Longitudinal and Transverse Response Functions in ^(56)Fe(e,e') at Momentum Transfer near 1 GeV/c

Inclusive electron-scattering cross sections have been measured for ^(56)Fe in the quasielastic region at electron energies between 0.9 and 4.3 GeV, at scattering angles of 15° and 85°. Longitudinal and transverse response functions at a q of 1.14 GeV/c have been extracted using a Rosenbluth separation. The experimental Coulomb sum has been obtained with aid of an extrapolation. The longitudinal response function, after correction for Coulomb distortion, is lower than quasifree-scattering-model predictions at the quasielastic peak and on the high-ω side

The Cowl - v.10 - n.5 - Nov 5, 1947

The Cowl - student newspaper of Providence College. Volume 10, Number 5 - Nov 5, 1947. 6 pages

Concerning Stephen Hawking’s Claim that Philosophy is Dead

The article begins from Stephen Hawking's well-known claim that philosophy is dead, and considers several other quotations in which philosophy is either belittled or subordinated outright to the natural sciences. This subordination requires a downward reductionism that is paralleled by the upward reductionism of the linguistic turn and social constructionist theories. Rather than undermining or overmining mid-sized individual entities, philosophy must deal with objects on their own terms. This suggests a possible tactical alliance between philosophy and the arts

The Cowl - v.13 - n.7 - Nov 15, 1950

The Cowl - student newspaper of Providence College. Volume 13, Number 7 - November 15, 1950. 6 pages

Characterization of the Small RNA Transcriptome of the Marine Coccolithophorid, Emiliania huxleyi

Small RNAs (smRNAs) control a variety of cellular processes by silencing target genes at the transcriptional or post-transcription level. While extensively studied in plants, relatively little is known about smRNAs and their targets in marine phytoplankton, such as Emiliania huxleyi (E. huxleyi). Deep sequencing was performed of smRNAs extracted at different time points as E. huxleyi cells transition from logarithmic to stationary phase growth in batch culture. Computational analyses predicted 18 E. huxleyi specific miRNAs. The 18 miRNA candidates and their precursors vary in length (18-24 nt and 71-252 nt, respectively), genome copy number (3-1,459), and the number of genes targeted (2-107). Stem-loop real time reverse transcriptase (RT) PCR was used to validate miRNA expression which varied by nearly three orders of magnitude when growth slows and cells enter stationary phase. Stem-loop RT PCR was also used to examine the expression profiles of miRNA in calcifying and non-calcifying cultures, and a small subset was found to be differentially expressed when nutrients become limiting and calcification is enhanced. In addition to miRNAs, endogenous small RNAs such as ra-siRNAs, ta-siRNAs, nat-siRNAs, and piwiRNAs were predicted along with the machinery for the biogenesis and processing of si-RNAs. This study is the first genome-wide investigation smRNAs pathways in E. huxleyi. Results provide new insights into the importance of smRNAs in regulating aspects of physiological growth and adaptation in marine phytoplankton and further challenge the notion that smRNAs evolved with multicellularity, expanding our perspective of these ancient regulatory pathways

Computational modelling of molecular nexopathies

Neurodegenerative diseases are an ever-increasing health problem, requiring substantial human and financial resources. They are caused by pathogenic proteins, which accumulate and spread in the brain's neural network, causing neuronal loss and brain atrophy. However, the mechanisms that govern pathogenic protein accumulation, spread, and toxic effects are still poorly understood, and many competing hypotheses regarding them have been presented by researchers. A better understanding of these mechanisms can help inform which hypotheses are more likely to be true, improve prognosis tools, and assist in drug development. Clinically, brain atrophy follows specific spatiotemporal patterns in each neurodegenerative disease, and each disease is linked to specific pathogenic proteins. This observation led to the `molecular nexopathies' hypothesis, which states that clinical phenotypes can be predicted if the specific pathogenic protein variant and the neural network characteristics are both known. However, little computational work has been done that links pathogenic protein mechanisms, the brain's neural network, and clinical phenotypes. In this thesis, I developed computational models for a variety of hypotheses regarding pathogenic protein mechanisms of accumulation, spread, and toxic effects on the brain, which occur at the neuronal scale, while linking them to neuroimaging data, which is acquired at the brain scale. After running simulations with the modelled mechanisms within a neural network, I compared simulation results over time against empirical data for Alzheimer's disease and three genetic variants of frontotemporal dementia. For each disease, the model that best fitted its atrophy progression was found, discovering differences among diseases with regards to what degree each mechanism played a role. I also analysed how each mechanism affected disease progression, discovered each disease's seed location, and found mechanisms that showed potential as candidate targets for therapies, in particular, increasing the firing frequency of neurons

Vision during manned booster operation Final report

Retinal images and accomodation control mechanism under conditions of space flight stres