The reaction of substituted acetylacetonates with R₃B compounds leads to the production of an interesting series of chelates containing the pseudo-metal ion moiety, BR₂. [see document for image of chemical compound] When the substituents on the acetylacetone are capable of extensive delocalization with the chelate ring (e.g., benzoylacetomethane) and/or when the R groups on boron are sufficiently withdrawing (R = F, C₆H₅), these species are capable of reversible one-electron reduction to the radical ion. These ion radicals are extremely stable, having been kept for many months at room temperature under argon atmosphere. Previous studies have indicated that the dianion radical of the substituted acetylacetonate ligand itself is extremely unstable. It has been trapped at extremely low temperatures and its spectral properties have been reported. Obviously, the main group chelate radical ions that we have studied represent a case where the inherently unstable dianion radical system is stabilized by coordination to the pseudometal ion. The spin densities and charge distribution in the boron chelate radicals and the neutral parent have been calculated by Pariser-Parr-Pople SCF techniques, extended Hückel molecular orbital calculations, and CNDO and INDO methods. The ligand dianion radicals have also been successfully handled. In all cases, good agreement between experimentally observed ESR hyperfine coupling constants, assigned by satisfactory simulation, and calculated hyperfine constants have been obtained. The spin density calculations on the radical anions indicated that there are negligible spin delocalization over the moiety, BR₂. The net charge distribution in the neutral and the radical anions demonstrate that the effect of BR₂ on the radical stability is due to its withdrawing effect. The electronic energy levels and electronic transitions allowed in the neutral and the radical ions have been calculated by closed-shell and open-shell (RSCF) methods of Longuet-Higgins and Pople with the CI treatment of Ishitani and Nagakura. Good agreement with the experimental data is observed. Correlation diagrams connecting the MO levels for the neutral and radical ion species reveal information about the perturbations of energy levels caused by the injection of an extra electron into the previous spin-paired system. / Ph. D.

This research investigated the effects of age, sex, male vs female voice, and unfamiliar vs familiar voice upon the infants body movements. The sample consisted of 40 middle-class infants, balanced according to sex, at four age levels -- 3, 6, 9, 12 months. Four tape-recorded stimulus conditions -- mother's voice, father's voice, female stranger’s voice, and male stranger's voice -- were presented to each infant. The body movements of the infants were recorded at one frame per second by an 8mm. camera. Analyses of variance were performed to determine any differences among the four stimulus conditions and control periods. The 12-month-old infants showed more activity to the father's voice than to the male stranger's voice or to the mother's voice. These subjects also showed more activity to the female stranger's voice than to the male stranger's voice. Female subjects were more active than male subjects to the unfamiliar voices on Trial 1. On Trial 2 females showed greater activity than males to the familiar voice. Females exhibited greater activity than males overall. Males showed greater activity than females to the cessation of the female voice and to the initiation of their father's voice. Results were discussed in terms of the infant's development as affected by sex of the infant and the cross-over effect found by Friedlander (1970). / Master of Science

During apoptosis, changes occur in T-lymphocyte membranes that render them susceptible to hydrolysis by secretory phospholipase A2 (sPLA2). To study the relevant mechanisms, a simplified model of apoptosis using a calcium ionophore was first applied. Kinetic and flow cytometry experiments provided key observations regarding ionophore treatment: initial hydrolysis rate was elevated, total reaction product was increased four-fold, and adsorption of the enzyme to the membrane surface was unaltered. Analysis of these results suggested that susceptibility during calcium-induced apoptosis is limited by substrate availability rather than enzyme adsorption. Fluorescence experiments identified three membrane alterations that might affect substrate access to the sPLA2 active site. First, intercalation of merocyanine 540 into the membrane was improved, suggesting increased lipid spacing. Second, laurdan detected increased solvation of the lower head group region of the membrane. Third, the rate at which fluorescent lipids could be removed from the membrane by albumin was enhanced, implying greater vertical mobility of phospholipids. Thus, it was proposed that the apoptotic membranes become susceptible to sPLA2 through a reduction in lipid-neighbor interactions which facilitates migration of phospholipids into the enzyme active site. This proposal was then examined in T-lymphocytes treated with glucocorticoid, a more physiologically relevant apoptotic stimulant, using similar techniques. The following observations corresponded to induction of membrane susceptibility: increased merocyanine 540 intercalation; phosphatidylserine flip-flop, detected by annexin binding; and alterations in laurdan fluorescence properties. These observations implied a relationship among sPLA2 susceptibility, lipid spacing, and phosphatidylserine exposure. To clarify this relationship, additional assays were also performed using dibutyryl-cAMP to induce apoptosis, a drug reported to induce apoptosis in S49 cells without the typical translocation of phosphatidylserine. Our results indicated that in cells treated with dibutyryl-cAMP, the merocyanine 540 response and its correlation with sPLA2 susceptibility was similar to that observed with dex-treated samples. This suggests that the underlying mechanisms which promote sPLA2 hydrolysis lead to alterations that may be facilitated by but do not require phosphatidylserine exposure. Taken together, all of the results suggest that direct regulation of the biophysical microenvironment of the membrane is the mode of control of membrane susceptibility to the hydrolytic activity of sPLA2.