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Biomedical subjects

K Yokochi

Publications and source records attributed to K Yokochi.

At least 73 records · Page 4Linked to original sources
PubMed1986

A case of ataxic diplegia, mental retardation, congenital nystagmus and abnormal auditory brain stem responses showing only waves I and II.

A three-year-old boy who had ataxic diplegia, mental retardation, horizontal pendular nystagmus with head nodding and abnormal auditory brain stem responses showing only waves I and II was presented. His clinical features coincided with recent reports in the Japanese literature of cases of a new syndrome that is congenital in origin and seen only in boys.

Auditory Pathways↗
PubMed1986

Infective endocarditis in children: a current diagnostic trend and the embolic complications.

Twenty-three cases of IE, of which 91% had underlying congenital heart diseases were diagnosed by positive blood culture or vegetative lesion detected by 2-D ECHO when a patient revealed clinically suspicious episodes. VSD and TOF were the most common underlying heart diseases. The vegetation was detected successfully by 2-D ECHO in 91% of the cases. The causative organisms were identified in 83% of the cases. Streptococcus viridans and Staphylococcus aureus were the two major organisms detected. Candida albicans was found in 3 postoperative and fatal cases. Embolic complications occurred in 7 cases (30.5%): five cases of pulmonary infarction and two of cerebral infarction. The overall mortality was 22%. We recommend early surgical intervention whenever a patient reveals a very large vegetation with animated movability, and emphasize the importance of a proper prophylaxic regimen.

Adolescent↗
PubMed1986

[Unusual cardiac hypertrophy in neonates with congestive heart failure: report of three cases].

We experienced three cases of unusual cardiac hypertrophy of the right ventricle or interventricular septum with severe congestive heart failure in the neonatal period. One patient had congenital heart disease consisting of membranous tricuspid atresia, absent pulmonary valve, patent ductus arteriosus, left single coronary artery and a hypoplastic pouch-like right ventricle. Very marked cardiac hypertrophy was observed in the right ventricle and interventricular septum. Histologically, there was no appreciable disorganization of the cardiac muscle. The etiology of the unusual hypertrophy of cardiac muscle in this patient is uncertain. The other two patients had asymmetrical septal hypertrophy of the left ventricle evidenced by two-dimensional echocardiography. Cardiac catheterization was performed for these two patients. There was no evidence of congenital heart disease; however, one patient had a significant pressure gradient in the outflow tracts of the left and right ventricles. These two patients' faces appeared unusual and they had minor anomalies of their fingers and ears. This unusual cardiac hypertrophy associated with cardiac anomalies and minor anomalies of the face and extremities comprise a specific type of cardiomyopathy in neonates. This should be distinguished from hypertropic cardiomyopathy of older children and adults.

Cardiomegaly↗
PubMed1986

[Carnitine deficiency: a treatable cardiomyopathy].

This is a report of two brothers, six and five years of age, with systemic carnitine deficiency and cardiomyopathy, whose symptoms were improved after oral administrations of DL-carnitine. They had had progressive muscle weakness since three years of age. The elder brother's radiograph on admission showed cardiomegaly with a cardiothoracic ratio of 60%, and his electrocardiogram showed left ventricular hypertrophy and tall, peaked T waves in the precordial leads. The echocardiogram showed slight thickening of the cardiac muscle and decreased ejection fraction. Skeletal muscle biopsy specimens and sera were assessed for carnitine content. The skeletal muscle specimens revealed lipid storage myopathy, and the carnitine contents of the skeletal muscle and sera were both decreased. Myocardial biopsy for the elder brother revealed mitochondrial accumulation. Cardiomyopathy caused by carnitine deficiency is often fatal, but may be cured. Carnitine deficiency should be considered whenever a patient with cardiomegaly and progressive skeletal muscle weakness is encountered.

Cardiomyopathies↗
PubMed1985

Skeletal muscle involvement in Escobar syndrome.

In addition to the clinical characteristics of Escobar syndrome, including an anomalous facial expression, multiple joint contractures, multiple pterygia and a short stature, two female siblings developed proximal dominant muscle weakness from birth and slowly progressive scoliosis. Biopsied specimens obtained from the paravertebral and gluteus maximums muscles at the time of spinal surgery showed variation in fiber size, increased numbers of fibers with central nuclei, interstitial fibrosis and disorganized intermyofibrillar networks with occasional core/targetoid formations. The most outstanding histochemical abnormality in both cases was an abnormal fiber type distribution (type 2 fiber deficiency) which might be the result of an abnormal or deficient neural supply to the developing muscles. The defective neural influence on the muscle is assumed to produce the above-mentioned muscle changes, inducing multiple joint contractures and scoliosis.

Adolescent↗
PubMed1985

Congenital muscular dystrophy with severe infantile scoliosis.

A girl with congenital muscular dystrophy with severe scoliosis from birth was presented. No positive family history was obtainable. She developed muscle hypotonia and weakness, and feeding difficulty during the neonatal period. Her developmental milestones were delayed; she learned to walk at the age of 2 years when she walked with a "waddling gait" and stood up with Gowers' maneuver. On physical examination at 2 years old, she had mild proximal dominant muscle weakness and atrophy, and severe scoliosis with a Cobb's angle of 74 degrees but no joint contractures in the extremities. Creatine kinase was slightly elevated. Biopsied muscle showed myopathic changes, including variation in fiber size, moderate fibrous tissue proliferation, some necrotic and regenerating fibers and type 1 fiber predominance, consistent with those seen in chronic progressive muscular dystrophy.

Biopsy↗
PubMed1985

Prostaglandins and fetal cardiac output distribution in the lamb.

With the use of a triple thermodilution technique in 17 fetal lambs, combined with microsphere estimations in 7, the effects of indomethacin prostaglandin (PG) I2 and PGE2 on cardiac output and its distribution were measured. Indomethacin (0.2 mg/kg) induced a main pulmonary artery-to-aorta pressure gradient, which peaked within 45-60 min and persisted for 2-3 h. PGE2 abolished this gradient (threshold 50 ng X kg-1 X min-1), while PGI2 in doses up to 100 ng X kg-1 X min-1 increased it. Indomethacin did not change total cardiac output but altered its distribution (right ventricular output, left ventricular output) and increased the percentage of right ventricular output flowing to the lungs. Ductal flow decreased concomitantly. After indomethacin, PGI2 further decreased ductal flow, increased pulmonary flow, and decreased pulmonary vascular resistance. PGE2 restored the original right ventricular-to-total cardiac output ratio, although ductus flow did not return to base-line levels. Pulmonary resistance increased slightly, reflecting decreased pulmonary flow, associated with decreased right ventricular output. Thus PGE2 was more effective on the ductus than on the pulmonary circulation. PGI2 did not relax the ductus but was a potent pulmonary vasodilator. Neither PGI2 nor PGE2 nor indomethacin changed total cardiac output but all altered its distribution.

Animals↗
PubMed1985

[Anomalous origin of the right coronary artery from the pulmonary artery: report of a case].

An asymptomatic 5-year-old boy with anomalous origin of the right coronary artery from the pulmonary artery was reported. He was referred to us for evaluation of an apical continuous murmur. The chest radiograph, and electrocardiograms at rest and during exercise were unremarkable. This anomaly, whose echocardiographic findings have not been described before, were visualized first by two-dimensional echocardiography, and confirmed by coronary angiography. There have been some reports of sudden death occurring in patients with this rare congenital heart defect. We believe that careful follow-up study is indicated.

Child, Preschool↗
PubMed1984

Action of PGI2 analogs on the pulmonary and systemic circulations in the conscious newborn lamb.

Previous work (Lock et al., J. Pharm . Exp. Ther. 215:156, 1980) has shown that conventional screening procedures for vasoactive PGI2 analogs were little value in predicting pulmonary vasodilator activity in the newborn lamb. To gain a better insight into the structural requirements for pulmonary vasoactivity and possibly identify useful compounds for the management of neonatal pulmonary hypertensive disorders, we have tested the following PGI2 analogs in normoxic and hypoxic newborn lambs: 15(S)-9-deoxy-15-methyl-9 alpha,6- nitrilo -PGF1 (analog I); 9-deoxy-9 alpha,5- nitrilo -PGF1 (analog II); (6S, 15S)-15-methyl-PGI2 (analog III); and ( 6R , 15S)-15-methyl-PGI1 (analog IV). A prostaglandin analog mimicking PGI2 (compound BW245C ; (+/-)-5-(6- carboxyhexyl )-1-(3-cyclohexyl-3-hydroxypropyl)hydantoin ) was tested as well. Compounds were injected into a branch pulmonary artery and any local pulmonary effect could be assessed from the change in the ratio of blood flow to the injected lung over total flow. None of the analogs tested proved to be a selective pulmonary dilator. BW245C was a potent peripheral vasodilator (threshold around 0.5 microgram/kg) and indirectly lowered pulmonary vascular resistance through its systemic effects. Analog I also dilated the systemic circulation, but only at the highest dose tested (100 micrograms/kg). The latter finding is surprising because it was previously shown that the parent, non-methylated compound is a fairly potent and selective pulmonary vasodilator. Analog II and IV were inactive at a dose up to, respectively, 30 and 20 micrograms/kg. Analog III, on the other hand, weakly constricted the systemic circulation at a dose of 10 micrograms/kg.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

Effects of betazole hydrochloride and cyclic AMP on the pepsinogen secretion by rabbit gastric mucosa in organ culture.

The effects of betazole hydrochloride, dibutyryl cyclic AMP (DB-cyclic AMP) and betazole hydrochloride plus aminophylline on pepsinogen secretion by rabbit gastric mucosa were studied in organ culture. Betazole hydrochloride alone did not stimulate pepsinogen secretion at the concentrations of 10(-8), 10(-6), 10(-5) and 10(-4) M. However, 10(-3) M DB-cyclic AMP produced a significant stimulation of pepsinogen secretion into the culture medium when compared with the control. In the presence of 3 x 10(-3) M aminophylline, betazole hydrochloride in the concentration of 10(-5) and 10(-4) M stimulated pepsinogen secretion into the culture medium, and the magnitude of this increase was 2.0- and 2.8-fold, respectively, compared with the control. Aminophylline alone could not change pepsinogen secretion into the culture medium. These results suggested that the pepsinogen secretion, stimulated by betazole hydrochloride, was mediated by cyclic AMP in the chief cells.

Aminophylline↗
PubMed1982

Phenytoin--allopurinol interaction: Michaelis--Menten kinetic parameters of phenytoin with and without allopurinol in a child with Lesch--Nyhan syndrome.

We analyzed Michaelis--Menten pharmacokinetic parameters of phenytoin with and without the coadministration of allopurinol (150 and 200 mg/day) in a child with Lesch--Nyhan syndrome. The Vmax and Km were estimated from at least two different sets of serum concentration--dosage data of phenytoin. The Vmax values (mg/kg/day) were 16.1 without allopurinol, and 12.4 and 10.9 with allopurinol (150 and 200 mg/day), respectively, whereas those for Km remained relatively constant (3.9 to 4.9 microgram/ml). Our results suggest that allopurinol is a drug that inhibits the hepatic metabolism of phenytoin.

Adolescent↗
PubMed1981

Placental transfer of anticonvulsants (phenobarbital, phenytoin, valproic acid) and the elimination from neonates.

In six full-term newborn infants born to epileptic mothers, the cord-to-maternal concentration ratios of anticonvulsants and the plasma disappearance of the drugs transferred across the placenta were studied. The respective mean +/- SEM values for the ratio of the cord-to-maternal blood concentration were: 0.95 +/- 0.05 (n = 5) for phenobarbital (PB), 0.97 +/- 0.04 (n = 3) for phenytoin (PHT), and 1.71 +/- 0.23 (n = 4) for valproic acid (VPA). The disappearance from the plasma of neonates showed a discernible two-component (initially slow and then fast) curve for all cases with PB, for one with PHT, and for two with VPA. Half-lives calculated from the terminal elimination phase were: 74.0 +/- 8.8 hours for PB (n = 5) and 26.8 +/- 4.8 hours (n = 4) for VPA. The half-life value of PB observed in this study was found to be shorter than that observed postnatally in the previous reports, while that of VPA was two to three times as long as that reported from children or adults, but shorter than that from a neonate in the literature.

Anticonvulsants↗
PubMed1981

[Application of two dimensional echocardiography for the intracardiac manipulation: the evaluation of atrial septal movement before and after balloon atrial septostomy (author's transl)].

Two-dimensional echocardiography was applied to intracardiac catheter manipulation (especially balloon atrial septostomy: BAS) in 6 babies with complete transposition of the great arteries and 2 with total anomalous pulmonary venous drainage. Under the usual roentgenoscopic investigation, intracardiac catheter manipulation was observed by two-dimensional echocardiography directly representing the right atrium, left atrium, atrial septum, right ventricle, left ventricle and interventricular septum by the subcostal approach. Also, formation and movement of the atrial septum and intra-atrial shunt before and after BAS was evaluated by contrast echocardiography. 1. It was confirmed that the catheter tip was inserted into the left atrium from the right atrium. 2. It was clearly demonstrated that the balloon was expanding in the left atrium. 3. When the balloon was pulled out to the right atrium from the left atrium, the movement of the atrial septum and the balloon was observed. 4. The formation and movement of atrial septal defect by BAS was demonstrated and the shunt of this site was estimated by using contrast echocardiography. The relation between the catheter tip and the intracardiac structures can be judged more correctly by two-dimensional echocardiography than roentgenoscopic investigation. Also the structural and hemodynamic changes by BAS can be clearly estimated by the observation of the atrial septum by two-dimensional echography.

Cardiac Catheterization↗