Predictive Modeling of a Two-stage Gearbox towards Fault Detection

This research presents a systematic approach to health monitoring using dynamic gearbox models (DGM) and the harmonic wavelet transforms (HWT) for vibration response analysis. A comprehensive DGM is developed, the model parameters are identified through correlated numerical and experimental investigations, and HWT analysis is performed to illustrate the fault detection and diagnosis procedure and capability of this approach. The model fidelity is validated first by spectrum analysis, using constant speed experimental data, and secondly by HWT analysis, using non-stationary experimental data. The comparison confirms that both the frequency content and the predicted, relative response magnitudes match with physical measurements. Model prediction and experimental data are compared for healthy gear operation and seeded gear faults including a pinion with a missing tooth, tooth root crack, tooth spall and varying tooth chip severities, demonstrating that fault type and severity are distinguishable. The research shows fault modeling in combination with HWT data analysis is able to identify fault types, evaluate fault relative severity, and greatly reduce pattern recognition library development. This approach can facilitate successful fault detection, diagnosis and prognosis for gearbox systems, providing a physically meaningful connection of fault indicators to the actual fault patterns thus paving the way to real-time condition monitoring

Extension Professionals\u27 Information Use, Protective Behaviors, and Work-Life Stress During the COVID-19 Pandemic

In the context of the COVID-19 pandemic, we asked Extension professionals about sources used to inform their work, means used to inform clientele, and management of their own health and well-being. Survey data revealed that Extension professionals sought information from trusted sources and that large majorities were involved in disseminating online information to clientele. Extension professionals felt well supported, were prepared to address the pandemic\u27s challenges, and were practicing recommended health behaviors. However, respondents reported high levels of stress and difficulty balancing professional and personal needs. Recommendations focus on collaborative opportunities for Extension as well as professional development and other resources for Extension personnel

Regulatory effects of interleukin‐11 during acute lung inflammatory injury

The role of interleukin‐11 (IL‐11) was evaluated in the IgG immune complex model of acute lung injury in rats. IL‐11 mRNA and protein were both up‐regulated during the course of this inflammatory response. Exogenously administered IL‐11 substantially reduced, in a dose‐dependent manner, the intrapulmonary accumulation of neutrophils and the lung vascular leak of albumin. These in vivo anti‐inflammatory effects of IL‐11 were associated with reduced NF‐κB activation in lung, reduced levels of tumor necrosis factor α (TNF‐α) in bronchoalveolar lavage (BAL) fluids, and diminished up‐regulation of lung vascular ICAM‐1. It is interesting that IL‐11 did not affect BAL fluid content of the CXC chemokines, macrophage inflammatory protein‐2 (MIP‐2) and cytokine‐inducible neutrophil chemoattractant (CINC); the presence of IL‐11 did not affect these chemokines. However, BAL content of C5a was reduced by IL‐11. These data indicate that IL‐11 is a regulatory cytokine in the lung and that, like other members of this family, its anti‐inflammatory properties appear to be linked to its suppression of NF‐κB activation, diminished production of TNF‐α, and reduced up‐regulation of lung vascular ICAM‐1. J. Leukoc. Biol. 66: 151–157; 1999.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141937/1/jlb0151.pd

White paper on nuclear astrophysics and low energy nuclear physics Part 1: Nuclear astrophysics

This white paper informs the nuclear astrophysics community and funding agencies about the scientific directions and priorities of the field and provides input from this community for the 2015 Nuclear Science Long Range Plan. It summarizes the outcome of the nuclear astrophysics town meeting that was held on August 21–23, 2014 in College Station at the campus of Texas A&M University in preparation of the NSAC Nuclear Science Long Range Plan. It also reflects the outcome of an earlier town meeting of the nuclear astrophysics community organized by the Joint Institute for Nuclear Astrophysics (JINA) on October 9–10, 2012 Detroit, Michigan, with the purpose of developing a vision for nuclear astrophysics in light of the recent NRC decadal surveys in nuclear physics (NP2010) and astronomy (ASTRO2010). The white paper is furthermore informed by the town meeting of the Association of Research at University Nuclear Accelerators (ARUNA) that took place at the University of Notre Dame on June 12–13, 2014. In summary we find that nuclear astrophysics is a modern and vibrant field addressing fundamental science questions at the intersection of nuclear physics and astrophysics. These questions relate to the origin of the elements, the nuclear engines that drive life and death of stars, and the properties of dense matter. A broad range of nuclear accelerator facilities, astronomical observatories, theory efforts, and computational capabilities are needed. With the developments outlined in this white paper, answers to long standing key questions are well within reach in the coming decade

Mechanism-Based Screen for G1/S Checkpoint Activators Identifies a Selective Activator of EIF2AK3/PERK Signalling

Human cancers often contain genetic alterations that disable G1/S checkpoint control and loss of this checkpoint is thought to critically contribute to cancer generation by permitting inappropriate proliferation and distorting fate-driven cell cycle exit. The identification of cell permeable small molecules that activate the G1/S checkpoint may therefore represent a broadly applicable and clinically effective strategy for the treatment of cancer. Here we describe the identification of several novel small molecules that trigger G1/S checkpoint activation and characterise the mechanism of action for one, CCT020312, in detail. Transcriptional profiling by cDNA microarray combined with reverse genetics revealed phosphorylation of the eukaryotic initiation factor 2-alpha (EIF2A) through the eukaryotic translation initiation factor 2-alpha kinase 3 (EIF2AK3/PERK) as the mechanism of action of this compound. While EIF2AK3/PERK activation classically follows endoplasmic reticulum (ER) stress signalling that sets off a range of different cellular responses, CCT020312 does not trigger these other cellular responses but instead selectively elicits EIF2AK3/PERK signalling. Phosphorylation of EIF2A by EIF2A kinases is a known means to block protein translation and hence restriction point transit in G1, but further supports apoptosis in specific contexts. Significantly, EIF2AK3/PERK signalling has previously been linked to the resistance of cancer cells to multiple anticancer chemotherapeutic agents, including drugs that target the ubiquitin/proteasome pathway and taxanes. Consistent with such findings CCT020312 sensitizes cancer cells with defective taxane-induced EIF2A phosphorylation to paclitaxel treatment. Our work therefore identifies CCT020312 as a novel small molecule chemical tool for the selective activation of EIF2A-mediated translation control with utility for proof-of-concept applications in EIF2A-centered therapeutic approaches, and as a chemical starting point for pathway selective agent development. We demonstrate that consistent with its mode of action CCT020312 is capable of delivering potent, and EIF2AK3 selective, proliferation control and can act as a sensitizer to chemotherapy-associated stresses as elicited by taxanes

Genome-wide analyses as part of the international FTLD-TDP whole-genome sequencing consortium reveals novel disease risk factors and increases support for immune dysfunction in FTLD

Frontotemporal lobar degeneration with neuronal inclusions of the TAR DNA-binding protein 43 (FTLD-TDP) represents the most common pathological subtype of FTLD. We established the international FTLD-TDP whole genome sequencing consortium to thoroughly characterize the known genetic causes of FTLD-TDP and identify novel genetic risk factors. Through the study of 1,131 unrelated Caucasian patients, we estimated that C9orf72 repeat expansions and GRN loss-of-function mutations account for 25.5% and 13.9% of FTLD-TDP patients, respectively. Mutations in TBK1 (1.5%) and other known FTLD genes (1.4%) were rare, and the disease in 57.7% of FTLD-TDP patients was unexplained by the known FTLD genes. To unravel the contribution of common genetic factors to the FTLD-TDP etiology in these patients, we conducted a two-stage association study comprising the analysis of whole-genome sequencing data from 517 FTLD-TDP patients and 838 controls, followed by targeted genotyping of the most associated genomic loci in 119 additional FTLD-TDP patients and 1653 controls. We identified three genome-wide significant FTLD-TDP risk loci: one new locus at chromosome 7q36 within the DPP6 gene led by rs118113626 (pvalue=4.82e-08, OR=2.12), and two known loci: UNC13A, led by rs1297319 (pvalue=1.27e-08, OR=1.50) and HLA-DQA2 led by rs17219281 (pvalue=3.22e-08, OR=1.98). While HLA represents a locus previously implicated in clinical FTLD and related neurodegenerative disorders, the association signal in our study is independent from previously reported associations. Through inspection of our whole genome sequence data for genes with an excess of rare loss-of-function variants in FTLD-TDP patients (n≥3) as compared to controls (n=0), we further discovered a possible role for genes functioning within the TBK1-related immune pathway (e.g. DHX58, TRIM21, IRF7) in the genetic etiology of FTLD-TDP. Together, our study based on the largest cohort of unrelated FTLD-TDP patients assembled to date provides a comprehensive view of the genetic landscape of FTLD-TDP, nominates novel FTLD-TDP risk loci, and strongly implicates the immune pathway in FTLD-TDP pathogenesis

Binary systems and their nuclear explosions

Peer ReviewedPreprin

Discovery of a z = 0.65 post-starburst BAL quasar in the DES supernova fields

We present the discovery of a z = 0.65 low-ionization broad absorption line (LoBAL) quasar in a post-starburst galaxy in data from the Dark Energy Survey (DES) and spectroscopy from the Australian Dark Energy Survey (OzDES). LoBAL quasars are a minority of all BALs, and rarer still is that this object also exhibits broad Fe II (an FeLoBAL) and Balmer absorption. This is the first BAL quasar that has signatures of recently truncated star formation, which we estimate ended about 40 Myr ago. The characteristic signatures of an FeLoBAL require high column densities, which could be explained by the emergence of a young quasar from an early, dust-enshrouded phase, or by clouds compressed by a blast wave. The age of the starburst component is comparable to estimates of the lifetime of quasars, so if we assume the quasar activity is related to the truncation of the star formation, this object is better explained by the blast wave scenario