[The causative mechanisms of mitral valve prolapse in progressive muscular dystrophy. Thorax and thoracic spine deformity and left ventricular dysfunction].
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Adolescent↗
Biomedical subjects
N Takasawa
Publications and source records attributed to N Takasawa.
[Spectral analysis of finger photoelectric plethysmogram in its relation to emotion: visual display of baseline deflection and pulse wave].
The present study applied spectral analysis of finger photoelectric plethysmogram (PTG) to describe the emotional factor involved in baseline deflection of PTG. Using 23 normal male students as subjects, PTG was measured under rest, verbal instruction, and electric shock conditions. PTG spectral analysis via fast Fourier transform was carried out on the consecutive 10 X 9 ms X 1 024 points X 4(398.64 s) samples in each condition with frequency resolution at 0.0109 Hz. In the analysis of power spectra, two distinct power peaks were observed in all conditions; below 0.3 Hz and around 1.0 Hz. It was confirmed that the former was baseline deflection and the latter was heart beat component. There were no differences in each peak frequency among conditions. Whereas peak power below 0.3 Hz tended to increase all through verbal instruction and electric shock conditions as compared to rest one. These results were discussed in relation to anxiety involved in emotion.
Adult↗
[Regional wall motion of the left ventricle in congestive cardiomyopathy: in comparison with progressive muscular dystrophy of Duchenne type (author's transl)].
The features of regional wall motion abnormalities of the left ventricle were analysed in 11 patients of congestive cardiomyopathy (CCM) in comparison with 22 patients of progressive muscular dystrophy (DMD) of Duchenne type who showed an abnormal motion of the left ventricle by echocardiography. Real time two-dimensional echocardiographic study demonstrated the following results: I) In CCM, (1) only 2 or less of 11 cases preserved a normal motion in each left ventricular segment, and the depression of wall motion of the left ventricle were thought to be generalized; (2) there were 9 cases with segmental wall motion abnormalities and 3 of them demonstrated ventricular aneurysms, and (3) the localizations of the segmental abnormalities varied in each case, and there was no apparent accumulation to any segments. II) In DMD, (1) all the cases showed depressed motions and 8 of them demonstrated a ventricular aneurysm in the posterior wall of the left ventricle (LVPW), (2) while, there was no case showing ventricular aneurysm in the segments other than LVPW, and about one third of all cases showed normal motion in those segments. From these results, we concluded as follows: 1) Although the depression of a wall motion of the left ventricle was generalized in CCM, this was not always uniform and the segmental abnormalities of a wall motion were frequently observed. The localization of the most severely disturbed segment varied in each case. 2) On the other hand, in DMD, the wall motion was disturbed more frequently and more severely in LVPW than in other ventricular segments.
Adolescent↗
[Treatment of Mycobacterium intracellular infection with antibacterial drugs (author's transl)].
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Aged↗
Nemaline myopathy: histological, histochemical and ultrastructural studies.
Histological, histochemical and ultrastructural studies were performed on muscle biopsies from three siblings with congenital nemaline myopathy. Histological studies revealed type I fibre atrophy and type II fibre paucity. Ultrastructural studies of intramuscular nerves showed that the axonal diameters were very narrow compared with the width of myelin lamellae. Granular or membranous osmiophilic material occurred in the adaxonal Schwann cell cytoplasm and had a periodicity of 33--38 A. The neuromuscular junctions showed degenerative features such as glycogen granules or myelin figures in 27.1% of total terminal axons. The secondary synaptic clefts were markedly decreased in number and short in length. Myotendinous junction-like structures were found in 5.5% of the muscle fibres near the neuromuscular junctions, and often near sites of fibre-splitting. Rods in nemaline myopathy might be caused as a result of longitudinal splitting and disruption of fibres due to deficient regeneration of the muscle fibres associated with neurotrophic abnormalities.
Adolescent↗