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New nonlinear image processing techniques, in particular smoothing based on the understanding of the image, may create computerized tomography (CT) images of good quality using less radiation. Such techniques may be applied before the reconstruction and particularly after it. Current CT scanners use strong linear low-pass filters applied to the CT projections, reducing noise but also deteriorating the resolution of the image. The method in this study was to apply a weak low-pass filter on the projections, to perform the reconstruction, and only then to apply a nonlinear filter on the image. Various kinds of nonlinear filters were investigated based on the fact that the image is approximately piecewise constant. The filters were applied with many values of several parameters and the effects on the spatial resolution and the noise reduction were evaluated. The signal-to-noise ratio of a high-contrast phantom image processed were compared with the nonlinear filter, with the SNR of the phantom images obtained with the built-in CT linear filters in two scanning modes, the normal and the ultra high resolution modes. It was found that the nonlinear filters improve the SNR of the image, compared to the built-in filters, about three times for the normal mode and twice for the UHR scanning mode. The most successful filter on low-contrast phantom image was applied and it also seems to lead to promising results. These results seem to show that applying nonlinear filters on CT images might lead to better image quality than using the current linear filters.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac glycosides such as digoxin or ouabain have long been known to influence the strength of contraction of cardiac muscle. Although the mechanism of action of these compounds remains unknown, all the proposed modes of action are based on initial binding to specific membrane receptors which are part of the (Na+ + K+)ATPase complex. These receptors, well characterized and defined, suggest the existence of an endogenous substance capable of binding to them, in analogy with endogenous opiates, discovered long after morphine and its receptors. As glycosides affect (Na+ + K+)ATPase activity, an endogenous substance may be a regulator of this important enzyme. Indeed, the search for endogenous regulators of the (Na+ + K+)ATPase or ouabain-like compounds (OLC) has recently intensified. These compounds, extracted and partially purified from mammalian brain, heart, blood and urine, and from toad skin and plasma, have been shown to inhibit 3H-ouabain binding and (Na+ + K+)ATPase activity. We report here that in addition to these effects, the OLC, highly purified from toad skin and sheep brain, increases the force of contraction of frog and guinea pig atrium.

Images obtained by digital fluorography were checked for compressability. These images include images of coronary vessels and images of peripheral vessels. These images have a very low signal-to-noise ratio compared to the optical images usually used for developing compression methods. Configurational entropy was used to represent the information content of these images. Reversible prediction algorithms were extensively checked in a search for minimal residual information, enabling more efficient reversible compression. Optimal results were obtained for algorithms based on two or three neighboring pixels and a semiempirical rule, based on the noise level, was found which decides on the best approach. It was found that raw data images are more predictable than subtracted images although the latter are visually preferred.

The effects of adrenaline and the beta-agonist isoprenaline on the time course of tension reactivation were studied in several cardiac tissues. The aim of the study was to assess whether experimental evidence can be found for a role of the sarcoplasmic reticulum in the reactivation of tension. It was assumed that calcium recycles between different parts of the reticulum, and that this recycling may affect tension repriming. Isoprenaline was assumed to enhance such recycling by increasing the uptake of calcium, following its release during a preceding contraction. Isoprenaline (in the range of 40 nM to 4 microM) was found to enhance tension repriming in adult guinea pig atria. However, in adult rat atria, isoprenaline often gave a complex effect, with a smaller degree of repriming at short intervals, and enhanced repriming at longer intervals. This was thought to reflect the balance between the enhancing effect of the drug on calcium recycling and an augmented release from the sarcoplasmic reticulum (SR). In striking contrast, there was no effect of isoprenaline on tension repriming in neonatal guinea pig atria and a retardation in neonatal rat atria. This was interpreted as reflecting the lack of a sarcoplasmic network in the neonatal tissue. The effects of isoprenaline on tension repriming in the frog atrium (which also has a sparse sarcoplasmic reticulum network) were also found to be complex; low concentrations (40 nM) enhanced the process, and high concentrations (0.4 microM) retarded it. Intermediate levels often produced a 'crossover' effect: more reactivation at short intervals, and less at long intervals. The interpretation of these results was that there are two processes which interact to determine the amount of tension produced at short intervals after each contraction: the basal reactivation process and some augmenting mechanism superimposed on it. This mechanism is probably related to other behavioural features of cardiac muscle, such as rate-dependent increases in membrane calcium currents. It is relevant mainly in those cases where tension repriming depends on membrane calcium currents. Further experiments (in the frog atrium) with elevated calcium and with the alpha-adrenergic agonist phenylephrine (both of which slowed down the reactivation process) also support this idea. These agents elevate internal calcium levels, and presumably saturate the augmenting mechanism (by producing maximal tension responses).(ABSTRACT TRUNCATED AT 400 WORDS)

The process of tension repriming and the phenomenon of tension potentiation after premature stimulation (post-extrasystolic potentiation, PESP) were studied in the adult guinea pig atrium. The following results were obtained. (i) Reducing extracellular calcium, [Ca]o, to 50% of normal did not significantly change the rate of tension repriming. However, in the presence of 5 microM isoprenaline (which greatly speeded up repriming) the same reduction in [Ca]o slowed down the repriming process. (ii) Increases in the rate of stimulation enhanced the rate of tension repriming in a control medium, but this rate-dependence was absent in the presence of isoprenaline. (iii) Isoprenaline (20 microM) abolished PESP. A reduction in [Ca]o or the addition of verapamil (still with isoprenaline) partly restored tension potentiation. In neonatal guinea pig atria, a large PESP was evident, which was only slightly reduced by isoprenaline. These results are interpreted as reflecting changes induced by isoprenaline in the degree of filling of sarcoplasmic reticulum (SR) stores with calcium, and in the rate of calcium recycling between uptake and release sites within the SR network. The large PESP found in the neonate, and its relative insensitivity to isoprenaline was interpreted as reflecting a scarcity of SR. This implies that tension potentiation may also reflect changes in sarcolemmal calcium currents.

The time course of reactivation of the calcium current in isolated single cardiac cells is complex. The rising phase is sigmoid and there is an overshoot. Catecholamines increase the initial rate of reactivation but reduce or abolish the overshoot. This combination of effects results in a 'crossover', so that the net effect of adrenaline depends on the pulse interval used. Acetylcholine not only reduces the current amplitude, it also substantially slows recovery. At short intervals the effect of acetylcholine is therefore very large. Agents that increase intracellular cyclic AMP levels affect the amplitude of the current but do not have a large effect on the reactivation time course. It is suggested that the autonomic transmitters exert their effects by controlling the local calcium concentration near the inner surface of the channels. This is supported by the fact that there are natural variations in reactivation time course between different cells and that these are correlated with their calcium loading, as judged by other electrophysiological criteria, such as the speed of calcium current inactivation and the presence of the calcium-dependent slow inward current.

Stage XIII chick blastoderms deprived of the marginal zone, the area opaca and the posterior half of the hypoblast, when incubated further developed axes whose orientation in 50% of the cases was according to the original blastoderm's orientation, whilst in 50% of the cases they developed at 90 degrees from the posterior side. Those results illustrate the quantitative differences in inductivity between the anterior and the posterior hypoblastic halves. Normally the posterior region has the highest effect but other regions can also bring about the development of an embryonic axis if allowed to act upon the epiblast for a sufficiently long period of time. The possible ways in which a chick hypoblast influences the epiblast to develop an embryo are examined in the light of recent findings and of new experiments described below.

Beat rate, contractility and viability of cultured myocardial cells perfused with solutions containing various concentrations of T-2 toxin were studied. While doses below 50 micrograms/ml had no immediate effect, those above 250 micrograms/ml decreased beat rate and amplitude. After 10-30 min of perfusion most cells stopped beating and did not restart after withdrawal of toxin. Nevertheless, most cells remained viable as judged by morphology and trypan blue exclusion. A 24-h exposure to doses of 5 or 2.5 micrograms/ml of toxin decreased the beat rate and inotropic responses of the myocytes. After 48 h cell death ensued. Thus T-2 toxin has some direct toxicity to myocardial cells but the lethal dose seems too high to make this the cause of cardiovascular failure.

The pattern of contraction of the endocardial wall of the left ventricle in the right anterior oblique cineangiogram was studied by using a frame by frame radial technique and a fixed centroid without correction for rotation and translation motion during the cardiac cycle. Spatial defects of contraction were quantitated by measuring the shortening fraction of each radius and temporospatial defects by using a time-contraction integral. Twelve normal subjects were used as a basis for comparison. Thirty-two patients with isolated disease of the left anterior descending (LAD) coronary artery were divided into seven arbitrary clinicopathological subsets. Five subsets showed significant quantitative differences in contraction from the normal subjects but there was no significant difference between the subsets. They had a typical defect of contraction in the distal two thirds of the anterior wall, the apex and distal quarter of the inferior wall of the left ventricle. The subsets included: (1) patients who had undergone an anterior myocardial infarction and who had total occlusion of the LAD artery and a large anterior infarction on ECG; (2) patients with a previous classical myocardial infarction but with only 95% residual narrowing of the LAD; (3) patients with an anterior infarction and total occlusion of the LAD with return of the R waves in the anterior precordial leads; (4) patients with anterior infarction, LAD obstruction and left bundle branch block and (5) patients with anterior infarction but with early successful reperfusion with intracoronary streptokinase. Two other subsets, (1) patients with total obstruction of the LAD without a clinical myocardial infarction or (2) subtotal occlusion of the LAD without infarction, had mild left ventricular dysfunction at rest and did not differ significantly from normal.

T-2 toxin is the major lethal component of several Fusarium fungi implicated in the disease of man and animals. We used isolated rats hearts to test the T-2 toxin cardiotoxicity. Electrodynamics and ultrastructural parameters were studied. The main changes consisted of decreased contractility and electrocardiographic abnormalities without much effect on heart rate or QRS and QT intervals. Ultrastructurally, swelling of myofibers and their mitochondria occurred and damage to the plasma membrane was seen. It is possible that the T-2 effect is mediated through soluble thiol to cause cytoplasmic calcium decrease and loss of plasma membrane integrity.