Henri Temianka Correspondence; (landfield)

This collection contains material pertaining to the life, career, and activities of Henri Temianka, violin virtuoso, conductor, music teacher, and author. Materials include correspondence, concert programs and flyers, music scores, photographs, and books.https://digitalcommons.chapman.edu/temianka_correspondence/4075/thumbnail.jp

Friend over Foe: Friendship Quality and Chronic Peer Victimization

The present research builds on the extensive literature in the field of peer victimization. Specifically, it examines whether friendship acts as a buffer in the relation between implicit socio-cognitive biases and peer victimization among 82 children ages 9-13. Children completed two implicit measures of victimization in order to detect cognitive biases in socioemotional processing among chronically victimized children. Levels of friendship quality were assessed and shown to have a main effect on peer victimization indices. The emotional Stroop task related negatively to peer victimization, indicating a cognitive avoidance of emotionally-salient stimuli. The IAT and peer victimization were related such that chronic victims displayed greater identification of self as a victim. Implications for various social interventions among these peer groups are discussed

Sensitivity of Neutrino-Driven Core-Collapse Supernova Models to the Microphysical Equation of State

The aim of this dissertation is to explore the sensitivity of neutrino-driven core collapse supernova physics to the microphysical equation of state of the stellar matter. Core collapse supernovae result from the gravitational collapse and ensuing explosion of massive stars. The most fundamental question in core collapse supernova (CCSN) theory is the mechanism of shock revival leading to the observed supernova explosion. The leading scenario is that neutrinos trapped in the proto-neutron star (PNS) during its formation escape and reheat the inner shock, reviving the shockwave, which expands outward, ejecting the star\u27s outer shells into space. Given the central importance of the delayed heating mechanism to the dynamics of CCSNe, detailed studies of the dynamics of the neutrino heating mechanism, neutrino and gravitational wave (GW) signatures, and the dependence on both neutrinomatter interaction rates and the nuclear equation of state (EOS) are needed. The first direct detection of a GW emission from a CCSN would allow for a qualitative investigation into the accuracy of existing nuclear-force models via the EOS. Hence accurate CCSN numerical models are imminently necessary to predict and interpret such GW signatures. A tandem measurement of neutrino signature modulations and GWs would provide direct information about the CCSN mechanism and further our insight into the origins of neutron star rotation and kicks. In order to enhance the computational capability of the ORNL/UTK CCSN simulations, firstly I have developed the capacity to implement different pre-processed state-of- the-art EOS tables in the ORNL/UTK multi-D SN code CHIMERA. I have developed the multi-purpose EOS/Opacity table repository WeakLib for this purpose. Secondly, I have implemented these different EOS in 1D and 2D CHIMERA to study the impact of the EOS on the collapse, bounce, and post-bounce dynamics of the CCSNe explosion, as well as the impact on neutrino emission signals

Method of Protecting Against Neuron Loss

The present invention pertains to a method of protecting against neuron loss in a subject by administering a compound that protects against neuron loss by acting through a vitamin D receptor. Some of these compounds may prevent or retard neuron loss by regulating intraneuronal and/or peripheral calcium and phosphate levels. Other compounds of the invention act through a vitamin D receptor to protect against neuron loss through mechanisms not involving calcium or phosphate regulation. A preferred compound is a biologically active form of vitamin D, a precursor, metabolite, or analog of vitamin D. A preferred form of vitamin D is calcitriol. In another embodiment, the compound is a compound that acts by modulating the biological activity of vitamin D, a precursor, metabolite, or analog of vitamin D. For example, the compound may modulate the biological activity of the vitamin D compound by regulating the amount of the vitamin D compound which is available to protect against neuron loss or it may act by altering the ability of the vitamin D compound to protect against neuron loss. In an alternative embodiment, the compound is a compound that protects against neuron loss through a mechanism similar to that of the vitamin D compound but not involving a vitamin D receptor. The compound is administered to a subject in an amount and over a period of time effective to protect against neuron loss

Neural Network Model for Instruments That Store and Retrieve Sequential Information

A method and design is provided for distributing and storing sets of temporally ordered information in a systematic and sequential fashion. This method is based on a model of how the brain functions in the distribution and storage of temporally ordered memories, but it can also be applied to the design of new biological, electronic or optical devices. These devices may be used in the testing and development of new therapeutic drugs, in the detection of toxic agents or impaired performance, or in the development of new industrial and consumer devices in which the orderly storage of sequential information is important

Method for Storing and Retrieving Sequential Information

A method and design is provided for distributing and storing sets of temporally ordered information in a systematic and sequential fashion. This method is based on a model of how the brain functions in the distribution and storage of temporally ordered memories, but it can also be applied to the design of new biological, electronic or optical devices. These devices may be used in the testing and development of new therapeutic drugs, in the detection of toxic agents or impaired performance, or in the development of new industrial and consumer devices in which the orderly storage of sequential information is important

Expansion of the Calcium Hypothesis of Brain Aging and Alzheimer\u27s Disease: Minding the Store

Evidence accumulated over more than two decades has implicated Ca2+ dysregulation in brain aging and Alzheimer\u27s disease (AD), giving rise to the Ca2+ hypothesis of brain aging and dementia. Electrophysiological, imaging, and behavioral studies in hippocampal or cortical neurons of rodents and rabbits have revealed aging-related increases in the slow afterhyperpolarization, Ca2+ spikes and currents, Ca2+transients, and L-type voltage-gated Ca2+ channel (L-VGCC) activity. Several of these changes have been associated with age-related deficits in learning or memory. Consequently, one version of the Ca2+ hypothesis has been that increased L-VGCC activity drives many of the other Ca2+-related biomarkers of hippocampal aging. In addition, other studies have reported aging- or AD model-related alterations in Ca2+ release from ryanodine receptors (RyR) on intracellular stores. The Ca2+-sensitive RyR channels amplify plasmalemmal Ca2+ influx by the mechanism of Ca2+-induced Ca2+ release (CICR). Considerable evidence indicates that a preferred functional link is present between L-VGCCs and RyRs which operate in series in heart and some brain cells. Here, we review studies implicating RyRs in altered Ca+ regulation in cell toxicity, aging, and AD. A recent study from our laboratory showed that increased CICR plays a necessary role in the emergence of Ca2+-related biomarkers of aging. Consequently, we propose an expanded L-VGCC/Ca2+ hypothesis, in which aging/pathological changes occur in both L-type Ca2+ channels and RyRs, and interact to abnormally amplify Ca2+ transients. In turn, the increased transients result in dysregulation of multiple Ca2+-dependent processes and, through somewhat different pathways, in accelerated functional decline during aging and AD

Expansion of the calcium hypothesis of brain aging and Alzheimer's disease: minding the store

Evidence accumulated over more than two decades has implicated Ca2+ dysregulation in brain aging and Alzheimer's disease (AD), giving rise to the Ca2+ hypothesis of brain aging and dementia. Electrophysiological, imaging, and behavioral studies in hippocampal or cortical neurons of rodents and rabbits have revealed aging-related increases in the slow afterhyperpolarization, Ca2+ spikes and currents, Ca2+ transients, and L-type voltage-gated Ca2+ channel (L-VGCC) activity. Several of these changes have been associated with age-related deficits in learning or memory. Consequently, one version of the Ca2+ hypothesis has been that increased L-VGCC activity drives many of the other Ca2+-related biomarkers of hippocampal aging. In addition, other studies have reported aging- or AD model-related alterations in Ca2+ release from ryanodine receptors (RyR) on intracellular stores. The Ca2+-sensitive RyR channels amplify plasmalemmal Ca2+ influx by the mechanism of Ca2+-induced Ca2+ release (CICR). Considerable evidence indicates that a preferred functional link is present between L-VGCCs and RyRs which operate in series in heart and some brain cells. Here, we review studies implicating RyRs in altered Ca2+ regulation in cell toxicity, aging, and AD. A recent study from our laboratory showed that increased CICR plays a necessary role in the emergence of Ca2+-related biomarkers of aging. Consequently, we propose an expanded L-VGCC/Ca2+ hypothesis, in which aging/pathological changes occur in both L-type Ca2+ channels and RyRs, and interact to abnormally amplify Ca2+ transients. In turn, the increased transients result in dysregulation of multiple Ca2+-dependent processes and, through somewhat different pathways, in accelerated functional decline during aging and AD

Biomarkers for Aging

A statistical and functional correlation strategy to identify changes in cellular pathways specifically linked to impaired cognitive function with aging. Analyses using the strategy identified multiple groups of genes expressed in the hippocampi of mammals, where the genes were expressed at different levels for several ages. The aging changes in expression began before mid-life. Many of the genes were involved in specific neuronal and glial pathways with previously unrecognized relationships to aging and/or cognitive decline. These identified genes and the proteins they encode can be used as novel biomarkers of brain aging and as targets for developing treatment methods against age-related cognitive decline, Alzheimer\u27s Disease and Parkinson\u27s Disease

Method for Analyzing Molecular Expression or Function in an Intact Single Cell

A method for obtaining molecules from a substantially intact single cell is disclosed. The method differs from prior methods that obtain a variable fraction of a cell\u27s contents and therefore cannot quantitatively estimate the number of molecules in the cells. The present method comprises isolating and harvesting a substantially intact single cell from its organ tissue comprising the steps of subjecting a tissue mass to a dissociation method so that the cells are dissociated from the tissue to expose cell bodies or cell processes, contacting a dissociated cell with a device capable of collecting the cell from the tissue substantially intact, withdrawing device with the cell attached, and then isolating or detecting the molecules in the single cell