101,654 research outputs found
Evaluation of the implementation of nursing diagnostics. A study of the use of nursing diagnoses, interventions and outcomes in nursing documentation.
Contains fulltext :
40179.pdf (Publisher’s version ) (Open Access)RU Radboud Universiteit Nijmegen, 09 juli 2007Promotor : Achterberg, T. van Co-promotores : Lavin, M.A., Needham, I.175 p
Reception - Guest, Kevin Martin, Terry Lavin
Kevin T. Martin (Class of 1967), Terrence J. Lavin (Class of 1983), and a guest at the 125 Alumni of Distinction reception.https://scholarship.kentlaw.iit.edu/alumni_125/1134/thumbnail.jp
C-0664: 309 East Center, Smithfield, Utah, Lutie Burnell/Lavin C. Winn residence. Sec 27 T 13N R 1 E. Built 1925
C-0664: 309 East Center, Smithfield, Utah, Lutie Burnell/Lavin C. Winn residence. Sec 27 T 13N R 1 E. Built 192
Letter, [Author unclear] to Paulina T. Merritt
Handwritten letter to Paulina Merritt from an unknown author, October 1, 1876.
Fault injections on mission-critical computer systems
This thesis presents two unique sets of fault injections on mission-critical computer systems with the goal of (1) understanding the impact of faults, errors and failures, and (2) evaluating fault-tolerance and resilience of the targeted systems in the presence of failures.
Our first fault injection campaign studies the effects of failures on high-performance computing (HPC) systems. We target the Cray XE Blue Waters JYC testbed at the National Center for Supercomputing Applications, with the goal of improving the understanding of failure causes and propagation observed in the field failure data analysis of Blue Waters. We use data collected from system logs and network performance counters to (1) characterize fault-error-failure sequences and recovery mechanisms in Gemini interconnection networks and in Cray compute elements, (2) understand the impact of failures on the system and user applications at different scales, and (3) identify and recreate fault scenarios that induce unrecoverable failures, to create new tests for system and application design. We utilize HPCArrow, a newly developed software-implemented fault injection tool with the ability to disable and restore user-specified network links, directional connections, compute nodes and blades. We observe failures manifesting in the form of applications not making forward progress and network quiescence operations causing extended system recovery times.
Our second fault injection campaign studies the effects of faults, attacks and failures on a smart power grid utilizing software-defined networking (SDN) to orchestrate its data acquisition network. We evaluate our fault models on a smart power grid simulation running Raincoat, an SDN application that reroutes and spoofs network traffic to thwart attackers. Additionally, we propose an application- and data plane-based solution to pro-actively monitor system state and enforce user defined policies. We show that under certain faults, (1) applications orchestrating the network become ineffective, and (2) periodically monitoring the state of the network can identify faults or attacks before they manifest as failures. The results obtained from this work can aid in enhancing the resiliency of future SDN applications.Submission published under a 24 month embargo labeled 'Closed Access', the embargo will last until 2020-08-01The student, Lavin Devnani, accepted the attached license on 2018-07-18 at 13:24.The student, Lavin Devnani, submitted this Thesis for approval on 2018-07-18 at 13:28.This Thesis was approved for publication on 2018-07-18 at 14:19.DSpace SAF Submission Ingestion Package generated from Vireo submission #12626 on 2018-09-27 at 11:33:12Made available in DSpace on 2018-09-27T16:45:31Z (GMT). No. of bitstreams: 2
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Previous issue date: 2018-07-18Embargo set by: Seth Robbins for item 107856
Lift date: 2020-09-27T16:45:39Z
Reason: Author requested closed access (OA after 2yrs) in Vireo ETD systemEmbargo set by: Seth Robbins for item 107856
Lift date: 2020-09-27T16:47:41Z
Reason: Author requested closed access (OA after 2yrs) in Vireo ETD systemLimited Restriction Lifted for Item 107856 on 2020-09-28T09:15:13Z
An anaplerotic approach to correct the mitochondrial dysfunction in ataxia-telangiectasia (A-T)
Background: ATM, the protein defective in the human genetic disorder, ataxia-telangiectasia (A-T) plays a central role in response to DNA double-strand breaks (DSBs) and in protecting the cell against oxidative stress. We showed that A-T cells are hypersensitive to metabolic stress which can be accounted for by a failure to exhibit efficient endoplasmic reticulum (ER)-mitochondrial signalling and Ca2+ transfer in response to nutrient deprivation resulting in mitochondrial dysfunction. The objective of the current study is to use an anaplerotic approach using the fatty acid, heptanoate (C7), a metabolic product of the triglyceride, triheptanoin to correct the defect in ER-mitochondrial signalling and enhance cell survival of A-T cells in response to metabolic stress. Methods: We treated control cells and A-T cells with the anaplerotic agent, heptanoate to determine their sensitivity to metabolic stress induced by inhibition of glycolysis with 2- deoxyglucose (2DG) using live-cell imaging to monitor cell survival for 72 h using the Incucyte system. We examined ER-mitochondrial signalling in A-T cells exposed to metabolic stress using a suite of techniques including immunofluorescence staining of Grp75, ER-mitochondrial Ca2+ channel, the VAPB-PTPIP51 ER-mitochondrial tether complexes as well as proximity ligation assays between Grp75-IP3R1 and VAPB1-PTPIP51 to establish a functional interaction between ER and mitochondria. Finally, we also performed metabolomic analysis using LC-MS/MS assay to determine altered levels of TCA intermediates A-T cells compared to healthy control cells. Results: We demonstrate that heptanoate corrects all aspects of the defective ER-mitochondrial signalling observed in A-T cells. Heptanoate enhances ER-mitochondrial contacts; increases the flow of calcium from the ER to the mitochondrion; restores normal mitochondrial function and mitophagy and increases the resistance of ATM-deficient cells and cells from A-T patients to metabolic stress-induced killing. The defect in mitochondrial function in ATM-deficient cells was accompanied by more reliance on aerobic glycolysis as shown by increased lactate dehydrogenase A (LDHA), accumulation of lactate, and reduced levels of both acetyl CoA and ATP which are all restored by heptanoate. Conclusions: We conclude that heptanoate corrects metabolic stress in A-T cells by restoring ER-mitochondria signalling and mitochondrial function and suggest that the parent compound, triheptanoin, has immense potential as a novel therapeutic agent for patients with A-T.Full Tex
Handwritten biographical information on Paulina T. McClung Merritt
A handwritten biography of Paulina T. McClung Merritt by an unknown author, 1892.
Heterogeneous and tissue-specific regulation of effector T cell responses by IFN-gamma during Plasmodium berghei ANKA infection.
IFN-γ and T cells are both required for the development of experimental cerebral malaria during Plasmodium berghei ANKA infection. Surprisingly, however, the role of IFN-γ in shaping the effector CD4(+) and CD8(+) T cell response during this infection has not been examined in detail. To address this, we have compared the effector T cell responses in wild-type and IFN-γ(-/-) mice during P. berghei ANKA infection. The expansion of splenic CD4(+) and CD8(+) T cells during P. berghei ANKA infection was unaffected by the absence of IFN-γ, but the contraction phase of the T cell response was significantly attenuated. Splenic T cell activation and effector function were essentially normal in IFN-γ(-/-) mice; however, the migration to, and accumulation of, effector CD4(+) and CD8(+) T cells in the lung, liver, and brain was altered in IFN-γ(-/-) mice. Interestingly, activation and accumulation of T cells in various nonlymphoid organs was differently affected by lack of IFN-γ, suggesting that IFN-γ influences T cell effector function to varying levels in different anatomical locations. Importantly, control of splenic T cell numbers during P. berghei ANKA infection depended on active IFN-γ-dependent environmental signals--leading to T cell apoptosis--rather than upon intrinsic alterations in T cell programming. To our knowledge, this is the first study to fully investigate the role of IFN-γ in modulating T cell function during P. berghei ANKA infection and reveals that IFN-γ is required for efficient contraction of the pool of activated T cells
Dispelling the Myths Behind First-author Citation Counts
We conducted a full-scale evaluative citation analysis study of scholars in the XML research field to explore just how different from each other author rankings resulting from different citation counting methods actually are, and to demonstrate the capability of emerging data and tools on the Web in supporting more realistic citation counting methods. Our results contest some common arguments for the continued
use of first-author citation counts in the evaluation of scholars, such as high correlations between author rankings by first-author citation counts and other citation
counting methods, and high costs of using more realistic citation counting methods that are not well-supported by the ISI databases. It is argued that increasingly available digital full text research papers make it possible for citation analysis studies to go beyond what the ISI databases have directly supported and to employ more
sophisticated methods
Pelevin’s Trinity in the novel “t”: author – protagonist – reader
The article attempts to interpret Pelevin's artistic strategy in the novel "T" by exploring its subject organization and addressing the key problems of the author, the protagonist, and the reader as they are seen by the researcher. The article analyzes the peculiarities of constructing the narrative reality in the novel "T", and goes on to discuss Pelevin's philosophic models of the development of the humankind, and the emergence of his new anthropology
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