Biomedical subjects
Publications and source records attributed to Y Ochiai.
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The patient had been employed in an asbestos factory for four years from the age of 16. Five years ago, she complained of sputum and cough, and she was treated for chronic bronchitis. From March, 1977, when she was 53 years old, hydrothorax and ascites increased, her weight decreased and she was hospitalized for cachexia. The clinical diagnosis of malignant diffuse mesothelioma was made on the presence of atypical cells in the effusions. Atypical cells showed a positive colloidal iron staining test and positive hyaluronidase digestion test. Asbestos bodies were found in the sputum. The patient died on February 1978. Postmortem confirmed asbestosia and mesothelioma which was scattered over the pleura, pericardial sac, diaphragma, peritoneum and pancreas. In addition, bronchiolo-alveolar cell type lung cancer was found localized in the lower lobe of the left lung. The electron beam diffraction disclosed the asbestos as amosite (brown asbestos).
A high incidence of autoantibody against the neutral glycolipid "asialo GM1" was observed in sera from patients with systemic lupus erythematosus (SLE) with neurological disorders, using an immunoflocculation test. The sera from 14 out of 17 cases of SLE with neurological disorders showed antibody activity against asialo GM1 but not against the following glycolipids: asialo GM2 GM1, and galactocerebroside. In another 87 cases of SLE without any history of seizures, as well as 61 cases of other autoimmune diseases (rheumatoid arthritis, progressive systemic sclerosis, mixed connective tissue disease, etc.) and 20 cases of various neurological diseases (epilepsy, multiple sclerosis, etc.), no antibody could be detected. In general, the antibody titer was high several months, even years, before and/or after the seizure, though the titer was low at the time that patients showed definite neurological symptoms. Immunochemical characterization with Sephadex G-200 chromatogrphy and protein A-Sepharose CL-4B affinity column indicated that the antiasialo GM1 was probably an autoantibody belonging to the immunoglobulin G class. The above results suggest that this newly found autoantibody plays a role in the pathogenesis of neurological disorders accompanying SLE.
A new benzoquinonoid ansamycin, herbimycin B was isolated from the culture broth of Streptomyces hygroscopicus No. AM-3672, a herbimycin A-producing strain. Herbimycin B showed potent anti-TMV activity. Herbicidal effect of herbimycin B was less than that of herbimycin A.
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All seventeen black rats collected from Mauritius Island were characterized by having many extra small acrocentric autosomes. Their basic karyotype was of Oceanian type, because of the presence of the large metacentric M1 and M2 pairs, but chromosome numbers in 13 specimens among them were 42, those of 3 specimens 43, and those of the remaining one specimen 44. Although the Oceanian type rat had 2 small acrocentric autosomes (pair no. 13), 16 Mauritius rats had 10 small acrocentrics, and the remaining one had 8 small acrocentrics. Comparative karyotype analysis between Oceanian and Mauritius type rats showed that the extra small acrocentrics found in Mauritius rats were due to Robertsonian fission of small metacentric pairs no. 14 and 18 of the original Oceanian type rat. Only one rat with 8 small acrocentrics showed the heteromorphic pair no. 18 consisting of one metacentric and two acrocentrics. The large metacentric M1 chromosome in 13 of 17 rats examined showed homologous pair, but two of them were heteromorphic by involving one metacentric M1 and two acrocentrics. In the remaining two rats M1 chromosome was not observed, but acrocentric pairs no. 4 and 7 were included. These acrocentrics were also suggested to be originated from Robertsonian fission of the large metacentric M1 chromosome. Robertsonian fission seemed to be one of the important mechanism found in karyotype evolution.
Clinical, electrical and biochemical studies in an eight years old boy with movement-induced seizures were reported. The attack was usually triggered by sudden initiation of movement, but rarely occurred without any apparent movement. Repeated jumping provoked attacks constantly, which was recorded cinematographically. No abnormality was found either in ictal or interictal EEGs. Haloperidol aggravated the condition, but 1-DOPA had no effect, while DPH (100 mg/day) controlled attacks perfectly with the serum DPH concentration of just 2.0 ug/dl. In overnight sleep analysis, sleep rhythms and characters of REM sleep were not differed significantly from the standard. After DPH therapy, stabilization of sleep in general was noticed; that is, total sleep time prolonged, number of sleep stages decreased and interrupting awakening disappeared. Probenecid loading test revealed that 5-HIAA was normal, HVA high, and large amount of octopamine was detected in CSF.
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Tissue extracts from human heart, lung, liver, kidney, skeletal muscle and cerebrum displayed at least 3 distinct cyclic 3':5'-nucleotide phosphodieterase (EC 3.1.4.17) activity peaks (FI, FII, FIII) on DEAE-cellulose chromatography and various properties of these forms were compared in each tissue. FI eluted at about 0.08 M sodium acetate, hydrolyzed cyclic GMP more rapidly than it did cyclic AMP, and cyclic GMP hydrolysis by FI in most tissues was enhanced by a protein activator in the presence of CaCl2. As only high concentrations of cyclic AMP inhibited cyclic GMP hydrolytic activity of FI, the enzyme probably has a low affinity for cyclic AMP. FII eluted at about 0.2 M sodium acetate, hydrolyzed both nucleotides at equal rates, and substrate affinities were relatively low. Cyclic GMP hydrolysis by FII was also stimulated by addition of a protein activator in the presence of CaCl2 and cyclic AMP hydrolysis in this fraction was accelerated by a micromolar fraction of cyclic GMP. FII eluted at about 0.35 M hydrolyzed cyclic AMP preferentially and was insensitive to protein activator. These two cyclic nucleotides act as mutual inhibitors of the hydrolysis in this fraction. Ratio of the cyclic GMP to cyclic AMP hydrolysis was in the order FI, FII, FIII. Four activity peaks were eluted from the cerebral extract and enzymes from this tissue exhibited much the same properties as observed in the other tissues examined herein.
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Two infants had congenital atlantoaxial dislocation associated with myelopathy. One of them, a 3-month-old girl, showed anterior dislocation of the atlas on the axis, and had extreme weakness of the extremities. Another patient, an 8-month-old boy, showed tetraplegia, and posterior dislocation with absent odontoid process was demonstrated radiologically. These cases add another cause to the varied etiologies of floppiness in early infancy.
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In order to investigate flexor hypertonia of the extremities in newborns, a neurological examination and superficial electromyogram (EMG) recordings were carried out on 50 full-term infants both before and after the first 48 hours of life (the 'birth-shock period). EMG amplituds on the flexor side of the upper arm in the traction response were low during the first 48 hours despite flexion of the elbow (hypertonia); after the first 48 hours EMG amplitudes increased in a large percentage of the infants although elbow flexion decreased (hypotonia). This finding suggests that the frflex response to passive movement (traction) is weaker during the first two days of life than after this time. Flexor tone of the upper arm in recoil of the forearm increased during the first 48 hours in spite of low EMG amplitudes; after the first 48 hours the amplitudes increased although flexor tone of the upper arm decreased. The popliteal angle was more than 90 degrees in 27 infants and less than 90 degrees in 23 infants during the first 48 hours; after this period the angle was more than 90 degrees in 11 infants and less than 90 degrees in 39 infants. EMG amplitudes on the flexor side of the thigh in most cases increased after the first 48 hours for both groups of infants, i.e. those with an angle more than 90 degrees and those with an angle less than 90 degrees. It is suggested that flexor hypertonia of the extremities in newborn infants is not a result of muscle contraction (i.e. real muscle strength) but rather is residual from the infant's position in utero.