The representation of metric information in scenes

Four experiments were conducted that investigated the role of metric information in the identification and episodic recognition of scenes. A fifth experiment examined whether scene identification showed any hemispheric advantage. For scene identification, a priming paradigm was used in which participants were required to identify scenes that were identical, that changed size, or that changed location in the visual field relative to a previously viewed scene. For episodic recognition, participants were required to indicate whether a scene had been viewed previously while ignoring any changes in size or position. The results found a reduced identification or episodic recognition advantage for previously viewed scenes that had changed their size or position in the visual field relative to scenes that were identical to one viewed previously. In addition, no evidence of laterality was found. The results challenge the notion that scenes are treated in the same way by the visual system as objects or faces

A Combined Limit on the Neutrino Mass from Neutrinoless Double-Beta Decay and Constraints on Sterile Majorana Neutrinos

We present a framework to combine data from the latest neutrinoless double-beta decay experiments for multiple isotopes and derive a limit on the effective neutrino mass using the experimental energy distributions. The combined limits on the effective mass range between 130-310 meV, where the spread is due to different model calculations of nuclear matrix elements (NMEs). The statistical consistency (p values) between this result and the signal observation claimed by the Heidelberg-Moscow experiment is derived. The limits on the effective mass are also evaluated in a (3+1) sterile neutrino model, assuming all neutrinos are Majorana particles.Comment: 8 pages, 8 figures. Version accepted by Phys Rev D, including latest CUORE-0 result

Online Education and Contingent Faculty: An Exploratory Analysis of Issues and Challenges for Higher Education Administrators (Perspectives on Online Education)

With the growth of the popularity and accessibility of online courses, higher education administrators are under tremendous pressure to keep pace with rapidly evolving conditions related to online learning

Susceptibility of Mutant SOD1 to Form a Destabilized Monomer Predicts Cellular Aggregation and Toxicity but Not In vitro Aggregation Propensity

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the rapid and progressive degeneration of upper and lower motor neurons in the spinal cord, brain stem and motor cortex. The first gene linked to ALS was the gene encoding the free radical scavenging enzyme superoxide dismutase-1 (SOD1) that currently has over 180, mostly missense, ALS-associated mutations identified. SOD1-associated fALS patients show remarkably broad mean survival times (~17 years death post-diagnosis) that are mutation dependent. A hallmark of SOD1-associated ALS is the deposition of SOD1 into large insoluble aggregates in motor neurons. This is thought to be a consequence of mutation induced structural destabilization and/or oxidative damage leading to the misfolding and aggregation of SOD1 into a neurotoxic species. Here we aim to understand the relationship between SOD1 variant toxicity, structural stability, and aggregation propensity using a combination of cell culture and purified protein assays. Cell based assays indicated that aggregation of SOD1 variants correlate closely to cellular toxicity. However, the relationship between cellular toxicity and disease severity was less clear. We next utilized mass spectrometry to interrogate the structural consequences of metal loss and disulfide reduction on fALS-associated SOD1 variant structure. All variants showed evidence of unfolded, intermediate, and compact conformations, with SOD1G37R, SOD1G93A and SOD1V148G having the greatest abundance of intermediate and unfolded SOD1. SOD1G37R was an informative outlier as it had a high propensity to unfold and form oligomeric aggregates, but it did not aggregate to the same extent as SOD1G93A and SOD1V148G in in vitro aggregation assays. Furthermore, seeding the aggregation of DTT/EDTA-treated SOD1G37R with preformed SOD1G93A fibrils elicited minimal aggregation response, suggesting that the arginine substitution at position-37 blocks the templating of SOD1 onto preformed fibrils. We propose that this difference may be explained by multiple strains of SOD1 aggregate and this may also help explain the slow disease progression observed in patients with SOD1G37R

Blight Remediation and Affordable Housing Finance: A Potential Future Model for Hartford Homeownership

This report is designed to aid the Hartford Land Bank (HLB) in its efforts to remediate blight as well as lay the groundwork for a more frictionless path to homeownership for residents in the City of Hartford. Over the course of the semester, the team has conducted research and analysis on various models and state funding systems that could increase property ownership among city residents. In collaboration with the HLB and Cleveland Housing Network (CHN), the team has focused on existing rent-to-own (RTO) and lease-purchase models of homeownership with decades of high success rate

Susceptibility of mutant SOD1 to form a destabilized monomer predicts cellular aggregation and toxicity but not in vitro aggregation propensity

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the rapid and progressive degeneration of upper and lower motor neurons in the spinal cord, brain stem and motor cortex. The first gene linked to ALS was the gene encoding the free radical scavenging enzyme superoxide dismutase-1 (SOD1) that currently has over 180, mostly missense, ALS-associated mutations identified. SOD1-associated fALS patients show remarkably broad mean survival times (~17 years death post-diagnosis) that are mutation dependent. A hallmark of SOD1-associated ALS is the deposition of SOD1 into large insoluble aggregates in motor neurons. This is thought to be a consequence of mutation induced structural destabilization and/or oxidative damage leading to the misfolding and aggregation of SOD1 into a neurotoxic species. Here we aim to understand the relationship between SOD1 variant toxicity, structural stability, and aggregation propensity using a combination of cell culture and purified protein assays. Cell based assays indicated that aggregation of SOD1 variants correlate closely to cellular toxicity. However, the relationship between cellular toxicity and disease severity was less clear. We next utilized mass spectrometry to interrogate the structural consequences of metal loss and disulfide reduction on fALS-associated SOD1 variant structure. All variants showed evidence of unfolded, intermediate, and compact conformations, with SOD1G37R, SOD1G93A and SOD1V148G having the greatest abundance of intermediate and unfolded SOD1. SOD1G37R was an informative outlier as it had a high propensity to unfold and form oligomeric aggregates, but it did not aggregate to the same extent as SOD1G93A and SOD1V148G in in vitro aggregation assays. Furthermore, seeding the aggregation of DTT/EDTA-treated SOD1G37R with preformed SOD1G93A fibrils elicited minimal aggregation response, suggesting that the arginine substitution at position-37 blocks the templating of SOD1 onto preformed fibrils. We propose that this difference may be explained by multiple strains of SOD1 aggregate and this may also help explain the slow disease progression observed in patients with SOD1G37R