290 research outputs found

    Predicting Employee Performance Using Text Data from Resumes

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    Text analytics using term frequency was proposed as an extension of biodata for predicting job performance and addressing criticisms of biodata and predictor methods—that they do not identify the constructs they are measuring or their predictive elements. Linguistic Inquiry and Word Count software was used to analyze and sort text into validated categories. Prolific Academic was used to recruit full-time workers who provided a copy of their resume and were assessed on impression management (IM), cognitive ability, and job performance. Predictive analyses used resumes with 100+ words (n = 667), whereas correlational analyses used the full sample (N = 809). Third-person plural pronouns, impersonal pronouns, sadness words, certainty words, non-fluencies, and colons emerged as significant predictors of job performance (χ2 = 26.01 (10), p = .006). As hypothesized, impersonal pronouns were positively correlated with self-oriented IM (r = .07, p \u3c .05), and first-person singular pronouns were positively correlated with other-oriented IM (r = .07, p \u3c .05), however, first-person plural pronouns were negatively correlated (r = -.07, p \u3c .05). Pronouns and verbs were not predictive of job performance. Positive and negative emotion words did not show hypothesized relationships to OCBs, CWBs, or job performance. Finally, differentiation words (r = .09, p \u3c .01), conjunctions (r = .28, p \u3c .01), words longer than six characters (r = .29, p \u3c .01), prepositions (r = .20, p \u3c .01), cognitive process words (r = .19, p \u3c .01), causal words (r = .20, p \u3c .01), and insight words (r = .06, p \u3c .05) correlated with cognitive ability, but did not predict job performance. An exploratory regression analysis in which cognitive ability as measured by the Spot-The-Word Test (β = .10, p \u3c .05) and a composite of cognitive ability created from text analytics (β = .15, p \u3c .05) both uniquely and significantly predicted job performance (F(1,805) = 18.79, p \u3c .001), demonstrating that word categories can serve as a proxy for cognitive ability. Overall, the method of text analytics sidesteps some of the limitations of biodata predictor methods, while demonstrating the potential to automate resume reviews and mitigate unconscious bias inherent in human judgment

    MARCKS phosphorylation is modulated by a peptide mimetic of MARCKS effector domain leading to increased radiation sensitivity in lung cancer cell lines

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    Lung cancer is the leading cause of cancer-associated mortality in the United States. Kinase hyperactivation is a known mechanism of tumorigenesis. The phosphorylation status of the plasma membrane-associated protein myristoylated alanine rich C-kinase substrate (MARCKS) effector domain (ED) was previously established as being important in the sensitivity of lung cancer to radiation. Specifically, when MARCKS ED was in a non-phosphorylated state, lung cancer cells were more susceptible to ionizing radiation and experienced prolonged double-strand DNA breaks. Additional studies demonstrated that the phosphorylation status of MARCKS ED is important for gene expression and in vivo tumor growth. The present study used a peptide mimetic of MARCKS ED as a therapeutic intervention to modulate MARCKS phosphorylation. Culturing A549, H1792 and H1975 lung cancer cell lines with the MARCKS ED peptide led to reduced levels of phosphorylated MARCKS and phosphorylated Akt serine/threonine kinase 1. Further investigation demonstrated that the peptide therapy was able to reduce lung cancer cell proliferation and increase radiation sensitivity. In addition, the MARCKS peptide therapy was able to prolong double-strand DNA breaks following ionizing radiation exposure. The results of the present study demonstrate that a peptide mimetic of MARCKS ED is able to modulate MARCKS phosphorylation, leading to an increase in sensitivity to radiation. Keywords: lung cancer, myristoylated alanine rich C-kinase substrate, radiation sensitivity, effector domain, peptide mimeti

    Compaction of Hyaloclastite from the Active Geothermal System at Krafla Volcano, Iceland

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    Hyaloclastites commonly form high-quality reservoir rocks in volcanic geothermal provinces. Here, we investigated the effects of confinement due to burial following prolonged accumulation of eruptive products on the physical and mechanical evolution of surficial and subsurface (depths of 70 m, 556 m, and 732 m) hyaloclastites from Krafla volcano, Iceland. Upon loading in a hydrostatic cell, the porosity and permeability of the surficial hyaloclastite decreased linearly with mean effective stress, as pores and cracks closed due to elastic (recoverable) compaction up to 22-24 MPa (equivalent to ~1.3 km depth in the reservoir). Beyond this mean effective stress, denoted as P∗, we observed accelerated porosity and permeability reduction with increasing confinement, as the rock underwent permanent inelastic compaction. In comparison, the porosity and permeability of the subsurface core samples were less sensitive to mean effective stress, decreasing linearly with increasing confinement as the samples compacted elastically within the conditions tested (to 40 MPa). Although the surficial material underwent permanent, destructive compaction, it maintained higher porosity and permeability than the subsurface hyaloclastites throughout the experiments. We constrained the evolution of yield curves of the hyaloclastites, subjected to different effective mean stresses in a triaxial press. Surficial hyaloclastites underwent a brittle-ductile transition at an effective mean stress of ~10.5 MPa, and peak strength (differential stress) reached 13 MPa. When loaded to effective mean stresses of 33 and 40 MPa, the rocks compacted, producing new yield curves with a brittle-ductile transition at ~12.5 and ~19 MPa, respectively, but showed limited strength increase. In comparison, the subsurface samples were found to be much stronger, displaying higher strengths and brittle-ductile transitions at higher effective mean stresses (i.e., 37.5 MPa for 70 m sample, >75 MPa for 556 m, and 68.5 MPa for 732 m) that correspond to their lower porosities and permeabilities. Thus, we conclude that compaction upon burial alone is insufficient to explain the physical and mechanical properties of the subsurface hyaloclastites present in the reservoir at Krafla volcano. Mineralogical alteration, quantified using SEM-EDS, is invoked to explain the further reduction of porosity and increase in strength of the hyaloclastite in the active geothermal system at Krafla

    Targeting the effector domain of the myristoylated alanine rich C-kinase substrate enhances lung cancer radiation sensitivity

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    Lung cancer is the leading cause of cancer related deaths. Common molecular drivers of lung cancer are mutations in receptor tyrosine kinases (RTKs) leading to activation of the phosphatidylinositol 3-kinase (PI3K)/Akt pro-growth, pro-survival signaling pathways. Myristoylated alanine rich C-kinase substrate (MARCKS) is a protein that has the ability to mitigate this signaling cascade by sequestering the target of PI3K, phosphatidylinositol (4,5)-bisphosphate (PIP2). As such, MARCKS has been implicated as a tumor suppressor, though there is some evidence that MARCKS may be tumor promoting in certain cancer types. Since the MARCKS function depends on its phosphorylation status, which impacts its subcellular location, MARCKS role in cancer may depend highly on the signaling context. Currently, the importance of MARCKS in lung cancer biology is limited. Thus, we investigated MARCKS in both clinical specimens and cell culture models. Immunohistochemistry scoring of MARCKS protein expression in a diverse lung tumor tissue array revealed that the majority of squamous cell carcinomas stained positive for MARCKS while other histologies, such as adenocarcinomas, had lower levels. To study the importance of MARCKS in lung cancer biology, we used inducible overexpression of wild-type (WT) and non-phosphorylatable (NP)-MARCKS in A549 lung cancer cells that had a low level of endogenous MARCKS. We found that NP-MARCKS expression, but not WT-MARCKS, enhanced the radiosensitivity of A549 cells in part by inhibiting DNA repair as evidenced by prolonged radiation-induced DNA double strand breaks. We confirmed the importance of MARCKS phosphorylation status by treating several lung cancer cell lines with a peptide mimetic of the phosphorylation domain, the effector domain (ED), which effectively attenuated cell growth as measured by cell index. Thus, the MARCKS ED appears to be an important target for lung cancer therapeutic development

    Circadian clock proteins regulate neuronal redox homeostasis and neurodegeneration

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    Brain aging is associated with diminished circadian clock output and decreased expression of the core clock proteins, which regulate many aspects of cellular biochemistry and metabolism. The genes encoding clock proteins are expressed throughout the brain, though it is unknown whether these proteins modulate brain homeostasis. We observed that deletion of circadian clock transcriptional activators aryl hydrocarbon receptor nuclear translocator–like (Bmal1) alone, or circadian locomotor output cycles kaput (Clock) in combination with neuronal PAS domain protein 2 (Npas2), induced severe age-dependent astrogliosis in the cortex and hippocampus. Mice lacking the clock gene repressors period circadian clock 1 (Per1) and period circadian clock 2 (Per2) had no observed astrogliosis. Bmal1 deletion caused the degeneration of synaptic terminals and impaired cortical functional connectivity, as well as neuronal oxidative damage and impaired expression of several redox defense genes. Targeted deletion of Bmal1 in neurons and glia caused similar neuropathology, despite the retention of intact circadian behavioral and sleep-wake rhythms. Reduction of Bmal1 expression promoted neuronal death in primary cultures and in mice treated with a chemical inducer of oxidative injury and striatal neurodegeneration. Our findings indicate that BMAL1 in a complex with CLOCK or NPAS2 regulates cerebral redox homeostasis and connects impaired clock gene function to neurodegeneration
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