The relationship between sensation seeking, psychopathy, and deception

Psychopathy has many implications for society at large. These individuals are likely to commit violent crimes, manifest other antisocial behavior, and make up a large portion of the prison population. This study aims to establish a relationship between sensation seeking, psychopathy, and deception. A sample of 100 undergraduate students enrolled in psychology courses in a southern university completed three questionnaires assessing their level of sensation seeking (SSS-V), deception (MACH-IV), and psychopathy (TriPM). Each of the three distinct phenotypic constructs measured by the TriPM were also correlated with total SSS-V and MACH-IV scores. Pearson and Spearman correlations revealed significant relationships between TriPM and MACH-IV (rho = .28, r = .288, p = .01); TriPM and SSS-V (rho = .583, r = .587, p = .01); MACH-IV and SSS-V (rho = .201, r = .247, p = .05). Pearson correlations revealed TriPM phenotypic construct relationships with SSS-V and MACH-IV as well. Meanness was related to MACH-IV (r =.457, p = .01) and SSS-V (r = .457, p = .01). The relation between Disinhibition and MACH-IV (r = .287, p = .01) and SSS-V (r = .324, p = .01). Boldness was significantly related to SSS-V (r = .428, p = .01), but was not related to the MACH-IV (r = -.102). Implications from this study could serve to further research in understanding the precursors and correlations of psychopathy and may allow the identification of this mental disorder in its early stages so that an effective treatment regime may be established

Short GRB 130603B: Discovery of a jet break in the optical and radio afterglows, and a mysterious late-time X-ray excess

We present radio, optical/NIR, and X-ray observations of the afterglow of the short-duration 130603B, and uncover a break in the radio and optical bands at 0.5 d after the burst, best explained as a jet break with an inferred jet opening angle of 4-8 deg. GRB 130603B is only the third short GRB with a radio afterglow detection to date, and the first time that a jet break is evident in the radio band. We model the temporal evolution of the spectral energy distribution to determine the burst explosion properties and find an isotropic-equivalent kinetic energy of (0.6-1.7) x 10^51 erg and a circumburst density of 5 x 10^-3-30 cm^-3. From the inferred opening angle of GRB 130603B, we calculate beaming-corrected energies of Egamma (0.5-2) x 10^49 erg and EK (0.1-1.6) x 10^49 erg. Along with previous measurements and lower limits we find a median short GRB opening angle of 10 deg. Using the all-sky observed rate of 10 Gpc^-3 yr^-1, this implies a true short GRB rate of 20 yr^-1 within 200 Mpc, the Advanced LIGO/VIRGO sensitivity range for neutron star binary mergers. Finally, we uncover evidence for significant excess emission in the X-ray afterglow of GRB 130603B at >1 d and conclude that the additional energy component could be due to fall-back accretion or spin-down energy from a magnetar formed following the merger.Comment: Submitted to ApJ; emulateapj style; 10 pages, 1 table, 3 figure

Inflammatory Activity of Epithelial Stem Cell Variants from Cystic Fibrosis Lungs Is Not Resolved by CFTR Modulators

Rationale CFTR (cystic fibrosis transmembrane conductance regulator) modulator drugs restore function to mutant channels in patients with cystic fibrosis (CF) and lead to improvements in body mass index and lung function. Although it is anticipated that early childhood treatment with CFTR modulators will significantly delay or even prevent the onset of advanced lung disease, lung neutrophils and inflammatory cytokines remain high in patients with CF with established lung disease despite modulator therapy, underscoring the need to identify and ultimately target the sources of this inflammation in CF lungs. Objectives To determine whether CF lungs, like chronic obstructive pulmonary disease (COPD) lungs, harbor potentially pathogenic stem cell “variants” distinct from the normal p63/Krt5 lung stem cells devoted to alveolar fates, to identify specific variants that might contribute to the inflammatory state of CF lungs, and to assess the impact of CFTR genetic complementation or CFTR modulators on the inflammatory variants identified herein. Methods Stem cell cloning technology developed to resolve pathogenic stem cell heterogeneity in COPD and idiopathic pulmonary fibrosis lungs was applied to end-stage lungs of patients with CF (three homozygous CFTR:F508D, one CFTR F508D/L1254X; FEV1, 14–30%) undergoing therapeutic lung transplantation. Single-cell–derived clones corresponding to the six stem cell clusters resolved by single-cell RNA sequencing of these libraries were assessed by RNA sequencing and xenografting to monitor inflammation, fibrosis, and mucin secretion. The impact of CFTR activity on these variants after CFTR gene complementation or exposure to CFTR modulators was assessed by molecular and functional studies. Measurements and Main Results End-stage CF lungs display a stem cell heterogeneity marked by five predominant variants in addition to the normal lung stem cell, of which three are proinflammatory both at the level of gene expression and their ability to drive neutrophilic inflammation in xenografts in immunodeficient mice. The proinflammatory functions of these three variants were unallayed by genetic or pharmacological restoration of CFTR activity. Conclusions The emergence of three proinflammatory stem cell variants in CF lungs may contribute to the persistence of lung inflammation in patients with CF with advanced disease undergoing CFTR modulator therapy

Cloning a Profibrotic Stem Cell Variant in Idiopathic Pulmonary Fibrosis

Idiopathic pulmonary fibrosis (IPF) is a progressive, irreversible, and rapidly fatal interstitial lung disease marked by the replacement of lung alveoli with dense fibrotic matrices. Although the mechanisms initiating IPF remain unclear, rare and common alleles of genes expressed in lung epithelia, combined with aging, contribute to the risk for this condition. Consistently, single-cell RNA sequencing (scRNA-seq) studies have identified lung basal cell heterogeneity in IPF that might be pathogenic. We used single-cell cloning technologies to generate libraries of basal stem cells from the distal lungs of 16 patients with IPF and 10 controls. We identified a major stem cell variant that was distinguished from normal stem cells by its ability to transform normal lung fibroblasts into pathogenic myofibroblasts in vitro and to activate and recruit myofibroblasts in clonal xenografts. This profibrotic stem cell variant, which was shown to preexist in low quantities in normal and even fetal lungs, expressed a broad network of genes implicated in organ fibrosis and showed overlap in gene expression with abnormal epithelial signatures identified in previously published scRNA-seq studies of IPF. Drug screens highlighted specific vulnerabilities of this profibrotic variant to inhibitors of epidermal growth factor and mammalian target of rapamycin signaling as prospective therapeutic targets. This profibrotic stem cell variant in IPF was distinct from recently identified profibrotic stem cell variants in chronic obstructive pulmonary disease and may extend the notion that inappropriate accrual of minor and preexisting stem cell variants contributes to chronic lung conditions

Automobile Prices, Gasoline Prices, and Consumer Demand for Fuel Economy

The relationship between gasoline prices and the demand for vehicle fuel efficiency is important for environmental policy but poorly understood in the academic literature. We provide empirical evidence that automobile manufacturers price as if consumers respond to gasoline prices. We derive a reduced-form regression equation from theoretical micro-foundations and estimate the equation with nearly 300,000 vehicle-week-region observations over the period 2003-2006. We find that vehicle prices generally decline in the gasoline price. The decline is larger for inefficient vehicles, and the prices of particularly efficient vehicles actually rise. Structural estimation that ignores these effects underestimates consumer preferences for fuel efficiency

The Recombinases Rad51 and Dmc1 Play Distinct Roles in DNA Break Repair and Recombination Partner Choice in the Meiosis of Tetrahymena

Repair of programmed DNA double-strand breaks (DSBs) by meiotic recombination relies on the generation of flanking 3′ single-stranded DNA overhangs and their interaction with a homologous double-stranded DNA template. In various common model organisms, the ubiquitous strand exchange protein Rad51 and its meiosis-specific homologue Dmc1 have been implicated in the joint promotion of DNA–strand exchange at meiotic recombination sites. However, the division of labor between these two recombinases is still a puzzle. Using RNAi and gene-disruption experiments, we have studied their roles in meiotic recombination and chromosome pairing in the ciliated protist Tetrahymena as an evolutionarily distant meiotic model. Cytological and electrophoresis-based assays for DSBs revealed that, without Rad51p, DSBs were not repaired. However, in the absence of Dmc1p, efficient Rad51p-dependent repair took place, but crossing over was suppressed. Immunostaining and protein tagging demonstrated that only Dmc1p formed strong DSB–dependent foci on meiotic chromatin, whereas the distribution of Rad51p was diffuse within nuclei. This suggests that meiotic nucleoprotein filaments consist primarily of Dmc1p. Moreover, a proximity ligation assay confirmed that little if any Rad51p forms mixed nucleoprotein filaments with Dmc1p. Dmc1p focus formation was independent of the presence of Rad51p. The absence of Dmc1p did not result in compensatory assembly of Rad51p repair foci, and even artificial DNA damage by UV failed to induce Rad51p foci in meiotic nuclei, while it did so in somatic nuclei within one and the same cell. The observed interhomologue repair deficit in dmc1Δ meiosis is consistent with a requirement for Dmc1p in promoting the homologue as the preferred recombination partner. We propose that relatively short and/or transient Rad51p nucleoprotein filaments are sufficient for intrachromosomal recombination, whereas long nucleoprotein filaments consisting primarily of Dmc1p are required for interhomolog recombination

Unsymmetric Aryl–Alkyl Disulfide Growth Inhibitors of Methicillin-Resistant \u3ci\u3eStaphylococcus aureus\u3c/i\u3e and \u3ci\u3eBacillus anthracis\u3c/i\u3e

This study describes the antibacterial properties of synthetically-produced mixed aryl alkyl disulfide compounds as a means to control the growth of Staphylococcus aureus and Bacillus anthracis. Some of these compounds exerted strong in vitro bioactivity. Our results indicate that among the twelve different aryl substituents examined, nitrophenyl derivatives provide the strongest antibiotic activities. This may be the result of electronic activation of the arylthio moiety as a leaving group for nucleophilic attack on the disulfide bond. Small alkyl residues on the other sulfur provide the best activity as well, which for different bacteria appears to be somewhat dependent on the nature of the alkyl moiety. The mechanism of action of these lipophilic disulfides is likely similar to that of previously reported N-thiolated β-lactams, which have been shown to produce alkyl-CoA disulfides through a thiol-disulfide exchange within the cytoplasm, ultimately inhibiting type II fatty acid synthesis. However, the mixed alkyl-CoA disulfides themselves show no antibacterial activity, presumably due to the inability of the highly polar compounds to cross the bacterial cell membrane. These structurally simple disulfides have been found to inhibit β-ketoacyl-acyl carrier protein synthase III, or FabH, a key enzyme in type II fatty acid biosynthesis, and thus may serve as new leads to the development of effective antibacterials for MRSA and anthrax infections