Smart built-in test

The work which built-in test (BIT) is asked to perform in today's electronic systems increases with every insertion of new technology or introduction of tighter performance criteria. Yet the basic purpose remains unchanged -- to determine with high confidence the operational capability of that equipment. Achievement of this level of BIT performance requires the management and assimilation of a large amount of data, both realtime and historical. Smart BIT has taken advantage of advanced techniques from the field of artificial intelligence (AI) in order to meet these demands. The Smart BIT approach enhances traditional functional BIT by utilizing AI techniques to incorporate environmental stress data, temporal BIT information and maintenance data, and realtime BIT reports into an integrated test methodology for increased BIT effectiveness and confidence levels. Future research in this area will incorporate onboard fault-logging of BIT output, stress data and Smart BIT decision criteria in support of a singular, integrated and complete test and maintenance capability. The state of this research is described along with a discussion of directions for future development

Scholarship in Review 84(2)

Scholarship in Review was a magazine highlighting research and scholarly activities at Central Washington University, published by the Office of Graduate Studies and Research.https://digitalcommons.cwu.edu/scholarship_in_review/1000/thumbnail.jp

Suicide and Pesticide Use among Pesticide Applicators and Their Spouses in the Agricultural Health Study

Background: An association may exist between pesticide exposure and suicide

Maintaining fertility of Grande Ronde Valley soils

Published March 1933. Facts and recommendations in this publication may no longer be valid. Please look for up-to-date information in the OSU Extension Catalog: http://extension.oregonstate.edu/catalo

Observational constraints on the co-evolution of supermassive black holes and galaxies

The star formation rate (SFR) and black hole accretion rate (BHAR) functions are measured to be proportional to each other at z < ~3. This close correspondence between SF and BHA would naturally yield a BH mass-galaxy mass correlation, whereas a BH mass-bulge mass correlation is observed. To explore this apparent contradiction we study the SF in spheroid-dominated galaxies between z=1 and the present day. We use 903 galaxies from the COMBO-17 survey with M* >2x10^10M_sun, ultraviolet and infrared-derived SFRs from Spitzer and GALEX, and morphologies from GEMS HST/ACS imaging. Using stacking techniques, we find that <25% of all SF occurs in spheroid-dominated galaxies (Sersic index n>2.5), while the BHAR that we would expect if the global scalings held is three times higher. This rules out the simplest picture of co-evolution, in which SF and BHA trace each other at all times. These results could be explained if SF and BHA occur in the same events, but offset in time, for example at different stages of a merger event. However, one would then expect to see the corresponding star formation activity in early-stage mergers, in conflict with observations. We conclude that the major episodes of SF and BHA occur in different events, with the bulk of SF happening in isolated disks and most BHA occurring in major mergers. The apparent global co-evolution results from the regulation of the BH growth by the potential well of the galactic spheroid, which includes a major contribution from disrupted disk stars.Comment: 14 pages, 5 figures, accepted for publication in Ap

AMPK Is Essential to Balance Glycolysis and Mitochondrial Metabolism to Control T-ALL Cell Stress and Survival

T cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy associated with Notch pathway mutations. While both normal activated and leukemic T cells can utilize aerobic glycolysis to support proliferation, it is unclear to what extent these cell populations are metabolically similar and if differences reveal T-ALL vulnerabilities. Here we show that aerobic glycolysis is surprisingly less active in T-ALL cells than proliferating normal T cells and that T-ALL cells are metabolically distinct. Oncogenic Notch promoted glycolysis but also induced metabolic stress that activated 5' AMP-activated kinase (AMPK). Unlike stimulated T cells, AMPK actively restrained aerobic glycolysis in T-ALL cells through inhibition of mTORC1 while promoting oxidative metabolism and mitochondrial Complex I activity. Importantly, AMPK deficiency or inhibition of Complex I led to T-ALL cell death and reduced disease burden. Thus, AMPK simultaneously inhibits anabolic growth signaling and is essential to promote mitochondrial pathways that mitigate metabolic stress and apoptosis in T-ALL

Genome-wide association study identifies 30 loci associated with bipolar disorder.

Bipolar disorder is a highly heritable psychiatric disorder. We performed a genome-wide association study (GWAS) including 20,352 cases and 31,358 controls of European descent, with follow-up analysis of 822 variants with P &lt; 1 × 10-4 in an additional 9,412 cases and 137,760 controls. Eight of the 19 variants that were genome-wide significant (P &lt; 5 × 10-8) in the discovery GWAS were not genome-wide significant in the combined analysis, consistent with small effect sizes and limited power but also with genetic heterogeneity. In the combined analysis, 30 loci were genome-wide significant, including 20 newly identified loci. The significant loci contain genes encoding ion channels, neurotransmitter transporters and synaptic components. Pathway analysis revealed nine significantly enriched gene sets, including regulation of insulin secretion and endocannabinoid signaling. Bipolar I disorder is strongly genetically correlated with schizophrenia, driven by psychosis, whereas bipolar II disorder is more strongly correlated with major depressive disorder. These findings address key clinical questions and provide potential biological mechanisms for bipolar disorder

Sixty-five common genetic variants and prediction of type 2 diabetes.

We developed a 65 type 2 diabetes (T2D) variant-weighted gene score to examine the impact on T2D risk assessment in a U.K.-based consortium of prospective studies, with subjects initially free from T2D (N = 13,294; 37.3% women; mean age 58.5 [38-99] years). We compared the performance of the gene score with the phenotypically derived Framingham Offspring Study T2D risk model and then the two in combination. Over the median 10 years of follow-up, 804 participants developed T2D. The odds ratio for T2D (top vs. bottom quintiles of gene score) was 2.70 (95% CI 2.12-3.43). With a 10% false-positive rate, the genetic score alone detected 19.9% incident cases, the Framingham risk model 30.7%, and together 37.3%. The respective area under the receiver operator characteristic curves were 0.60 (95% CI 0.58-0.62), 0.75 (95% CI 0.73 to 0.77), and 0.76 (95% CI 0.75 to 0.78). The combined risk score net reclassification improvement (NRI) was 8.1% (5.0 to 11.2; P = 3.31 × 10(-7)). While BMI stratification into tertiles influenced the NRI (BMI ≤24.5 kg/m(2), 27.6% [95% CI 17.7-37.5], P = 4.82 × 10(-8); 24.5-27.5 kg/m(2), 11.6% [95% CI 5.8-17.4], P = 9.88 × 10(-5); >27.5 kg/m(2), 2.6% [95% CI -1.4 to 6.6], P = 0.20), age categories did not. The addition of the gene score to a phenotypic risk model leads to a potentially clinically important improvement in discrimination of incident T2D

The potency of the fs260 connexin43 mutant to impair keratinocyte differentiation is distinct from other disease-linked connexin43 mutants

Although there are currently 62 mutants of Cx43 (connexin43) that can cause ODDD (oculodentodigital dysplasia), only two mutants have also been reported to cause palmar plantar hyperkeratosis. To determine how mutants of Cx43 can lead to this skin disease, REKs (rat epidermal keratinocytes) were engineered to express an ODDD-associated Cx43 mutant always linked to skin disease (fs260), an ODDD-linked Cx43 mutant which has been reported to sometimes cause skin disease (fs230), Cx43 mutants which cause ODDD only (G21R, G138R), a mouse Cx43 mutant linked to ODDD (G60S), a non-disease-linked truncated Cx43 mutant that is trapped in the endoplasmic reticulum (Δ244*) or full-length Cx43. When grown in organotypic cultures, of all the mutants investigated, only the fs260-expressing REKs consistently developed a thinner stratum corneum and expressed lower levels of Cx43, Cx26 and loricrin in comparison with REKs overexpressing wild-type Cx43. REKs expressing the fs260 mutant also developed a larger organotypic vital layer after acetone-induced injury and exhibited characteristics of parakeratosis. Collectively, our results suggest that the increased skin disease burden exhibited in ODDD patients harbouring the fs260 mutant is probably due to multiple additive effects cause by the mutant during epidermal differentiation