SB30-10/11: Federal Pell Grants

SB30-10/11: Federal Pell Grants. This resolution passed 12Y-8N on a roll call vote during the March 23, 2011 meeting of the Associated Students of the University of Montana (ASUM)

Parallel Mechanism with Large Joint Clearances for Precise Motion

Final report and prototype photo for Project 17 of ME450, Fall 2009 semester.This project aims to build a planar parallel mechanism with three degrees of freedom, whose motion is controlled by linear motors. The platform will be subjected to an external force, and will be indicated by markers that will be used to calculate the accuracy of its motion, by means of a camera. Strain gauges will be integrated on the links, in order to know the forces along them.Yoram Koren (Mechanical Engineering, U of M); ERC-RMS (U of M)http://deepblue.lib.umich.edu/bitstream/2027.42/86208/1/ME450 Fall2009 Final Report - Project 17 - Parallel Mechanism with Large Joint Clearances for Precise Motion.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/86208/2/ME450 Fall2009 Prototype Photo - Project 17 - Parallel Mechanism with Large Joint Clearances for Precise Motion.jp

Chemical inertness of UV-cured optical elastomers within the printed circuit board manufacturing process for embedded waveguide applications

Embedding polymer optical waveguides (WGs) into printed circuit boards (PCBs) for intra-board or board-to-board high speed data communications requires polymer materials that are compatible and inert when exposed to common PCB manufacturing processes. Ensuring both WG functionality after chemical exposure and maintaining PCB manufacturing integrities within the production process is crucial for successful implementation. The PCB manufacturing flow is analyzed to expose major requirements that would be required for the successful implementation of polymer materials for embedded WG development. Chemical testing and analysis were performed on Dow Corning ® OE-4140 UV-Cured Optical Elastomer Core and Dow Corning® OE-4141 UV-Cured Optical Elastomer Cladding which are designed for low loss embedded optical WGs. Contamination testing was conducted to demonstrate polymer compatibility in both cured and uncured form. Various PCB chemicals were treated with uncured polymer material and tested for effective contamination. Fully polymerized multimode WGs were fabricated and exposed to PCB chemicals at temperatures and durations comparable to PCB manufacturing conditions. Chemical analysis shows that the chosen polymer is compatible and inert with most common PCB manufacturing processes. © 2014 SPIE

Two Hypomorphic Alleles of Mouse Ass1 as a New Animal Model of Citrullinemia Type I and Other Hyperammonemic Syndromes

Citrullinemia type I (CTLN1, OMIM# 215700) is an inherited urea cycle disorder that is caused by an argininosuccinate synthetase (ASS) enzyme deficiency. In this report, we describe two spontaneous hypomorphic alleles of the mouse Ass1 gene that serve as an animal model of CTLN1. These two independent mouse mutant alleles, also described in patients affected with CTLN1, interact to produce a range of phenotypes. While some mutant mice died within the first week after birth, others survived but showed severe retardation during postnatal development as well as alopecia, lethargy, and ataxia. Notable pathological findings were similar to findings in human CTLN1 patients and included citrullinemia and hyperammonemia along with delayed cerebellar development, epidermal hyperkeratosis, and follicular dystrophy. Standard treatments for CTLN1 were effective in rescuing the phenotype of these mutant mice. Based on our studies, we propose that defective cerebellar granule cell migration secondary to disorganization of Bergmann glial cell fibers cause cerebellar developmental delay in the hyperammonemic and citrullinemic brain, pointing to a possible role for nitric oxide in these processes. These mouse mutations constitute a suitable model for both mechanistic and preclinical studies of CTLN1 and other hyperammonemic encephalopathies and, at the same time, underscore the importance of complementing knockout mutations with hypomorphic mutations for the generation of animal models of human genetic diseases