[Estimation of uranium, thorium and alpha emitters in LSI (large scale integration) components].
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Biomedical subjects
Publications and source records attributed to K Kudo.
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The administration of 2 i.p. injections of 2 x 10(7) ovalbumin- (OA) pulsed, syngeneic, adherent, peritoneal exudate cells (OA-pulsed macrophages [M phi]) to (C57BL/6 x DBA/2)F1 (B6D2F1) mice promoted a persistent and high-titer anti-OA IgE response in these mice. Similarly, 2 i.p. injections of OA-pulsed DBA/2 parental M phi also induced the generation of an anti-OA IgE response in B6D2F1 mice; an identical procedure using OA-pulsed C57BL/6 parental M phi, on the other hand, elicited in most cases a very weak to negligible anti-OA IgE response. The administration of 3 i.p. injections of OA-pulsed syngeneic M phi to SJL mice also induced these "IgE nonresponder" mice to develop an anti-OA IgE response that was both boosterable and of moderate to high titer. The significance of these results with regard to the induction and regulation of the IgE antibody response is discussed.
A 2-year-old girl with a ring of chromosome 11[46,XX,r(11)(p15q25)] was reported. Her clinical features included growth and psychomotor retardation, microbrachycephaly, hypertelorism, strabismus externus, short nose, low nasal bridge, low-set ears, microretrognathism, short neck, small opening of vagina with large clitoris, deformity of nails, café-au-lait spot of the skin, general hirsutism, congenital heart disease, generalized convulsions, and pancytopenia. Most of these features are those characteristic of the 11q- syndrome. The fact that the patients with the deletion distal from q22 (reported cases) to q25 (our case) had a common phenotype suggests that the loss of the q25 leads to qter segment is mainly responsible for the characteristic clinical features of the 11q- syndrome.
A total of 19 patients consisted of 10 cases with hypertrophic cardiomyopathy (HCM), 6 with hypertensive heart disease (HHD) and 3 with professional bicycle racers with myocardial hypertrophy, showing giant negative T waves greater than 10 mm in precordial leads (GNT-group) was examined by catheterization, cineangiography and endomyocardial biopsy. Fourteen patients of myocardial hypertrophy consisted of 5 cases with HCM, 4 with HHD and 4 with professional bicycle racers without giant negative T (non-GNT-group) were selected as the control. The average of mid-ventricular wall thickness (Tm = 17.4 +/- 4.6 mm) and that of apical wall thickness (Ta = 18.5 +/- 3.6 mm) obtained from the left ventriculogram in GNT group were significantly greater than those in non-GNT group. The average of the apical hypertrophic index (Ta/Tm = 1.1 +/- 0.3) was also greater than that in non-GNT group. For the evaluation of hypertrophy of the papillary muscles, pattern of the hypertrophy was divided into 2 types by the feature of the left ventriculogram in systolic phase of right anterior oblique view, i.e., normal to moderate (type I) and severe (type II). In GNT group, 79% of patients belonged to the type II, whereas 71% of patients in non-GNT group belonged to type I. Histopathologically, the hypertrophy of heart muscle cells in GNT group was higher grade than in non-GNT group. Disarray of the muscle cells and myocardial fibrosis was not so prominent in GNT group. It was concluded that the mode of hypertrophy in GNT group was characterized by the existence of papillary muscle hypertrophy and had similarity to the hypertrophy of known etiologies such as mechanically overloaded myocardium which suggested to the secondary heart muscle diseases.
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Two tumor cell-aggregation factors of glycoprotein nature, separated from rat ascites hepatoma AH136B cells (forming cell islands in vivo), had different antigenicity; one was not absorbed by immunoadsorbent chromatography with anti-rat serum antibody and the other was. The unabsorbed factor induced aggregation (as shown in the form of simple apposition) of rat ascites hepatoma AH109A cells (present as a free form in vivo) and cell adhesiveness characterized by well-defined tripartite junctional complexes, including intermediate junctions, desmosomes, and tight junctions. In contrast, the absorbed factor from AH136B cells, AH109A cells or normal rat serum aggregated AH109A cells but failed to develop the junctional complexes; only simple apposition was observed. AH109A cells themselves contained the absorbed factor but not the unabsorbed factor. AH136B cells proliferating in the skin developed the junctional complexes, while AH109A cells proliferating in the skin did not from any junctional complexes.
IgE levels in nude mice were estimated by the one-step single radial radiodiffusion method antisera prepared by immunization of guinea pigs with an IgE-rich fraction obtained from sera of normal mice infected with Nippostrongylus brasiliensis and immunized with DNP-ovalbumin in alum gel. 3 out of 8 nude mice had IgE levels significantly higher than those of normal mice.
The peripheral nerves of alloxan and streptozotocin diabetes rats six months after the induction of diabetes were morphologically investigated. The effect of insulin treatment was also examined. Prominent segmental demyelination and remyelination were observed in both alloxan and streptozotocin diabetes rats by isolated nerve fiber studies. Axonal degeneration and globular swelling were also recognized in some nerve fibers. Transmission electron microscopic findings were characterized by the figures of destructed myelin sheaths and axons. Reduplication and thickening of basal lamina of vasa nervorum were noted in the diabetes rats. Scanning electron microscopy revealed three dimensional architectures of degenerated nerve fibers and rough surface of Schwann cells in the diabetes rats. Insulin treated diabetes rats showed less structural changes of nerve fibers. It was indicated that the peripheral nerve lesions of experimental diabetes rats were caused by metabolic impairment of both axons and Schwann cells. Insulin treatment seemed to be effective on the experimental diabetic neuropathy.
Anti-ovalbumin (OA) IgE antibody responses were measured in B6D2F1 mice as a function of time and antigen dose. One hundred to 200 microgram of OA in Al(OH)3 elicited transient responses, whereas 1 to 10 microgram of OA in Al(OH)3 elicited persistent anti-OA IgE responses of high titer. T cells isolated from the spleens of mice mounting either a persistent or a transient response strongly suppressed primary anti-DNP IgE responses in unirradiated recipient mice that were immunized with DNP-OA in Al(OH)3; it was, therefore, concluded that suppressor T cells (Ts cells) were activated during both the persistent and transient IgE responses. Nevertheless, in the present study it was not possible to completely rule out the contention that IgG antibodies may also have been suppressing the IgE response. With a modified adoptive transfer system, it was shown that these Ts cells were sensitive to low doses (250 R) of x-irradiation. The suppressive activity of long-term OA primed cells was also shown to be markedly enhanced when cultured for 24 hr with soluble OA; this finding was interpreted to indicate the presence of memory suppressor cells.
A ferredoxin was purified from Clostridium perfringens by DEAE-cellulose chromatography and Sephadex G-50 gel filtration. It had absorption maxima at 390 and 280 nm. The molecular weight was estimated to be 6,000 by Sephadex gel filtration and from the results of amino acid analysis. The isoelectric point was 3.0. It contained four atoms of iron, four atoms of labile sulfur, and six cysteine residues. This ferredoxin as well as ferredoxin from C. pasteurianum acted as an electron donor for nitrate reductase from C. perfringens. The ferredoxin could also act as an electron donor for the hydrogenase from C. pasteurianum in hydrogen evolution.
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The antibody response to mite antigen in several mouse strains was studied. BALB/c, CBA, C3H/He, and C57B1 strains showed good responses against mite antigen. The AKR strain, on the other hand, showed a relatively poor response. When BALB/c mice were immunized with DNP-mite conjugate in aluminum hydroxide gel (alum), anti-DNP IgE antibody and IgG1 antibody were induced. When these mice were boosted with mite antigen alone in alum, both anti-mite IgE antibody and IgG1 antibody were induced, although these antibodies were not observed after the first immunization. Both IgE antibody responses were high and persistent. Mite antigen was denatured by alkylation and reduction in the presence of 8 M urea. Native antigen remaining in the chemically denatured antigen was removed by an immunoadsorbent method. The modified mite antigen could stimulate the carrier-specific helper cells, at least when it was injected with alum. It was also found that repeated injections of the modified mite antigen resulted in the suppression of an established IgE antibody response against mite antigen. These findings suggest possible clinical application for hyposensitization therapy.
Two tumour-cell-aggregation factors, derived from rat ascites hepatoma cells, had different antigenicity; one was not absorbed by immunoadsorbent chromatography with anti-rat serum antibody and the other was. Their activities were both lost by digestion with trypsin, but remained unchanged by oxidation with periodate, suggesting the role of the protein portions in their molecules. The potency of the unabsorbed factor was inhibited specifically by alpha-methyl-D-mannoside or D-mannose, while that of the absorbed factor was inhibited specifically by N-acetyl-D-glucosamine, suggesting that these carbohydrates may be concerned with the respective receptor structures at the tumour-cell surface. The unabsorbed factor induced not only cell aggregation (as shown in the form of simple apposition) but also cell adhesiveness characterized by development of intermediate junctions, desmosomes and tight junctions, while the absorbed factor produced only simple apposition, suggesting their functional difference.
Thirty-eight patients with discontinuity defects of the mandible were hospitalized at Iwate Medical University School of Dentistry during the 12-year period from 1965 to 1976. Treatment consisted of grafting autogenous ilium and rib in 35 patients and isologous ilium and Kiel bone in three patients. No bony union was noted in four of 28 cases involving benign tumors, three of eight cases involving malignant tumors, and one of two cases involving old fractures. Postoperative infection was the main cause for lack of union.