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Biomedical subjects

J L Morgan

Publications and source records attributed to J L Morgan.

54 records · Page 3Linked to original sources
PubMed1980

Immunological differences between actins from cardiac muscle, skeletal muscle, and brain.

The antigenic similarities and differences between various actins were explored by use of antisera against purified bovine cardiac actin and chicken embryo brain actin. In double-antibody coprecipitation tests, purified iodinated actins from bovine cardiac muscle, rabbit skeletal muscle, chicken embryo brain, and bovine brain all bound to antiserum against chicken embryo brain actin. This result demonstrates the presence of shared antigenic determinants among these actins. Cardiac actin antiserum, on the other hand, bound cardiac and skeletal actin, but failed to bind significantly either brain actin. In radioimmunoassay, all four unlabeled actins were capable of some degree of inhibition of binding of (125)I-labeled chicken embryo brain actin to homologous antiserum. The results confirm the existence of shared or similar antigenic determinants, but also show that the molecules are not antigenically identical. In the cardiac actin radioimmunoassay, unlabeled cardiac and skeletal muscle actins inhibited the binding of (125)I-labeled cardiac actin to homologous antiserum, but neither brain actin inhibited the binding. Thus, the muscle actins possess at least one antigenic determinant not expressed by the brain actins, in addition to the shared determinants. Furthermore, cardiac actin and skeletal actin generated different inhibition curves in the cardiac actin radioimmunoassay, demonstrating that, although antigenically related, they are not identical. Correlations with existing sequence data imply that substitutions in only a few residues alter the antigenic properties of actin.

Actins↗
PubMed1980

Effects of neomycin on the waveform of auditory-evoked brain stem potentials in dogs.

Neomycin sulfate was administered intravenously to eight mixed-breed dogs at a dosage of 30 mg/kg/day for as long as 50 days. Auditory-evoked brain stem potentials (AEBP) were recorded from the dogs three times a week. The AEBP amplitudes and latencies from the eight treated and the eight control dogs were compared. All treated dogs eventually exhibited an isoelectric AEBP. The time required for the AEBP waveform loss to occur in the treated dogs varied between 22 and 50 days. The AEBP waveforms were still isoelectric when measured as long as 150 days after neomycin administration was stopped. The fact that AEBP did not return would tend to support the findings of others that the loss of the receptors in the inner ear, due to neomycin toxicity, is permanent. The results of this electrophysiologic study indicate that the organ of Corti (organum spirale) is the site of pathologic changes in the auditory system that result from neomycin treatment.

Animals↗
PubMed1978

Species-dependent immunological differences between vertebrate brain tubulins.

The antigenic similarities and differences between highly purified brain tubulins from lamb, mouse, and chick embryo have been examined using rabbit antisera prepared against each of these tubulins. These antisera are capable of binding 125I-labeled tubulin in homologous or heterologous combinations, demonstrating immunological similarity between the tubulins. However, there are quantitative differences in the maximum amount of binding observed. Differences between the tubulins were further resolved by radioimmunoassays, comparing the ability of each of the tubulins to inhibit the binding of each 125I-labeled tubulin to each antiserum. Competition curves generated for all possible combinations revealed quantitative immunological differences between the tubulins that imply different densities of shared antigenic determinants on all three tubulins and a unique determinant on the chick tubulin molecule.

Animals↗
PubMed1977

Quantitation of cytoplasmic tubulin by radioimmunoassay.

A radioimmunoassay has been developed for the quantitation of crytoplasmic tubulin. It measures tubulin between 20 and 1500 nanograms and does so independently of decay in colchicine-binding activity. In addition, the state of tubulin as subunit or polymer does not alter the measurement.

Animals↗
PubMed1977

Identification of the major urinary metabolite of thromboxane B2 in the monkey.

Thromboxane B2 (TxB2) was biosynthesized from prostaglandin endoperoxides (PGG2, PGH2) using guinea pig lung microsomes and infused into an unanesthetized monkey. Urine was collected and TxB2 metabolites were isolated by reversed phase partition chromatography and high performance liquid chromatography. A major metabolite (TxB2-M) was found to be excreted in greater than two-fold abundance relative to other metabolites. Its structure was determined by gas chromatography-mass spectrometry to be dinor-thromboxane B2. In vitro incubation of TxB2 with rat liver mitochondria yielded a C18 derivative with a mass spectrum identical to that of TxB2-M, substantiating that the major urinary metabolite of TxB2 in the monkey is a product of a single step of beta-oxidation.

Animals↗
PubMed1975

Prostaglandins as mediators of hypercalcemia associated with certain types of cancer.

We investigated the role of prostaglandins in the hypercalcemia associated with neoplasia. In patients with hypercalcemia and solid tumors the excretion of the major urinary metabolite of the E prostaglandins, 7 alpha-hydroxy-5, 11-diketotetranorprostane-1, 16-dioic acid (PGE-M), was significantly greater than normal, P LESS THAN 0.01 (median of 58.4 and 7.1 ng per milligram of creatinine respectively). Slightly elevated values were seen in normocalcemic patients with solid tumors (14.3 ng per milligram). The levels of the metabolite were normal in hypercalcemic patients with either hematologic neoplasia or primary hyperparathyroidism. Immunoreactive parathyroid hormone was undetectable in the plasma of all hypercalcemic patients with solid tumors. Inhibition of prostaglandin synthesis by aspirin or indomethacin reduced excretion of both the urinary metabolite and serum calcium in six hypercalcemic patients with solid tumors and elevated excretion of the metabolite. These findings support the concept that prostaglandins are mediators of the hypercalcemia caused by certain solid tumors.

Aspirin↗
PubMed1975

Tubulin constancy during morphological differentiation of mouse neuroblastoma cells.

Clonal cell lines N18 and N103 of the mouse neuroblastoma C1300 possess an undifferentiated neuroblast morphology under optimal growth conditions; however, when deprived of serum, N18 can be induced to extend long neurites. Although initial neurite outgrowth is rapid, very long fibers are found only after several days. Both initial outgrowths and established neurites contain microtubules; however, the number and density of these polymerized tubules increase markedly during this time. Optimum conditions have been established for assessing the colchicine-binding activity of neuroblastoma sonicates. A time-decay colchicine-binding assay was used to make a comparative study of the tubulin content of both undifferentiated and differentiated N18 as well as the nondifferentiating N103 and the rat glioma C6. Both morphologies of clone N18 possessed similar concentrations of tubulin (130-140 pmol/10(6) cells). Although cells of clone N103 contain 20% less tubulin than N18 cells, this is considerably more tubulin than is present in the glioma C6 (30 pmol/10(6) cells) which has a similar generation time. Quantitative densitometry of neuroblastoma extracts electrophoresed on SDS-polyacrylamide gels confirmed the constancy of tubulin. Radiolabeled proteins from neuroblastoma cells subjected to both growth conditions show that neurite outgrowth does not create a disproportionate demand for tubulin synthesis. Thus, the morphological differentiation of neuroblastoma cells probably reflects the regulation of tubulin storage and microtubule polymerization.

Cell Differentiation↗
PubMedDate not supplied

Composite grafts of human keratinocytes grown on a polyglactin mesh-cultured fibroblast dermal substitute function as a bilayer skin replacement in full-thickness wounds on athymic mice.

We have developed and tested in athymic mice a new, cultured, dermal-epidermal graft composed of two human cell types coupled with a biodegradable dermal scaffold. Cultured, proliferating human keratinocytes (HK) were applied to the surface of a living dermal tissue replacement that is composed of human fibroblasts cultured on a polyglactin mesh. After 4 to 6 days of coculture, proliferating HKs achieved confluency on the surface of the living dermal tissue replacement. Grafts were then transferred to full-thickness wounds on the dorsum of athymic mice. Sixteen animals were grafted, and the mean percentage of graft take (original wound area covered) on day 20 after grafting was 51.25%. Staining with antibody specific for human involucrin confirmed the presence of HKs on closed wounds, and staining with antibody specific for human laminin revealed a continuous layer of laminin at the dermal-epidermal junction on day 20. Animals closed with living dermal tissue replacement alone markedly contracted, whereas application of living dermal tissue replacement-HK grafts appeared to retard contraction. Because polyglactin mesh fibers are absorbed by hydrolysis rather than by enzymatic degradation, this living composite graft may be more resistant to destruction when placed on excised human wounds than are composite grafts, which are composed of a collagen matrix. The inclusion of the living dermal substitute may ultimately provide better skin quality than is achieved from the use of cultured keratinocytes alone. Fragility of the epidermal layer is probably due to the short-term culture of HKs on the living dermal tissue replacement, and further efforts to develop a thicker epithelial layer may improve graft durability.

Animals↗