Nanocrystalline materials could exhibit high mechanical yield strength. Nevertheless, with a high volume fraction in nanocrystalline material, grain boundaries and triple junctions which store a relatively high free energy, are thermally instable which potentially contribute to grain growth. On the other hand, since both grain boundaries and triple junctions are prior sites of impurity enrichment which could in return reduce the triple junction energy, alloys with impurity enriched in grain boundaries and triple junctions are widely applied to stabilize the nanostructures. However, past studies mainly focused on grain boundaries and the kinetic properties of triple junctions and their influences on the thermal stability of nanocrystalline metals is less studied. In this work, triple junction mobility and impurity diffusivity in triple junction are studied by molecular dynamics simulations. Specifically, interface random walk method due to thermal fluctuation which has been widely applied to extract grain boundary mobility is extended to study triple junction motion.

<p>We report on graphene-based Superconductor-Normal metal-Superconductor Joseph- son junctions with contacts made from lead. The high transition temperature of this superconductor allows us to observe the supercurrent branch at temperatures up to &#1113094; 2 K. We are able to detect a small, but non-zero, resistance despite the Josephson junctions being in the superconducting state. We attribute this resistance to the phase diffusion regime, which has not been yet identified in graphene. By measuring the resistance as a function of temperature and gate voltage, we can further charac- terize the nature of electromagnetic environment and dissipation in our samples. In addition we modulate the critical current through grapehene by an external magnetic field; the resulting Fraunhofer interference pattern shows several periods of oscilla- tions. However, deviations from the perfect Fraunhofer pattern are observed, and their cause is explained by a simulation that takes into account the sample design.</p> / Dissertation

<p>The development and function of the nervous system relies on complex regulation of gene expression programs. MicroRNAs (miRNAs) are small RNAs that have diverse functions in mammalian development and disease. In concert with the RNA-induced silencing complex, miRNAs repress translation by binding to target mRNAs. The nervous system contains the largest proportion of miRNAs, yet few have been functionally characterized <italic>in vivo</italic>. </p><p>miR-133b is a highly conserved miRNA embedded in the sequence of 7H4, a noncoding RNA that is enriched at the neuromuscular junction (NMJ), a large synapse that is essential for eliciting muscle contraction and movement. I have found that, like 7H4, miR-133b expression is enriched at the NMJ and upregulated postnatally, coinciding with important events in synaptic maturation, including synaptic growth and elimination. Knockdown of miR-133b in postnatal muscle by electroporation of modified antisense oligonucleotides gave rise to abnormally large synapses, indicating a role for miR-133b in synaptic maturation. To specifically remove miR-133b <italic>in vivo</italic>, I generated a mouse containing a targeted deletion of the miR-133b stemloop. NMJ maturation and synapse elimination proceeded normally in miR-133b knockout mice, suggesting that miR-133b may have other functions at the synapse. The expression of 7H4 and miR-133b is upregulated following nerve transection, consistent with a role in synaptic regeneration. Indeed, NMJ reinnervation is delayed in miR-133b KO mice following nerve crush, but not nerve cut. These data suggest that miR-133b may have a specific protective function at the synapse that could be relevant to disease states, including amyotrophic lateral sclerosis (ALS), where NMJ denervation occurs following motor neuron cell death. However, loss of miR-133b did not affect survival or disease progression in the SOD1(G93A) mouse model, differentiating its role from that of miR-206, another miRNA found in 7H4.</p><p>miR-133b has recently been proposed to regulate the development and maintenance of midbrain dopaminergic (mDA) neurons. mDA neurons have critical functions in the control of movement and emotion, and their degeneration leads to motor and cognitive defects in Parkinson's disease. miR-133b is enriched in the midbrain and regulates mDA neuron differentiation <italic>in vitro</italic> by targeting Pitx3, a transcription factor required for appropriate development of substantia nigra DA neurons. However, the function of miR-133b in the intact midbrain has not been determined. miR-133b KO mice have normal numbers of midbrain dopaminergic neurons during development and aging. Moreover, dopamine neurotransmitter levels are unchanged in the striatum and other brain regions, while expression of dopaminergic genes including Pitx3 is also unaffected. Finally, miR-133b null mice display normal motor coordination and activity, suggesting that miR-133b does not play a significant role in the development or maintenance of the mDA neuron population.</p> / Dissertation

The cytoskeletal component of the muscle membrane, dystrophin and its associated proteins (DAPs), are essential for the maintenance of muscle integrity, since the absence of these molecules results in a variety of muscular dystrophies. The purpose of this work was to create and characterize monoclonal antibodies (mAbs) designed to recognize components of the DAP complex (DAPC), in order to provide tools for the study of its structure and function. / The first mAb generated, 1137, was raised against a 33 amino acid sequence of the core protein at the c-terminus of alpha-dystroglycan (alpha DG), a cell surface member of the DAPC linked to dystrophin via its co-transcript, the transmembrane protein, beta-dystroglycan. 1B7 was used to perform a comparative study in denervated rat muscle tissue in parallel with IIH6, a mAb which recognizes a different, more glycosylated form of alpha DG. The second and third mAbs were raised against a complex of proteins purified by succinylated Wheat Germ Agglutinin (sWGA) following extraction from rabbit skeletal muscle. (Abstract shortened by UMI.)

国立情報学研究所で電子化したコンテンツを使用している。

Thesis (Ph. D.)--University of Alabama at Birmingham, 2007. / Title from first page of PDF file (viewed Feb. 6, 2008). Includes bibliographical references (p. 81-92).

Heidelberg, Univ., Diss., 2008.

Thesis (M. Phil.)--Hong Kong University of Science and Technology, 2004. / Includes bibliographical references (leaves 102-115). Also available in electronic version. Access restricted to campus users.

Thesis (Ph. D.)--University of Texas at Austin, 1999. / Vita. Includes bibliographical references (leaves 110-117). Available also in a digital version from Dissertation Abstracts.

Includes bibliographical references (p. 100-114).