Testing of the multi-application small light water reactor (MASLWR) passive safety systems

Experimental thermal hydraulic research has been conducted at Oregon State University for the purpose of assessing the performance of a new reactor design concept, the multi-application small light water reactor (MASLWR). The MASLWR is a pressurized light water reactor design with a net output of 35 MWe that uses natural circulation in both normal and transient operation. Due to its small size, portability and modularity, the MASLWR design is well suited to help fill the potential need for grid appropriate reactor designs for smaller electricity grids as may be found in developing or remote regions. The purpose of the OSU MASLWR test facility is to assess the operation of the MASLWR under normal full operating pressure and full temperature conditions and to assess the passive safety systems under transient conditions. The data generated by the testing program will be used to assess computer code calculations and to provide a better understanding of the thermal-hydraulic phenomena in the design of the MASLWR NSSS. During this testing program, four tests were conducted at the OSU MASLWR test facility. These tests included one design basis accident and one beyond design basis accident. During the performance of these tests, plant operations to include start up, normal operation and shut down evolutions were demonstrated successfully.     

Microstructural development and creep deformation in equiaxed γ, γ+α 2, and γ+α 2+B2 titanium aluminides

The development of microstructure and its influence on creep properties have been studied for structures including equiaxed γ, duplex, and other structures of varying α ₂ morphology in two Ti-48Al-2Cr-2Nb alloys. Heat treatments at 1125 °C have been utilized to produce equiaxed γ microstructures in alloys with or without Mo additions. The γ → α transformation produces α ₂ plates with several orientation variants within γ grains during subsequent annealing of the equiaxed γ microstructures below the α transus. Formation of this α ₂ morphology results from rapid up-quenching (UQ), and this structure persists through annealing, cooling, and creep testing. Differences in minimum creep rates for several microstructures containing varying amounts of multi- or single variant γ/α ₂ grains are shown to be minimal. The presence of Mo has also resulted in improved creep resistance in equiaxed γ and γ+α ₂+B2 structures, as compared to similar microstructures in the Ti-48Al-2Cr-2Nb alloy. Deformation during creep at 760 °C at stresses between 200 and 400 MPa occurs by a combination of twinning and dislocation glide without recrystallization, resulting in power-law stress exponents in the range of 6 to 9. Only minimal strain path dependence of the minimum creep rate is detected in a comparison of creep rates in stress jump, stress drop, and single stress tests. This article is based on a presentation made in the symposium “Fundamentals of Gamma Titanium Aluminides,” presented at the TMS Annual Meeting, February 10–12, 1997, Orlando, Florida, under the auspices of the ASM/MSD Flow & Fracture and Phase Transformations Committees.     

Cytosolic and nuclear distribution of PPARgamma2 in differentiating 3T3-L1 preadipocytes

In light of the pivotal role that PPARgamma2 plays in the expression of fat specific genes (e.g., A-FABP), we have examined the hypothesis that a rise in PPARgamma2 protein is required for the expression of A-FABP, and that the acceleration of fat cell differentiation by the thiazolidinedione agent, pioglitazone (PIOG), reflects an increase in the abundance of PPARgamma2 mRNA and protein. Western analyses surprisingly revealed that undifferentiated 3T3-L1 fibroblasts contained significant levels of PPARgamma2 protein; that the amount of total cellular PPARgamma2 only increased 2-fold during differentiation; and that the levels of PPARgamma2 protein and mRNA were not increased by PIOG even though fat cell differentiation was accelerated by PIOG as revealed by a 20-fold increase in A-FABP expression. Cell fractionation studies revealed that PPARgamma2 was evenly distributed between the cytosolic and nuclear compartments in both undifferentiated and differentiating 3T3-L1 cells. Immunocytochemical studies with a PPARgamma2-specific antibody indicated that PPARgamma2 was diffusely distributed throughout the cytosol of undifferentiated 3T3-L1 cells, but as the differentiation progressed, the PPARgamma2 became focused around the developing lipid droplets. In contrast to PPARgamma2, undifferentiated 3T3-L1 cells contained no measurable quantities of RXRalpha, but once fat cell differentiation was initiated by treatment with IBMX and dexamethasone, the cellular content of RXRalpha increased several fold. The rise in RXRalpha content paralleled the induction of A-FABP, but the expression of RXRalpha was not enhanced by PIOG. Although the amount of PPARgamma2 and RXRalpha was unaffected by PIOG, gel shift assays revealed that PIOG stimulated PPARgamma2/RXRalpha binding to the adipose response element of A-FABP by 5-fold in less than 12 h. Apparently, RXRalpha rather than PPARgamma2 is the pivotal trans-factor essential for the initiation of terminal fat cell differentiation. However, the high cytsolic content of PPARgamma2 and its association with the lipid droplet of differentiating 3T3-L1 cells suggests PPARgamma2 may possess a cytosolic function in the developing fat cell.     

Caring for dying children: nurses' experiences

Interviews with 25 nurses in this grounded theory study show that when nurses recognized that a child's death was inevitable, they struggled with both grief distress and moral distress. Their distress occurred within the context of the nurse-patient relationship. Nurses employed a range of strategies to manage their distress. Several conditions facilitated or constrained nurses' strategies, and resulted in far-reaching implications both professionally and personally.     

Cooperation between glutathione depletion and protein synthesis inhibition against naturally occurring neuronal death

It is generally agreed that naturally-occurring neuronal death in developing animals is dependent on the synthesis of proteins. Oxidative stress, as when intracellular concentrations of free radicals are raised or when cell constituents such as membrane lipids or protein thiols are oxidized, is also involved in various types of neuronal death. In the present report, we show that the number of naturally dying retinal cells in the chick embryo can be reduced by intraocular injections of cycloheximide, an inhibitor of protein synthesis. L-buthionine-[S,R]-sulfoximine, an inhibitor of glutathione synthesis, can either enhance or diminish the cell death, depending on the conditions of treatment. Moreover, when the two inhibitors are combined, L-buthionine-[S,R]-sulfoximine potentiates the neuroprotective effects of cycloheximide. Measurements of retinal glutathione concentration and protein synthesis show the specificity of the treatments: buthionine-sulfoximine diminishes glutathione concentrations but not protein synthesis whereas cycloheximide inhibits protein synthesis without decreasing glutathione concentrations. Naturally-occurring neuronal death thus seems to involve the synthesis of proteins, and is also influenced by oxidative phenomena. Our results extend previous data in tectal-lesioned embryos, and suggest that a moderate, non-lethal oxidative stress can enhance the resistance of ganglion cells that might otherwise have died (spontaneously or following axotomy) owing to insufficient retrograde trophic support.     

PRMT 3, a type I protein arginine N-methyltransferase that differs from PRMT1 in its oligomerization, subcellular localization, substrate specificity, and regulation

Methylation is one of the many post-translational modifications that modulate protein function. Although asymmetric NG,NG-dimethylation of arginine residues in glycine-arginine-rich domains of eucaryotic proteins, catalyzed by type I protein arginine N-methyltransferases (PRMT), has been known for some time, members of this enzyme class have only recently been cloned. The first example of this type of enzyme, designated PRMT1, cloned because of its ability to interact with the mammalian TIS21 immediate-early protein, was then shown to have protein arginine methyltransferase activity. We have now isolated rat and human cDNA orthologues that encode proteins with substantial sequence similarity to PRMT1. A recombinant glutathione S-transferase (GST) fusion product of this new rat protein, named PRMT3, asymmetrically dimethylates arginine residues present both in the designed substrate GST-GAR and in substrate proteins present in hypomethylated extracts of a yeast rmt1 mutant that lacks type I arginine methyltransferase activity; PRMT3 is thus a functional type I protein arginine N-methyltransferase. However, rat PRMT1 and PRMT3 glutathione S-transferase fusion proteins have distinct enzyme specificities for substrates present in both hypomethylated rmt1 yeast extract and hypomethylated RAT1 embryo cell extract. TIS21 protein modulates the enzymatic activity of recombinant GST-PRMT1 fusion protein but not the activity of GST-PRMT3. Western blot analysis of gel filtration fractions suggests that PRMT3 is present as a monomer in RAT1 cell extracts. In contrast, PRMT1 is present in an oligomeric complex. Immunofluorescence analysis localized PRMT1 predominantly to the nucleus of RAT1 cells. In contrast, PRMT3 is predominantly cytoplasmic.     

Error handling in a parallel LR substring parser

Parallel parsing is currently receiving attention but there is little discussion about the adaptation of sequential error handling techniques to these parallel algorithms. We describe a noncorrecting error handler implemented with a parallel LR substring parser. The parser used is a parallel version of Cormack's LR substring parser. The applicability of noncorrecting error handling for parallel parsing is discussed. The error information provided for a standard set of 118 erroneous Pascal programs is analysed. The programs are run on the sequential LR substring parser.     

Evidence of successful river spawning by lake trout (Salvelinus namaycush) in the Lower Niagara River,Lake Ontario

Restoration of a wild-produced lake trout Salvelinus namaycush population in Lake Ontario has not been successful despite the adult population often meeting or exceeding restoration targets. Lack of high-quality spawning habitat in Lake Ontario is suggested as one impediment to recruitment of wild lake trout, although the quantity and location of spawning habitat is poorly understood. If high-quality spawning habitat is limited in Lake Ontario, lake trout may be using uncommon spawning locations such as rivers. Anecdotal angler accounts point to the Niagara River as a lake trout spawning location. To better understand the potential of the Niagara River as a spawning location, egg and juvenile fish collections were conducted 12–14 river kilometers from the mouth of the Niagara River from 2010 to 2012; and mature female lake trout with surgically implanted acoustic tags were monitored from 2015 to 2019. Genetic analyses confirmed 60% of collected eggs and 93% of collected post-hatch juvenile fish in the Niagara River were lake trout. Tagged female lake trout returned to the Niagara River over consecutive years during the spawning season. The short duration of lake trout presence in the river (mean = 56 days/year) suggests female lake trout use the Niagara River primarily for spawning. Diversity in spawning locations may provide lake trout population’s resilience against environmental variability through a portfolio effect. Improved identification of riverine spawning locations, including their overall contribution to wild recruitment, may be a useful tool for managers to restore a wild-produced population of lake trout in Lake Ontario.