Monolithic Solid Oxide Fuel Cell development

The Monolithic Solid Oxide Fuel Cell (MSOFC) is an oxide-ceramic structure in which appropriate electronic and ionic conductors are fabricated in a honeycomb shape similar to a block of corrugated paperboard. These electronic and ionic conductors are arranged to provide short conduction paths to minimize resistive losses. The power density achievable with the MSOFC is expected to be about 8 kW/kg or 4 kW/L, at fuel efficienceis over 50 percent, because of small cell size and low resistive losses in the materials. The MSOFC operates in the range of 700 to 1000 C, at which temperatures rapid reform of hydrocarbon fuels is expected within the nickel-YSZ fuel channels. Tape casting and hot roll calendering are used to fabricate the MSOFC structure. The performance of the MSOFC has improved significantly during the course of development. The limitation of this system, based on materials resistance alone without interfacial resistances, is 0.093 ohm-sq cm area-specific resistance (ASR). The current typical performance of MSOFC single cells is characterized by ASRs of about 0.4 to 0.5 ohm-sq cm. With further development the ASR is expected to be reduced below 0.2 ohm-sq cm, which will result in power levels greater than 1.4 W/sq cm. The feasibility of the MSOFC concept was proven, and the performance was dramatically improved. The differences in thermal expansion coefficients and firing shrinkages among the fuel cell materials were minimized. As a result of good matching of these properties, the MSOFC structure was successfully fabricated with few defects, and the system shows excellent promise for development into a practical power source

Cervical Ectopic Pregnancy

[West J Emerg Med. 2012;13(1):125–126.

Application of spent fuel treatment technology to plutonium immobilization

The purpose of the electrometallurgical treatment technology being developed at Argonne National Laboratory (ANL) is to convert certain spent nuclear fuels into waste forms that are suitable for disposal in a geological repository for nuclear waste. The spent fuels of interest are those that cannot be safely stored for a long time in their current condition, and those that cannot be qualified for repository disposal. This paper explores the possibility of applying this electrometallurgical treatment technology to immobilization of surplus fissile materials, primarily plutonium. Immobilization of surplus fissile materials by electrometallurgical treatment could be done in the same facilities, at the same time. and in the same equipment as the proposed treatment of the present inventory of spent nuclear fuel. The cost and schedule savings of this simultaneous treatment scheme would be significant

Chemical Technology Division. Annual technical report, 1995

Highlights of the Chemical Technology (CMT) Division`s activities during 1995 are presented. In this period, CMT conducted research and development in the following areas: (1) electrochemical technology, including advanced batteries and fuel cells; (2) methods for treatment of hazardous waste and mixed hazardous/radioactive waste; (3) the reaction of nuclear waste glass and spent fuel under conditions expected for an unsaturated repository; (4) processes for separating and recovering selected elements from waste streams, concentrating low-level radioactive waste streams with advanced evaporator technology, and producing {sup 99}Mo from low-enriched uranium; (5) electrometallurgical treatment of different types of spent nuclear fuel in storage at Department of Energy sites; and (6) physical chemistry of selected materials in environments simulating those of fission and fusion energy systems

Quantitative Analysis of Focused A-To-I RNA Editing Sites by Ultra-High-Throughput Sequencing in Psychiatric Disorders

A-to-I RNA editing is a post-transcriptional modification of single nucleotides in RNA by adenosine deamination, which thereby diversifies the gene products encoded in the genome. Thousands of potential RNA editing sites have been identified by recent studies (e.g. see Li et al, Science 2009); however, only a handful of these sites have been independently confirmed. Here, we systematically and quantitatively examined 109 putative coding region A-to-I RNA editing sites in three sets of normal human brain samples by ultra-high-throughput sequencing (uHTS). Forty of 109 putative sites, including 25 previously confirmed sites, were validated as truly edited in our brain samples, suggesting an overestimation of A-to-I RNA editing in these putative sites by Li et al (2009). To evaluate RNA editing in human disease, we analyzed 29 of the confirmed sites in subjects with major depressive disorder and schizophrenia using uHTS. In striking contrast to many prior studies, we did not find significant alterations in the frequency of RNA editing at any of the editing sites in samples from these patients, including within the 5HT2C serotonin receptor (HTR2C). Our results indicate that uHTS is a fast, quantitative and high-throughput method to assess RNA editing in human physiology and disease and that many prior studies of RNA editing may overestimate both the extent and disease-related variability of RNA editing at the sites we examined in the human brain

Genome-wide search for breast cancer linkage in large Icelandic non-BRCA1/2 families

Abstract Introduction: A significant proportion of high-risk breast cancer families are not explained by mutations in known genes. Recent genome-wide searches (GWS) have not revealed any single major locus reminiscent of BRCA1 and BRCA2, indicating that still unidentified genes may explain relatively few families each or interact in a way obscure to linkage analyses. This has drawn attention to possible benefits of studying populations where genetic heterogeneity might be reduced. We thus performed a GWS for linkage on nine Icelandic multiple-case non-BRCA1/2 families of desirable size for mapping highly penetrant loci. To follow up suggestive loci, an additional 13 families from other Nordic countries were genotyped for selected markers. Methods: GWS was performed using 811 microsatellite markers providing about five centiMorgan (cM) resolution. Multipoint logarithm of odds (LOD) scores were calculated using parametric and nonparametric methods. For selected markers and cases, tumour tissue was compared to normal tissue to look for allelic loss indicative of a tumour suppressor gene. Results: The three highest signals were located at chromosomes 6q, 2p and 14q. One family contributed suggestive LOD scores (LOD 2.63 to 3.03, dominant model) at all these regions, without consistent evidence of a tumour suppressor gene. Haplotypes in nine affected family members mapped the loci to 2p23.2 to p21, 6q14.2 to q23.2 and 14q21.3 to q24.3. No evidence of a highly penetrant locus was found among the remaining families. The heterogeneity LOD (HLOD) at the 6q, 2p and 14q loci in all families was 3.27, 1.66 and 1.24, respectively. The subset of 13 Nordic families showed supportive HLODs at chromosome 6q (ranging from 0.34 to 1.37 by country subset). The 2p and 14q loci overlap with regions indicated by large families in previous GWS studies of breast cancer. Conclusions: Chromosomes 2p, 6q and 14q are candidate sites for genes contributing together to high breast cancer risk. A polygenic model is supported, suggesting the joint effect of genes in contributing to breast cancer risk to be rather common in non-BRCA1/2 families. For genetic counselling it would seem important to resolve the mode of genetic interaction

Repression of Meiotic Genes by Antisense Transcription and by Fkh2 Transcription Factor in Schizosaccharomyces pombe

In S. pombe, about 5% of genes are meiosis-specific and accumulate little or no mRNA during vegetative growth. Here we use Affymetrix tiling arrays to characterize transcripts in vegetative and meiotic cells. In vegetative cells, many meiotic genes, especially those induced in mid-meiosis, have abundant antisense transcripts. Disruption of the antisense transcription of three of these mid-meiotic genes allowed vegetative sense transcription. These results suggest that antisense transcription represses sense transcription of meiotic genes in vegetative cells. Although the mechanism(s) of antisense mediated transcription repression need to be further explored, our data indicates that RNAi machinery is not required for repression. Previously, we and others used non-strand specific methods to study splicing regulation of meiotic genes and concluded that 28 mid-meiotic genes are spliced only in meiosis. We now demonstrate that the “unspliced” signal in vegetative cells comes from the antisense RNA, not from unspliced sense RNA, and we argue against the idea that splicing regulates these mid-meiotic genes. Most of these mid-meiotic genes are induced in mid-meiosis by the forkhead transcription factor Mei4. Interestingly, deletion of a different forkhead transcription factor, Fkh2, allows low levels of sense expression of some mid-meiotic genes in vegetative cells. We propose that vegetative expression of mid-meiotic genes is repressed at least two independent ways: antisense transcription and Fkh2 repression

Outcomes for Implementation Research: Conceptual Distinctions, Measurement Challenges, and Research Agenda

An unresolved issue in the field of implementation research is how to conceptualize and evaluate successful implementation. This paper advances the concept of “implementation outcomes” distinct from service system and clinical treatment outcomes. This paper proposes a heuristic, working “taxonomy” of eight conceptually distinct implementation outcomes—acceptability, adoption, appropriateness, feasibility, fidelity, implementation cost, penetration, and sustainability—along with their nominal definitions. We propose a two-pronged agenda for research on implementation outcomes. Conceptualizing and measuring implementation outcomes will advance understanding of implementation processes, enhance efficiency in implementation research, and pave the way for studies of the comparative effectiveness of implementation strategies

Mobile DNA elements in T4 and related phages

Mobile genetic elements are common inhabitants of virtually every genome where they can exert profound influences on genome structure and function in addition to promoting their own spread within and between genomes. Phage T4 and related phage have long served as a model system for understanding the molecular mechanisms by which a certain class of mobile DNA, homing endonucleases, promote their spread. Homing endonucleases are site-specific DNA endonucleases that initiate mobility by introducing double-strand breaks at defined positions in genomes lacking the endonuclease gene, stimulating repair and recombination pathways that mobilize the endonuclease coding region. In phage T4, homing endonucleases were first discovered as encoded within the self-splicing td, nrdB and nrdD introns of T4. Genomic data has revealed that homing endonucleases are extremely widespread in T-even-like phage, as evidenced by the astounding fact that ~11% of the T4 genome encodes homing endonuclease genes, with most of them located outside of self-splicing introns. Detailed studies of the mobile td intron and its encoded endonuclease, I-TevI, have laid the foundation for genetic, biochemical and structural aspects that regulate the mobility process, and more recently have provided insights into regulation of homing endonuclease function. Here, we summarize the current state of knowledge regarding T4-encoded homing endonucleases, with particular emphasis on the td/I-TevI model system. We also discuss recent progress in the biology of free-standing endonucleases, and present areas of future research for this fascinating class of mobile genetic elements