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Biomedical subjects

G N Beall

Publications and source records attributed to G N Beall.

At least 55 records · Page 3Linked to original sources
PubMed1977

Comparison of the bronchodilator effects of aerosol fenoterol and isoproterenol.

Aerosolized fenoterol in a dosage of 400 microgram was compared to isoproterenol 150 microgram in 31 asthmatic subjects during the course of a double-blind parallel 90-day study. Bronchodilator activities of the two drugs were evaluated for up to 6 hours on days 1, 45 and 90. Analysis of the data revealed that fenoterol consistently produced a significantly greater increase in FEV1, FEF25-75% and Gaw/VL. Specific airway conductance increased on each test day 25 percent or more above baseline for over three hours after use of fenoterol and for only one hour after use of isoproterenol. Fenoterol has less effect upon the cardiovascular and central nervous systems, but produced a greater incidence of shaking compared to isoproterenol. Patients used fenoterol less frequently than isoproterenol which can be attributed to the former having a greater peak effect and time course of bronchodilation. The therapeutic efficacy of fenoterol was sustained throughout this three-month study, and suggests that this relatively selective beta2 adrenergic drug will provide a well tolerated, alternative aerosol for chronic use in asthma.

Adult↗
PubMed1977

Assays for antigen-stimulated lymphocyte-derived migration enhancement and inhibition factors from patients with thyroid diseases and their relatives.

Cell-mediated immunity to thyroid antigens was studied by means of an assay for antigen-stimulated leukocyte migration inhibition factor (LIF) in 5 groups of subjects: patients with Graves' disease, Hashimoto's thyroiditis, their relatives and normal controls. We also sought evidence for the possibility that the hypothesized migration enhancement factor (MEF) might be produced by lymphocytes from patients with autoimmune disorders. We found little evidence of LIF production and none of MEF production by the leukocytes of patients with autoimmune thyroid diseases upon exposure to thyroid antigens. Similarly, either no or only minimal amounts of LIF were demonstrated in culture supernatants of leukocytes of their immediate relatives.

Antibodies↗
PubMed1975

Leukocytic epinephrine receptors of normal and asthmatic individuals.

To determine if the hypothesized beta adrenergic blockade in asthma is located at the level of the hormone receptor, we have compared the number and binding affinity of leukocytic epinephrine receptors in normal and asthmatic subjects. Human leukocytes, but not human erythrocytes, possess low-affinity epinephrine receptors. When saturated, each leukocyte binds approximately 1.0 times 10-6 molecules of epinephrine. Binding of 3H DL-epinephrine was largely inhibited by excess unlabeled L-epinephrine. The binding was reversible and involved both the D and L forms of 3H DL-epinephrine. Inhibition studies with nonradioactive isoproterenol, norepinephrine, propranolol, and tolazoline produced results consistent with the interpretation that the leukocytes contained both alpha and beta adrenergic receptors. Two procedures, subcellular fractionation of lymphocytes and incubation of leukocytes in 0.1 per cent trypsin, permitted the demonstration that most of the catecholamine binding occurred at the plasma membrane. Thin-layer chromatography of the bound 3H DL-epinephrine after its extraction from the leukocytes permitted the interpretation that the hormone had fully retained its chemical structure. In addition, epinephrine binding was associated with cAMP production. Leukocytic epinephrine receptors of 10 asthmatic and 9 normal individuals were compared and found not to be substantially different in number or binding affinity.

Adult↗
PubMed1973

Neutralizing and non-neutralizing antibodies to bovine thyroid-stimulating hormone and its subunits.

To test the possibility that the long-acting thyroid stimulator (LATS) might represent an immune complex either of thyroid-stimulating hormone (TSH) with anti-TSH or of a subunit of TSH with an appropriate antibody, we immunized rabbits with bovine TSH (bTSH), bLH (luteinizing hormone), and their alpha and beta subunits (bTSHalpha and bTSHbeta). Binding, neutralizing, and nonneutralizing antibodies were demonstrated in the antisera obtained. First, antisera to TSH, TSHbeta, and TSHalpha all bound [(125)I]TSH and [(125)I]TSHbeta. Anti-bTSHbeta antisera bound [(125)I]bTSHbeta better than did anti-TSH sera, while the binding of [(125)I]bTSH was similar with both types of antiserum. Second, the thyroid-stimulating activity (McKenzie bioassay) of TSH could be neutralized by incubation with various dilutions of anti-TSH or anti-TSHbeta. Finally, when incubation mixtures containing TSH and dilutions of anti-TSHbeta antisera that only partially neutralized TSH were treated with an antiserum against rabbit immunoglobulins to precipitate immune complexes, the bioassay response of the TSH was abolished. This phenomenon was not observed when antiserum to the intact hormone was substituted in the incubation mixture. The removal of TSH biological activity from a mixture of TSH and anti-bTSHbeta by addition of an anti-immunoglobulin indicated that biologically active immune complexes were formed between TSH and anti-TSHbeta but not between TSH and anti-TSH. The time-course of the bioactivity and several other characteristics of these complexes differentiate them from LATS.

Animals↗
PubMed1973

The effects on rabbits of immunization with bovine thyroid-stimulating hormone and its subunits.

Rabbits were immunized with bovine thyroid-stimulating hormone (bTSH), bovine Inteinizing hormone (bLH), and their subunits. In two immunization experiments, thyroid-stimulating activity was found in the serum of 6 out of 12 rabbits immunized with bTSHbeta subunits. The thyroid-stimulating activity in the anti-bTSHbeta sera was greater at 2 h than at 8, was eluted with the globulin fraction from Sephadex G-100, was completely neutralized by both anti-bTSH and anti-rabbit gamma globulin, and was completely suppressed by administration of triiodothyronine (T(3)) to the immunized rabbit. These findings led to the conclusion that the thyroid-stimulating activity resided in soluble complexes of rabbit TSH bound to anti-bTSHbeta. Two of nine rabbits immunized with bTSH developed thyroid-stimulating activity in their serum, but it was nonsuppressible by T(3). None of the animals immunized with bTSHalpha, bLH, bLHbeta, or bLHalpha developed serum thyroid-stimulating activity.Hypopituitary hypothyroidism, evidenced by decreased serum thyroxine (T(4)) and thyroidal (131)I uptake and by the histologic appearance of large follicles with flat cells, was found in the bTSHbeta- and bTSH-immunized animals, despite the presence of thyroid-stimulating activity in the serum of many. The reasons for this paradox are unclear; possibly the complexes block the effect of TSH on the rabbit thyroid.

Animals↗
PubMed1971

Radioimmunoassay for measurement of triiodothyronine in human serum.

A convenient, specific, precise, and reproducible radioimmunoassay system for measurement of triiodothyronine (T(3)) in human serum has been developed. The procedure compares the ability of standards and unknowns to compete with radioactive T(3) for binding sites on a T(3)-binding antiserum produced in rabbits by immunization with human thyroglobulin. The assay is set up in the presence of 250 ng thyroxine (T(4)) in all tubes, to mobilize T(3) from its binding with the thyronine-binding globulin (TBG), and athyreotic sheep serum in standards to correct for the TBG in the unknowns. The method regularly detected 0.4 ng T(3), which would correspond to a T(3) concentration of 100 ng/100 ml when 400 mul of serum is analyzed. The mean recovery of unlabeled T(3) added to normal serum pools was 106%. Serial dilution of hyperthyroid sera containing high concentrations of T(3) with athyreotic sheep serum yielded expected values. The serum T(3) concentration in 80% of 31 euthyroid normal subjects was less than 100 ng/100 ml (range < 100-170 ng/100 ml); it was greater than 170 ng/100 ml in 89% of 27 sera of hyperthyroid patients with untreated Graves' disease (range < 100-1300, mean 519 in 25 sera with detectable T(3)). The concentration of serum T(3) fell, frequently to undetectable levels, during treatment of hyperthyroid patients with antithyroid drugs. The serum T(3) concentration in four hypothyroid patients was less than 100 ng/100 ml.

Animals↗