As part of a research program to study the transitional region of N=88 isotones, ¹⁵²Tb was produced by the reaction ¹⁵¹Eu(α,3n)¹⁵²Tb in the 88" cyclotron located at LBNL. Gamma-ray spectroscopy of the radiation emitted from excited ¹⁵²Gd following the β⁺ decay of ¹⁵²Tb has been performed using an array of 20 germanium detectors. The large Q-value (3990 keV) of the ¹⁵²Tb 2⁻ decay allows for the population of many levels; study of coincidence and single events resulted in the establishment of 54 new levels and 266 new transitions. Angular correlation of the coincidences has determined spin and parity of many levels with several seen as key to the band structure, including two new 0⁺ levels. One new rotational band including the new 1475.2 keV 0⁺ level and the 1771.7 keV 2⁺ level is proposed. The overall band structure compared to collective excitation models demonstrates the position of ¹⁵²Gd in the transition from a spherical to deformed shape, also seen in other N=88 isotones. Monopole transition strength among bands indicates the possibility of mixing of both shapes among the excited states. The remarkable similarity of the band structure among these isotones is discussed. / Graduation date: 2005

Muc4, a heterodimeric transmembrane mucin containing EGF-like domains, has been described as an ErbB2-binding protein which modulates signaling via the ErbB2-ErbB3 pathway. In Muc4-transfected MCF-7 cells, Muc4 expression resulted in alteration of both the time course and phosphorylation levels of NRG beta 1 induced phosphorylation and activation of both ErbB2 and ErbB3. Muc4 significantly enhanced the autophosphorylation of ErbB2 over the early (defined 0-30 min) and intermediate (30-120 min) NRG beta 1 treatment times at three sites, Y1248, Y1221 and Y1139. The sites displayed differential maximal phosphorylation times. At Y1248 and Y1139, maximal phosphorylation occurred entirely during the early treatment phase. However, Y1221/2 showed maximal phosphorylation during the intermediate phase with a smaller peak during the early phase. The ratio of phosphorylated ErbB3 and total receptor level was significantly enhanced (in cells that expressed Muc4 compared without Muc4) over both the early and intermediate NRG beta 1 treatment time at the Y1289 site. This motif is one of several similar ErbB3 motifs whose phosphorylation mediates the binding of PI3-kinase. This phospholipid kinase is a key modulator of numerous cellular pathways leading to proliferation, motility and survival. Aberrancies in the ErbB2-ErbB3 signaling pathway have been implicated in the aggressive behavior of tumor cells, and the identification and characterization of modulators of this pathway are being sought as targets of potential therapeutic interventions. Muc4 significantly enhanced activated ERK in the absence of NRG beta 1 treatment while a NRG beta 1 mediated activation of AKT was observed. At early NRG beta 1 treatment time phases, Muc4 co-localized with phosphorylated ErbB2 (pY1248) independent of NRG beta 1 treatment; co-localization of Muc4 and ErbB2 receptor (activated/receptor forms) was observed at the apical surface or around the cell surface membrane. These data provide evidence in the Muc4-transfected MCF-7 cells for the biological NRG beta 1 mediated ErbB2 and ErbB3 activation. Our data suggests that Muc4 affects steady state phosphorylation levels and duration of the phosphorylation signal of both ErbB receptors, and that NRG beta 1 might affect ErbB2 and ErbB3 signaling differently. Additionally, the results of the timing of phosphorylation studies suggest the possibility that temporal aspects of phosphorylation at different sites may determine the pathways activated preferentially in the subsequent signaling cascades.

Thesis (Ph. D.)--University of Chicago, Dept. of Chemistry, June 1999. / Includes bibliographical references. Also available on the Internet

Thesis (Ph. D.)--Oregon State University, 2007. / Printout. Includes bibliographical references (leaves 107-113). Also available on the World Wide Web.

Thesis (Ph. D.)--University of Missouri-Columbia, 2006. / The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file viewed on (March 3, 2007) Vita. Includes bibliographical references.

Thesis (Ph. D.)--Ohio State University, 2006. / Full text release at OhioLINK's ETD Center delayed at author's request

Early research with beta-alanine (beta-ALA) supplementation has shown increases in muscle carnosine as well as improvements in body composition, exercise performance and blood lactate levels. Creatine monohydrate supplementation has been extensively researched for its effects on anaerobic exercise performance. Recently, a new line of studies have examined the combined effects beta-ALA and creatine supplementation on anaerobic exercise performance and lactate threshold. The purpose of the present study is to examine the acute and chronic effects of beta-ALA supplementation with and without creatine monohydrate on body composition, aerobic and anaerobic exercise performance, and muscle carnosine and phosphagen levels in college-aged recreationally active females. Thirty-two females were randomized in a double-blind placebo controlled manner into one of four supplementation groups including beta-ALA only, creatine only, beta-ALA and creatine combined and placebo. Participants supplemented for four weeks and reported for testing at baseline, day 7 and day 28. Testing sessions consisted of a resting muscle biopsy of the vastus lateralis, body composition measurements, a graded exercise test on the cycle ergometer for VO2max and lactate threshold, and multiple Wingate tests for anaerobic exercise performance. Results showed all supplementation strategies increasing muscle carnosine levels over placebo after four weeks, but not between groups. Muscle creatine increased for all groups after four weeks, but not between groups. There were improvements for all groups with body composition after four weeks, despite the present study not including a specific training protocol. There were no group differences observed for aerobic exercise, blood lactate levels, lactate threshold, ventilatory threshold, peak power, mean power, total work or rate of fatigue. There were some trends for anaerobic exercise indicating groups supplementing with creatine may have greater improvements, however, these findings were not statistically significant. The present study failed to show any additive effects of beta-ALA and creatine supplementation for body composition, aerobic exercise, lactate threshold or anaerobic exercise measures. This could be due to the small sample size resulting in low power and effect sizes. Previous research has demonstrated that four weeks of beta-ALA and creatine supplementation was enough time to increase muscle carnosine and phosphagen levels. However, perhaps more time is needed for performance adaptations to occur, especially without the addition of an exercise training component.

Muscle fatigue has always been of vital importance in most sports. A few possible factors have been reported to be the cause of muscular fatigue during high intensity exercise; depletion of glycogen, oxidative stress, disruption of contractile mechanisms and accumulation of metabolites. One of the theories of the cause of muscular fatigue, both in endurance and intermittent sports, is decreased pH levels due to increased concentration of H+ ions dissociated from lactic acid in muscle. Carnosine, a fairly unnoticed ergogenic aid, taken in the form of β-alanine has shown to potentially delay the onset of fatigue. Supplementation of β-alanine, would increase carnosine levels in muscle and may counteract the decrease in pH since carnosine functions as a H+ buffer. The purpose of the present study was to examine the effects of 8 weeks supplementation of β-alanine in distance runners and Swedish division four soccer players on aerobic capacity, intermittent recovery and muscular fatigue. The runners (n = 15) were tested in lactate profiling tests and the soccer players (n = 22) were tested in the Yo-Yo intermittent endurance test pre and post the 8-week test-period. The yo-yo test did not result in significant difference between the soccer players’ β-group and control-group (p = 0,29). Neither did the lactate test result in significant differences between the distance runners’ β-group and control-group in any of the five variables measured. However, a trend in difference was seen between groups in both velocity at lactate threshold (VLT) (p = 0,11) and recovery blood lactate (RBL) (p = 0,14) where the β-group had increased slightly from 16,8 ± 1,6 km/h to 17,0 ± 1,2 km/h in VLT and decreased from 4,5 ± 1,6 mmol∙L-1 to 3,1 ± 1,0 mmol∙L-1 in RBL. The results suggested that β-alanine may delay the onset of fatigue and improve performance in endurance sports such as running by increasing the removal of lactate acid from muscle.

The gulf toadfish (Opsanus beta) is a member of a group of teleosts that have retained their ornithine urea cycle (OUC) allowing them to excrete nitrogenous waste in the form of urea (ureotely). Urea-­N for the entire day is excreted in 1-­2 quick pulsing events (1-­3 h). This study evaluated the hypothesis that urea-­N pulsing events in gulf toadfish can be triggered by social signals from conspecifics via a specific waterborne messenger. Using a crowding protocol, we found that pre-­conditioned seawater induced a secondary urea pulsing event in naïve conspecifics. Furthermore, it was revealed that other factors such as signal concentration and donor body mass relay information to recipients as well. Fractionation of pre-­conditioned seawater was carried out to narrow possible signal candidates and the aqueous portion was found to contain the active molecule. Ammonia was found to be an important factor controlling the response of toadfish to pre-conditioned seawater.

The spatiotemporal dynamics of ongoing beta band (15-30 Hz) cortical oscillations and the modulation of this neural activity by tactile input and movement provide insight into how the brain achieves proper sensorimotor processing. Earlier studies have shown that the synchrony of the cortical beta rhythms within and between central and peripheral neuronal populations is modulated during and following somatosensation or movement, and correlated with effective motor control. In addition, abnormal levels of beta oscillations in the basal ganglia are correlated with motor dysfunction in Parkinson’s disease. Numerous functional roles for the beta rhythm have been proposed – ranging from inhibition to the facilitation of long-range communication. However, the neural network that generates the sensorimotor beta rhythm and the functional significance of this activity have not been fully specified. Thus, I used magnetoencephalography to complete three studies of the beta rhythm in healthy right-handed adults. In the first study, I hypothesized that finger vibration at beta frequencies would generate stimulus-coherent neuronal firing in the neural network that generates the beta rhythm – thus revealing the nodes of this network. Data were analyzed for nineteen subjects (10 females). The coherent activity was revealed using a novel analysis technique that generated whole-brain maps of inter-trial synchrony during passive repetitive finger vibration at 23 Hz. These maps identified contralateral primary somatosensory cortex (SI), posterior parietal cortex, supplementary motor area and primary motor cortex (MI), and ipsilateral brainstem as nodes in the network. In the second study, I correlated changes in focused attention with modulations in beta band cortical responses to specify the functional significance of this activity. Data were analyzed for twelve subjects (7 females). With increased focused attention to the stimulus, I hypothesized that the beta band responses to finger vibration would be enhanced in areas involved in somatosensory processing. A transient increase in the magnitude of beta oscillations in MI (event-related synchronization) following vibration offset was significantly enhanced by attention, as compared to passive stimulation. In addition, attention caused the suppression of beta oscillations (event-related desynchronization, ERD) in ipsilateral SI beginning 1 second prior to vibration offset. Strong attention-modulation of the beta rhythm outside of contralateral SI implies that these changes are indicative of higher-order processing of afferent information. In the third study, I tested the hypothesis that synchrony between beta rhythms in contralateral MI and the relevant muscle supports effective neuronal communication. I correlated changes in task performance with corticomuscular coherence (CMC) during the sustained application of force to match a visually-presented target. Data were analyzed for eighteen subjects (9 females). As predicted, CMC in MI was significantly increased during improved performance in this task. This suggests that central-peripheral synchrony plays an important functional role in sustaining isometric muscle control. Concurrent beta ERD in bilateral SI and primary visual cortices during the contraction indicates the importance of afferent feedback in this task. Gender-related effects were not investigated in these studies. Beta band neuromagnetic responses to movement and somatosensation identify a pervasive neural network that is involved in processing the relevant properties of somatic input and regulating sustained motor output.