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Biomedical subjects

M Wada

Publications and source records attributed to M Wada.

At least 757 records · Page 42Linked to original sources
PubMed1975

Body surface isopotential mapping in Wolff-Parkinson-White syndrome: noninvasive method to determine the localization of the accessory atrioventricular pathway.

The body surface isopotential maps of 22 patients with WPM syndrome were obtained from the 85 unipolar lead ECG's using the on-line minicomputer system newly devised by the author's group. The map patterns were classified into three types-I, II, and III (Type I, eight; Type II, seven; Type III, three; and unclassified, four cases). In Type I, the back surface displayed the negative potential throughout the entire ventricular activation, and at the terminal stage the lower precordial area displayed the positive potential and the upper precordial area, the negative one. Type II was characterized by two longitudinal lines, one staying at its place on the back and the other moving right to left on the precordial area following the process of ventricular activation. In Type III, the right precordial area displayed negative potential in the early stage, and in the terminal stage the upper part of the right side of chest surface displayed positive potential and the lower part, negative potential. It was surmised from these patterns that the pre-excited area was located at the posterior region of the ventricles in Type I, at the right ventricle in Type II, and the right ventricular base near the posterior margin of the ventricular septum in Type III. Type A patients in the conventional ECG classification fell under Type I; Type C patients, under Type III; Type B patients under either Type I or Type II.

Adolescent↗
PubMed1975

Ischemic heart disease and hyperlipidemia.

Studies on lipid and lipoprotein abnormalities which are associable with ischemic heart disease were presented. None of the subjects studied for this report had clinical signs or symptoms characteristic to "familial or sporadic" hyperlipoproteinemia. Only few showed gross abnormalities in lipid chemistries which are compatible with these clinical entities. Lipid abnormalities characteristic to the majority of ischemic heart patients were modest to moderate increase of serum total and free cholesterol and triglyceride; either independent increase or combined increase of these lipid fractions. Determination of free cholesterol may favor to detect such minute abnormality in modest hyperlipidemia as seen in ischemic heart patients. As expressed by our lipoprotein PAG electrophoresis pattern, B and Bp pattern (Fig. 1) seemed to be important lipoprotein abnormalities because of high incidence of ischemic heart disease (60 to 65%). Another feature of these hyperbeta lipoproteinemic state without (B pattern) or with (Bp pattern) moderate prebeta lipoprotein is highly suggestive of premature onset of ischemic heart suggestive premature onset of ischemic heart disease in the subjects with these lipoprotein patterns. Pb battern (hyperpre-beta lipoproteinemic state) was the next, because of frequent occurrence of this pattern (approx. 30%) among the cardiovascular patients and relatively high incidence (approx. 40%) of ischemic heart disease. PB pattern (combine hyperpre-beta and hyperbeta lipoproteinemic state) occurred rarely but incidence of ischemic heart disease in the subject with this pattern was high (approx. 40%). Midband lipoprotein which is one of the unique lipoprotein species detected by PAG electrophoresis may possibly reflect disordered lipoprotein metabolism. However, its association with ischemic heart disease seemed highly unlikely. However, further studies on this and other unusual lipoproteins detectable with PAG electrophoresis seems productive. Extensive studies on cine coronary angiographically established subjects (well characterized study subjects) with this new method in addition to the others would be highly productive to obtain more reliable conclusion on this subject, and hence, to obtain more effective guide line for early identification or for prevention of coronary atherosclerosis.

Adult↗
PubMed1975

A case report of Turner's syndrome with ring X chromosome.

A case of Turner's syndrome with short stature and 45, XO/46, XXr mosaicism in chromosome study was presented. With special emphasis on endocrinological study, the size of the breasts was normal in contrast to the poor development of the breasts in most of types of Turner's syndrome. She showed normal thyroid function, slightly low level of urinary 17-OHCS, decreased 17-KS, poor response in metopirone test and poor response of HGH to insulin.

17-Hydroxycorticosteroids↗
PubMed1975

Studies on the effects of hemodialysis on plasma lipoproteins.

Plasma Lps of the patients on maintenance hemodialysis and the patients with other specific renal diseases have been studied. The patients on hemodialysis frequently showed gross abnormality in their plasma Lps, which was differentiated from the abnormalities demonstrated in other renal diseases or clinical entities. An exception was type-III hyperlipoproteinemia; i.e. Lp electrophoretograms of the hemodialysis patients resembled those ultracentrifugal fractions had been made had VLDL of beta-migration in paper electrophoresis and another had VLDL or pre-beta-migration. During hemodialysis, intravascular lipolysis, accelerated by heparin infusion, affected all plasma Lps, producing an increase of alpha-Lps and cholestrol ester-rich-beta-Lp. The accelerated triglyceride hydrolysis under circumstances of high glucose availability may stimulate resynthesis of endogenous triglyceriderich Lps, which characterizes the plasma Lp abnormality in more than half of the hemodialysis patients. The abnormality may not be attribuate to the predisposing renal disease but due to an accumlation of the characteristic Lp during the course of maintenace hemodialysis. A possible cause of accelerated atherosclerosis in the hemodialysis patients may be the accumulation of remnants of plasma Lp catabolism and the stimulated synthesis of triglycerdie-rich plasma Lp.

Adult↗
PubMed1974

Sequential change in the different of potential distribution between a normal subject and simulated torso model.

Isopotential map was obtained every 3 msec after the onset of ventricular activation from 85 unipolar lead ECGs of a normal subject (Measured map) and similar map at the corresponding instant (Simulated map) was also obtained by means of mathematical calculation under the assumption that the cardiac electromotive force can be represented by a single electric dipole fixed at the heart center. These 2 maps were quantitatively compared and difference was delineated on a map (Difference map). Although, in major aspect, there was a fairly good agreement between Measured and Simulated maps during early stages of ventricular activation, a remarkable difference of potential distribution began to appear between them around the time of occurrence of epicardial breakthrough of the ventricular activation front. From that t me on, it became impossible to represent the cardiac electromotive force into 2 or more electric dipoles in Difference map. Difference maps around the instant of epicardial breakthrough of the ventricular activation were supposed to be helpful for the estimation of the spread of ventricular activation.

Action Potentials↗