Disability, Gender and Race: Does Educational Attainment Reduce Earning Disparity for All or Just Some?

Although interest in research on persons with disabilities has grown steadily, these individuals continue to encounter workplace discrimination and remain marginalized and understudied. We draw on human capital and discrimination theories to propose and test hypotheses on the effects of educational attainment on earnings (in)equality for persons with disabilities and the moderating influence of gender and race using 885,950 records, including 40,438 persons with disabilities from the American Community Survey 2015 (United States Census Bureau, 2015). Consistent with human capital theory, we find that persons with disabilities benefit from greater educational attainment, yet consistent with disability discrimination theories, we find evidence that they are less likely to convert educational gains for master’s and higher degrees into earning gains, and consistent with theories on multiple sources of discrimination, we find that women with disabilities may be doubly disadvantaged. These results, however, are mixed and complex. Considering the importance of harnessing diverse talent in organizations, we outline implications for research and practice toward reducing workplace discrimination

Disability Severity, Professional Isolation Perceptions, and Career Outcomes: When Does Leader–Member Exchange Quality Matter?

Employees with disability-related communication impairment often experience isolation from professional connections that can negatively affect their careers. Management research suggests that having lower quality leader relationships can be an obstacle to the development of professional connections for employees with disabilities. However, in this paper we suggest that lower quality leader–member exchange (LMX) relationships may not be a uniform hurdle for the professional isolation of employees with disability-related communication impairment. Drawing on psychological disengagement theory, we predict that employees with more severe, rather than less severe, communication impairment develop resilience to challenges in lower quality LMX relationships by psychologically disengaging from professional connections and, in turn, bear fewer negative consequences of professional isolation on career outcomes. In two studies of deaf and hard of hearing employees, we find that in lower quality LMX relationships employees with more severe communication impairment perceive being less isolated than employees with less severe communication impairment, and, in turn, report better career outcomes. Overall, our findings suggest that employees with more severe communication impairment may develop effective coping strategies to manage challenges of perceived professional isolation for career outcomes when in lower quality LMX relationships

Toward Greater Understanding of the Pernicious Effects of Workplace Envy

Despite the fact that envy is widely viewed as one of the most pernicious and dysfunctional workplace emotions, research has ignored its longer-term consequences. This oversight can largely be attributed to over reliance on the relatively static affective events framework that does not account for how envy-eliciting events can threaten an individual’s perceptions of social standing or trigger emotional schema from previous events. Hence, we propose an extension of this framework in order to address these shortcomings and in order to account more fully for the cumulative effects of prior envy-eliciting events. In particular, by integrating insights from social comparison and emotional schema theories into the current framework, we offer a deeper, more fine-grained explanation of the cumulative effects of emotionally congruent envious episodes. We believe that these additional insights will offer a perspective, for researchers and practitioners alike, into how envy-eliciting events can result in more malicious and chronic behavior. Future research and managerial implications are discussed.This is an author's peer-reviewed final manuscript, as accepted by the publisher. The published article is copyrighted by Taylor & Francis and can be found at: [http://www.tandfonline.com/toc/rijh20/current#.VEb6wmNPJm0.Keywords: social comparison, envy, emotion, emotional schema, affective events theor

Análisis sincrónico de la gobernanza universitaria: una mirada teórica a los años sesenta y setenta

Resumen Estudiar las perspectivas en el campo del gobierno de las universidades tiene cada día mayor preeminencia, especialmente si se toma en cuenta la incuestionable necesidad de avanzar hacía organizaciones más eficientes, conectadas con las expectativas que sobre ellas tiene la sociedad. Considerando este escenario, el trabajo se ha planteado como propósito central realizar un análisis de carácter sincrónico del concepto de gobernanza y la constitución de los gobiernos universitarios. Desde el punto de vista metodológico se utilizaron fuentes secundarias: una revisión de papers publicados esencialmente en revistas de habla inglesa. El estudio comprende las décadas del sesenta y el setenta. Se centra en las raíces del concepto de gobernanza universitaria, en la delineación de los actores que participan en sus gobiernos y en las relaciones de poder que fluyen entre ellos.Entre las principales conclusiones, se pueden destacar como el estamento académico desde el principio de las universidades ha ocupado el rol casi plenipotenciario en su respectivo gobierno, producto de esto, en el correr del desarrollo y mientras la complejidad organizacional se incrementaba, es que fue necesario incorporar nuevos actores a los sistemas de gestión; todo lo anterior, teniendo en cuenta que dos elementos han sido fundamentales para la sobrevivencia de este tipo de instituciones, la legitimidad otorgada por la sociedad y los principios de estrategias del ámbito de la gestión

A Novel Mutation in LEPRE1 That Eliminates Only the KDEL ER- Retrieval Sequence Causes Non-Lethal Osteogenesis Imperfecta

Prolyl 3-hydroxylase 1 (P3H1), encoded by the LEPRE1 gene, forms a molecular complex with cartilage-associated protein (CRTAP) and cyclophilin B (encoded by PPIB) in the endoplasmic reticulum (ER). This complex is responsible for one step in collagen post-translational modification, the prolyl 3-hydroxylation of specific proline residues, specifically α1(I) Pro986. P3H1 provides the enzymatic activity of the complex and has a Lys-Asp-Glu-Leu (KDEL) ER-retrieval sequence at the carboxyl terminus. Loss of function mutations in LEPRE1 lead to the Pro986 residue remaining unmodified and lead to slow folding and excessive helical post-translational modification of type I collagen, which is seen in both dominant and recessive osteogenesis imperfecta (OI). Here, we present the case of siblings with non-lethal OI due to novel compound heterozygous mutations in LEPRE1 (c.484delG and c.2155dupC). The results of RNA analysis and real-time PCR suggest that mRNA with c.2155dupC escapes from nonsense-mediated RNA decay. Without the KDEL ER- retrieval sequence, the product of the c.2155dupC variant cannot be retained in the ER. This is the first report of a mutation in LEPRE1 that eliminates only the KDEL ER-retrieval sequence, whereas other functional domains remain intact. Our study shows, for the first time, that the KDEL ER- retrieval sequence is essential for P3H1 functionality and that a defect in KDEL is sufficient for disease onset

Helicobacter pylori versus the Host: Remodeling of the Bacterial Outer Membrane Is Required for Survival in the Gastric Mucosa

Modification of bacterial surface structures, such as the lipid A portion of lipopolysaccharide (LPS), is used by many pathogenic bacteria to help evade the host innate immune response. Helicobacter pylori, a gram-negative bacterium capable of chronic colonization of the human stomach, modifies its lipid A by removal of phosphate groups from the 1- and 4′-positions of the lipid A backbone. In this study, we identify the enzyme responsible for dephosphorylation of the lipid A 4′-phosphate group in H. pylori, Jhp1487 (LpxF). To ascertain the role these modifications play in the pathogenesis of H. pylori, we created mutants in lpxE (1-phosphatase), lpxF (4′-phosphatase) and a double lpxE/F mutant. Analysis of lipid A isolated from lpxE and lpxF mutants revealed lipid A species with a 1 or 4′-phosphate group, respectively while the double lpxE/F mutant revealed a bis-phosphorylated lipid A. Mutants lacking lpxE, lpxF, or lpxE/F show a 16, 360 and 1020 fold increase in sensitivity to the cationic antimicrobial peptide polymyxin B, respectively. Moreover, a similar loss of resistance is seen against a variety of CAMPs found in the human body including LL37, β-defensin 2, and P-113. Using a fluorescent derivative of polymyxin we demonstrate that, unlike wild type bacteria, polymyxin readily associates with the lpxE/F mutant. Presumably, the increase in the negative charge of H. pylori LPS allows for binding of the peptide to the bacterial surface. Interestingly, the action of LpxE and LpxF was shown to decrease recognition of Helicobacter LPS by the innate immune receptor, Toll-like Receptor 4. Furthermore, lpxE/F mutants were unable to colonize the gastric mucosa of C57BL/6J and C57BL/6J tlr4 -/- mice when compared to wild type H. pylori. Our results demonstrate that dephosphorylation of the lipid A domain of H. pylori LPS by LpxE and LpxF is key to its ability to colonize a mammalian host

IFN-λ3, not IFN-λ4, likely mediates IFNL3-IFNL4 haplotype-dependent hepatic inflammation and fibrosis

Genetic variation in the IFNL3-IFNL4 (interferon-λ3-interferon-λ4) region is associated with hepatic inflammation and fibrosis. Whether IFN-λ3 or IFN-λ4 protein drives this association is not known. We demonstrate that hepatic inflammation, fibrosis stage, fibrosis progression rate, hepatic infiltration of immune cells, IFN-λ3 expression, and serum sCD163 levels (a marker of activated macrophages) are greater in individuals with the IFNL3-IFNL4 risk haplotype that does not produce IFN-λ4, but produces IFN-λ3. No difference in these features was observed according to genotype at rs117648444, which encodes a substitution at position 70 of the IFN-λ4 protein and reduces IFN-λ4 activity, or between patients encoding functionally defective IFN-λ4 (IFN-λ4-Ser70) and those encoding fully active IFN-λ4-Pro70. The two proposed functional variants (rs368234815 and rs4803217) were not superior to the discovery SNP rs12979860 with respect to liver inflammation or fibrosis phenotype. IFN-λ3 rather than IFN-λ4 likely mediates IFNL3-IFNL4 haplotype-dependent hepatic inflammation and fibrosis

Through-Bond Interactions in the Diradical Intermediates Formed in the Rearrangements of Bicyclo[ n

Article on through-bond interactions in the diradical intermediates formed in the rearrangements of bicyclo[n.m.0]alkatetraenes

Macrocephaly and developmental delay caused by missense variants in RAB5C

Rab GTPases are important regulators of intracellular vesicular trafficking. RAB5C is a member of the Rab GTPase family that plays an important role in the endocytic pathway, membrane protein recycling and signaling. Here we report on 12 individuals with nine different heterozygous de novo variants in RAB5C. All but one patient with missense variants (n = 9) exhibited macrocephaly, combined with mild-to-moderate developmental delay. Patients with loss of function variants (n = 2) had an apparently more severe clinical phenotype with refractory epilepsy and intellectual disability but a normal head circumference. Four missense variants were investigated experimentally. In vitro biochemical studies revealed that all four variants were damaging, resulting in increased nucleotide exchange rate, attenuated responsivity to guanine exchange factors and heterogeneous effects on interactions with effector proteins. Studies in C. elegans confirmed that all four variants were damaging in vivo and showed defects in endocytic pathway function. The variant heterozygotes displayed phenotypes that were not observed in null heterozygotes, with two shown to be through a dominant negative mechanism. Expression of the human RAB5C variants in zebrafish embryos resulted in defective development, further underscoring the damaging effects of the RAB5C variants. Our combined bioinformatic, in vitro and in vivo experimental studies and clinical data support the association of RAB5C missense variants with a neurodevelopmental disorder characterized by macrocephaly and mild-to-moderate developmental delay through disruption of the endocytic pathway

Evaluation of analgesic protocol effect on calf behavior after concurrent castration and dehorning

Castration and dehorning are common procedures in the US cattle industry, but the impact of analgesic programs on post-surgical behavior is not well documented. The research objective was to determine the impact of three different analgesic protocols: (sodium salicylate; a combination of xylazine, ketamine and butorphanol; and both treatments together) compared to the absence of analgesia on cattle behavior after concurrent castration and dehorning. Accelerometers recorded activity on 40 calves for three periods of time: prior to sham surgery, between sham and actual surgery, and 4 days post-surgery. Significant interactions (P<0.05) were found between treatment and time relative to surgery. Cattle treated with a combination of ketamine, butorphanol, and sodium salicylate spent more time lying after the procedures compared to cattle receiving only xylazine, ketamine, and butorphanol