[Lipiodol emulsion (Lip. (E)20) as a new contrast agent for selective visualization of the liver and spleen. Basic analysis and experimental studies in dogs by X-ray CT and ultrasound].
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Biomedical subjects
Publications and source records attributed to K Sugimura.
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Macrophage-chemotactic factor (MChF)-producing T cell hybridomas were established. These hybridomas produced MChF upon the specific antigenic stimulation with phosphorylcholine (PC)-conjugated protein in the presence of I-Ed-positive antigen-presenting cells. The hybridomas also secreted MChF after co-culture with concanavalin A in the absence of antigen-presenting cells. The MChF-secreting hybridomas were positive for Kd, Dd, Lyt-1.2 but negative for I-Ad, Lyt-2.2. The molecular weight of MChF produced by the hybridomas was 43000 and the factor was focused at pH 6.6-6.8 in the chromatofocusing procedure. The MChF was protease sensitive but resistant to neuraminidase treatment, and it was stable by heating at 80 degrees C for 15 min. The MChF-producing hybridomas established in this stud did not produce macrophage migration inhibitory factor (MIF), macrophage-activating factor (MAF) or interleukin 2, suggesting molecular nonidentity between MChF and these lymphokines. The MChF-producing T cell hybridomas reactive to specific antigens (PC) will be promising tools for analysis of molecular nature of MChF as well as molecular aspects of antigen recognition mechanism of T cells.
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In order to determine the difference between steroidogenesis in normal and polycystic ovaries (PCO), endocrinological analysis of follicular fluid and monolayer cell culture of human granulosa cells were carried out, and human LH and dibutyryl cyclic AMP were added to the cultures. The concentrations of LH and androstenedione in the follicular fluid from PCO ovaries were significantly higher than those found in normal ovaries in the early and mid-follicular phases. The cultured granulosa cells from the mid-follicular phase of normal women responded significantly to LH, showing an 8 to 10 fold increase in progesterone production. In contrast, exogenous LH caused only a slight stimulation (2 to 4 fold increase) in progesterone production by granulosa cells from PCO follicles. The cultured granulosa cells from normal women and PCO ovaries responded significantly to dibutyryl cyclic AMP, showing an 8 to 10 fold increase in progesterone production. These results strongly suggest that there is no alteration in the steroidogenic pathway after the cyclic AMP stage and that the persistent elevation of LH in serum and follicular fluid may lead to a disturbance of progesterone production in response to exogenous LH in the cultured granulosa cells from PCO ovaries.
A patient who had vesical leukoplakia with unusual macroscopic and histological findings was studied. The mucous membrane of the urinary bladder in this patient showed a tumor-like proliferation similar to verrucous hyperplasia which is often found in the oral mucosa. We propose a new classification of vesical leukoplakia, dividing it into three groups, atrophic, hypertrophic and verrucous types. The atrophic type has a heavily keratinized, flat and thin type of epithelium with features resembling lichen sclerosis et atrophius. Histologically, it shows a variable degree of hyperkeratosis but no parakeratosis. The hypertrophic type has histological characteristics resembling features of leukoplakia in sites elsewhere in the body, which is marked by hyperkeratosis and irregular hyperplasia of the prickle cell layer with lengthening and abnormality in shape of rete pegs. The verrucous type has very rare features of coral shape, white color and verrucous proliferation. Histologically, this type shows severe hyperkeratosis, parakeratosis and elongation of the rete pegs, but no irregular invasion can be observed.
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The function of IgE class-specific suppressor factor (IgE-TsF) from T hybridomas was studied by employing IgE-producing B hybridomas. IgE-TsF was obtained from IgE class-specific T hybridomas, which had been established by the fusion of a phosphorylcholine-conjugated Mycobacterium-primed T cell population with the T lymphoma cell line BW5147. The absorption experiments showed that IgE-TsF from T hybridomas was composed of the binding site(s) for IgE and I region gene products as observed in conventional IgE-TsF. Incubation of IgE-producing B hybridomas with IgE-TsF for 1 hr at 37 degrees C resulted in the reduction of the number of IgE-secreting cells when assessed by a reverse plaque assay. The proportions of surface IgE-positive cells were concomitantly reduced. After 24 hr incubation with IgE-TsF, the number of cytoplasmic IgE-positive cells was reduced, showing that IgE synthesis was inhibited by IgE-TsF. Antigen-specific TsF from phosphorylcholine-specific T hybridomas did not show any inhibitory effect, and IgE-TsF did not block the antibody production of IgM-producing B hybridomas. Precapping of IgE receptors by anti-epsilon antibody or the simultaneous addition of soluble IgE with IgE-TsF abrogated the suppressive function, suggesting that IgE-TsF acted directly on B epsilon cells through binding with IgE receptors.
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The effects of diffusion and ultrafiltration on cardiac output (CO) and organ blood flow (BF) in the uraemic dog were studied by a modified microsphere technique. In the diffusion phase of sequential therapy, a decrease in mean arterial pressure (MAP) and total peripheral resistance (TPR) was noted despite no change in circulatory plasma volume (CPV) and CO. In the ultrafiltration (UF) phase, MAP recovered with an increase in TPR despite the decrease in CPV and CO. Muscle vascular resistance increased in UF phase but not in the diffusion phase. The results suggest that the decrease in CPV through UF resulted in CO decrease, but that the compensation mechanism for the decrease is impaired by diffusion.
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The lumbosacral spinal cord, lumbar roots, L5 spinal ganglion, L5 segmental nerve and entire lengths of the sciatic, tibial, peroneal and sural nerves were taken at postmortem examination from 2 patients with insulin-dependent diabetes mellitus (IDDM) and a predominantly sensory symmetric distal polyneuropathy and compared with 2 non-diabetic control patients. Sections from proximal to middle levels of sciatic nerves of these patients showed a remarkable variability in myelinated fiber (MF) density within and between fascicles. Roots and segmental nerves appeared to be unaffected. Sections of peroneal, tibial and sural nerves showed only severe and diffuse fiber loss. The findings suggest that multifocal lesions at upper levels of sciatic nerve can summate distally to produce a symmetric diabetic neuropathy. The findings, if confirmed by using quantitative approaches in larger numbers of patients, suggest an underlying interstitial pathological process rather than a metabolic process.