[NMR-CT in muscular disorders--muscle T1 values in normal children and Duchenne muscular dystrophy patients].
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Biomedical subjects
Publications and source records attributed to N Fukuda.
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The relative importance of fatty acid synthesis in triglyceride secretion by perfused livers from lean (normal control) and obese Zucker rats was investigated. Livers from fed animals were perfused in a recirculating system with tritiated water and a constant infusion of oleic acid. Triglyceride secretion was 5 times greater and cholesterol secretion was 35% greater in the obese rat livers. The very-low-density lipoprotein hypersecreted by perfused livers from obese rats contained more apolipoprotein B and exhibited an increased B-48/B-100 ratio. Apo-B was also elevated in the hypertriglyceridemic plasma of obese rats in both fed and fasting states. The very-low-density lipoprotein isolated therefrom was likewise characterized by an increased B-48/B-100 ratio. Ketogenesis was depressed 40% in the obese rat livers and increased hepatic malonyl-CoA was implicated in this alteration. The de novo synthesis and secretion of newly synthesized cholesterol was moderately increased in the perfused livers from obese rats. Tritium incorporation into fatty acids was 15 times greater in the obese genotype. Most of the synthesized fatty acids remained in the liver and were recovered after perfusion in triglyceride and phospholipids. Newly synthesized fatty acids accounted for only 3 and 15% of the triglyceride secreted by the lean and obese rat livers, respectively. A large portion of the secreted triglyceride fatty acids was derived from endogenous liver lipids. When the turnover of newly synthesized fatty acids in these pools was considered, the contribution of de novo fatty acid synthesis to triglyceride secretion was estimated to be 9% in the lean and 44% in the obese rat livers. Therefore, the altered partition of free fatty acids (Fukuda, N., Azain, M. J., and Ontko, J. A. (1982) J. Biol. Chem. 257, 14066-14072) and increased fatty acid synthesis are both major determinants of the hypersecretion of triglyceride-rich lipoproteins by the liver in the genetically obese Zucker rat.
The effect of sublingual nifedipine on left ventricular (LV) function was assessed by analyzing LV inflow velocity patterns using pulsed Doppler echocardiography (PDE) and radioisotope (RI) angiography in 23 patients with hypertrophic cardiomyopathy (HCM), 13 with hypertensive heart disease (HHD) and 24 with ischemic heart disease (IHD). The results were as follows: LV inflow velocity pattern and M-mode echocardiography after the administration of nifedipine (Study-I). The deceleration time (DT) of the diastolic rapid filling wave was shortened after nifedipine in HCM and HHD, but not in IHD. The acceleration time (AT) of the diastolic rapid filling wave and the A/D ratio (amplitude of an atrial contraction wave/amplitude of a diastolic rapid filling wave) were not significantly changed in all groups. Peak negative Vcf was significantly improved after nifedipine in HCM, but unchanged in the other groups. Fractional shortening and peak Vcf did not change in all groups. LV inflow velocity pattern and RI angiography after nifedipine (Study-II). The mean LV rapid filling rate (V1) based on the LV volume curve by multi-gated blood pool scans increased during nifedipine in HCM and HHD, but other diastolic indices, such as the peak filling rate and 1/3 filling fraction, were unchanged. The DT-V1 relationship during nifedipine shifted toward the right and downward in HCM and HHD. In IHD, however, this relationship shifted toward the left and downward in cases with reduced LV function (V1 less than 1.0 EDC/sec), but toward the right and downward in patients whose LV function was maintained (V1 greater than or equal to 1.0 EDC/sec). Nifedipine therapy was associated with an improved LV filling in nearly all cases of HCM and HHD, and in some cases of IHD. PDE and RI angiography are useful for evaluating LV diastolic function during sublingual nifedipine in various heart diseases.
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Magnetic resonance imaging (MRI) was performed for 10 patients with cardiovascular thrombi using a 0.1-Tesla resistive type apparatus (ASAHI MARK-J). In all cases thrombi were clearly imaged by NMR and their shapes closely resembled those imaged by X-ray CT. Mural thrombi located within left ventricular aneurysms of two patients with old anteroseptal myocardial infarction were semilunar in form. A mural thrombus in the right ventricle of a patient with cardiovascular Behcet's disease was also clearly imaged. Mural thrombi within the enlarged left atrium of two patients with mitral valve stenosis and insufficiency were clearly demonstrated in both cross- and longitudinal sections. In three patients with thoracic aortic aneurysm, mural thrombi were recognized within the local dilatations of the aorta. In two patients with dissecting aortic aneurysm, mural thrombi were visualized within false lumen using MRI. Mean T1 values and standard deviations for the left ventricular cavity, the left ventricular wall, and the thrombi were 639 +/- 49, 349 +/- 17 and 316 +/- 84 msec, respectively. Mean T1 values of the thrombi were usually shorter than those of the left ventricular wall. Some supposedly fresh thrombi had longer T1 values, however.
To clarify the genesis of a protodiastolic extra heart sound (S3') which was occasionally recorded at about the beginning of a diastolic rumble in mitral stenosis (MS), phono-, apex- and echocardiography were performed for 33 patients with MS, and left ventricular (LV) cineangiography was performed for eight of them. The patients were classified as S3'(+) and S3'(-) groups, according to whether they had S3'. Results were as follows: The S3' was synchronous with the rapid filling (RF) wave of the apexcardiogram (ACG). Its amplitude was proportional to the size of the RF wave. The RF wave was significantly sharper in the S3'(+) group as compared with that of the S3'(-) group. The S3' always appeared after onset of dispersion of dots in the velocity pattern of blood flow at the mitral valve orifice according to pulsed Doppler echocardiography. There was no significant difference between the S3'(+) and S3'(-) groups in the region of the mitral valve orifice according to two-dimensional echocardiography, and at the peak rate of change of the LV dimension during diastole as determined by M-mode echocardiography. The peak rate of change of the long-axis dimension of the LV during diastole as determined by cineangiography was significantly greater in the S3'(+) group than in the S3'(-) group. However, there was no significant difference between the two groups regarding the peak rate of change in the short-axis dimension of the LV during diastole as determined by cineangiography. The amplitude of the early diastolic dip of the interventricular septum (IVS) was significantly greater in the S3'(+) group as compared with that of the S3'(-) group. The amplitude of the S3' and the size of the RF wave correlated positively with the amplitude of the early diastolic dip of the IVS in pts with atrial fibrillation. Fractional shortening of the LV ascertained by M-mode echocardiography was significantly greater in the S3'(+) group than in the S3'(-) group. The end-systolic dimension of the LV tended to be less in the former than in the latter group. In conclusion, the S3' in MS was considered to be a third heart sound. Expansion along the long-axis of the LV and its sudden change in early diastole may account for the genesis of the S3', and this expansion may be accentuated by restoring force and active diastolic suction of the LV, and by velocity, direction and spread toward the cardiac apex of the stenotic mitral jet flow.
To investigate the mechanism of an apical mid-diastolic rumble in hypertrophic cardiomyopathy (HCM), we recorded left ventricular (LV) inflow velocity patterns using pulsed Doppler echocardiography and apexcardiography for 10 HCM patients with rumble and 20 HCM patients without rumble. Controls consist of 17 normal subjects, three patients with complete atrioventricular block and two patients with artificial right ventricular pacemakers. The LV inflow velocity profiles were analyzed in terms of acceleration time (AT) and deceleration time (DT) of the rapid filling wave, and the ratio of peak velocity of the atrial contraction wave to that of the rapid filling wave (A/D ratio). The results were as follows: The apical mid-diastolic murmur in HCM had a crescendo-decrescendo character mainly of medium frequency, and increased in intensity after the inhalation of amyl nitrite. All patients with rumble had asymmetric septal hypertrophy and the five of these had LV outflow obstruction. In six of the 10 patients with rumble, mild mitral regurgitation was detected. In HCM with rumble, the AT tended to be shorter than that of HCM without rumble, but it was significantly longer than the AT of normal subjects. In HCM with rumble, the DT was significantly shorter than that of HCM without rumble, but it was significantly longer than the DT of normal subjects. There was no significant difference in the A/D ratio between the HCM with rumble and the normal subjects, but the A/H ratio of the apexcardiogram was significantly increased in HCM with rumble as compared with those of HCM without rumble and of the normal subjects. The LV dimension was significantly decreased in HCM with rumble as compared with those of HCM without rumble and the normal subjects. Peak negative VCF was significantly decreased in HCM with rumble as compared with that of HCM without rumble. But there was no significant difference in this parameter between HCM with rumble and the normal subjects. In simultaneous recordings of apical mid-diastolic rumble and LV inflow velocity patterns, the rumble appeared to start after the beginning of the diastolic rapid filling wave and to stop before or at the end of the diastolic rapid filling wave. In patients with complete atrioventricular block and with artificial right ventricular pacemakers, the apical mid-diastolic rumble appeared when the P wave was during the rapid filling phase of the left ventricle.(ABSTRACT TRUNCATED AT 400 WORDS)
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In fed rat livers perfused with [1-14C]oleic acid, Ro 22-0654 (4-amino-5-ethyl-3-thiophenecarboxylic acid methyl ester hydrochloride), an inhibitor of fatty acid synthesis, activated ketogenesis and decreased the secretion of triglyceride in very low density lipoproteins (VLDL). Ro 22-0654 was without effect on total oleic acid uptake and utilization by the liver. The liver triglyceride content, urea synthesis, and bile production were also unaffected. Ro 22-0654 increased the conversion of both exogenous and endogenous fatty acid substrates to ketone bodies, while decreasing the secretion of triglyceride synthesized from both of these sources. Depressed fatty acid synthesis accounted for a relatively small portion of the decrease in secretory triglyceride derived from endogenous sources. 14CO2 from [1-14C]oleic acid was unchanged by Ro 22-0654. This drug decreased the malonyl-CoA content of rat liver freeze-clamped in vivo, providing an explicable mechanism for its activation of fatty acid oxidation. Hepatic citrate was also diminished. The present studies indicate the following sequence of events in the liver of fed rats following the administration of Ro 22-0654: decreased formation of citrate and malonyl-CoA, decreased fatty acid synthesis via decreased carbon supply and increased fatty acid oxidation via stimulation of acylcarnitine formation, decreased synthesis of triglyceride from both endogenous and exogenous fatty acids, resulting in the decreased formation and secretion of VLDL.
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A 59-year-old female of facial myokymia with multiple sclerosis was reported. In this case, facial myokymia appeared at the same time as the first attack of multiple sclerosis, in association with paroxysmal pain and desesthesia of the neck, painful tonic seizures of the right upper and lower extremities and cervical transverse myelopathy. The facial myokymia consisted of grossly visible, continuous, fine and worm-like movement, which often began in the area of the left orbicularis oculi and spread to the other facial muscles on one side. Electromyographic studies revealed grouping of motor units and continuous spontaneous rhythmic discharges in the left orbicularis oris suggesting facial myokymia, but there were no abnormalities on voluntary contraction. Sometimes doublet or multiplet patterns occurred while at other times the bursts were of single motor potential. The respective frequencies were 3-4/sec and 40-50/sec. There was no evidence of fibrillation. The facial myokymia disappeared after 4-8 weeks of administration of prednisolone and did not recur. In the remission stage after disappearance of the facial myokymia, nuclear magnetic resonance (NMR) imaging by the inversion recovery method demonstrated low intensity demyelinated plaque in the left lateral tegmentum of the inferior pons, which was responsible for the facial myokymia, but X-ray computed tomography revealed no pathological findings. The demyelinated plaque demonstrated by NMR imaging seemed to be located in the infranuclear area of the facial nerve nucleus and to involve the intramedurally root.(ABSTRACT TRUNCATED AT 250 WORDS)
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We investigated the changes of behavioral, electrophysiological and biochemical parameters during and after global cerebral ischemia in rats. Global cerebral ischemia was produced by the temporary occlusion of both common carotid arteries 24 hr after the permanent electrocauterization of bilateral vertebral arteries. Just before recirculation following 10 or 30 min of cerebral ischemia, loss of righting reflex, flattenning of cortical EEG activity, and detrimental decrease of ATP content and marked increase of lactate content in the cerebrum were observed. The alterations of all parameters completely recovered within 60 min after recirculation in 10-min cerebral ischemic rats. However, the 30-min cerebral ischemic rats showed almost no recovery after recirculation, suggesting that some irreversible damages are produced in the cerebrum of the 30-min ischemic rat. On the other hand, it was found that the auditory brain stem evoked response (ABER) and ATP content in the pons plus medulla were only slightly affected by the ischemic procedure, which indicates that the ischemic damages do not ensue in the lower part of the brain stem.
Partially purified Okinawan sugar cane wax and fatty alcohol were fed to Wistar strain rats to examine the effects on serum and liver cholesterol (Chol), triglyceride (TG) and phospholipid (PL). The fecal excretion of neutral sterols in the rats was also determined. There were no significant differences found in the body weight gain, food intake and liver weight among the animals of experimental diet groups. An addition of 0.5% sugar cane wax to the diet significantly lowered the concentrations of serum and liver Chol in the rats. There were no significant differences observed in PL and TG levels either in serum or liver among the experimental groups. These results indicate that cane wax, one of the elements contained in sugar cane rind as well as in black sugar, may have a cholesterol-lowering effect on the serum and liver of the rats. The amount of feces excreted by the three experimental diet groups of rats were exactly the same and also no significant differences were found in the excretion of Chol.