Biomedical subjects
Publications and source records attributed to M Ogata.
The computed tomography (CT) was performed in 10 cases of neurofibromatosis. The CT scan showed the abnormal findings in 8 cases out of 10. Skull lesions were noted in 3 cases and intracranial tumors were found in 5 among which multiple neoplasms were seen in 3. Although reported cases were not large enough in number, the incidence and variety of the tumors were similar to others reported before CT era.
Using an immunoperoxidase antibody test, the serum immunoglobulin (Ig) A antibody titer was determined in swine naturally infected with transmissible gastroenteritis (TGE; group A), swine inoculated orally with high-virulent TGE virus (group B), and swine inoculated IM (group C) or orally (group D) with low-virulent TGE virus. Studies were then made on the relationship between active immunity to TGE and the serum IgA antibody titer. In group A swine, serum IgA antibody and virus-neutralizing (VN) antibody were absent in the serum collected in the acute stage, but were detected from the serum collected in the convalescent stage. In group B swine, serum IgA antibody and VN antibody began to be detected on postinoculation day (PID) 7 and were still detectable on PID 100. In group C and D swine, VN antibody was detected, but serum IgA antibody was not. Swine were inoculated orally with high-virulent TGE virus and were challenge exposed orally with the same strain of virus on PID 18, 21, 80, and 120 (group E). None of group E swine manifested clinical signs of infection. Their serum IgA antibody titers ranged from 2 to 512 at the time of inoculation. Swine were inoculated IM with low-virulent TGE virus and intranasally with the same virus on PID 60 (group F). They were challenge exposed with the high-virulent strain of TGE virus on PID 140, 200, and 260 (80, 140, and 200 days after the 2nd inoculation). At the time of challenge exposure, IgA antibody was undetected in serum at a 1:2 dilution. All group F swine had severe diarrhea 3 to 4 days after inoculation. Many of them vomited at the same time. In these swine, villous atrophy was observed in the jejunal portion of the small intestine. The VN antibody titer of porcine serum obtained at the time of challenge exposure was higher than was that determined in the group E swine. Seemingly, serum IgA antibody titer determined by the immunoperoxidase antibody test may be an indicator of active immunity to TGE.
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The effect of lead on the activities of erythrocyte pyrimidine 5'-nucleotidase (Py5N) and delta-aminolevulinate dehydratase (ALA-D) was studied in the mice which were given ad libitum a drinking water containing lead of 10, 50 and 250 ppm, for 27 days. The erythrocyte Py5N activity was not decreased in all groups of lead-exposed mice. However, the erythrocyte ALA-D activity was markedly decreased in the groups exposed to 50 and 250 ppm lead. These data indicate that erythrocyte ALA-D is more sensitive than Py5N to lead in vivo. On the other hand, from the in vitro study, it was demonstrated that the human erythrocyte Py5N is moderately inhibited by zinc and tin, and markedly by mercury, cadmium, silver, copper, and lead, at 10(-4) molar concentrations. In addition, it was observed that the erythrocyte Py5N is most remarkably inhibited by mercury while the ALA-D by lead, among metals tested.
The authors determined that the organic sulfur compounds usually contained in crude oil can be used as a marker of oil pollution in shellfish and fish. Short-necked clams (Tapes Angdala phillipinarum A. et Reeve) and eels were maintained in a controlled laboratory environment in water with suspension of crude oil. Mass spectra and mass chromatograms of short-necked clam extract showed the presence of organic sulfur compounds of alkyl- (from C1 to C10) benzothiophenes, dibenzothiophene, alkyl- (C1 to C8) dibenzothiophene, naphthalene, and alkyl- (C1 to C6) naphthalene. Alkyl benzothiophenes and alkyl dibenzothiophenes of low carbon numbers were more easily transferred to short-necked clams than those of higher carbon numbers. Capillary column gas chromatography-mass chromatograms of crude oil and extract from the soft body of a short-necked clam showed the presence of organic sulfur compounds of alkyl benzothiophene (from C2-C6), dibenzothiophene, and alkyl dibenzothiophene (C1-C4). Besides sulfur components, various other compounds were contained in crude oil and short-necked clam, namely alkyl benzene (C3-C9), naphthalene, alkyl naphthalene (C1-C5), phenanthrene, alkyl phenanthrene (C1-C6), n-paraffin (C12-C21), and probably pyrene and alkyl pyrene (C1-C2). Also, mass chromatograms of crude oil and the extract from eel flesh showed the presence of alkyl benzothiophene (C1-C5), dibenzothiophene, naphthalene, and alkyl naphthalene (C1-C5). Data indicated that the organic sulfur compounds and polyaromatic compounds could serve as markers of oil pollution in shellfish and fish. for the identification of sulfur compounds by capillary gas chromatography/mass spectrometry, a new intensity matching method was devised.
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Spinal cord tissue oxygen was measured by polarography at the dorsum of the spinal cord for 24 hours after acute spinal cord injury, and the effects of hypertension, hypercarbia, and hyperoxia were examined. Acute spinal cord injury was produced in mongrel dogs by constriction of the midthoracic cord with an epidural tourniquet inflated to 400 mm Hg, which was maintained for 5 minutes. At the injury site spinal cord tissue oxygen was slightly increased immediately after injury but was depressed significantly at 1 hour and remained unchanged thereafter. Hypertension induced by the intravenous infusion of norepinephrine elevated the tissue oxygen only slightly after 3 hours. Hypercarbia and hyperoxia produced by ventilation with a 95% O2:5% CO2 mixture did not elevate the depressed spinal cord oxygen content. When hypertension, hypercarbia, and hyperoxia were combined, the spinal cord oxygen value was elevated to the normal level even at 3 hours after injury, when the cord oxygen was at its lowest, and it increased steadily thereafter.
Combined hypertension and hypercarbia, which was found to improve post-traumatic spinal cord hypoxia and presumably ischemia in our previous study, was used in dogs subjected to experimental spinal cord injury to determine its therapeutic effects against acute spinal cord trauma. Intermittent hypertension and hypercarbia therapy, in which 15 minutes of hypertension and 95% O2:5% CO2 gas ventilation were alternated with 10 minutes of air ventilation, was given for 3 hours beginning 3 hours after injury. The treated dogs and untreated control dogs were checked neurologically and electrophysiologically at weekly intervals for up to 8 weeks. The treated dogs showed higher grades of neurological function within 1 week, but the results were statistically insignificant. Both groups demonstrated steady neurological improvement for the next 2 weeks and remained paraparetic thereafter with no group difference. The size of the intramedullary lesion was identical in both groups. Recovery of the somatosensory evoked potentials coincided well with neurological improvement, with again no difference between the two groups.
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In a study of 14 patients (11 Japanese and 3 white North Americans) with aldosterone-producing tumor carried out within 2 to 4 weeks after unilateral adrenalectomy, both plasma renin activity (PRA) and plasma aldosterone concentration (PAC) increased almost normally with short-term sodium depletion and upright posture. Aldosterone excretion rate (AER) also increased significantly with sodium depletion, and was normally suppressed by sodium loading. Highly significant correlations were observed between PRA and PAC (r=0.89, p < 0.001) or AER (r=0.88, p < 0.001) ater operation, whereas there had been no such correlation before operation. Either physiological or laboratory findings were normalized or markedly improved in all cases although pathohistological diagnosis was made as adenomatous hyperplasia in 10 out of 11. These results indicate that within 4 weeks of operation PRA and the remaining adrenal gland can almost normally respond to stimuli such as sodium depletion and upright posture regardless of the amount of spironolactone given preoperatively.