[Postwar activities of public health nurses (1). Ms. Noriko Fukuhara (Hokkaido)].
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Biomedical subjects
Publications and source records attributed to N Ishida.
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The feasibility of a bone mineral analyzer equipped with a single source of 241Am but with a specially designed water bath (Beam Scanner, Aloca Co. Ltd.) was evaluated both experimentally and clinically. The attenuation rate of 241Am gamma-ray showed an exponential decrease with the increase of the thickness of the plaster plate containing CaSO4. Measurements of the test tubes filled with Ca(OH)2 demonstrated the measured mineral values to be in good correlation with the amount of Ca(OH)2. The coefficient of variation (C.V.) of bone mineral values obtained by measuring the phantom 20 times was 4.06%. Reproducibility tests performed in 10 normal persons after an interval of 8 months revealed a C.V. of 2.0%. Bone mineral values seemed to reach their peak in the 4th decade and thereafter gradually decreased with aging in normal persons. A marked decrease of the bone mineral value was observed in 5 cases of osteoporosis. We conclude that the bone mineral measurement using the above described method is practical and reliable.
The incidence of non-A, non-B hepatitis in a cardiovascular surgical unit was examined among the 204 patients who received blood transfusion and extracorporeal circulation while undergoing open heart surgery during April 1979 to December 1981. Among 115 adult patients (20 to 69 years old) 46 (43%) developed non-A, non-B hepatitis, whereas the incidence in younger patients (1 to 19 years old) was much lower (21.8%, 19 out of 89). When monthly incidence was examined during the study period, two nosocomial epidemics, the first during September 1979 to February 1980 and second during October 1980 to January 1981, were found. When clinical features such as maximum ALT level and the proportion of icterus were examined, the features of the above two epidemics were taken to be different from those consistently observed through the study period. The epidemic type hepatitis not only resulted in more severe clinical features than the nonepidemic type, but the sera of the former contained immune complexes at a higher rate (80%) than did the latter (7.6%).
Risk factors related to the occurrence of non-A, non-B posttransfusion hepatitis (PTH) were statistically analyzed in 204 patients (115 adults and 89 children) who received blood transfusion and extracorporeal circulation during open-heart surgery. The PTH incidence, irrespective of age or body weight, was affected by both transfusion volume and circulation time, ie, the incidence increased cumulatively with the increment of these two variables. Based upon such statistical analysis, a "PTH-risk index," from which one can objectively predict the probability of PTH, was devised by the summation of standardized transfusion volumes (Vs) and circulation time (Ts). As a result, a high correlation between the obtained PTH-risk index and actual incidence was found. The obtained straight regression line between PTH-risk index and the actual incidence rate enabled us to predict the incidence of PTH in open-heart surgery patients.
The antigen/antibody systems specific for non-A, non-B hepatitis (NANB) were studied using urine samples as the antigen source and sera for the antibody source. Two immunologically distinct systems, SO-antigen/anti-SO and MI-antigen/anti-MI were discovered. This paper deals chiefly with the characterization of the SO-antigen, which was associated with an epidemic-type non-A, non-B hepatitis found during September 1979 to February 1980 (first outbreak) and October 1980 to January 1981 (second outbreak) in the Cardiovascular Surgical Unit of Tohoku University Hospital. All patients who developed non-A, non-B hepatitis during the first and second epidemic periods had SO-antigen in their urine (24 out of 24). After the epidemic, however, the detection rate of SO-antigen gradually decreased among patients in the same unit, although posttransfusion non-A, non-B hepatitis continued to be found. The final detection of SO-antigen occurred at or just after the elevation of alanine aminotransferase (ALT) levels during the episode of hepatitis and persisted in most cases throughout the elevated period. Anti-SO antibody was detected relatively late (eight months after blood transfusion, in most cases) and apparently persisted longer than five years. The immunological and physicochemical properties of SO-antigen were also studied. It appeared to be neither a plasma protein nor a liver tissue component when the cross-reactivity of SO-antigen was examined by the immunodiffusion method. Absorption with insolubilized human serum and liver tissues failed to affect the anti-SO antibody activity. The molecular weight of SO-antigen was estimated to be 250,000, the sedimentation coefficient to be 11.0 S, and the buoyant density in CsCl to be 1.215 g/cm3. Electron microscopy showed that the SO-antigen corresponded with uniform particles with a mean diameter of 11 nm. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) analysis of SO-antigen revealed only a single protein band corresponding to molecular weight 38,000.
The strains of H 1 N 4 influenza A virus isolated from feral ducks in Japan in 1977-78 were compared to swine-origin H 1 N 1 viruses antigenically and genetically. Homologous characteristics were found among the H 1 N 4 isolates from feral ducks in hemagglutination-inhibition (HI) tests, viral RNA patterns on polyacrylamide gel electrophoresis and oligonucleotide mapping. Although the hemagglutinins of duck-origin viruses employed in this study were identified as H 1, the viruses were distinguishable from A/New Jersey/8/76 (H 1 N 1), A/duck/Alberta/35/76 (H 1 N 1) and the virus isolated from swine in Japan in the cross HI test. Also, the viral RNA patterns of the duck- and swine-origin H 1 viruses were found to be quite different, indicating that genetic reassortment of HA genes between them is unlikely. After H 1 N 4 virus of duck-origin was intranasally inoculated into pigs, a brief period of virus recovery with no serological response was observed; whereas swine-origin H 1 N 1 virus produced seroconversion in the pigs inoculated.
OK-432, a killed preparation of Streptococcus pyogenes, as well as bacillus Calmette-Guérin (BCG) and Corynebacterium parvum are all known to induce immune interferon (IFN gamma) in mice. To examine the mechanisms of IFN gamma induction by OK-432, DDI mice were sensitized with various doses of OK-432, either by a single injection of a 1-mg dose or repeated injections of 0.1-mg doses given intraperitoneally. Spleen cells removed from the mice 7-9 days after the last injection produced high-titered IFN gamma (600-800 IU/ml) in vitro in the presence of 5 micrograms/ml of OK-432. In the absence of OK-432, however, in vitro IFN gamma production of sensitized spleen cells was quite limited. Moreover, when inducers of different antigenic entities such as serologically unrelated Streptococcus faecalis, Listeria monocytogenes, or Con A were added in vitro, instead of OK-432, to the OK-432-sensitized spleen cells, high-titered IFN gamma production also occurred. This may indicate that the signal required by T cells to produce IFN gamma in vitro need not necessarily be the same as that required to sensitize mouse macrophage in vivo. Once sensitized with OK-432, mice spleen cells continued to produce high-titered IFN gamma for more than 3 but less than 5 weeks.
A climatologic analysis of human rotavirus infection in inpatients with acute diarrhea was conducted over a seven-year period. The infection frequency appeared to be related to temperature, but not to relative humidity. Human rotavirus infection was found to appear abruptly when the mean temperature of any 10-day period became less than 5 C (November or December), reached a peak when it was less than 0 C (January and February), and waned when it became greater than 20 C (June and July) in the city of Yamagata in northern Japan.
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The antiviral effect of highly purified mouse interferon (IFN) was studied on influenza virus infection in mice, by changing the routes of administration. By repeated intravenous (i.v.) administrations of IFN, no antiviral effect was observed. However, IFN was effective when the infected mice received either intraperitoneal (i.p.) or intranasal (i.n.) administrations. While all of the untreated mice died within 10 days after infection, 20% of the i.p. treated mice and 67% of the i.n. treated mice survived more than 30 days. To explain these different effects after administration by different routes, the distribution of given IFN in mouse organs was examined. Fifteen min after i.v. injection, only a low-titered IFN was detected in the serum, lung, spleen and liver of the mice and soon disappeared. However, a relatively high-titered IFN was detected 30 min after i.p. administration in the lung and serum. After i.n. administration, high-titered IFN was detected in the lung within 15 min after administration and continued for 90 min. Thus the findings demonstrated that the maintenance of a detectable amount of IFN in mice organs is dependent on the route of administration, and the higher the titer of IFN in the lung, the higher the protective effect of IFN against influenza virus infection.
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Cholesterol derivatives, including 7 alpha-hydroxycholesterol (7 alpha-HC), 7 beta-hydroxycholesterol (7 beta-HC), and 7-ketocholesterol (7-KC), were isolated from the Cohn fraction IV-I of normal human sera and were shown to be the moieties responsible for the suppression of lymphocyte proliferation. When 5-10 micrograms/ml of 7 alpha-HC, 7 beta-HC or 7-KC were added in vitro to lymphocyte cultures, incorporation of 3H-thymidine (3H-TdR) into the lymphocyte DNA was suppressed by about 50% when compared with the control. When 10-50 mg/kg/day of 7 alpha-HC, 7 beta-HC and 7 KC were administered in vivo to skin grafts on rats, the prolongation of skin grafts was observed. The concentration of 7-KC in cancer patient sera was 2 to 3 times the amount in normal pooled human sera.
A low-molecular-weight factor (less than 1000) which impairs the capacity of normal mice to resist Listeria infection has been isolated from the ascitic fluid of tumor-bearing mice. The factor showed potent suppressive activity when as little as 0.2 ml of 1:10(5) dilution of the factor was given iv to mice. The factor impaired stage 2 (72 hr after infection) of Listeria elimination in the liver when circulating monocytes migrate from the blood to the liver to begin eliminating the bacteria, but not stage 1 (within 24 hr after infection) when Listeria elimination depends on resident liver macrophages. The factor also inhibited macrophage accumulation in the peritoneum of mice after ip injection of phytohemagglutinin and macrophage chemotaxis in vitro. The factor was heat labile and lost its suppressive activity after being heated at 56 degrees C for 30 min. The factor was detectable in the ascitic fluid rather late after tumor implantation and its production was closely related to tumor growth.
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Suppressed concanavalin A response of spleen cells which appeared on Day 21 in C3H/He mice bearing methylcholanthrene-induced fibrosarcoma was attributed to macrophages. These macrophages were not only immunoglobulin and Thy 1.2 negative and mitomycin C resistant but were also found in the light-specific-gravity (1.077) fraction and were completely removed by carbonyl iron treatment. These suppressor macrophages, however, disappeared 4 days after surgical resection of the tumor, suggesting that the control mechanism originally resides in tumor tissues. Immunosuppressive acidic protein (IAP) levels in the sera of these tumor-bearing mice increased along with the appearance of these suppressor macrophages. Inasmuch as the suppressor macrophages obtained from the spleens of tumor bearers and cultured in vitro produced 4 times more IAP (88 ng/ml) than did resident macrophages, the elevated levels of IAP in the sera of tumor-bearing mice at the late stage might be explained partly by the appearance of suppressor macrophages. On the other hand, an i.v. administration of IAP (5 mg/mouse) into normal mice not only induced the same unresponsiveness of spleen cells to concanavalin A shown by tumor-bearing mice but also induced suppressor macrophages in the spleens of these mice. This fact may indicate that IAP elevation, even though artificial, triggers the induction of suppressor macrophages in the spleen or at least points to a keen correlation between the appearance of suppressor macrophages and increased IAP level in the serum.