[A case of SLE, hypertrophic neuropathy, and uterine cancer].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Y Kitahara.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Cerebellar ataxic gait was compared with normals by a simple quantitative method. Strain gauges attached to the heel, the first and the fifth metatarsal areas of a shoe, were used and the gait was telemetrically recorded. A natural and one per second click sound-synchronized gait was analyzed. A contact sequence of the three areas of the sole, the stride time, the stance-phase time and the foot contact pattern were compared between patients and normals. All of these items disclosed different results in the two groups.
Explore the source record for details and available documents.
In order to evaluate the efficacy of cefmetazole (CMZ) against osseous and articular infections fundamentally, the sensitivity of clinically isolated strains of Staphylococcus aureus to the drug and its concentration in serum and bone marrow of tibia were determined. 1. The clinically isolated strains of S. aureus was found to be sensitive to 0.78 microgram-6.25 micrograms CMZ per milliliter when inoculated at 10(6) cells/ml and to 0.78 microgram-12.5 micrograms CMZ per milliliter when inoculated at 10(8) cells/ml. No strains were resistant to CMZ. 2. One gram of CMZ was injected intramuscularly before operation. Blood samples were collected from the bone marrow and the vein and measured for the concentration of CMZ. The mean concentration in the bone marrow of tibia were 30.5 microgram/ml, 16.8 micrograms/ml and 8.9 micrograms/ml 1, 2, and 3 hours later, respectively, and the mean transfer rate from serum to bone marrow was 104.8, 92.8 and 101.1% respectively. 3. CMZ concentration in bone marrow of tibia attained following an intramuscular injection of 1 g of CMZ were higher than the MIC values for most of the clinically isolated strains of S. aureus, suggesting the effectiveness of CMZ in clinical practice.
Explore the source record for details and available documents.
Resistance to Listeria monocytogenes (L.M.) in diabetic state was studied using streptozotocin (SZ)-induced diabetic mice. SZ-diabetic mice showed an enhanced resistance to primary listerial infection with a sublethal dose of inoculum, whereas there was no difference between normal and diabetic hosts when challenged with a lethal dose. The growth of L.M. in diabetic mice was inhibited at an early stage of infection. However viable Listeria survived in diabetic mice at a later stage, suggesting the trend of persisting infection. Such enhanced resistance to L.M. in diabetic mice was associated with increased rate of spreading of peritoneal macrophages and with reduction in the level of delayed type hypersensitivity (DTH) to L.M. Therefore, it seemed likely that the enhanced resistance to Listeria in diabetic mice would be due to nonspecifically activated macrophages. Secondary challenge in the immunized animals and transfer experiment with immune spleen cells revealed that the development of protective immunity in diabetic mice was inferior to that in normal mice. Treatment with insulin could hardly influence the altered resistance to L.M. in diabetic mice.
Antibacterial resistance in a diabetic state was studied using experimental Pseudomonas infection in streptozotocin (SZ) induced diabetic mice. The results obtained were as follows: (1) there was no difference in acute death rate between normal and diabetic mice when infected with Pseudomonas aeruginosa. However, a significant increase in the number of bacteria in the kidney and liver occurred at a later stage of infection in diabetic mice. (2) Active immunization with a phenolized vaccine resulted in 100% survival in either normal or diabetic mice; otherwise challenge was lethal. However, the organs examined in diabetic vaccinated mice contained distinctly increased numbers of bacteria as compared with normal vaccinated mice 7 days after infection. (3) There were no significant differences in antibody titre between normal and diabetic ice after infection, but passive protection with immune serum from diabetic vaccinated mice was less effective than that from vaccinated mice. Furthermore, immune serum from normal vaccinated mice exerted protective action less efficiently in diabetic recipients than in normal recipients. (4) The bactericidal effect of peripheral whole blood was apparently lower in diabetic mice than in normal mice. (5) Treatment with insulin restored such reduced resistance to Pseudomonas infection in diabetic mice. These findings suggest that the decreased resistance to Pseudomonas infection in diabetic mice should be ascribed to impaired function of antibody, abnormalities in phagocytic cells and disturbed microcirculation caused by the insulin-deficient state.
The immune responsiveness in streptozotocin (SZ)-induced diabetic mice was studied using the immune responses to sheep red blood cells (SRBC) as an indicator system. In SZ-diabetic mice, the weights of such lymphoid organs as the thymus and spleen were significantly decreased with time after SZ administration, whereas the weight of liver was markedly increased. In SZ-diabetic mice, the level of delayed type hypersensitivity (DTH) to SRBC was not lower than that in normal controls in most cases, although the level of DTH was significantly depressed, on occasion, in SZ-diabetic mice. In contrast, antibody-forming activity, measured as the number of plaque-forming cells (PFC), was markedly decreased in SZ-diabetic mice. It seems that antibody production is more profoundly depressed than is DTH in SZ-diabetic mice. The transfer of normal thymus and bone marrow cells into SZ-diabetic mice caused only a partial restoration of PFC activity. When normal spleen cells were transferred into diabetic irradiated mice, proliferation of spleen cells and production of splenic PFC was greatly reduced as compared with normal irradiated mice. Treatment with insulin completely reversed such depression in the transfer system. These findings suggest that the chronic insulin-deficient diabetic state caused a depression and delay in the proliferation and differentiation of lymphoid cells.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The kinetic effect of cyclophosphamide (CY) was investigated using the immune response to sheep red blood cells (SRBC), activation of the mononuclear macrophage system and altered susceptibity to pseudomonas infection. The level of delayed type hypersensitivity (DTH) was enhanced with suppressed antibody formation, when antigenic stimulation was given about 3 days after CY administration. In contrast, antibody formation increased markedly when challenged with antigen about 10 days after CY administration. Activity of macrophage system as measured by rate of carbon clearance and spreading of peritoneal macrophage was decreased within 6 days after CY, therefore increased to a peak at the 13th day of CY administration. CY increased a susceptibility to pseudomonas infection at the early time of its administration such as the 3rd day, whereas more increased resistance was observed at the later time such as the 13th day. These results indicated that B-lymphocyte depletion included by administration of sublethal dose of CY (200mg/kg) was followed by vigorous hyperplasia of B-lymphocyte.
Various antigenic activities of polyoma virus-transformed and embryonic mouse cells were retained after 3M KCl solubilization of surface components. Particularly, transplantation antigen (TSTA) demonstrated by homograft rejection, and surface (S) antigen, detected by inhibition of immunofluorescence on polyoma-virus-transformed mouse cells, could be demonstrated. The crude soluble extracts were partially purified by salting out with (NH4)2SO4. In the case of polyoma-virus-transformed cells, TSTA and a part of S antigen activity were found in the same fraction (60% (NH4)2SO4 saturation) while another part of S antigen was salted out at 80% saturation. By chromatography, S antigen activity was found in 2 zones for transformed cells and in one zone for embryonic cells. One of these zones was common to both cell extracts.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Pseudomonas septicemia in mice caused the early death in the first three days of infection without any localized lesions. Localized lesions such as abscess are observed in the kidney and liver after the third day of infection. The early death increased in the BCG infected mice showing an increased level of macrophage activation. It seemed that such early death is due to endotoxin produced by Pseudomonas aeruginosa. However, the BCG infected mice showing an enhanced antibody formation were more resistant to pseudomonas septicemia. Immune serum protected such death, but immune spleen cells did not. Furthermore immune serum also protected the increased death in BCG infected mice.
Explore the source record for details and available documents.