Graduate Student Seminar Scheduled for February 11

The Spring 2009 Beckman Institute Graduate Student Seminar series begins on Wednesday, February 11. The seminar will feature three short talks from graduate students Andrew R. Hamilton, Agatha E. Luszpak, and Justin Haldar. The seminar will be held in Beckman Institute Room 1005 and a pizza lunch will be served.

The Beckman Institute Graduate Student Seminar Series presents the work of outstanding graduate students working in Beckman research groups. The seminar starts at Noon in Beckman Institute Room 1005 and is open to the public. Lunch will be served.

Self-Healing in Epoxy-Matrix Microvascular Networks
Andrew R. Hamilton

Epoxy-Matrix Microvascular Networks

Healing in biological systems is accomplished by a pervasive vascular network that supplies the necessary biochemical components. Recent advances in soft lithographic and direct-write assembly methods have enabled the creation of materials with complex embedded microvascular networks that emulate many of the key responses of biological vascular systems. Toohey et al. have applied this concept to heal crack damage in a brittle coating on a ductile substrate.  Healing agent is delivered to cracks in the coating via a three-dimensional microvascular network embedded in the substrate, which remains undamaged.  In the current work, we explore the interaction of cracks with the microvascular network and the ability to repeatedly heal the damaged network in-situ.  A testing protocol based on the double cleavage drilled compression (DCDC) fracture specimen geometry is adopted to induce stable crack growth through a microvascular network of channels containing the sequestered components of a two-part epoxy system.  When released into the crack plane, the two components mix and cure, forming a bond between the crack faces.  We demonstrate recovery of over 100% of the virgin fracture toughness and as many as 10 healing cycles in a thermosetting epoxy matrix material.

Analysis of neuropeptide release in fragile X syndrome
Agatha E. Luszpak

Fragile X syndrome (FXS) is the most prevalent cause of inherited mental retardation with an incidence of 1/8000 in females and 1/3000-1/4000 in males. A single mutation in the fragile X mental retardation gene (Fmr1) causes a lack of fragile x mental retardation protein (FMRP). FMRP, most abundant in brain tissue, binds select mRNAs and regulates their transport and translation. Deficits associated with FXS are mental retardation, attention deficit, hyperactivity, and autism. Here, the first report of impaired vesicle release machinery in the Fmr1 KO mouse is presented. Rab3A, an mRNA cargo of FMRP involved in the docking and fusion of vesicles, is reduced by ~50% in Fmr1 KO synaptoneurosomes. In addition, the number of neuropeptide-housing dense-core vesicles (DCVs) is reduced in Fmr1 KO mice. Using mass spectrometry, a large decrease in peptide release is observed from both synaptoneurosomes and brain slices in Fmr1 KO mice compared to wild-type mice, for a surprisingly broad suite of neuropeptides. It is speculated that some deficits associated with FXS may reflect impaired peptide release due to faulty vesicle release mechanisms, leading to deficits in maturation and maintenance of synapses and dendritic spines.

Anatomically-Constrained Multi-Modal MR Neuroimaging
Justin Haldar

Multi-Modal MR Neuroimaging

Magnetic Resonance Imaging (MRI) can be used to probe the structure and function of biological tissues from a variety of different perspectives.  However, because of low sensitivity, many of these experiments have been limited due to inherent trade-offs between data acquisition time, signal-to-noise ratio, and resolution.  This talk will discuss a new scheme for MRI data acquisition and image reconstruction, which leverages the strong correlations found between different neuroimaging modalities to enable faster and more efficient experiments.  We will demonstrate applications to metabolic mapping and to identifying white-matter connectivity in the brain.