[18-month interaction with a delinquent boy].
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Biomedical subjects
Publications and source records attributed to M Nagashima.
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In three familial cases and one sporadic case of late-onset distal myopathy, muscle wasting started in the distal portions of the lower extremities. The most striking change seen by light microscopy was the appearance of rimmed vacuoles. These were presumed to be autophagic, because they were found by electron microscopy to contain membranous lamellar structures and other heterogenous materials enclosed by a limiting membrane. On the other hand, lysosomal activity was markedly increased in skeletal muscle. In 6% to 22% of affected muscle fibers there were acid phosphatase-positive granules deep in the sarcoplasm, whereas control muscles had no such granules. The degenerative process in distal myopathy may be different from that in other muscular dystrophies.
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Automated Edman degradation of alpha 1-acid glycoprotein from serum (serum AGP) was successful only after the desialylated, reduced, and alkylated protein had been treated with pyroglutamate aminopeptidase. The sequence is (less than Glu)-Asn-Pro-Glu-Pro-Ala-X-Ile-Thr-Leu-Gly-Ile-Pro-Ile-. For radioactive sequencing of the NH2 terminus of the intracellular precursor form (liver AGP) of serum AGP, protein was labeled by incubating liver cells in suspension with either [3H]proline or [3H]isoleucine for a 15-min period. Liver AGP was separated from serum AGP by ion exchange chromatography. Between 78 and 90% of the radioactivity incorporated into total AGP was associated with liver AGP, indicating that little conversion of newly synthesized liver AGP to serum AGP had occurred during the 15-min incubation period. Liver AGP was then isolated by immunoprecipitation. The antigen-antibody complex was exposed to 15 Edman degradation cycles; however, no radioactivity was released. Automated Edman degradation of liver AGP which had been extracted from the immunoprecipitate with dilute acid and subsequently treated with pyroglutamate aminopeptidase yielded a sequence of proline and isoleucine identical with that in serum AGP. We conclude that processing of the intracellular precursor form of AGP does not involve a proteolytic trimming near the NH2 terminus.
The long-term results of 1023 adult patients with congenital heart diseases, operated and non-operated, with atrial septal defect (ASD), patent ductus arteriosus (PDA), pulmonary stenosis (PS) and tetralogy of Fallot, were followed for up to 24 years, and the long-term results of operated and non-operated congenital heart diseases were compared. The survival rate of patients with operated isolated ASD was significantly higher than in patients with non-operated isolated ASD, and that of operated patients with VSD associated with other anomalies was also significantly higher than in non-operated VSD patients with such involvement. The survival rate showed no significant difference in the operated and non-operated patients with PDA, PS and tetralogy of Fallot. In all congenital heart diseases, there was a close correlation between the mean pulmonary artery pressure and the mortality rate both in operated and non-operated patients and a marked improvement of physical capacity of operated patients at the time of the last follow-up examination.
Electrophysiological studies were performed on 34 patients whose reentrant circuit of paroxysmal supraventricular tachycardia (PSVT) involved normal atrioventricular (AV) conduction system as the antegrade limb and either overt (25 patients) or concealed (9 patients) accessory AV pathway as the retrograde limb. The diagnosis of this mechanism was made by one or more of the following: 1) eccentric retrograde atrial activation sequence; 2) effect of bundle branch block on ventriculoatrial (VA) conduction time; 3) paradoxically premature atrial capture; 4) atrial capture by premature ventricular stimulation of VA conduction time with retrograde during PSVT; 5) no significant prolongation of VA conduction time with retrograde atrial activation sequence to that of PSVT during incremental and premature ventricular stimulation; 6) shortening of cycle length with constant H-V and V-A intervals after atropine administration. The participation of accessory pathway in PSVT circuit should be decided by as many of the above-mentioned findings or procedures as possible for optimal therapy. Electrophysiological studies have led to the recognition that accessory pathway, functionally silent during antegrade conduction, is responsible for some patients with PSVT. If the mechanisms of PSVT were more carefully analyzed, the recognition of PSVT cases involving accessory pathway would increase.
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With the improvement of recovery ratio of trophoblastic disease by means of primary chemotherapy, undetermined cases of trophoblastic diseases, whose morphological examination has not been conducted, have increased. The respective sickly constitutions of these cases are extremely complicated, and we have deviced a new close classification of these cases from clinical standpoint. For the purpose, we have chosen out the following items.: A. Major subdivision 1. Types of antecident pregnancy. 2. Duration between the antecident pregnancy and the commencement of chemotherapy. 3. Urinary hCG secretion pattern following molar pregnancy. 4. Following treatment of hydatidiform mole. B. Minor subdivision 1. Urinary hCG titer at the commencement of chemotherapy. 2. BBT pattern. 3. Chest x-ray findings. 4. PAG. 5. Clinical signs. 6. Development of focuses (clinical). 7. Necessary reasons for chemotherapy. These items are expressed respectively by figures. This close classification method is based on the combinations of these figures. The authors believe, this method will enable the easy classification of early chemotherapy examples and will present a strong key for the analysis of enormous cases.
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