NAU is abuzz about career

In 2013, NAU Career Development implemented a robust 3 year assessment strategy. Year One, showcased at the 2015 Assessment Fair, focused on assessing the Reach of our program. In Year Two, we continued to assess Reach and added measures of Perception, including satisfaction surveys targeted towards students, employers, and campus partners, as well as interviews with faculty. Assessing outcomes of both quantitative and qualitative data analyses, our results demonstrated something exciting….NAU is Abuzz about Career! The busy bees at NAU Career Development are having an impact, resulting in prepared students, engaged partners, and satisfied employers. Our data is reviewed throughout the year, and continues to inform future priorities and next steps. Come see what the buzz is about

Õpetussõnade raamatu esimese kogumiku 1–9 vahetekstide analüüs

Käesoleva uurimistöö eesmärk oli analüüsida Õpetussõnade raamatu peatükkides 1–9 esinevat viit vaheteksti (1:20–33; 3:13–20; 6:1–19; 8:1–36; 9:1–18) nende lähimas kontekstis ehk Õpetussõnade raamatu sissejuhatavas osas. Võrdlesin vahetekstide sisu ja vormi omavahel ning peatükkides 1–9 esineva kümne õpetuskõnega, et mõista, kuidas on vahetekstid ja õpetuskõned omavahel seotud, milline võiks olla vahetekstide ning nende osade kronoloogiline järjekord, ning milliste salmide ja lõikudega on neid täiendatud. Need eesmärgid on enamjaolt täidetud. Kirjanduskriitikat ja vormianalüüsi, s.h kolomeetrilist meetodit kasutades on võimalik tuvastada tekstides esinevaid lisandeid ja erisusi, mis omakorda võimaldavad määrata tekstides esinevaid kõrvalmõjusid. Võrreldes omavahel vahetekstide ja õpetuskõnede metafoorikat, semantikat ja sõnakasutust on võimalik tuvastada sarnasusi nii teiste vahetekstide kui ka õpetuskõnedega. Analüüsi tulemused on välja toodud iga peatüki lõpus ja kuuendas peatükis

Slow Wave Sleep and Long Duration Spaceflight

While ground research has clearly shown that preserving adequate quantities of sleep is essential for optimal health and performance, changes in the progression, order and /or duration of specific stages of sleep is also associated with deleterious outcomes. As seen in Figure 1, in healthy individuals, REM and Non-REM sleep alternate cyclically, with stages of Non-REM sleep structured chronologically. In the early parts of the night, for instance, Non-REM stages 3 and 4 (Slow Wave Sleep, or SWS) last longer while REM sleep spans shorter; as night progresses, the length of SWS is reduced as REM sleep lengthens. This process allows for SWS to establish precedence , with increases in SWS seen when recovering from sleep deprivation. SWS is indeed regarded as the most restorative portion of sleep. During SWS, physiological activities such as hormone secretion, muscle recovery, and immune responses are underway, while neurological processes required for long term learning and memory consolidation, also occur. The structure and duration of specific sleep stages may vary independent of total sleep duration, and changes in the structure and duration have been shown to be associated with deleterious outcomes. Individuals with narcolepsy enter sleep through REM as opposed to stage 1 of NREM. Disrupting slow wave sleep for several consecutive nights without reducing total sleep duration or sleep efficiency is associated with decreased pain threshold, increased discomfort, fatigue, and the inflammatory flare response in skin. Depression has been shown to be associated with a reduction of slow wave sleep and increased REM sleep. Given research that shows deleterious outcomes are associated with changes in sleep structure, it is essential to characterize and mitigate not only total sleep duration, but also changes in sleep stages

Sex-Specific Incompatibility Generates Locus-Specific Rates of Introgression Between Species

Disruption of interactions among ensembles of epistatic loci has been shown to contribute to reproductive isolation among various animal and plant species. Under the Bateson–Dobzhansky–Muller model, such interspecific incompatibility arises as a by-product of genetic divergence in each species, and the Orr–Turelli model indicates that the number of loci involved in incompatible interactions may “snowball” over time. We address the combined effect of multiple incompatibility loci on the rate of introgression at neutral marker loci across the genome. Our analysis extends previous work by accommodating sex specificity: differences between the sexes in the expression of incompatibility, in rates of crossing over between neutral markers and incompatibility loci, and in transmission of markers or incompatibility factors. We show that the evolutionary process at neutral markers in a genome subject to incompatibility selection is well approximated by a purely neutral process with migration rates appropriately scaled to reflect the influence of selection targeted to incompatibility factors. We confirm that in the absence of sex specificity and functional epistasis among incompatibility factors, the barrier to introgression induced by multiple incompatibility factors corresponds to the product of the barriers induced by the factors individually. A new finding is that barriers to introgression due to sex-specific incompatibility depart in general from multiplicativity. Our partitioning of variation in relative reproductive rate suggests that such departures derive from associations between sex and incompatibility and between sex and neutral markers. Concordant sex-specific incompatibility (for example, greater impairment of male hybrids or longer map lengths in females) induces lower barriers (higher rates of introgression) than expected under multiplicativity, and discordant sex-specific incompatibility induces higher barriers

Automated Framework for the Optimisation of Spatial Layouts for Concrete Structures Reinforced with Robotic Filament Winding

Concrete is a major contributor to the environmental impact of the construction industry, due to its cement content but also its reinforcement. Reinforcement has a significant contribution because of construction rationalisation, resorting to regular mats or cages of steel bars, despite layoutoptimisation algorithms and additive-manufacturing technologies. This paper presents an automated framework, connecting design and fabrication requirements for the optimisation of spatial layouts as of reinforcement of concrete structures, by the means of robotic filament winding

Extension-Led Training for Human Services Providers on Use of a Financial Empowerment Tool

We investigated the effectiveness of an Extension-led training for human services providers on Your Money, Your Goals: A Financial Empowerment Toolkit, a resource developed by the Consumer Financial Protection Bureau. Results from pretests, posttests, and focus group research indicate that participants significantly increased confidence in their ability to understand, access, and convey financial information. Recommendations include making adjustments to improve future trainings and addressing the need for additional financial literacy professional development. We offer lessons learned that Extension professionals can use to expand the reach of financial empowerment education and can apply to other trainings for professionals, regardless of discipline

Absence of keratin 8 or 18 promotes antimitochondrial autoantibody formation in aging male mice

Human mutations in keratin 8 (K8) and keratin 18 (K18), the intermediate filament proteins of hepatocytes, predispose to several liver diseases. K8‐null mice develop chronic liver injury and fragile hepatocytes, dysfunctional mitochondria, and Th2‐type colitis. We tested the hypothesis that autoantibody formation accompanies the liver damage that associates with K8/K18 absence. Sera from wild‐type control, K8‐null, and K18‐null mice were analyzed by immunoblotting and immunofluorescence staining of cell and mouse tissue homogenates. Autoantibodies to several antigens were identified in 81 % of K8‐null male mice 8 mo or older. Similar autoantibodies were detected in aging K18‐null male mice that had a related liver phenotype but normal colon compared with K8‐null mice, suggesting that the autoantibodies are linked to liver rather than colonic disease. However, these autoantibodies were not observed in nontransgenic mice subjected to 4 chronic injury models. The autoantigens are ubiquitous and partition with mitochondria. Mass spectrometry and purified protein analysis identified, mitochondrial HMG‐CoA synthase, aldehyde dehydrogenase, and catalase as the primary autoantigens, and glutamate dehydrogenase and epoxide hydrolase‐2 as additional autoantigens. Therefore, absence of the hepatocyte keratins results in production of anti‐mitochondrial autoantibodies (AMA) that recognize proteins involved in energy metabolism and oxidative stress, raising the possibility that AMA may be found in patients with keratin mutations that associate with liver and other diseases.—Toivola, D. M., Habtezion, A., Misiorek, J. O., Zhang, L., Nyström, J. H., Sharpe, O., Robinson, W. H., Kwan, R., Omary, M. B. Absence of keratin 8 or 18 promotes antimitochondrial autoantibody formation in aging male mice. FASEB J. 29, 5081–5089 (2015). www.fasebj.orgPeer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/154363/1/fsb2029012032.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/154363/2/fsb2029012032-sup-0002.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/154363/3/fsb2029012032-sup-0003.pd

Cardiac-Specific Inactivation of LPP3 in Mice Leads to Myocardial Dysfunction and Heart Failure

Lipid Phosphate phosphatase 3 (LPP3), encoded by the Plpp3 gene, is an enzyme that dephosphorylates the bioactive lipid mediator lysophosphatidic acid (LPA). To study the role of LPP3 in the myocardium, we generated a cardiac specific Plpp3 deficient mouse strain. Although these mice were viable at birth in contrast to global Plpp3 knockout mice, they showed increased mortality ~ 8 months. LPP3 deficient mice had enlarged hearts with reduced left ventricular performance as seen by echocardiography. Cardiac specific Plpp3 deficient mice had longer ventricular effective refractory periods compared to their Plpp3 littermates. We observed that lack of Lpp3 enhanced cardiomyocyte hypertrophy based on analysis of cell surface area. We found that lack of Lpp3 signaling was mediated through the activation of Rho and phospho-ERK pathways. There are increased levels of fetal genes Natriuretic Peptide A and B (Nppa and Nppb) expression indicating myocardial dysfunction. These mice also demonstrate mitochondrial dysfunction as evidenced by a significant decrease (P \u3c 0.001) in the basal oxygen consumption rate, mitochondrial ATP production, and spare respiratory capacity as measured through mitochondrial bioenergetics. Histology and transmission electron microscopy of these hearts showed disrupted sarcomere organization and intercalated disc, with a prominent disruption of the cristae and vacuole formation in the mitochondria. Our findings suggest that LPA/LPP3-signaling nexus plays an important role in normal function of cardiomyocytes