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B Miller

Publications and source records attributed to B Miller.

At least 379 records · Page 21Linked to original sources
PubMed1981

Photoaffinity labeling of the insulin receptor in H4 hepatoma cells: lack of cellular receptor processing.

Photoaffinity labeling techniques were used to identify insulin-binding components of the plasma membrane in insulin-responsive, monolayer-cultured hepatoma cells. The activated, photosensitive reagent, an n-hydroxysuccinimide ester of 4-azidobenzoic acid, was coupled with highly purified insulin, and the hormone derivative was subsequently iodinated, bound to cell surface receptors of intact H4 cells, and photoactivated. Ater dissolution of the cells, labeled proteins were analyzed by SDS/polyacrylamide gel electrophoresis under reducing conditions. The main labeled band exhibited an apparent molecular weight of 130,000. Two minor components of apparent mol wt 95,000 and 40,000 were also identified. Specific labeling of all 3 bands was inhibited by simultaneous incubation of the cells with native insulin, but not by the heterologous hormone, glucagon, prior to photoactivation. Binding of azidobenzoyl insulin to H4 cells was time-dependent, as was the correlated labeling of receptor components. Band-labeling by the photosensitive insulin derivative was totally light-dependent; spontaneous covalent linking of insulin and receptor was not observed. The labeled receptor-related proteins were not degraded by the cells under our experimental conditions.

Affinity Labels↗
PubMed1981

Ocular malignant melanoma in South African blacks.

The incidence of primary ocular malignant melanoma in blacks during the last 25 years in a large part of the Transvaal Province of South Africa is reported. Only 8 cases were diagnosed, 1 uveal, 4 conjunctival, and 3 orbital. During this same period 153 cases of primary ocular malignant melanoma were diagnosed in whites. The rarity of these tumours among blacks is stressed and the reasons for this infrequent incidence discussed.

Adult↗
PubMed1981

Relationship of steroid receptor, cell kinetics, and clinical status in patients with breast cancer.

The fractions of cells in the different phases of the cell cycle were determined by flow cytometry in 70 human breast tumors and six human benign breast tissues. This procedure showed that 44% of the tumors and none of the benign tissues were aneuploid as determined by mixing experiments using normal peripheral blood as a standard for DNA content per nucleus. The mean percent S-phase fraction (% S) values +/- S.D. for benign and malignant tissues were 6.9 +/- 1.6 and 13.7 +/- 6.5, respectively. By our procedure, aneuploid tumors seem to have significantly higher mean % S value than do diploid tumors. Breast cancer tissue which contained steroid receptors had a mean % S value of 11.3, while those tumors which had neither the estrogen nor progesterone receptors had a mean % S value of 17.1 (p less than 0.01). The estrogen receptor status had a better inverse relationship to the cell kinetic data than did the progesterone receptor status. The use of molecular forms of the steroid receptor was of some assistance in improving the inverse relationship between cell kinetics and steroid receptor status. A trend was observed between lack of steroid receptors and higher probability of the tumor being aneuploid. From the limited clinical data, there was no relationship between cell kinetic and aneuploid data with respect to nodal status, metastatic disease, and menopausal status. The possible use of these data is discussed.

Aneuploidy↗
PubMed1980

Double-blind placebo controlled crossover evaluation of levamisole in rheumatoid arthritis.

During levamisole therapy, 14 of 20 patients with previously unresponsive rheumatoid arthritis had significant improvement (P less than 0.05) in clinical measures of disease activity, erythrocyte sedimentation rate, and rheumatoid factor titer in a 32-week double-blind placebo controlled crossover trial. Levamisole was shown to alter antibody responses to tetanus and typhoid antigens, lymphocyte blastogenesis to phytohemagglutinins, and the number of null cells in peripheral blood. Agranulocytosis and rash resulted in discontinuation of the drug in one patient in each group. Though clearly effective, routine use of levamisole as a disease suppressant in rheumatoid arthritis must await more complete clarification of its association with agranulocytosis.

Adult↗
PubMed1980

HLA antigens in acute anterior uveitis in South African blacks.

Fifty-three black patients with acute nongranulomatous anterior uveitis (AAU) were tissue typed and the results compared to those from a panel of 200 healthy unrelated black volunteers. No statistically significant deviation from the norm with regard to the frequencies of 38 HLA antigens could be observed.

Acute Disease↗
PubMed1980

Cultured hepatoma cells as a model system for studying insulin processing and biologic responsiveness.

Monolayer cultures of minimal deviation hepatoma cells (H4-II-E-C3') bound and degraded insulin specifically, the apparent Ki value for insulin inhibition of both processes being 1 x 10(-8) M, indicating that cell-bound 125I-insulin is the substrate for subsequent hormone degradation in these cells as in isolated hepatocytes.1 The time course of insulin binding to its receptor depended on hormone concentration and temperature. Degradation of insulin also depended highly on temperature, with little or no degradation occurring at less than 20 degrees C, a temperature below which a membrane-lipid phase transition may block homone translocation or uptake. The effects of various agents on the binding and degradation of 125I-insulin also were tested. Agents believed to inhibit intralysosomal degradation of various proteins also inhibited the degradation of 125I-insulin by H4 cells (chloroquine, ammonium chloride, procaine, and lidocaine); inhibitors of energy production (dinitrophenol, sodium cyanide) inhibited degradation; an agent which inhibits microtubule function (vinblastine) blocked insulin degradation; and methylamine, reported to prevent receptor aggregation,2 also interfered with insulin processing. These findings are consistent with a model for cellular insulin processing, comprising receptor binding, clustering of receptors, endocytotic uptake, intralysosomal degradation, and extracellular release of some degradation products. H4 cells were highly sensitive to insulin. The KE for a half-maximal response of hormone-stimulated incorporationof 14C-glucose into glycogen was 10(-11) M insulin, corresponding to less than 1% receptor occupancy. This response was also mimicked by concanavalin A at a concentration of 10 microgram/ml. Vinblastine and chloroquine both significantly inhibited insulin-stimulated glucose incorporation into glycogen without affecting basal levels. However, since these inhibitory effects were not relieved by addition of excess insulin, it seems unlikely that their action on glycogen synthesis was exerted only at the level of the generation of an active intermediate or degradation product from hormone-receptor complexes. The hormone-sensitive H4 cells thus provide a useful system for further studies examining the role of insulin-receptor uptake in hormone action, receptor regulation, and signal termination.

Animals↗
PubMed1980

The incident.

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History, Modern 1601-↗
PubMed1979

Tetracaine blocks the responses of isolated acinar cells from rat parotid to carbachol but not to substance P.

Carbachol and substance P stimulated 45Ca2+ flux changes, 86Rb+ efflux, and amylase secretion from acinar cells isolated from rat parotid. The local anesthetic tetracaine blocked all of these measured responses to carbachol, but none of the responses to substance P. Tetracaine must act at either the cholinergic receptor or at a subsequent transducing step in the cholinergic stimulus-response sequence. If tetracaine acts at one of the transducing steps between cholinergic receptor occupation and the physiological responses then the action of tetracaine must be at a locus in the cholinergic reaction scheme not shared by substance P, because tetracaine did not block any response of the parotid to substance P.

Amylases↗