Ground Water Contamination: What You Need to Know

14 pages. Contains references

Ground Water Contamination: What You Need to Know

14 pages. Contains references

Specific yield by geophysical logging potential for the Denver basin

Research project technical completion report.Project A-052-COLO, agreement no. 14-34-0001-1106, 14-34-0001-2106; partially funded by the U.S. Dept. of the Interior as authorized by the Water Research and Development Act of 1978

Infiltration affected by flow of air

May 1971.Bibliography: pages 31-32

Salt transport in soil profiles with application to irrigation return flow: the dissolution and transport of gypsum in soils

Submitted to Office of Water Research and Technology.Bibliography: pages 85-88.January 1976.Experimental information on the dissolution of gypsum and the subsequent transport of the dissolved species in a soil-water system was obtained by measuring the calcium concentration in the solution phase as a function of time at different positions in columns filled with a soil-gypsum mixture that were leached with distilled water. These gypsum leaching experiments were performed with two different soils for a range of flow rates of the solution phase, solution contents and particle sizes of the gypsum material. The measured concentration-time curves were compared with results from two models, the first based on equilibrium chemical principles and the mixing cell concept and a second based on the one-dimensional convection-dispersion equation combined with a first-order kinetic rate equation describing the gypsum dissolution process. The formulation of the rate equation was based on the hypothesis that the rate of dissolution was proportional to the product of the saturation deficit and a function of the mass of gypsum present in the system. The equations in the kinetic model were solved numerically and a graphical and an optimization procedure were used to determine those values of the kinetic parameters for which the best possible agreement was obtained between the measured concentration-time curves and curves calculated from the kinetic model. It was concluded from the comparison between the experimental data, the mixing cell model and the kinetic model that the dissolution reaction of the gypsum was time dependent and was not controlled by the solubility product relationship, as assumed in the mixing cell model. The qualitative agreement between the kinetic model and the experimental results seems to support the hypothesis used in the formulation of the rate equation.OWRT Project no. A-017-COLO; supported (in part) by funds provided by the U. S. Department of the Interior, Office of Water Research and Technology, as authorized by the Water Resources Research Act of 1964 and pursuant to Grant Agreement Nos. 14-31-0001-3806, 14-31-0001-4006, and 14-31-0001-5006

Introductory programming: a systematic literature review

As computing becomes a mainstream discipline embedded in the school curriculum and acts as an enabler for an increasing range of academic disciplines in higher education, the literature on introductory programming is growing. Although there have been several reviews that focus on specific aspects of introductory programming, there has been no broad overview of the literature exploring recent trends across the breadth of introductory programming. This paper is the report of an ITiCSE working group that conducted a systematic review in order to gain an overview of the introductory programming literature. Partitioning the literature into papers addressing the student, teaching, the curriculum, and assessment, we explore trends, highlight advances in knowledge over the past 15 years, and indicate possible directions for future research

Modeling Spinal Muscular Atrophy in Drosophila

Spinal Muscular Atrophy (SMA), a recessive hereditary neurodegenerative disease in humans, has been linked to mutations in the survival motor neuron (SMN) gene. SMA patients display early onset lethality coupled with motor neuron loss and skeletal muscle atrophy. We used Drosophila, which encodes a single SMN ortholog, survival motor neuron (Smn), to model SMA, since reduction of Smn function leads to defects that mimic the SMA pathology in humans. Here we show that a normal neuromuscular junction (NMJ) structure depends on SMN expression and that SMN concentrates in the post-synaptic NMJ regions. We conducted a screen for genetic modifiers of an Smn phenotype using the Exelixis collection of transposon-induced mutations, which affects approximately 50% of the Drosophila genome. This screen resulted in the recovery of 27 modifiers, thereby expanding the genetic circuitry of Smn to include several genes not previously known to be associated with this locus. Among the identified modifiers was wishful thinking (wit), a type II BMP receptor, which was shown to alter the Smn NMJ phenotype. Further characterization of two additional members of the BMP signaling pathway, Mothers against dpp (Mad) and Daughters against dpp (Dad), also modify the Smn NMJ phenotype. The NMJ defects caused by loss of Smn function can be ameliorated by increasing BMP signals, suggesting that increased BMP activity in SMA patients may help to alleviate symptoms of the disease. These results confirm that our genetic approach is likely to identify bona fide modulators of SMN activity, especially regarding its role at the neuromuscular junction, and as a consequence, may identify putative SMA therapeutic targets

Conserved Genes Act as Modifiers of Invertebrate SMN Loss of Function Defects

Spinal Muscular Atrophy (SMA) is caused by diminished function of the Survival of Motor Neuron (SMN) protein, but the molecular pathways critical for SMA pathology remain elusive. We have used genetic approaches in invertebrate models to identify conserved SMN loss of function modifier genes. Drosophila melanogaster and Caenorhabditis elegans each have a single gene encoding a protein orthologous to human SMN; diminished function of these invertebrate genes causes lethality and neuromuscular defects. To find genes that modulate SMN function defects across species, two approaches were used. First, a genome-wide RNAi screen for C. elegans SMN modifier genes was undertaken, yielding four genes. Second, we tested the conservation of modifier gene function across species; genes identified in one invertebrate model were tested for function in the other invertebrate model. Drosophila orthologs of two genes, which were identified originally in C. elegans, modified Drosophila SMN loss of function defects. C. elegans orthologs of twelve genes, which were originally identified in a previous Drosophila screen, modified C. elegans SMN loss of function defects. Bioinformatic analysis of the conserved, cross-species, modifier genes suggests that conserved cellular pathways, specifically endocytosis and mRNA regulation, act as critical genetic modifiers of SMN loss of function defects across species

Self-oligomerization regulates stability of survival motor neuron protein isoforms by sequestering an SCF^Slmb degron

Spinal muscular atrophy (SMA) is caused by homozygous mutations in human SMN1. Expression of a duplicate gene (SMN2) primarily results in skipping of exon 7 and production of an unstable protein isoform, SMNΔ7. Although SMN2 exon skipping is the principal contributor to SMA severity, mechanisms governing stability of survival motor neuron (SMN) isoforms are poorly understood. We used a Drosophila model system and label-free proteomics to identify the SCFSlmb ubiquitin E3 ligase complex as a novel SMN binding partner. SCFSlmb interacts with a phosphor degron embedded within the human and fruitfly SMN YG-box oligomerization domains. Substitution of a conserved serine (S270A) interferes with SCFSlmb binding and stabilizes SMNΔ7. SMA-causing missense mutations that block multimerization of full-length SMN are also stabilized in the degron mutant background. Overexpression of SMNΔ7S270A, but not wild-type (WT) SMNΔ7, provides a protective effect in SMA model mice and human motor neuron cell culture systems. Our findings support a model wherein the degron is exposed when SMN is monomeric and sequestered when SMN forms higher-order multimers