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Reports on the investigation into the removal of mutagen precursors from wastewaters. How removal extent of mutagen precursor was evaluated by the mutagen formation potential (MFP) which is mutagenicity of pollutants capable of forming mutagens when chlorinated under the conditions of water purification processes.

The distribution of human IgG subclasses among the glomerular deposits in human membranous nephropathy was examined by immunofluorescence with subclass specific monoclonal antibodies, Large amounts of granular deposits of IgG4 were identified along the capillary loops in all 12 patients, and seven patients had small amounts of IgG1 deposits. Neither IgG2 nor IgG3 deposits were detcetable in any or the patients. On the contrary. all four IgG subclasses were detected in membranoproliferative glomerulonephntis and lupus nephritis with a predominance of IgG1 and IgG3. The results indicate that IgG4 is predominant in the glomerular deposits in membranous nephropathy and may play an important role in its pathogenesis. [ABSTRACT FROM AUTHOR]

Fc∊ receptor (Fc∊R) expression on several human cell lines (U937, RPMI 8866, HL 60, THP-1, and Molt 4) and its regulation were examined by immunofluorescent analysis using a monoclonal antihuman Fc∊R antibody, H107, Phorbol ester (PMA), recombinant gamma interferon (IFN-γ) and H107 itself enhanced Fc∊R expression on a FC∊R positive cell line LI937, whereas these reagents did not induce FC∊R expression on the Fc∊R negative cell lines. Molt 4, HL 60 and THP-1. Dexamethasone not only suppressed by 50%, the spontaneous Fc∊R expression on U937 cells but also completely inhibited the enhancement of their Fc∊R expression on U937 cells induced by PMA, IFN-γ or H107. Dexamethasone caused a little suppression of Fc∊R expression by RPMI 8866 cells. The results showed that Fc∊R expression on a human monoblast cell line IJ937 was up- or down-regulated by a variety of physiological or pharmacological agents. These experimental systems provide a good model for the investigation of the regulatory mechanisms of Fc∊R expression. [ABSTRACT FROM AUTHOR]

The mechanisms involved in the inhibition of growth of a human B lymphoma cell line, B104, by anti-MHC class II antibodies (Ab) were compared with those in anti-IgM Ab-induced B104 growth inhibition. Two anti-MHC class II Ab, L227 and 2.06, inhibited the growth of B104 cells, although 2.06, but not L227, needed to be further cross-linked with a goat anti-mouse IgG Ab (GAM) to show the effect. L227 induced an increase in intracellular free Ca2+ concentration [Ca2+]i from the intracellular pool and little or no protein tyrosine phosphorylation, phosphatidyl inositol turnover, or expression of Egr-I mRNA, whereas 2.06 plus GAM induced an increase in [Ca2+]i from both the intracellular and, in particular, the extracellular pools. The inhibition of B104 cell growth induced by anti-MHC class II Ab was Ca2+ -independent and not inhibited by actinomycin D or cyclosporin A, and cell cycle arrest at the G₂/M interphase was not observed. These features are very different from those observed in B104 cell death induced by anti-IgM Ab. Neither DNA fragmentation nor the morphology of apoptosis was observed. These findings demonstrate that cross-linking of MHC class II molecules transduced the negative signals through intracellular mechanisms different from those present in the cross-linking of surface IgM. [ABSTRACT FROM AUTHOR]

Unlabelled: In order to clarify the clinical significance of serum interleukin 4 (IL-4) levels, we measured serum IL-4 concentrations in allergic and non-allergic children using a highly sensitive sandwich ELISA. The limit of detection of the assay was 0.15 pg/ml in serum samples. Serum IL-4 was detected in 96.3% (53/55) of non-allergic controls, in 92.9% (183/197) of allergic children, in 70% (7/10) of cord blood samples and in 86.7% (26/30) of neonates. The IL-4 levels in sera from non-allergic controls were relatively constant during the ages examined and all samples were under 1.5 pg/ml. In allergic children, the serum levels of IL-4 were significantly elevated, particularly at age 13-24 months. The serum levels of IL-4 did not differ in children with different clinical manifestations of allergy, such as bronchial asthma, and atopic dermatitis. The serum level of soluble CD23 (sCD23) showed an age-dependent change in allergic and non-allergic children and was significantly higher in allergic than in non-allergic infants aged 7 to 12 months, but not in other age groups. There was no significant correlation among serum levels of IL-4, sCD23 and IgE.Conclusion: It is suggested that the measurement of serum IL-4 and sCD23 is helpful in the examination of allergic patients in infancy and early childhood, but neither the serum level of IL-4 nor sCD23 directly reflects in vivo IgE production. [ABSTRACT FROM AUTHOR]

To study the roles of eosinophils and catecholamines in the pathophysiology of exercise-induced asthma (EIA), an exercise challenge test was performed in 22 asthmatic children, using a bicycle ergometer, and the changes in lung function, plasma norepinephrine (NE), epinephrine (E) and eosinophil cationic protein (ECP) levels with exercise were eval-uated. Subjects were classified into three groups from the results of lung function test, respectively: EIA-negative group. EIA-positive groups with good recovery and poor reccovery. Eosinophil counts before exercise in the EIA-positive groups were significantly higher than those in the EIA negative group. The ECP levels rose with exercise in all groups. Five minutes after exercise. ECP values fell to the pre-exercise level in the EIA-negative group, but rose to higher levels in EIA-positive groups. Plasma E levels rose with exercise and showed 4-fold increase in the EIA-negative group, whereas only 1.5 fold increase of plasma E levels was observed in the EIA-positive group with poor recovery. From these findings, a possible contribution of sympathoadrenal hypofunction and a probable involvement of eosinophils in the patho-physiology of EIA have been suggested. [ABSTRACT FROM AUTHOR]

In the previous paper we reported that human natural killer (NK) cell activity was augmented greatly by preincubation with Staphylococcus aureus Cowan I bacteria (SpA CoI) or its Protein A. We examined here whether the augmentation with these stimulants is ascribable to the direct activation of NK cells or mediated by some soluble factors produced by the stimulants. It was found that a significant amount of interferon (IFN) was produced by the SpA CoI-stimulation but not by the Protein A-stimulation, although the latter usually induced augmentation of NK-cell activity not less than SpA CoI-stimulation. IFN produced by SpA CoI was considered to belong to α-type IFN, because it was stable at pH 2.0 and could be neutralized effectively by anti-IFNα antibody. Kinetics of NK-cell activation by SpA CoI (but not by Protein A) were very similar to those by IFNα. Furthermore, augmentation of NK-cell activity with SpA CoI-stimulated supernatant was inhibited almost completely by diluted anti-IFNα antibody, whereas augmentation with Protein A-stimulated supernatant could not be abolished by the same treatment. It was, therefore, suggested that augmentation of NK-cell activity with SpA CoI might be ascribable in most part to the IFN induced, whereas Protein A can stimulate NK or T cells directly or soluble factors other than IFN might work as well. [ABSTRACT FROM AUTHOR]

An immune adherence receptor exists on the surface of primate erythrocytes, and has been characterized as a receptor for the activated third component of complement (C3b). We have applied human red blood cells (RBCs, blood group O) to a sensitive determination of complement-fixing, soluble immune complexes in serum. The method involved the binding of immune complexes with RBCs in the presence of complement and the detection of cell-bound IgG molecules by radiolabelled anti-human IgG antibodies. Since the binding of RBCs with monomeric IgG was minimal, cell-bound IgG molecules were taken as representing immune complexes. When aggregated human gammaglobulin (AHG) was used as a model of immune complexes, as littLe as 5 μg dissolved in 1 ml of normal human serum were detected. The binding of RBCs with AHG was inhibited in EDTA solution where the classical complement pathway could not be activated. The RBC radioimmune assay was successfully applied to the determination of soluble immune complexes in pathological serum samples obtained from the patients with systemic lupus erythematosus and those with fulminant Type B hepatitis. False-positive results by autoantibodies against RBCs could be excluded by performing a Coombs test and by comparing the binding in the presence of complement with that in EDTA solution. The ubiquitous availability of RBCs coupled with a high sensitivity would allow the RBC radioimmune assay to be added to the battery of previous methods to determine immune complexes in the serum. [ABSTRACT FROM AUTHOR]

Antigenic determinants of Australia antigen (AuAg) may be determined by haemagglutination inhibition with ease and high sensitivity. The reaction depends on the inhibitory effect of the test antigen-positive sample on the agglutination by specific antibody of glutaraldehyde-fixed sheep erythrocytes which have been tanned and coated with AuAg of different specificities. The standard monospecific antibody reactants are directed against one or other of the common antigens, a and Re, or against the subtypic determinants, d,y,w and r. Because it is more sensitive than conventional immunodiffusion or electrosyneresis, and more convenient than radioimmunoassay, haemagglutination inhibition is most suited to large-scale determinations of AuAg subtypes in samples of relatively low antigenic activity. [ABSTRACT FROM AUTHOR]

To investigate the involvement of nitric oxide (NO) in childhood meningitis, we measured the concentrations of NO-[sub 2] (a stable metabolite of NO) in serial samples of cerebrospinal fluid (CSF) from 11 children with septic and 7 with aseptic meningitis and 26 control patients without meningitis. The mean concentration of NO-[sub 2] in samples obtained during the early stages of septic meningitis, but not aseptic meningitis, was significantly higher than in control samples. Clinical and laboratory improvement following administration of antibiotics and dexamethasone was associated with a fall in CSF [NO-[sub 2]] to normal levels in these patients. CSF [NO-[sub 2]] remained almost consistently within the normal range in patients with aseptic meningitis. Our findings indicate that NO production is enhanced in the CSF compartment of children with septic meningitis and support the hypothesis that NO is involved in the pathophysiology of septic meningitis. [ABSTRACT FROM AUTHOR]

A patient with intestinal lymphangiectasia (IL) was studied for his immunological abnormalities. The patient had hypoproteinaemia with severe hypogammaglobulinaemia. The results of lymphocyte subpopulation studies revealed a decrease of CD4+ cells and a decrease of surface immunoglobulin (sIg)-positive B lymphocytes. T cell functions determined by the proliferative responses against Concanavalin A (Con A) or phytohaemagglutinin (PHA) and by delayed type cutaneous hypersensitivity (DTH) response to purified protein derivatives (PPD) and PHA were normal. No immunoglobulin (Ig)-secreting cells were induced when his peripheral blood lymphocytes (PBL) were cultured with pokeweed mitogen (PWM). His T cells showed suppressor function to the PWM- induced differentiation of normal B cells. This suppressor activity was sensitive to 3000 rads irradiation. His B cells also failed to differentiate into Ig-producing cells with the help of normal T cells and PWM. Thus, in this patient, the decrease of Ig-synthesis in vitro could be attributed to suppressor T cells, lack of T helper cells and an intrinsic B cell defect. Therefore, this patient appears to have immunological abnormalities which differ from previously reported IL patients. [ABSTRACT FROM AUTHOR]

Using a monoclonal anti-human Fc∊R antibody (Hi07), we found that lymphocytosis promoting factor (LPF), phytohaemagglutinin (PHA-P) and Concanavalin A (Con A) could induce Fc∊R. detected by immunofluorescence study, on normal human peripheral blood lymphocytes without IgE. The number of Fc∊R bearing lymphocytes was increased by stimulation with 3, 10 and 10 μ/ml of LPF. PHA-P and Con A. respectively, from 6.0 ± 3.0 /1000 cells to 26.0 ± 7.9., 54.0 ± 6.7 and 24.8±7.1/1000 cells, respectively. Although the induction of Fc∊R occurred neither in the separated T-enriched fraction (TEF) nor the T-depleted fraction (TDF), it recovered when the two fractions were mixed. The cell free supernatants from TEF stimulated with LPF or PHA-P could increase Fc∊R( + ) cells in TDF, whereas those from TDF failed to increase them in TEF. The results suggest that the induction of FCER occurs mainly on B lymphocytes by the soluble factor(s) formed by T cells stimulated with LPF or PHA-P. The induction of Fc∊R by stimulants was completely inhibited by 10-6M dexamethasone. It was demonstrated that the effects of dexamethasone on lymphocytes were dual: one was on B cells to inhibit responsive increases of Fc∊R, and the other was on T cells to suppress the formation of the soluble factor(s) which induced Fc∊R on B cells. [ABSTRACT FROM AUTHOR]

Hepatitis B subviral particles, purified from plasma of asymptomatic carriers seropositive for hepatitis B e antigen, were treated with various conditions reported for the processing of vaccines. Thereafter, antigenic activities displayed by the translation products of pit- S(1), pre-(2) regions and the S gene were determined with monoclonal antibodies, and the reactivity for polyalbumin receptor was tested. Heating at 100°C for 1.5 mm and then at 65°C for 10 h preserved more than 1/2 of antigenic activities representing products of pre- S(1), pre-S(2) regions and the S gene. After incubation in the presence of 8 M urea at 37°C for 4 h, more than 2/3 of antigenic activities still remained. The antigenic activity of the S gene product was decreased to 2/3 and that of pre-S(2) region product to 1/3, after treatment with formalin at the final concentration of 1:4000 at 37°C for 72 h, whereas the activity of pre-S(1) region product was affected drastically. Although 1/5 of the antigenic activity of the S gene product survived the digestion with pepsin for 18 h, antigenic activities of pre-S(l) and pre-S(2) region products were destroyed almost completely. Polyalbumin receptor, borne by the pre-S(2) region product, was lost by pepsin digestion also. Based on the results obtained, heating may be most appropriate for sterilizing plasma-derived hepatitis B particles for use as a vaccine, because it is reliably virucidal and would not affect the protective efficacy to an extent as the other virucidal methods would. [ABSTRACT FROM AUTHOR]

Serum samples containing hepatitis B e antigen (HBeAg) were subjected to electrophoresis in agarose, and fast-migrating 'small' HBeAg and slow-migrating "large" IgG-associated HBeAg were pooled separately. HBeAg of each category was determined by a two-site radioimmunoassay that sandwiched HBeAg between monoclonal antibody (anti-HBe) against one epitope of HbeAg, fixed on a solid support, and anti-HBe against another epitope, labelled with radioiodine. Eighteen sera in which small HBeAg dominated revealed activities of hepatitis B surface antigen-associated DNA polymerase significantly higher than 14 sera in which large HBeAg dominated (logarithm of et/min. mean±s.e. 3.36±0.08 versus 2.14 ± 0.11, P<0.01). Shift from small HBeAg lo large HBeAg was observed, along with the disappearance of DNA polymerase, in the serum from two carriers who seroconverted to anti-HBe. [ABSTRACT FROM AUTHOR]