[Bartter's syndrome, a case report with some references to the pathogenesis (author's transl)].
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Biomedical subjects
Publications and source records attributed to M Gotoh.
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Cellular localization of 2,4-dinitrophenyl (DNP) groups in the peripheral lymphoid system of guinea-pigs was studied at various times after painting the skin with 2,4-dinitrochlorobenzene (DNCB) by the immunofluorescent method using anti-DNP antibody. The cells taking up the stain (DNP cells) were shown to be mainly lymphocytes. At 1-6 h after painting the majority of DNP cells were found in the peripheral blood and the spleen but the maximum number was reached in the lymph node draining the site of DNCB application 12 h after painting. Injecting cyclophosphamide (CY) 3 days before painting with DNCB, heightened the number of DNP cells residing in the draining node. The animals treated with the tolerogen, 2,4-dinitrobenzene sulphonic acid sodium salt (DNBSO3Na), and then painted with DNCB, had fewer DNP cells than those animals which had simply been painted once with DNCB. The culture supernatants prepared from the draining nodes of both normal and tolerant animals partially blocked the anti-DNP antibody binding with DNP cells. It is suggested that the cells associated with DNP groups residing in the draining lymph node act as immunogens in the immunizing process of contact sensitivity.
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The factors causing heart rate variability (HRV) were investigated under various kinds of workloads and flight conditions. Frequency analysis of heart rate, and cross-correlation analysis with blood pressure and respiration, were performed by using the fast Fourier analyser. Consequently, the main frequency of HRV at rest consisted of 0.1 Hz and 0.25-0.3 Hz. These fluctuations disappeared under physical loads, but the value of 0.1 Hz at first increased under moderate mental load and thereafter decreased as the mental load increased. It was suggested that the behavior of the frequency 0.1 Hz under mental load was influenced partly by higher brain centers. For the actual flight, the frequency decreased under takeoff and landing, and remained as at rest during the gunnery and acrobatic training flight. It was concluded that the evaluation of workloads under flight conditions by using the analysis of the factors of HRV was very useful to improve a man-machine interface.
Peroxisomes in hepatomas and hyperplastic preneoplastic liver lesions induced in mice by 500 ppm alpha-benzene hexachloride were examined histochemically and electron microscopically. Although most of the hepatomas were well-differentiated tumors and contained a considerable number of peroxisomes, the tumor cells did not respond to ethyl-alpha-p-chlorophenoxyisobutyrate with proliferation of peroxisomes. At the 16th week of carcinogen feeding, hyperplastic nodules appeared and advanced to further stages. A majority of the nodules showed a considerable number of peroxisomes and the inductive proliferation of peroxisomes. Within the nodules, foci of proliferation of the cells that showed no inducibility of proliferation of peroxisomes appeared. These cells proliferated further, replacing the most part of the nodules, and with this process hepatomas appeared to have been formed. No abnormal matrical inclusions of peroxisomes were formed in the cells of hyperplastic nodules by ethyl-alpha-p-chlorophenoxyisobutyrate unlike in the case of rats.
DNCB-sensitized guinea pigs demonstrated an accelerated reactivity on retest of DNCB at the site of prior contact reaction, though presenting normal contact sensitivity at the virgin site. The retest reaction reached maximal at 9 h and waned at 24 h after antigenic challenge. Massive accumulation of eosinophils in either the epidermis or dermis was its distinguishing histologic feature. The reaction was induced at the site of delayed skin reaction to DNP-GPE in the animals sensitized with DNCB or DNP-GPE. A retest reaction in delayed sensitivity to DNP-GPE was also elicited at the site of contact reaction to DNCB in the animals. The significance of these findings is discussed.
The incidence of dinitrophenylated cells in guinea pig lymphocytes incubated with 0-30 mM concentrations of DNBSO3Na in phosphate-buffered saline was examined by an immunofluorescence method using fluorescence-labelled anti-DNP antibody. Under our experimental conditions, the incidence was roughly proportional to the concentration used. Using DNP-lymphocytes as an antigen for skin testing, a marked delayed reaction was induced in guinea pigs sensitized by painting with DNCB and intradermal injection of Freund's complete adjuvant. The significance of these findings is discussed.
The distribution of DNP groups in various tissues of guinea-pigs following intravenous injection of DNBSO3Na was investigated by an immunofluorescent method using FITC-labelled anti-DNP antibody. DNP groups were detected either in the cytoplasms of epidermal cells or on/in lymphoid tissue cells. The epidermal distribution of DNP groups was shown in the skin obtained from 5 min to 3 days after injection. There was no fundamental difference in the epidermal localization of DNP groups between at the previously tested site and at virgin site in DNCB sensitized animals. Unreacted DNBSO3Na was demonstrated in the blood plasma of DNBSO3Na injected animals. The injection of either DNP-lysine or 2,4-dinitrophenol was found incapable of inducing flare up reaction and no epidermal localization of DNP groups in the sensitized animals was observed. A possibility that intravenously injected DNBSO3Na forms a complete antigen by conjugation with epidermal proteins and sensitized cells, which have been indicated by Polak, Turk & Frey (1973) to remain at the site of old contact reaction, react with the antigen resulting in flare up reaction, is suggested.
In order to analyze the relationship between heart rate variability (HRV) and the flight tasks of pilots, HRV of various mental and physical work stresses were investigated. For the physical stress on the treadmill, S.D. of heart rate sequence showed a minimum value at medium stresses and remained there until the maximum stress. However, the centrifuge acceleration test presupposed special physical stresses, and S.D. was almost same as the resting findings. In the tracking tasks, which presupposed maximum interpretative actions, the increase in the mean heart rate (MHR) was small with the S.D. increased a greater amount than for resting results. Consequently, preflight checks and level flight phases presupposed medium interpretative actions and mental stress with reserve capacity. Takeoff and landing phases were considered as both high interpretative action and high emotional stress situations. Acrobatic and gunnery training flight phases were considered physical load, strong interpretative actions, and emotional stress tasks.
The number of DNP group-bearing lymphocytes in the regional lymph node, thoracic duct and peripheral blood was determined at various time intervals after painting normal guinea pigs with DNCB by the immunofluorescent method using anti-DNP antibody. The incidence of such cells in the regional node was maximal at 12 hours whereas in the thoracic duct and peripheral blood the maximum incidence was found at 0.1-2 hours after painting. Unreacted DNCB was demonstrated in both the thoracic lymph duct and the blood at least for 12 or 24 hours respectively following exposure to DNCB. The authors therefore suggest that DNCB reacts directly in vivo with the lymphocyte cell membrane of guinea pig following epicutaneous application of the chemical.
A case of Schonlein-Henoch-purpura is presented. The immunofluorescent study of skin lesions of the patient showed granular deposits of IgA and C3 in the blood vessel walls perivascular deposits of plasminogen and diffuse localization of fibrin and fibrinogen in the upper dermis. Complement activation via the alternative pathway through IgA, C3 and plasminogen deposits was suggested.
To obtain better arterio grafts, we prepared three samples from adventitia of swine carotid arteries, and their antigenicity was studied with immunological procedures. Sample I was prepared from swine carotid arteries, by eliminating the extraneous fat and connective tissues. Sample II was prepared from Sample I by treatment with chymotrypsin, and Sample III was prepared from Sample II by treatment with 3% glutaraldehyde for 14 days. From the three samples, the water soluble protein fractions were extracted, and abbreviated as E-I, E-II and E-III, respectively. Immunopharmacological tests in guinea pigs and rabbits including active and passive anaphylaxis, passive cutaneous anaphylaxis, Schultz-Dale test and Arthus's phenomenon among these extracts revealed cross reactions between E-I and E-II. Also, precipitin test and Ouchterlony's method, precipitation was observed between E-I and E-II, and it was suggested that there might be at least a common antigen between E-I and E-II. The rabbits which had been implanted subcutaneously at the back with the minced Sample I evoked severe reactions and died after intravenous injection of E-I at the 3rd or 5th month after implantation. No reaction was observed between Sample III and E-III in the same experiment. From the above results, it was suggested that the antigenicity of swine carotid arteries could be eliminated by the treatment with chymotrypsin and glutaraldehyde.
Feeding of acetylsalicylic acid (ASA), clofibrate and dimethrin induces formation of matrical plates in heptaic microbodies. Administration of sodium citrate prevents formation of matrical plates in rats fed ASA, but not in rats treated with clofibrate or dimethrin. Propionate has a similar effect on rats fed ASA but not those fed clofibrate. Feeding of aminotriazole prevents formation of matrical plates in rats fed ASA without inhibiting the proliferation of microbodies. Sodium citrate and aminotriazole and feeding decrease also the activity of hepatic catalase in rats fed ASA.
Regulation of the formation of microbodies in Morris hepatoma 9618A was studied by examination of the response of the organelles to clofibrate. The fine structures of microbodies in the hepatoma cells closely resembled those in hepatocytes of normal adult rats. In clofibrate-treated rats, the tumor cells showed a slight increase in the size of microbodies and in catalase activity; however, the tumor microbodies did not increase in number. In contrast, in adult clofibrate-treated rats and rats on the day of birth whose mothers received clofibrate during the gestation period, the hepatocytes showed microbodies that were greater in both number and size, and the catalase activity in the liver was definitely elevated.
Abnormal inclusions in microbodies were induced by clofibrate in hepatocytes of hyperplastic liver nodules in rats fed 2-acetylaminofluorene. These were matrical tubules and plates, each with the same ultrastructural features as those reported previously by other investigators. A hyperplastic state of hepatocytes induced by hepatocarcinogens might be related to the formation of these inclusions in response to clofibrate.