Simply diluting serum before radioimmunoassay does not prevent binding of prednisolone to protein.
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Biomedical subjects
Publications and source records attributed to Y Asano.
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It has recently been demonstrated that the Lyb-5+ and Lyb-5- B cell subpopulations differ in their requirements for major histocompatibility complex (MHC)-restricted activation by T helper (TH) cells. To determine whether these MHC-restricted and -unrestricted pathways of B cell activation result from differences in the participating TH cell populations or reflect differences exclusively in the responding B cell subpopulations, experiments were carried out using cloned TH cells for in vitro antibody responses to trinitrophenyl-keyhole limpet hemocyanin. The same cloned T helper cells were able to activate both CBA/N (Lyb-5-) B cells and CBA/CaHN (Lyb-5+ + Lyb-5-) B cells under different experimental conditions. The activation of Lyb-5-B cells by cloned T helper cells required both MHC-restricted TH cell-B cell interaction and carrier-hapten linkage. In contrast, the activation of Lyb-5+ B cells required only MHC-restricted T helper cell interaction with accessory cells, while T-B interaction was MHC unrestricted and did not require carrier-hapten linkage. Thus, the differences in activation requirements observed for the Lyb-5- and Lyb-5+ B cell subsets do not result from differences in the TH cell populations activating these B cells, but rather reflect differences in the ability of these B cells to respond to signals from the same TH cells.
The present studies have been carried out to characterize the regulatory influences acting upon defined pathways of T cell-dependent B cell activation. In these studies, it was demonstrated that high concentrations of free carrier strongly inhibited the MHC-restricted in vitro T cell-dependent antibody responses of primed Lyb-5- B cells to the corresponding carrier-hapten conjugate. In contrast, these same concentrations of free carrier failed to inhibit the T cell dependent responses of Lyb-5+ B cells to the same antigen. The inhibition of Lyb-5- B cell responses by free carrier was shown to result from active suppression mediated by carrier-specific primed Lyt-1+2- T cells and to require the additional participation of unprimed Lyt-1-2+ T cells. The activation of this suppression was antigen-specific, but suppression once activated was antigen nonspecific in its effect. These findings thus demonstrate that distinct pathways of B cell activation can be independently regulated by T suppressor network influences, and that these pathways therefore constitute potentially independent components of the immune response to a given antigenic stimulus.
Antibody to varicella-zoster virus was measured in Vero cell cultures by a conventional and an enhanced plaque neutralization test. In the latter, heterologous antibody to human immunoglobulin was added to the virus-serum mixture to potentiate the neutralization reaction. The antibody to human immunoglobulin enhanced the sensitivity of the neutralization test seven- to 107-fold as compared with the conventional procedure. The test was highly reproducible in that individual serum titers fluctuated in a twofold range on repeated testing. A prozone phenomenon was observed in the enhanced neutralization test in low-titered sera, but not with high-titered sera or with specimens of cerebrospinal fluid. The specificity of the test was confirmed by the detection of seroconversion in recipients of live varicella virus vaccine.
We studied the efficiency of in vitro and in vivo charcoal hemoperfusion for the removal of paraquat. At a flow rate of 200 ml/min, 93-99% of paraquat in 4 L of solution (5, 10, 100 ppm) was removed in less than 160 min. The disappearance half-time was 16 min 10 sec. At 100 ml/min, it was 49 min 30 sec. Of 23 paraquat poisoning cases, 15 patients underwent hemoperfusion (HP) of which 10 died of respiratory failure within 28 days (7.6 +/- 2.9) and 5 survived without pulmonary complications. Of eight patients who did not receive HP, six died of respiratory failure within 97 days (33.4 +/- 18.8), even when their general condition was good upon admission. Two who vomited the ingested paraquat immediately survived without HP, and their paraquat concentration in urine was less than one ppm on admission. In one patient, whose paraquat concentration in blood was followed serially, 99% of the paraquat was removed from circulating blood by a single hemoperfusion. We conclude that charcoal hemoperfusion is effective for the removal of paraquat from blood in vivo and from solution in vitro. Hemoperfusion may also improve survival after paraquat ingestion, but further data are needed.
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The protective effect on 45 household contacts of immediate inoculation of a live varicella vaccine was examined in relation to the viral dose and days after exposure to varicella. The viral doses used were 300 PFU to 15,000 PFU, and the intervals between exposure and vaccination were 0 to 5 days. All 30 contacts given viral doses of 800 to 15,000 PFU within 3 days after exposure were protected from clinical varicella. With lower viral doses of 300 to 600 PFU within 3 days after exposure, 6 to 10 contacts developed rashes 13 to 25 days after vaccination, but all showed mild symptoms. When vaccine was given 5 days after exposure, even with a dose of 1,500 to 4,000 PFU, typical varicella symptoms appeared 6 to 9 days after vaccination. These results suggest that vaccination of household contacts with viral doses of over 500-800 PFU within 3 days after exposure is effective in preventing manifestation of clinical varicella and that clinical symptoms may be modified to a mild form by vaccination with even a lower viral dose when given within 3 days after exposure.
The hypotensive effect of 4-(2'-nitrophenyl)-2,6-dimethyl-1,4-dihydropyridine-3,5-dicarboxydimethylester (nifedipine, Adalat) was studied in 15 hypertensive patients with chronic renal failure. The decrease of blood pressure lasted for approximately 3 h and maximum decrement was achieved in 1 h after oral administration of nifedipine (10 mg). Hypotensive action of the drug was associated with a constant decrease in total peripheral resistance and an increase in cardiac output, plasma renin activity (PRA), and plasma norepinephrine (noradrenaline). Initial PRA was apparently the major determinant of the rise in PRA since a close correlation was present between the initial value and the increase induced by nifedipine (r = 0.93, p less than 0.05). Marked reduction of blood pressure without noticeable side effects was observed in two cases who had not responded to previous antihypertensive treatment. These data suggest that nifedipine exerts its hypotensive action through peripheral vasodilation and may be an effective drug for treatment of hypertension during chronic renal failure.
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