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Biomedical subjects

S Hirata

Publications and source records attributed to S Hirata.

At least 217 records · Page 12Linked to original sources
PubMed1981

[Detection of aortic valve prolapse by cross-sectional echocardiography (author's transl)].

Echocardiography has been widely used for a detection of mitral and tricuspid valve prolapse. However, no extensive study has been made for a recognition of aortic valve prolapse. In this study, an echocardiographic search for aortic valve prolapse was attempted on 1700 consecutive cases at our laboratory including 70 cases with aortic regurgitation and 30 with mitral valve prolapse. Criteria of aortic valve prolapse by cross-sectional echocardiography were as follows: (1) eccentric coaptation point of aortic valve cusps, (2) asymmetric enlargement of the aortic valve cusp, and (3) downward displacement of the cusps. Using the above-mentioned criteria, five cases were recognized as having aortic valve prolapse, and it was divided into the following three morphological patterns: (1) prolapse of the right coronary cusp (1 case), (2) prolapse of the left coronary cusp (1) case, and (3) prolapse of the noncoronary cusp (3 cases). All 5 cases showed apparent aortic regurgitation, while none of these cases had any evidence of mitral valve prolapse. From the present observations, it might be suggestive that aortic valve prolapse is one of the common causes of aortic regurgitation. Elucidation of a spectrum of aortic valve prolapse should wait for a further extensive study.

Aged↗
PubMed1981

[Heart sounds and heart murmurs in progressive muscular dystrophy of Duchenne type (author's transl)].

Phonocardiographic and echocardiographic investigation was performed in patients with progressive muscular dystrophy of Duchenne type (PMD). The clinical materials consisted of 90 patients with PMD (aged 8 to 21 yrs, a mean of 14.5), and 90 normal subjects (aged 6 to 19 yrs, a mean of 11.7). The patients with PMD were classified into 8 stages from the mildest, S(1), to the severest, S(8), according to Swinyard-Deaver' criteria. In the 90 normal subjects the diminished first heart sound was noted in 12 cases (13.3%), presystolic murmurs in 4 cases (4.4%), and diastolic rumbles in 9 cases (10%), whereas, in the patients with PMD the diminished first heart sound was noted in 47 cases (52.2%), presystolic murmurs in 41 cases (45.6%), and diastolic rumbles in 44 cases (48.9%). There was a significant difference in the incidence of the above-mentioned three phonocardiographic findings between the PMD patients and the normal subjects. But there was no significant difference in the incidence of a systolic click between these two groups. The incidence of the diminished first heart sound increased with the progress of Swinyard-Deaver' classification. A presystolic murmur was observed with the highest incidence in the stage of S(8). The incidence of a rumble was also augmented with increasing severity of the disorder from the stages of S(1) to S(7), but decreased in S(8). Another attenpt was made to relate the phonocardiographic findings to those of the echocardiogram. In the cases with anterior mitral leaflet fluttering, there were diastolic rumble in 69% whereas 16.7% of the patients without anterior mitral leaflet fluttering had diastolic rumbles. In two-dimensional echocardiography, the anterior and posterior mitral leaflets looked like pennants fluttering in the wind. All these observations positively indicate that anterior mitral leaflet fluttering was closely associated with the genesis of rumbles. Consequently, it can be concluded that the diminished first heart sound, presystolic murmurs and diastolic rumbles might be useful clinical signs in the assessment of the myocardial involvement in PMD.

Adolescent↗
PubMed1981

[Detection of left ventricular thrombi by echotomography and computed tomography (author's transl)].

Left ventricular (LV) thrombi are rarely recognized during life, though they are not infrequent at the post-mortem examination of patients succumbed to valvular disease, acute myocardial infarction, and cardiomyopathy. We presented five cases in which LV thrombi were detected by cross-sectional echocardiography (CSE) and confirmed by computed tomography. The main purpose of this study was to compare the echocardiographic findings of the LV thrombi with the manifestations of the LV thrombi on the computed tomograms, with a hope to augment the clinical utility of CSE in the detection of LV thrombi. CSE was recorded from the apical and four-chamber views in addition to the conventional approach. A computed tomographic whole-body scanner which utilized a continuously rotating gantry and pulsed anode with X-ray radiation collimated to form a thin fan-shaped beam was used. A complete section scan was performed in 3 seconds. Sustained enhancement was obtained with a rapid intravenous infusion of 30% meglumine iothalanate. Most of the LV thrombi showed an abnormal echo with irregular borders and/or a mobile mass echo at the apex by CSE. Computed tomographic findings suggestive of LV thrombi appeared as a defect, which was apparently different in quality from the surrounding myocardium or valvular apparatus. These findings were quite consistent with those of CSE with respect to the number and the location of the LV thrombi. Consequently, it may be concluded that CSE is a useful adjunct in the detection of LV thrombi and an additional use of computed tomograph will certainly open up a promising way to make the secure diagnosis of LV thrombi.

Aged↗
PubMed1979

Prevention by tiopronin (2-mercaptopropionyl glycine) of methylmercuric chloride-induced teratogenic and fetotoxic effects in mice.

Previous investigations (Fuyuta et al., '76, '79) have shown that a single oral administration of 25 mg/kg methylmercuric chloride (MMC) to pregnant ICR mice on day 10 of pregnancy induced cleft palate in a remarkably high incidence in fetuses. Based on these findings, the present study dealing with the prevention of cleft palate by Tiopronin, (2-mercaptopropionyl glycine, Tp), was initiated. Twenty females in the positive control group were given 25 mg/kg MMC orally on day 10 of pregnancy and then given physiological saline intraperitoneally. Twenty females in the negative control group were given distilled water orally and then given saline intraperitoneally. Cleft palate was found in 98.1% of fetuses in the positive control group and none of them in the negative control group. Twenty females were pretreated with a single oral dose of 25 mg/kg MMC on day 10 of pregnancy and were posttreated with Tp intraperitoneally, immediately and at every 24, 48 and 72 hours after the MMC treatment. The doses of Tp were 320, 160 and 80 mg/kg/day. The incidences of cleft palate in fetuses were reduced to 1.49, 31.3 and 47.8% in the Tp-treated groups with the doses of 320, 160 and 80 mg/kg/day, respectively. Tiopronin could effectively prevent the expected incidence of cleft palate. Other types of abnormalities as well as fetotoxicity represented by reduced fetal body weight were also effectively prevented with the Tp-treatment.

Abnormalities, Drug-Induced↗
PubMed1979

Esophagoplasty with an autogenous tubed gastric flap.

As an esophageal substitute, a tubed gastric flap 2.5 cm in inner diameter and 38 cm in length, was constructed from the gastric wall along the greater curvature; a pedicle was attached to the gastric antrum, and its oral stump was brought up into the left supraclavicular fossa through a retrosternal tunnel to perform an esophagogastrostomy. Anastomotic breakdown occurred in only three of fifty cases in which this procedure was used.

Esophageal Neoplasms↗
PubMed1978

Embryotoxic effects of methylmercuric chloride administered to mice and rats during orangogenesis.

Pregnant C57BL mice were given a daily dose of 7.5, 6.0, 5.0 or 2.5 mg/kg methylmercuric chloride (MMC) orally from the sixth through the thirteenth day of pregnancy. Pregnant Wistar rats were given a daily dose of 7.5, 5.0 or 2.5 mg/kg MMC orally from the seventh through the fourteenth day of pregnancy. Fetal examinations were performed on days 18 and 20 in mice and rats, respectively. In mice, the dose of 7.5 mg/kg was embryocidal. The dose of 6.0 mg/kg also caused a high incidence of fetal death, decreased fetal weight and a marked increase in malformations. A dose of 5.0 mg/kg caused a decrease in fetal weight and a marked increase in the incidence of malformations. The most common malformations were cleft palate and fused thoracic vertebrae. In rats, the dose of 7.5 mg/kg caused a high incidence of fetal death and malformations. The most frequent malformations were cleft palate, generalized edema, brain lesions and wavy ribs. A dose of 5.0 mg/kg caused a significant decrease in fetal weight and a significant increase in the incidence of malformations.

Abnormalities, Drug-Induced↗
PubMed1978

Inhibition of cell division of Escherichia coli by a new synthetic penicillin, piperacillin.

The mechanism of the action of piperacillin against Escherichia coli was investigated. This drug converted cells to filaments, but did not show lytic action in a range of concentrations below 25 mug/ml. In some of the filaments, stretched constrictions with various diameters were observed. Addition of piperacillin to a synchronous culture inhibited cell division immediately at any stage of the cell cycle. The results of morphological examination of synchronous cultures show that the percentage of filaments with a stretched constriction corresponds to that of normally septated cells before addition of the drug. Furthermore, peptidoglycan synthesis and cross-linking were not inhibited by this drug. It is likely that this drug inhibits only septum formation, but not the growth of wall, and that stretched constrictions are a result of longitudinal growth of septation caused by the drug. Examination of affinity of the drug to penicillin-binding proteins shows that protein 3 is the most sensitive, proteins 2 and 7 are moderately so, and protein 1 is sensitive only to high concentrations of the drug.

Bacterial Proteins↗
PubMed1977

Changes in blood catecholamine levels and ultrastructure of dog adrenal medullary cells during hemorrhagic shock.

Blood catcholamine levels and ultrastructural changes in adrenal medullary cells were followed during the course of oligemic and normovolemic shock in dogs. Blood adrenaline concentration rose promptly after hemorrhage, reaching a maximum that was 10-fold greater than normal during the early period of hemorrhagic hypotension. Thereafter, adrenaline levels gradually declined until the end of the critical stage of hemorrhagic shock when the blood concentration rose to a level 8-fold that of normal. Following the critical stage, and throughout the irreversible stages of shock, adrenaline levels remained near normal. Noradrenaline, which was initially undetectable, first appeared in the impending stage of hemorrhagic hypotension and showed little change during the course of severe hemorrhagic hypotension. Ultrastructural studies demonstrated A-cell degranulation as early as 5 min after initiation of hemorrhage. Degranulation continued throughout the impending stage of hemorrhagic hypotension and was associated with an increasing number of autophagic vacuoles containing empty vesicles. At the end of the critical stage, all A cells showed complete degranulation and degenerative hydropic change. Progression to necrosis rather than arrest or reversal of hydropic change was observed after reinfusion of blood. In contrast to the marked alterations in A cells, most N cells were morphologically unchanged.

Adrenal Medulla↗