Envirocare of Utah: Expanding Waste Acceptance Criteria to Provide Low-Level and Mixed Waste Disposal Options.

Envirocare of Utah operates a low-level radioactive waste disposal facility 80 miles west of Salt Lake City in Clive, Utah. Accepted waste types includes NORM, 11e2 byproduct material, Class A low-level waste, and mixed waste. Since 1988, Envirocare has offered disposal options for environmental restoration waste for both government and commercial remediation projects. Annual waste receipts exceed 12 million cubic feet. The waste acceptance criteria (WAC) for the Envirocare facility have significantly expanded to accommodate the changing needs of restoration projects and waste generators since its inception, including acceptable physical waste forms, radiological acceptance criteria, RCRA requirements and treatment capabilities, PCB acceptance, and liquids acceptance. Additionally, there are many packaging, transportation, and waste management options for waste streams acceptable at Envirocare. Many subcontracting vehicles are also available to waste generators for both government and commercial activities

Camera distortion self-calibration using the plumb-line constraint and minimal Hough entropy

In this paper we present a simple and robust method for self-correction of camera distortion using single images of scenes which contain straight lines. Since the most common distortion can be modelled as radial distortion, we illustrate the method using the Harris radial distortion model, but the method is applicable to any distortion model. The method is based on transforming the edgels of the distorted image to a 1-D angular Hough space, and optimizing the distortion correction parameters which minimize the entropy of the corresponding normalized histogram. Properly corrected imagery will have fewer curved lines, and therefore less spread in Hough space. Since the method does not rely on any image structure beyond the existence of edgels sharing some common orientations and does not use edge fitting, it is applicable to a wide variety of image types. For instance, it can be applied equally well to images of texture with weak but dominant orientations, or images with strong vanishing points. Finally, the method is performed on both synthetic and real data revealing that it is particularly robust to noise.Comment: 9 pages, 5 figures Corrected errors in equation 1

Structural basis for +1 ribosomal frameshifting during EF-G-catalyzed translocation [preprint]

Frameshifting of mRNA during translation provides a strategy to expand the coding repertoire of cells and viruses. Where and how in the elongation cycle +1-frameshifting occurs remains poorly understood. We captured six ∼3.5-Å-resolution cryo-EM structures of ribosomal elongation complexes formed with the GTPase elongation factor G (EF-G). Three structures with a +1-frameshifting-prone mRNA reveal that frameshifting takes place during translocation of tRNA and mRNA. Prior to EF-G binding, the pre-translocation complex features an in-frame tRNA-mRNA pairing in the A site. In the partially translocated structure with EF-G, the tRNA shifts to the +1-frame codon near the P site, whereas the freed mRNA base bulges between the P and E sites and stacks on the 16S rRNA nucleotide G926. The ribosome remains frameshifted in the nearly post-translocation state. Our findings demonstrate that the ribosome and EF-G cooperate to induce +1 frameshifting during mRNA translocation

Mortality in paediatric burns victims: A retrospective review from 2009 to 2012 in a single centre

Background. Childhood mortality is high in low- and middle-income countries. Burns are one of the five leading causes of childhood injury mortality in South Africa (SA). While there is an abundance of literature on burns in the developed world, there are far fewer publications dealing with childhood mortality related to burns in Africa and SA.Objective. To describe the mortality of children admitted to a dedicated paediatric burns unit, and investigate factors contributing to reducing mortality.Methods. A retrospective review was performed of patients admitted to the Johnson & Johnson Paediatric Burns Unit, Chris Hani Baragwanath Academic Hospital, Johannesburg, SA, between May 2009 and April 2012.Results. During the study period, 1 372 patients aged ≤10 years were admitted to the unit. There were 1 089 admissions to the general ward and 283 admissions to the paediatric burns intensive care unit (PBICU). The overall mortality rate was 7.9% and the rate for children admitted to the PBICU 29.3%; 90.8% of deaths occurred in children aged ≤5 years. Of children admitted with an inhalational injury, 89.5% died. No child with a burn injury >60% of total body surface area (TBSA) survived.Conclusions. Our overall mortality rate was 7.9%, and the rate declined significantly over the 3-year study period from 11.7% to 5.1%. Age ≤5 years, the presence of inhalational injury, burn injury >30% of TBSA and admission to the PBICU were significant risk factors for mortality

Structural basis for +1 ribosomal frameshifting during EF-G-catalyzed translocation

Frameshifting of mRNA during translation provides a strategy to expand the coding repertoire of cells and viruses. How and where in the elongation cycle +1-frameshifting occurs remains poorly understood. We describe seven ~3.5-A-resolution cryo-EM structures of 70S ribosome complexes, allowing visualization of elongation and translocation by the GTPase elongation factor G (EF-G). Four structures with a + 1-frameshifting-prone mRNA reveal that frameshifting takes place during translocation of tRNA and mRNA. Prior to EF-G binding, the pre-translocation complex features an in-frame tRNA-mRNA pairing in the A site. In the partially translocated structure with EF-G*GDPCP, the tRNA shifts to the +1-frame near the P site, rendering the freed mRNA base to bulge between the P and E sites and to stack on the 16S rRNA nucleotide G926. The ribosome remains frameshifted in the nearly post-translocation state. Our findings demonstrate that the ribosome and EF-G cooperate to induce +1 frameshifting during tRNA-mRNA translocation

Ribosome*RelA structures reveal the mechanism of stringent response activation

Stringent response is a conserved bacterial stress response underlying virulence and antibiotic resistance. RelA/SpoT-homolog proteins synthesize transcriptional modulators (p)ppGpp, allowing bacteria to adapt to stress. RelA is activated during amino-acid starvation, when cognate deacyl-tRNA binds to the ribosomal A (aminoacyl-tRNA) site. We report four cryo-EM structures of E. coli RelA bound to the 70S ribosome, in the absence and presence of deacyl-tRNA accommodating in the 30S A site. The boomerang-shaped RelA with a wingspan of more than 100 A wraps around the A/R (30S A-site/RelA-bound) tRNA. The CCA end of the A/R tRNA pins the central TGS domain against the 30S subunit, presenting the (p)ppGpp-synthetase domain near the 30S spur. The ribosome and A/R tRNA are captured in three conformations, revealing hitherto elusive states of tRNA engagement with the ribosomal decoding center. Decoding-center rearrangements are coupled with the step-wise 30S-subunit \u27closure\u27, providing insights into the dynamics of high-fidelity tRNA decoding

Genetic evidence that SMAD2 is not required for gonadal tumor development in inhibin-deficient mice

<p>Abstract</p> <p>Background</p> <p>Inhibin is a tumor-suppressor and activin antagonist. Inhibin-deficient mice develop gonadal tumors and a cachexia wasting syndrome due to enhanced activin signaling. Because activins signal through SMAD2 and SMAD3 in vitro and loss of SMAD3 attenuates ovarian tumor development in inhibin-deficient females, we sought to determine the role of SMAD2 in the development of ovarian tumors originating from the granulosa cell lineage.</p> <p>Methods</p> <p>Using an inhibin α null mouse model and a conditional knockout strategy, double conditional knockout mice of Smad2 and inhibin alpha were generated in the current study. The survival rate and development of gonadal tumors and the accompanying cachexia wasting syndrome were monitored.</p> <p>Results</p> <p>Nearly identical to the controls, the Smad2 and inhibin alpha double knockout mice succumbed to weight loss, aggressive tumor progression, and death. Furthermore, elevated activin levels and activin-induced pathologies in the liver and stomach characteristic of inhibin deficiency were also observed in these mice. Our results indicate that SMAD2 ablation does not protect inhibin-deficient females from the development of ovarian tumors or the cachexia wasting syndrome.</p> <p>Conclusions</p> <p>SMAD2 is not required for mediating tumorigenic signals of activin in ovarian tumor development caused by loss of inhibin.</p