Biomedical subjects
N A Harris
Publications and source records attributed to N A Harris.
Quantum defect theory of dipole and vibronic mixing in Rydberg states of CaF.
The Rydberg spectra of CaF combine the simplicity of a single electron outside a doubly closed-shell Ca2+F- ion core with the exceptional polarity of the ion core. A global multichannel quantum defect (MQDT) fit to 612 previously assigned levels, 507 from n approximately = 12-18, N=0-14, v+=1, 97 from n approximately = 9-10, N=0-14, v+=2, and 8 from n approximately = 7, N=3-10, v+=3, produces the complete L=0-3 quantum defect matrix mu (with the exception of one element) and 19 of 20 elements of the partial differentialmu/differentialR matrix, as well as the molecular constants of the CaFX 1sigma+ state [omega(e)+=694.58(14), omega(e)x(e+)=2.559(40), B(e+)=0.373 07(16) cm(-1), and the v=0, N=0 to v(+)=0, N(+)=0 ionization energy, 46,996.40(8) cm(-1)]. This experimentally determined mu(R) matrix is unusual in the completeness of its representation of the spectrum of both core-penetrating and nonpenetrating Rydberg series, including both local perturbations and vibrational autoionization rates, as well as all dynamical processes encoded in the spectrum that result from the scattering (at negative energy) of the Rydberg electron off the Ca2+F- ion core. The MQDT theory is presented in a form that clarifies the relationships of the reaction (K) and phase (P) matrices of MQDT to effective Hamiltonian models for local interactions between accidentally near degenerate levels. In particular, a Hund's case (b) like representation of the Hamiltonian is described in which the rovibronic K matrix is diagonalized and the P matrix, which contains information about the v+, N+ eigenstates of the ion, becomes nondiagonal.
Florence Henderson. The art of open-drop ether.
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Tobacco craving: intensity-related effects of imagery scripts in drug abusers.
Two experiments were conducted to determine whether active imagery would elicit tobacco craving in smokers with histories of drug abuse who were not interested in quitting smoking. In Experiment 1, the authors used scripts that contained positive, negative, or neutral affective content with and without descriptions of smoking urge. Scripts with urge content and negative affect scripts increased subjective reports of tobacco craving. An interaction between affective manipulation and urge content was observed on self-reported mood. In Experiment 2, positive affect scripts that varied in amount of urge content produced an orderly increase in tobacco craving as a function of urge intensity, suggesting that changes were specific to the imagery manipulation. In both experiments, increases in tobacco craving were positively correlated with craving for drug of choice, suggesting that stimuli that engender smoking urges may occasion craving for other drugs of abuse.
Suppression of DNA synthesis in NEL-M1 human melanoma cells by triamcinolone acetonide.
The present study characterizes the biological response of a cloned human melanotic melanoma cell line (NEL-M1) to glucocorticoid treatment. Scatchard analysis of the binding of [3H]-triamcinolone acetonide to the glucocorticoid receptor showed a binding capacity of 170 fmol/mg protein and a dissociation constant (KD) of 1.76 X 10(-9) M. When the 3H-labeled cytosol was warmed to 25 degrees C for 30 min and then incubated with DNA-cellulose at 4 degrees C for 45 min, 32% of the specific glucocorticoid-receptor complexes were bound to DNA-cellulose. Additional studies showed that when NEL-M1 cells were cultured for 72 h with 1 X 10(-7) M triamcinolone acetonide, a 36% reduction in cellular growth was observed compared to the control cultures. The calculated population doubling time for the control cells was 17.5 h compared to 20.3 h for the triamcinolone acetonide-treated cells. Analysis of the effect of triamcinolone acetonide on macromolecular synthesis revealed that, over a 24-h incubation period, triamcinolone acetonide (a) inhibited [3H]thymidine incorporation by 51%; (b) increased the incorporation of the melanin precursor, L-3,4-dihydroxy[3H]phenylalanine, by 59%; and (c) had essentially no effect on [3H]leucine or [3H]uridine incorporation. During this same incubation period, triamcinolone acetonide inhibited [3H]glucose uptake by 19%. Further studies using synchronized NEL-M1 cells clearly show that the earliest detectable action of triamcinolone acetonide was the inhibition [3H]thymidine incorporation during the S phase of the cell cycle. Thus, these findings show that the human melanoma cell line, NEL-M1, is biologically responsive to glucocorticoid treatment. Continued studies using NEL-M1 cells may eventually lead to ascertaining the exact mechanism by which glucocorticoids regulate DNA synthesis.
Effect of triamcinolone acetonide on tyrosinase activity in a human melanoma cell line.
The synthetic glucocorticoid, triamcinolone acetonide, was found to increase melanogenesis in the human melanoma cell line NEL. Treatment of NEL cells for 24 hr with triamcinolone acetonide (1 X 10(-7) M) increased the activity of the enzyme tyrosinase by 43% and the incorporation of the melanin precursor, L-3,4-dihydroxyphenylalanine, by 23%. Additional studies revealed no change in cyclic AMP levels over an 18-hr test period. A 2-hr preincubation of NEL cells with actinomycin D (10 micrograms/ml) prevented the increase in tyrosinase activity by triamcinolone acetonide. When triamcinolone acetonide was added to a synchronized population of NEL cells, an increase in tyrosinase activity was observed at 16 hr, coinciding with the late S phase of the cell cycle. These results suggest that glucocorticoids are involved in the regulation of melanogenesis in NEL cells by increasing the activity of the rate-controlling enzyme tyrosinase.
Transient respiratory depression of the newborn. Its occurrence after succinylcholine administration to the mother.
A baby born after a cesarean section experienced transient respiratory depression. The mother had a postsuccinylcholine apnea caused by homozygosity for the atypical allele for serum pseudocholinesterase; the baby was heterozygous for this allele and the usual allele for serum pseudocholinesterase. The possible relationship between the genotype of the baby and the respiratory difficulty at birth is raised.