Upper Atmosphere Research Satellite (UARS) trade analysis

The Upper Atmosphere Research Satellite (UARS) which will collect data pertinent to the Earth's upper atmosphere is described. The collected data will be sent to the central data handling facility (CDHF) via the UARS ground system and the data will be processed and distributed to the remote analysis computer systems (RACS). An overview of the UARS ground system is presented. Three configurations were developed for the CDHF-RACS system. The CDHF configurations are discussed. The IBM CDHF configuration, the UNIVAC CDHF configuration and the vax cluster CDHF configuration are presented. The RACS configurations, the IBM RACS configurations, UNIVAC RACS and VAX RACS are detailed. Due to the large on-line data estimate to approximately 100 GB, a mass storage system is considered essential to the UARS CDHF. Mass storage systems were analyzed and the Braegan ATL, the RCA optical disk, the IBM 3850 and the MASSTOR M860 are discussed. It is determined that the type of mass storage system most suitable to UARS is the automated tape/cartridge device. Two devices of this type, the IBM 3850 and the MASSTOR MSS are analyzed and the applicable tape/cartridge device is incorporated into the three CDHF-RACS configurations

The UARS and open data concept and analysis study

Alternative concepts for a common design for the UARS and OPEN Central Data Handling Facility (CDHF) are offered. Costs for alternative implementations of the UARS designs are presented, showing that the system design does not restrict the implementation to a single manufacturer. Processing demands on the alternative UARS CDHF implementations are then discussed. With this information at hand together with estimates for OPEN processing demands, it is shown that any shortfall in system capability for OPEN support can be remedied by either component upgrades or array processing attachments rather than a system redesign. In addition to a common system design, it is shown that there is significant potential for common software design, especially in the areas of data management software and non-user-unique production software. Archiving the CDHF data are discussed. Following that, cost examples for several modes of communications between the CDHF and Remote User Facilities are presented. Technology application is discussed

Characterization of TCDD-inducible poly-ADP-ribose polymerase (TIPARP/ARTD14) catalytic activity

YesHere, we report the biochemical characterization of the mono-ADP-ribosyltransferase 2,3,7,8-tetrachlorodibenzo-p-dioxin poly-ADP-ribose polymerase (TIPARP/ARTD14/PARP7), which is known to repress aryl hydrocarbon receptor (AHR)-dependent transcription. We found that the nuclear localization of TIPARP was dependent on a short N-terminal sequence and its zinc finger domain. Deletion and in vitro ADP-ribosylation studies identified amino acids 400–657 as the minimum catalytically active region, which retained its ability to mono-ADP-ribosylate AHR. However, the ability of TIPARP to ADP-ribosylate and repress AHR in cells was dependent on both its catalytic activity and zinc finger domain. The catalytic activity of TIPARP was resistant to meta-iodobenzylguanidine but sensitive to iodoacetamide and hydroxylamine, implicating cysteines and acidic side chains as ADP-ribosylated target residues. Mass spectrometry identified multiple ADP-ribosylated peptides in TIPARP and AHR. Electron transfer dissociation analysis of the TIPARP peptide 33ITPLKTCFK41 revealed cysteine 39 as a site for mono-ADP-ribosylation. Mutation of cysteine 39 to alanine resulted in a small, but significant, reduction in TIPARP autoribosylation activity, suggesting that additional amino acid residues are modified, but loss of cysteine 39 did not prevent its ability to repress AHR. Our findings characterize the subcellular localization and mono-ADP-ribosyltransferase activity of TIPARP, identify cysteine as a mono-ADP-ribosylated residue targeted by this enzyme, and confirm the TIPARP-dependent mono-ADP-ribosylation of other protein targets, such as AHR.This work was supported by Canadian Institutes of Health Research (CIHR) operating grants [MOP-494265 and MOP-125919]; CIHR New Investigator Award; an Early Researcher Award from the Ontario Ministry of Innovation [ER10-07-028]; the Johan Throne Holst Foundation; Novo Nordic Foundation; and the Norwegian Cancer Society to J.M. This work was also funded by grants from the Johan Throne Holst Foundation; and the Novo Nordic Foundation to H.I.N

Cross-talk between fatty acid and cholesterol metabolism mediated by liver X receptor-alpha

LXR alpha (liver X receptor, also called RLD-1) is a nuclear receptor, highly expressed in tissues that play a role in lipid homeostasis. In this report we show that fatty acids are positive regulators of LXR alpha gene expression and we investigate the molecular mechanisms underlying this regulation. In cultured rat hepatoma and primary hepatocyte cells, fatty acids and the sulfur-substituted fatty acid analog, tetradecylthioacetic acid, robustly induce LXR alpha (up to 3.5- and 7-fold, respectively) but not LXR beta (also called OR-1) mRNA steady state levels, with unsaturated fatty acids being more effective than saturated fatty acids. RNA stability and nuclear run-on studies demonstrate that changes in the transcription rate of the LXR alpha gene account for the major part of the induction of LXR alpha mRNA levels. A similar induction of protein level was also seen after treatment of primary hepatocytes with the same fatty acids. Consistent with such a transcriptional effect, transient transfection studies with a luciferase reporter gene, driven by 1.5 kb of the 5'-flanking region of the mouse (m)LXR alpha gene, show a peroxisome proliferator-activated receptor-alpha-dependent increase in luciferase activity upon treatment with tetradecylthioacetic acid and the synthetic peroxisome proliferator-activated receptor-alpha activator, Wy 14.643, suggesting that the mLXR alpha 5'-flanking region contains the necessary sequence elements for fatty acid responsiveness. In addition, in vivo LXR alpha expression was induced by fatty acids, consistent with the in vitro cell culture data. These observations demonstrate that LXR alpha expression is controlled by fatty acid signaling pathways and suggest an important cross-talk between fatty acid and cholesterol regulation of lipid metabolism

Perilipin 5 is protective in the ischemic heart

Background: Myocardial ischemia is associated with alterations in cardiac metabolism, resulting in decreased fatty acid oxidation and increased lipid accumulation. Here we investigate how myocardial lipid content and dynamics affect the function of the ischemic heart, and focus on the role of the lipid droplet protein perilipin 5 (Plin5) in the pathophysiology of myocardial ischemia. Methods and results: We generated Plin5(-/-) mice and found that Plin5 deficiency dramatically reduced the triglyceride content in the heart. Under normal conditions, Plin5(-/-) mice maintained a close to normal heart function by decreasing fatty acid uptake and increasing glucose uptake, thus preserving the energy balance. However, during stress or myocardial ischemia, Plin5 deficiency resulted in myocardial reduced substrate availability, severely reduced heart function and increased mortality. Importantly, analysis of a human cohort with suspected coronary artery disease showed that a common noncoding polymorphism, rs884164, decreases the cardiac expression of PLIN5 and is associated with reduced heart function following myocardial ischemia, indicating a role for Plin5 in cardiac dysfunction. Conclusion: Our findings indicate that Plin5 deficiency alters cardiac lipid metabolism and associates with reduced survival following myocardial ischemia, suggesting that Plin5 plays a beneficial role in the heart following ischemia. (C) 2016 The Authors. Published by Elsevier Ireland Ltd