Adolescent Literacy in the Common Core Classroom

This project focuses on the advantages of utilizing reading fluency assessments and targeted reading instruction in adolescent language arts classrooms. Typically, as students progress beyond about sixth grade, many teachers do not continue to instruct and assess students specifically on their reading fluency; however, research shows that continuing to focus on these skills is beneficial to students, especially with the increased pressures for students to be college and career ready from forces such as the Common Core State Standards. Learning to read is a skill that grows as students grow - the data in this project shows that when students are encouraged to continue to learn to read as well as read to learn, students can make great improvements in their reading ability in a single year

ENG 3140: The Post-Colonial Nature of Disney: The Ruining of a Childhood

Savages, savages! scream the English colonizers at the Native Americans in the Disney film, Pocahontas. This quote exemplifies the postcolonial tensions that are present in several of Disney\u27s movies. However, the characters in Disney movies tend to be romanticized. Thus, we judged that Disney\u27s children\u27s characters were the perfect basis for our Post-Colonial video. The princesses we chose to look at were Ariel (and Ursula), Jasmine, Pocahontas, Cinderella, and Rapunzel (with focus on Mother Gothel). Each of these princesses had their own cultures and were oppressed by a colonizer, either literally or figuratively. Yet, the classic Disney movies glossed over this colonization in favor of a romantic, happy-ending plot. By creating song parodies of each princess\u27s song, we highlighted the already existing colonial nature of the movies, while also connecting to the post-colonial literature read in class

Landslide-dammed paleolake perturbs marine sedimentation and drives genetic change in anadromous fish

Large bedrock landslides have been shown to modulate rates and processes of river activity by forming dams, forcing upstream aggradation of water and sediment, and generating catastrophic outburst floods. Less apparent is the effect of large landslide dams on river ecosystems and marine sedimentation. Combining analyses of 1-m resolution topographic data (acquired via airborne laser mapping) and field investigation, we present evidence for a large, landslide-dammed paleolake along the Eel River, CA. The landslide mass initiated from a high-relief, resistant outcrop which failed catastrophically, blocking the Eel River with an approximately 130-m-tall dam. Support for the resulting 55-km-long, 1.3-km^3 lake includes subtle shorelines cut into bounding terrain, deltas, and lacustrine sediments radiocarbon dated to 22.5 ka. The landslide provides an explanation for the recent genetic divergence of local anadromous (ocean-run) steelhead trout (Oncorhynchus mykiss) by blocking their migration route and causing gene flow between summer run and winter run reproductive ecotypes. Further, the dam arrested the prodigious flux of sediment down the Eel River; this cessation is recorded in marine sedimentary deposits as a 10-fold reduction in deposition rates of Eel-derived sediment and constitutes a rare example of a terrestrial event transmitted through the dispersal system and recorded offshore

Expanding Coverage Initiatives: 2015-2016 Evaluation Report

This report from the Missouri Foundation for Health Expanding Coverage Initiative describes external evaluation findings for year five of the evaluation which covers the time period of August 1, 2015 to July 31, 2016.https://openscholarship.wustl.edu/cphss/1093/thumbnail.jp

Loss of Mitochondrial Ndufs4 in Striatal Medium Spiny Neurons Mediates Progressive Motor Impairment in a Mouse Model of Leigh Syndrome

Inability of mitochondria to generate energy leads to severe and often fatal myoencephalopathies. Among these, Leigh syndrome (LS) is one of the most common childhood mitochondrial diseases; it is characterized by hypotonia, failure to thrive, respiratory insufficiency and progressive mental and motor dysfunction, leading to early death. Basal ganglia nuclei, including the striatum, are affected in LS patients. However, neither the identity of the affected cell types in the striatum nor their contribution to the disease has been established. Here, we used a mouse model of LS lacking Ndufs4, a mitochondrial complex I subunit, to confirm that loss of complex I, but not complex II, alters respiration in the striatum. To assess the role of striatal dysfunction in the pathology, we selectively inactivated Ndufs4 in the striatal medium spiny neurons (MSNs), which account for over 95% of striatal neurons. Our results show that lack of Ndufs4 in MSNs causes a non-fatal progressive motor impairment without affecting the cognitive function of mice. Furthermore, no inflammatory responses or neuronal loss were observed up to 6 months of age. Hence, complex I deficiency in MSNs contributes to the motor deficits observed in LS, but not to the neural degeneration, suggesting that other neuronal populations drive the plethora of clinical signs in LS

Bioenergetic Phenotyping of DEN-Induced Hepatocellular Carcinoma Reveals a Link Between Adenylate Kinase Isoform Expression and Reduced Complex I-Supported Respiration

Hepatocellular carcinoma (HCC) is the most common form of liver cancer worldwide. Increasing evidence suggests that mitochondria play a central role in malignant metabolic reprogramming in HCC, which may promote disease progression. To comprehensively evaluate the mitochondrial phenotype present in HCC, we applied a recently developed diagnostic workflow that combines high-resolution respirometry, fluorometry, and mitochondrial-targeted nLC-MS/MS proteomics to cell culture (AML12 and Hepa 1-6 cells) and diethylnitrosamine (DEN)-induced mouse models of HCC. Across both model systems, CI-linked respiration was significantly decreased in HCC compared to nontumor, though this did not alter ATP production rates. Interestingly, CI-linked respiration was found to be restored in DEN-induced tumor mitochondria through acute in vitro treatment with P1, P5-di(adenosine-5′) pentaphosphate (Ap5A), a broad inhibitor of adenylate kinases. Mass spectrometry-based proteomics revealed that DEN-induced tumor mitochondria had increased expression of adenylate kinase isoform 4 (AK4), which may account for this response to Ap5A. Tumor mitochondria also displayed a reduced ability to retain calcium and generate membrane potential across a physiological span of ATP demand states compared to DEN-treated nontumor or saline-treated liver mitochondria. We validated these findings in flash-frozen human primary HCC samples, which similarly displayed a decrease in mitochondrial respiratory capacity that disproportionately affected CI. Our findings support the utility of mitochondrial phenotyping in identifying novel regulatory mechanisms governing cancer bioenergetics

Bioenergetic Phenotyping of DEN-Induced Hepatocellular Carcinoma Reveals a Link Between Adenylate Kinase Isoform Expression and Reduced Complex I-Supported Respiration

Hepatocellular carcinoma (HCC) is the most common form of liver cancer worldwide. Increasing evidence suggests that mitochondria play a central role in malignant metabolic reprogramming in HCC, which may promote disease progression. To comprehensively evaluate the mitochondrial phenotype present in HCC, we applied a recently developed diagnostic workflow that combines high-resolution respirometry, fluorometry, and mitochondrial-targeted nLC-MS/MS proteomics to cell culture (AML12 and Hepa 1-6 cells) and diethylnitrosamine (DEN)-induced mouse models of HCC. Across both model systems, CI-linked respiration was significantly decreased in HCC compared to nontumor, though this did not alter ATP production rates. Interestingly, CI-linked respiration was found to be restored in DEN-induced tumor mitochondria through acute in vitro treatment with P1, P5-di(adenosine-5′) pentaphosphate (Ap5A), a broad inhibitor of adenylate kinases. Mass spectrometry-based proteomics revealed that DEN-induced tumor mitochondria had increased expression of adenylate kinase isoform 4 (AK4), which may account for this response to Ap5A. Tumor mitochondria also displayed a reduced ability to retain calcium and generate membrane potential across a physiological span of ATP demand states compared to DEN-treated nontumor or saline-treated liver mitochondria. We validated these findings in flash-frozen human primary HCC samples, which similarly displayed a decrease in mitochondrial respiratory capacity that disproportionately affected CI. Our findings support the utility of mitochondrial phenotyping in identifying novel regulatory mechanisms governing cancer bioenergetics

Controlled microdroplet transport in an atmospheric pressure microplasma

We report the controlled injection of near-isolated micron-sized liquid droplets into a low temperature He-Ne steady-state rf plasma at atmospheric pressure. The H2O droplet stream is constrained within a 2 mm diameter quartz tube. Imaging at the tube exit indicates a log-normal droplet size distribution with an initial count mean diameter of 15 micrometers falling to 13 micrometers with plasma exposure. The radial velocity profile is approximately parabolic indicating near laminar flow conditions with the majority of droplets travelling at >75% of the local gas speed and having a plasma transit time of < 100 microseconds. The maximum gas temperature, determined from nitrogen spectral lines, was below 400 K and the observed droplet size reduction implies additional factors beyond standard evaporation, including charge and surface chemistry effects. The successful demonstration of controlled microdroplet streams opens up possibilities for gas-phase microreactors and remote delivery of active species for plasma medicine