Confusing data on skin testing devices.
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Biomedical subjects
Publications and source records attributed to H M Brown.
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The effects of treating the environment of 25 dust mite-allergic patients with an acaracide are reported. Remarkable symptomatic improvements in asthma, eczema, or rhinitis were observed. Many patients could reduce or stop medication, and these benefits have persisted for up to a year after using Acarosan once only. Relapse of symptoms following exposure to untreated dusty environments was observed on many occasions confirming that the improvements were due to removal of the mite allergen.
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A 1% (v/v) solution of dimethyl sulfoxide (DMSO) added to the saline bath of isolated Balanus eburneus photoreceptors increased receptor potential amplitude by 40-50% and shortened time to peak amplitude and latency by 20-25%. The light-sensitive membrane current of voltage-clamped cells was increased systematically as DMSO concentration was increased from 1% to 10%. The null potential of the light sensitive current was unaffected by DMSO with short pulses of light, indicating that DMSO has no direct effect on ion selectivity of the light-sensitive channel. Absorbance changes of cell injected with the calcium indicator arsenazo III show that DMSO elevates intracellular Ca2+ (Cai). Current-voltage relations in darkness reveal that DMSO induces a small sustained inward current (approximately 5 nA) which has a null potential similar to the light-induced current. DMSO may activate the light-sensitive conductance via the increase in Cai. However, the altered kinetics and increased amplitude of the receptor current are opposite to the desensitizing effects normally observed with increased Cai.
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A substrain of the human monocyte-like cell line U937, which is a cholesterol auxotroph, was used to study the effect of cellular cholesterol depletion on the expression of the type I Fc receptor for IgG (Fc gamma RI). Measurement of Fc gamma RI expression was performed by immunofluorescence and flow cytometry using the monoclonal antibody (mAb) 32.2, which is specific for an epitope on Fc gamma RI, and monomeric IgG2a, which binds to the ligand binding site of Fc gamma RI. Incubation of these cells for 24 h in growth medium containing delipidated fetal calf serum depletes cellular cholesterol without affecting growth or viability. While incubation of U937 cells with human interferon-gamma (IFN-gamma) increased Fc gamma RI expression, cholesterol depletion after cell growth in media containing delipidated serum and IFN-gamma resulted in reduced binding of both mAb 32.2 and IgG2a. A significant decrease in the number of cell surface binding sites, as measured by mean fluorescence intensity, was observed after cholesterol depletion. Supplementation of the delipidated serum medium with pure cholesterol in an ethanol/bovine serum albumin mixture, which replenished cellular cholesterol and supported growth, failed to restore antibody binding significantly. In contrast, low-density lipoprotein (LDL) which also delivered cholesterol to the cells restored binding both in terms of the number of the reactive cells and cell surface receptor density. High-density lipoprotein (HDL3), which does not deliver cholesterol to the cells, showed results similar to those obtained with pure cholesterol. This indicates that either LDL cholesterol is better utilized for membrane synthesis than pure cholesterol or that LDL provides another component, in addition to cholesterol, which is required for expression of Fc gamma RI, but not for growth. These studies indicate a role for LDL in regulating the expression of Fc gamma RI on the cell surface.
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The cellular basis for the generation of antigen-specific T8 suppressor cells with high doses of antigen has been studied. We separated the T4 subset of human T cells into T4+2H4+ and T4+2H4- subpopulations with a recently developed monoclonal anti-2H4 antibody. T8 cells could be consistently activated to suppress a primary anti-2,4-dinitrophenyl (DNP) antibody response in vitro with unfractionated T4 cells or with the T4+2H4+ subset but not the T4+2H4- subset. In contrast, the T4+2H4- subset functioned as the helper inducer for the anti-DNP antibody response. With keyhole limpet hemocyanin (KLH)-stimulated T4+2H4+ cells we could efficiently induce antigen-specific suppressor activity of fresh T8 cells. In contrast, the T4+2H4+ subset could not effect suppression in the absence of T8 cells. Our findings indicate that the T4+2H4+ subset of human T cells is the suppressor inducer of specific T8 cells in an antigen-specific DNP-KLH system.
ELISA plates coated with highly pure IgG4 were employed to detect IgM antiglobulin in atopic sera. The use of IgG4, rather than whole IgG, on the solid-phase was to provide direct evidence for the IgG4 reactivity of the antiglobulin. Bound IgM was shown to be antiglobulin in that binding can be inhibited by pre-absorption of serum with IgG. Some 75% of asthmatic patients and 29% of eczema patients were found to have significantly raised level of IgM antiglobulin. This antiglobulin resembles rheumatoid factor in that it appears to be directed against antigenic determinants common to human and rabbit IgG. Isolated antiglobulin-enriched IgM fractions released histamine from leucocytes of 7 out of 12 atopic patients. The histamine-releasing capacity of the IgM antiglobulin was shown to be operating via basophil-bound IgG in that the process can be blocked by pre-absorption of the antiglobulin with IgG. Furthermore, heating the antiglobulin-enriched IgM fraction did not affect its histamine-releasing capacity. We conclude that the IgM antiglobulin detectable in our atopic patients may contribute to the pathological changes in them.
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IgE and IgG4 antibodies to bovine milk fat globule membrane (FGM) were measured in atopic eczema patients to determine whether their presence would account for allergy to milk in cases where whole or individual milk protein-specific antibodies are not detectable. The study demonstrates that the measurements of IgE and IgG4 antibodies to FGM do not offer any additional diagnostic value in milk exacerbated cases of atopic eczema. Furthermore, cross-inhibition studies with four milk proteins showed that these FGM-reactive IgE and IgG4 antibodies are directed against alpha-casein.
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The absolute photoelectron quantum yield spectra for benzo[a]pyrene and dimethylbenzanthracene are presented in the wavelength range 180--230 nm. These polycyclic aromatic carcinogens have photoelectron quantum yields of approximately 2 x 10(-3) electrons per incident photon at 180 nm. The quantum yields fall off quickly and monotonically at wavelengths longer than 210 nm (5.9 eV). Threshold values for benzo[a]pyrene and dimethylbenzanthracene are 5.25 +/- 0.06 cV and 5.27 +/- 0.04 eV, respectively. The photoelectron quantum yields of benzo[a]pyrene and dimethylbenzanthracene are several orders of magnitude greater than typical components of biological membranes (amino acids, phospholipids, and polysaccharides). Preliminary micrographs of benzo[a]pyrene and dimethylbenzanthracene sublimed onto poly(L-lysine) and onto dimyristoyl phosphatidylcholine demonstrate the high contrast of small crystallites of carcinogens against a background of membrane components. These results and calculations involving relative contrast factors suggest that the distribution of these carcinogens in biological membranes can be determined by using photoelectron microscopy.