED40 values for the negative inotropic effects of these drugs were 0.097, 10 and 0.74 mmol/l in this order. BUC (50 mumol/l), NAD (0.5 mmol/l) and NIF (0.2 mmol/l) produced about 60, 20 and 20% reduction of Vmax at 1 Hz. The frequency-dependent reductions at these and higher concentrations were greatest for BUC, intermediate for NAD and least for NIF. These potencies at certain frequencies were, as a whole, consistent with log P-potency relationship established in our previous papers (Harada et al. 1981; Ban et al. 1985). The reductions of Vmax in APs in response to premature stimuli during basic stimuli at the rate of 0.25 or 0.027 Hz decayed exponentially during diastolic intervals (DI). The time constants of these decay process (tau) estimated by linear and nonlinear regression analyses and by eye were 12.2-9.6 s for BUC (50-100 mumol/l) and 2.9-4.8 s for NAD (1-2 mmol/l) and 57-87 ms for NIF (0.2-1 mmol/l). In terms of the molecular weight (MW)-log tau relationship (Ban et al. 1985), these tau values are within the 95% fiducial limit for BUC and NAD and deviated from the lower fiducial limit for NIF. The frequency-dependent reductions of Vmax by these drugs were explained in terms of a function of tau and the intercept Ao. Based on the study made by Cohen et al.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed1986

Reactivation processes of three inward current systems involved in the rising phase of the action potentials in embryonic chick hearts.

In embryonic chick hearts during development, there are three inward current systems which are involved in the rising phases of the action potentials (APs): fast INa, slow ICa, and tetrodotoxin-insensitive slow INa. To assess reactivation processes for these three types of inward current channels (fast Na+, slow Ca2+, and slow Na+ channels), diastolic recovery of Vmax was examined in embryonic chick hearts using a paired-pulse protocol. In all cases, the diastolic recoveries were approximated by single exponential functions. The time constants of recovery (tau(V)) and T90% (the diastolic interval which allows 90% recovery of Vmax of the premature AP) were, respectively, 53.1 +/- 5.2 and 61.5 +/- 8.6 ms for Na+-dependent fast AP (n = 10), 376.9 +/- 49.3 and 659.2 +/- 113.1 ms for the Ca2+-dependent slow AP (n = 10), and 40.7 +/- 5.3 and 45.6 +/- 12.0 ms for the Na+-dependent slow AP (n = 10). In the presence of lidocaine, the recovery kinetics also appeared to be single exponentials for diastolic intervals up to 500 ms (fast APs) or 250 ms (slow APs). The reactivation processes for the Na+-dependent fast and slow channels were significantly slowed by 100 microM lidocaine. In addition, in the presence of 100 microM lidocaine, Vmax was depressed in a frequency-dependent manner; the higher the stimulation frequency, the greater the depression. Hence, the fast Na+ channels and the slow Na+ channels had the following similarities: rapid reactivation, reactivation slowed by lidocaine, and frequency-dependent depression in the presence of lidocaine.

Action Potentials↗

PubMed1986

Depressant action of Ca-antagonists on slow action potentials in guinea pig ventricular muscles.

The depressant action of four Ca antagonists, including a novel drug, tiapamil, on Ca channels was investigated using a conventional microelectrode technique. "All or none" slow action potentials were recorded in K+-depolarized guinea-pig papillary muscles. Verapamil and diltiazem decreased the amplitude and maximum rate of rise (Vmax) of the slow action potentials at concentrations up to 2 microM. The depressant effect of a novel Ca-antagonist, tiapamil, on the slow action potentials was as marked as that of verapamil and diltiazem. However, prenylamine was less potent than the other 3 drugs. In addition, the action of all drugs on the slow action potentials was enhanced as the frequency of stimulation was increased between 0.0083 and 1 Hz. It was concluded that tiapamil, as verapamil and diltiazem, produced a frequency-dependent blockade of the slow Ca channel.

Action Potentials↗

PubMed1985

Effects of diacetyl monoxime (DAM) on slow and fast action potentials of young and old embryonic chick hearts and rabbit hearts.

The effects of the negative inotropic agent, diacetyl monoxime (DAM), were studied on cardiac action potentials in young (3 day old) and old (13-18 day old) embryonic chick hearts and in rabbit papillary muscles. DAM (5-10 mM) decreased the action potential (AP) amplitude, the maximum rate of rise (Vmax), and AP duration of slow and fast APs in both young and old embryonic chick hearts. Concomitantly with these changes, the spontaneous beating rate was increased in young hearts. At 20 mM DAM, the maximum diastolic potential (MDP) was decreased. In fast APs of old embryonic chick hearts, the most prominent effect of DAM was a shortening of AP duration, the effects on AP amplitude, Vmax, and resting potential being less. In rabbit papillary muscles, DAM had little effect on the slow AP parameters except for shortening of AP duration. The onset of the DAM effects was rapid, the peak effect being attained by 5 min in all preparations. Reversal of the effects of DAM upon washout were fast, complete recovery being attained within 10 min. We conclude that DAM suppressed the slow Na+ current present in young chick embryonic hearts. The effects of DAM, up to 10 mM, on Vmax of the fast Na+-dependent APs in old embryonic chick hearts was less, and there was no effect on rabbit hearts. DAM suppressed the slow Ca2+-dependent APs in old embryonic chick hearts but not in rabbit papillary muscles, suggesting that the effect of DAM on the Ca2+ slow channels depends on the species.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed1985

Effects of para-substituted beta-adrenoceptor blocking agents and methyl-substituted phenoxypropanolamine derivatives on maximum upstroke velocity of action potential in guinea-pig papillary muscles.

The effects of atenolol (2-5 mmol/l), sotalol (1-2 mmol/l) and pamatolol (0.1-1 mmol/l), together with N-tertiary butyl phenoxypropanolamines with o-methyl (D-2T: 50-100 mumol/l) m-methyl (D-3T: 50-100 mumol/l) and p-methyl (D-4T: 100-200 mumol/l) group as well as with o,p-methyl groups (D-24T) (50-100 mumol/l) on action potentials (APs) were investigated in isolated guinea-pig papillary muscles. All the drugs in these concentrations produced a concentration-dependent reduction of the maximum upstroke velocity (Vmax). The reduction of Vmax in premature APs induced by stimuli interpolated between the basic driving rate of 0.25, 0.1 or 0.027 Hz decayed exponentially during diastolic intervals. The time constants of these decay processes tau for atenolol, pamatolol and sotalol ranged between 260-541 ms, those for D-3T and D-4T between 655-1,166 ms, and D-2T and D-24T between 1,565-1,931 ms. A drug which provided larger tau values caused the reduction of Vmax in a wider range of the frequency.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed1985

The calcium channel agonist, Bay K-8644, antagonizes effects of diacetyl monoxime on cardiac tissues.

Effects of a novel slow channel activator, Bay K-8644 (Bay K), were studied on slow action potential (APs) in young and old embryonic chick hearts, and on its antagonism of the effects of diacetyl monoxime (DAM). The slow APs of young hearts are mediated by slow Na+ channels, whereas those of old hearts are mediated by slow Ca2+ channels. In slow APs of old (13-18 days old) embryonic chick hearts superfused with a high (22 mM) K+ solution, Bay K (10-6 M) gradually increased the amplitude, maximum rate of rise (Vmax), and duration of the slow APs. The actions of Bay K persisted for a long time (greater than 30 min) after washout of the drug. DAM (10 mM) depressed the Vmax, duration and amplitude of the slow APs. Some of the changes in slow AP parameters produced by DAM, e.g., Vmax decrease, were antagonized by the addition of Bay K (10(-6) M). In 3-day-old embryonic chick hearts. Bay K potentiated the slow APs and DAM depressed them; Bay K antagonized these effects of DAM. Thus, the actions of Bay K and DAM are likely to be produced, respectively, via the activation and depression of slow Ca2+ channels in old embryonic chick hearts. In addition, the drugs seem to influence slow Na+ channels found in young embryonic chick hearts.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMedDate not supplied

Actions of the slow channel activator, Bay-K-8644, on the electrical activity of 3-day-old embryonic chick hearts.

In order to assess the effects of Bay-K-8644 on electrical activities of young embryonic chick hearts in which the rising phase of the action potential (AP) depends on tetrodotoxin-insensitive slow Na+ currents, slow AP were recorded in spontaneously beating 3-day-old embryonic chick hearts. Bay-K-8644(10(-6) mol/l) caused increases in the maximum rate of rise, amplitude, and duration of the slow AP; there was a slow increase in the spontaneous firing rate. Thus, Bay-K-8644 stimulates Na+ influx through TTX-insensitive slow channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗