[Stress analysis of posterior bridge. Case of abutment teeth with reduced supporting tissues. Part I (Finite element method)].
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Biomedical subjects
Publications and source records attributed to K Miyatake.
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Pyruvate:NADP+ oxidoreductase was homogeneously purified from crude extract of Euglena gracilis. The Mr of the enzyme was estimated to be 309,000 by gel filtration. The enzyme migrated as a single protein band with Mr of 166,000 by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, suggesting that the enzyme consists of two identical polypeptides. The absorption spectrum of the native enzyme exhibited maxima at 278, 380, and 430 nm, and a broad shoulder was observed around 480 nm; the maximum at 430 nm was eliminated by reduction of the enzyme with dithionite. Reduction of the enzyme with pyruvate and CoA and reoxidation with NADP+ were proved from changes of absorption spectra. The enzyme contained 2 molecules of FAD and 8 molecules of iron. It was also indicated that the enzyme was thiamine pyrophosphate-dependent. The enzyme was oxygen-sensitive, and the reaction was affected by the presence of oxygen. Pyruvate was the most active substrate, but the enzyme was slightly active for 2-oxobutyrate, 3-hydroxypyruvate, and oxalacetate, but not for glyoxylate and 2-oxoglutarate. The native electron acceptor was NADP+, whereas NAD+ was completely inactive. Methyl viologen, benzyl viologen, FAD, and FMN were utilized as artificial electron acceptors, whereas spinach and Clostridium ferredoxins were inactive. Pyruvate synthesis by reductive carboxylation of acetyl-CoA with NADPH as the electron donor occurred by the reverse reaction of the enzyme. The enzyme also catalyzed a pyruvate-CO2 exchange reaction and electron-transfer reaction from NADPH to other electron acceptors like methyl viologen. These results indicate that pyruvate:NADP+ oxidoreductase in E. gracilis is clearly distinct from either the pyruvate dehydrogenase multienzyme complex or pyruvate:ferredoxin oxidoreductase.
The aim of the present study was to elucidate the mechanisms of mitral regurgitation accompanying myocardial infarction. Severity and site of mitral regurgitation was evaluated by the real-time two-dimensional Doppler flow imaging technique in 81 patients with old myocardial infarction. The incidence of mitral regurgitation did not depend on the region of infarction. There was, however, a close relationship between the site of regurgitation and the region of infarction. In patients with mitral regurgitation spurting from the posteromedial area of the valve, the inferior wall was involved in infarction without exception and in some of these patients, the posteromedial papillary muscle was also found to be affected by myocardial infarction; in those with regurgitation spurting from the anterolateral area, the anterior wall showed asynergy. On the other hand in patients with mitral regurgitation spurting from the central area, the region of infarction varied. In these patients, however, the larger the diameter of the mitral anulus, the more severe the grade of regurgitation. The extent of asynergy was another factor related to the severity of mitral regurgitation. Both longitudinally and transversely, broad infarction leads to the enlargement of the mitral anulus. However, even if the mitral anulus is not so dilated, severe involvement of either commissural area results in severe mitral regurgitation from the same commissural side. Thus, there are two major causative factors of mitral regurgitation: (1) asynergy of the papillary muscle or the ventricle that results in mitral regurgitation located in the commissural area of the same side as asynergy, and (2) enlargement of mitral anulus, which results in regurgitation from the central area of the orifice.(ABSTRACT TRUNCATED AT 250 WORDS)
The validity of continuous wave Doppler ultrasound estimation of the peak pressure gradient between the aorta (Ao) and pulmonary artery (PA) in patients with patent ductus arteriosus (PDA) was evaluated. Ten patients, all without other anomalies, underwent cardiac catheterization and cine-angiography, and the peak pressure gradient between the Ao and PA (dP(C)) was measured during catheterization. In all cases the mean PA pressure was less than 35 mmHg. According to the angiographic findings, the patients were categorized as Group A, consisting of seven patients whose features of the ductus were wedge- or tube-like in configuration; Group B, consisting of two patients whose features were termed "orifice-like" stenosis including one with abrupt narrowing on the PA side of the ductus and the other with a short segmental ductus. Group C consisted of one patient who had a long curved segmental ductus. The maximum velocity of ductus flow was measured by continuous wave Doppler ultrasonography, and the estimated peak pressure gradient between the Ao and PA by Doppler (dP(D] was calculated using the simplified Bernoulli equation (dP = 4V2). In group A, dP(D) was overestimated compared to dP(C) in all patients by 19 to 51 mmHg (mean 34 mmHg). However, in group B, the difference between dP(D) and dP(C) was small, 5 mmHg and 7 mmHg, respectively. In group C, dP(D) was underestimated as opposed to dP(C). Thus, in the limited cases, the simplified Bernoulli equation could be used in estimating the peak pressure gradient between the Ao and PA. However, this equation leads to overestimation in many cases.(ABSTRACT TRUNCATED AT 250 WORDS)
Using pulsed Doppler echocardiography, the effects of postural change on the blood flow pattern in the superior vena cava and in the right ventricular inflow tract were investigated to evaluate the physiological role of the pericardium. Eight cases of left-sided pericardial defect and eight healthy subjects were examined. 1. Suppressed inflow into the right atrium during systole in left-sided pericardial defect was manifested as a reduction of the systolic wave (S) in the superior caval vein and impairment of the systolic shift of the tricuspid annulus. This suppression suggested unsatisfactory volume expansion in the right atrium due to the absence of negative intrapericardial pressure. 2. In left-sided pericardial defect, the right ventricular inflow pattern differed from the normal, most distinctly in the right lateral recumbent position, though the cardiac motion was nearly identical with that of the normal in this position. In this position, the ratio of the peak velocity of presystolic filling to that of rapid filling was increased, and the deceleration half time of rapid filling was prolonged. These findings indicated that the right ventricular rapid filling was retarded, and was compensated by the filling due to atrial contraction. It is assumed that right ventricular filling is influenced by hydrostatic pressure due to changes in posture in the absence of restriction by the pericardium. 3. It is concluded that the pericardium maintains negative intrapericardial pressure, so that each cardiac chamber is uniformly expanded for its filling, and that this function minimizes the influence of posture on cardiac hemodynamics.
The purpose of this study was (1) to analyze the factors responsible for errors in the two-dimensional Doppler echographic measurements of cardiac output (C.O.) and (2) to establish a noninvasive method for measuring C.O. The subjects were 50 cardiac patients who had neither aortic valve disease nor intracardiac shunts. The C.O. was calculated using the following formula: C.O. (l/min) = mean flow velocity (cm/sec) x pi(aortic ring diameter/2)2 (cm2) x 60/10(3) Left ventricular ejection flow velocity was recorded in the center of the aortic ring from the apical approach. Mean velocity was calculated by integration of instantaneous mean velocity in the ejection phase divided by the cardiac cycle length, and was corrected by the Doppler incident angle. The inner diameter of the aortic ring was measured in the parasternal long-axis view at the time of the maximum ejection flow velocity. The following results were obtained: 1. Sources of error in the measurement of cardiac output. 1) Accuracy of instantaneous mean velocity calculating circuit: This calculating circuit was accurate in model experiments using pulsatile flow. 2) Effect of high-pass filter: In model circuits, application of high-pass filter overestimated flow velocity. The higher the cut-off frequency of the high-pass filter, the larger the overestimation. This was probably due to the parabolic flow velocity profile in the circuit. 3) Flow velocity profile in the aortic ring: The flow velocity profile seemed to be flat in the aortic ring except near the anterior aortic wall. Therefore, the effect of the high-pass filter was considered to be negligible in case of clinical application. 4) The effects of shift and size of sample volume: The location of sample volume relative to the aortic valve ring shifted about 7 mm during systole. However, the shift and size of sample volume seemed to have little effect on the measured C.O., because the flow velocity profile was nearly flat in the aortic ring. 5) Ultrasound beam incident angle: From a practical viewpoint, it was necessary to set an incident angle of less than 50 degrees for minimizing the error. We were able to set the angle within 50 degrees in all but one of patients. 6) Diameter of the aortic ring: Two-dimensional echographic measurement of the aortic ring diameter was not so accurate; it seemed to become a major source of error in the calculation of C.O.(ABSTRACT TRUNCATED AT 400 WORDS)
To determine the optimum time for surgical intervention in pure mitral regurgitation, 39 patients were studied by echocardiography before and after surgery. Pure mitral regurgitation included mitral valve prolapse with or without ruptured chordae tendineae. Twenty-two patients had mitral valve replacement and 17 had mitral valve reconstruction. Serial echocardiograms were obtained from all 39 patients (average follow-up: 40 months). Two of the 39 patients died suddenly at home on 26 and 62 months after surgery. One of the 39 patients now suffers from congestive heart failure. These three patients had preoperative left ventricular end-diastolic dimensions greater than 70 mm and left ventricular end-systolic dimension greater than 50 mm. Operation is recommended for patients with end-diastolic dimension less than 70 mm and end-systolic dimension less than 50 mm.
Although two-dimensional echocardiography is a standard for diagnosing mitral valve prolapse, the diagnostic criteria are controversial. Regardless of valve ballooning we have used our criteria which are based on the dislocation of the mitral valve coaptation. The purpose of this study was to clarify the relationship between the location and the degree of mitral valve prolapse assessed by two-dimensional echocardiography and those of mitral regurgitation evaluated by color Doppler flow imaging, which enables us detailed analysis of regurgitation. Twenty-three patients with idiopathic mitral valve prolapse diagnosed by our criteria were studied. They were 14 men and nine women, ranging in age from 19 to 72 years (mean 44.7). In any patients, prolapse of either the anterior or posterior leaflet does not satisfy the Gilbert's criteria. Twenty of the 23 patients had mitral regurgitation by color Doppler flow imaging, and the grade was II, III or IV in 16 of these 20 patients. In 19 of 20 patients, the localization of the regurgitant jet flow from the mitral orifice coincided with the two-dimensional echocardiographic site of dislocation of mitral valve coaptation. Therefore, it was concluded that the dislocation of mitral leaflet coaptation detected by two-dimensional echocardiography is an abnormal finding regardless of the protrusion of the valve beyond the mitral ring.
An attempt was made to determine whether mitral regurgitation could be detected and its severity evaluated semiquantitatively by newly developed real-time two-dimensional Doppler flow imaging in 109 patients who underwent left ventriculography. In the Doppler flow imaging technique, Doppler signals due to blood flow in the cardiac chambers are processed using a high speed autocorrelation technique, so that the direction, velocity and turbulence of the intracardiac blood flow are displayed in the color-coded mode on the monochrome B-mode echocardiogram in real time. Mitral regurgitant flow was imaged as a jet spurting out from the mitral valve orifice into the left atrial cavity. It was noted that the regurgitant jet in the left atrial cavity had a variety of orientations and dynamic features when studied by the present technique. The sensitivity of the technique in the detection of mitral regurgitation was 86% as compared with that of left ventriculography. Mitral regurgitation in the false negative cases was mostly mild. On the basis of the farthest distance reached by the regurgitant flow signal from the mitral valve orifice, the severity of regurgitation was graded on a four point scale and these results were compared with those of angiography. A significant correlation (r = 0.87) was found between Doppler imaging and angiography in the evaluation of the severity of mitral regurgitation. A similar result was obtained for the evaluation based on the area covered by the regurgitant signals in the left atrial cavity. Thus, noninvasive semiquantitative evaluation by real-time two-dimensional Doppler flow imaging appears to be a promising clinical technique.
It has been difficult to diagnose mitral regurgitation due to valve perforation using either noninvasive or invasive methods, differentiating it from that resulting from incomplete coaptation of the mitral valve. This report describes three patients with infective endocarditis and mitral valve perforation, which was definitively diagnosed by the real-time two-dimensional Doppler flow imaging technique. In these three patients, B-mode echocardiography demonstrated an echo interruption on the anterior mitral leaflet. However, it was not certain whether this interruption was simply an echo dropout or indicated an interruption of the valve tissue. Doppler flow imaging then demonstrated unusual flow in the vicinity of the echo interruption, which appeared to flow from the left ventricular cavity into the left atrial cavity across the midportion of the anterior mitral valve leaflet during systole and in the opposite direction during diastole. This was interpreted as mitral valve perforation. In general, Doppler flow imaging may play a complementary role with B-mode echocardiography in cardiac diagnosis.
The pattern of normal blood flow in the right atrial cavity was studied using the newly developed real-time two-dimensional Doppler flow imaging technique as a standard reference for the Doppler diagnosis of heart diseases with intracardiac shunts at the atrial level. The study was performed primarily with use of the apical four chamber and the parasternal right ventricular inflow tract views in 21 healthy subjects. The following patterns were observed: blood from the inferior vena cava flowed up along the posterior wall of the right atrium and joined with blood from the superior vena cava in the posterocranial part of the right atrial cavity; the flow then coursed along the roof of the right atrium toward the tricuspid valve in the atrial relaxation phase. This flow was always noted along the interatrial septum in the four chamber view. During and after mid-systole of the right ventricle, additional blood flow away from the tricuspid valve appeared, moving from the valve to the central part of the right atrial cavity, that is, at the lower right of the preceding inflow; this flow was interpreted as arising from eddy currents caused by the preceding inflow. In early diastole of the right ventricle, the flow signal area along the interatrial septum and the roof of the right atrium extended into the right ventricular cavity through the tricuspid valve. In the atrial contraction phase only the blood near the tricuspid valve in the right atrial cavity appeared to flow into the right ventricular cavity. Inflow from the coronary sinus was almost undetectable.(ABSTRACT TRUNCATED AT 250 WORDS)
Short chain-length specific trans-2-enoyl-CoA reductase (reductase I), which contributed to mitochondrial fatty acid synthesis, was purified about 200-fold from crude extract of mitochondria in Euglena gracilis. It had a molecular weight of 39,000, and consisted of two dissimilar subunits with molecular weights of 15,000 and 25,000. The enzyme utilized crotonyl-CoA as the most active substrate and showed negative cooperativity in the reaction with the substrate. NADH was the sole electron donor. Some divalent cations were inhibitory to the enzyme when incubated with the enzyme prior to the start of the reaction. The reductase apparently contained loosely bound FAD.
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The clinical validity and some problems concerning pulsed Doppler echocardiography (PD) in non-invasive estimates of pressure difference (delta P) across a ventricular septal defect were studied. The maximum velocity (max V) of the left to right shunt flow in the right ventricle was converted to delta P using the simplified Bernoulli equation: delta P = 4V2. We also used the equation: delta P = 4(V2(2) - V1(2)) to estimate the delta P in cases who had left to right shunt flows of high velocity in the left ventricle. Simulatenous recordings of both left and right ventricular pressures and PD were obtained during cardiac catheterization of 11 cases. Accurate Doppler estimates of delta P only from the maximum velocity of the left to right shunt flow in the right ventricle were impossible in nine cases whose actual delta P's were large (more than 41 mmHg) and also in eight cases whose right ventricular systolic pressure was high (either equal to or higher than left ventricular systolic pressure). Besides these 17 cases, delta P estimated by PD using the simplified Bernoulli equation in 39 cases, with pansystolic left to right shunt flows in the right ventricle, correlated well with the actually measured delta P (Y = 0.99X + 2.77, r = 0.91, p less than 0.01). The difference in the maximal instantaneous pressure gradient and Doppler delta P was considered insignificant (between 0 and 7 mmHg, mean 4 mmHg). In nine cases, the left to right shunt flows of relatively high speed (0.63 approximately 2.00 m/sec, mean 1.31 m/sec) were observed also in the left ventricle, and calculated delta P using the simplified Bernoulli equation overestimated the actually measured delta P by 2 to 16 mmHg (Y = 1.52X + 4.88, r = 0.95, p less than 0.01). However, if the delta P is estimated by using the equation, delta P = 4(V2(2) - V1(2)), without ignoring the maximum speed in the left ventricle (V1), it correlates well with the actually measured delta P (Y = 1.07X + 0.76, r = 0.98, p less than 0.01). Thus, in cases with left to right shunt flows with high speeds in the left ventricle, the equation: delta P = 4(V2(2) - V1(2)) was more accurate in estimating the delta P by pulsed Doppler echocardiography.
In Euglena gracilis a malonyl-CoA-independent fatty acid-synthetic system, in which fatty acids are synthesized directly from acetyl-CoA as both primer and C2 donor, occurs in mitochondria, and the system contributes to the wax ester fermentation. The activity of fatty acid synthesis in the mitochondrial system was enhanced about six times when an artificial acetyl-CoA-regenerating system was present, indicating that the fatty acid-synthetic activity is controlled by the ratio of acetyl-CoA against CoA. When fatty acids were synthesized using pyruvate instead of acetyl-CoA as substrate, a high activity, about 30 times higher than that from acetyl-CoA, was found under anaerobic conditions (below 10(-5) M oxygen), while in aerobiosis fatty acids were not synthesized at all. CoA, NADH, and NADP+ were required as cofactors for fatty acid synthesis from pyruvate. It was indicated that high activity of fatty acid synthesis from pyruvate due to the high ratio of acetyl-CoA against CoA was maintained by the action of the oxygen-sensitive pyruvate dehydrogenase found in Euglena mitochondria. When [2-14C]pyruvate was fed into intact mitochondria under anaerobic conditions, radioactive fatty acids were formed in the presence of malate, which provided reducing power for the matrix.
Doppler echocardiography was used to evaluate the features of interventricular septal rupture in six patients with acute myocardial infarction and to substantiate the hemodynamic data and morphologic findings at surgery or autopsy. Although echocardiographic visualization of the septal rupture was obtained in only two of the six patients, unusual Doppler flow signals were detected in the apical portion of the right ventricle in all six patients. Five patients had unusual flow signals during both systole and diastole; one had such signals only during systole. The location of these unusual flow signals coincided with the site of septal rupture confirmed at surgery or autopsy. The pattern of the flow signals in one cardiac cycle was very similar to that of the pressure difference between the left and right ventricular cavities. These findings indicate that the unusual flow signals represent the left to right shunt flows resulting from septal rupture. In conclusion, Doppler echocardiography may be a very useful tool for diagnosing interventricular septal rupture easily and noninvasively in patients with acute myocardial infarction.
It is appreciated that, linked with B-mode echocardiography, the real-time two-dimensional Doppler flow imaging technique provides information on the heart, which has never been available with conventional methods, greatly improving the capabilities of cardiac ultrasound. In general, the concept of major heart disease consists of anatomical abnormalities and those in intracardiac flow condition. The present method provides information on these two aspects simultaneously; consequently, it is regarded as a closer approach to heart diseases, compared with conventional examinations and techniques. The equipment is also convenient to operate. The combination of real-time two-dimensional Doppler flow imaging and B-mode echocardiography is expected to become a standard tool of the ultrasound examination of the heart.
Mitral regurgitation was detected and quantitatively evaluated using two-dimensional Doppler-echocardiography. The subjects consisted of 74 cases having a variety of heart diseases, who underwent left ventriculography within one week before or after the Doppler study. Among 50 patients with mitral regurgitation confirmed by left ventriculography, the Doppler study detected mitral regurgitant flow signals in 46, for a sensitivity of 92%. Minimal mitral regurgitation in four cases could not be detected by Doppler studies. Twenty-four patients had no mitral regurgitation according to left ventriculography; all but one also had no mitral regurgitation by Doppler study, for a specificity of 96%. In one false positive case, typical mitral regurgitant flow signals were detected in an area localized within the left atrial cavity near the mitral valve orifice. The possibility remains that left ventriculography missed this minimal regurgitation. For quantitative assessment of mitral regurgitation, the following two methods were used. Three long-axis views through the lateral, middle and medial parts of the mitral valve, and a short-axis view at the level of the mitral orifice were imaged via the parasternal approach. The area where mitral regurgitant flow signals were detected was mapped on each cross-sectional echocardiogram, then the distance attained by the regurgitant flow from the mitral valve and the area covered by the regurgitant flow were determined. The maximal distance among the three long-axis views and the sum of the distances in these views was parallel to the severity of mitral regurgitation as assessed by left ventriculography.(ABSTRACT TRUNCATED AT 250 WORDS)