Unlocking the mask: A look at the process by which authentic leaders impact follower attitudes and behaviors

The conceptual and empirical links between authentic leadership and follower attitudes, behaviors, and performance outcomes have not been fully developed. Although we have a number of articles developing the theory of authentic leadership and testing propositions that will appear in a forthcoming special issue of The Leadership Quarterly (Vol. 16, Issue 3, 2005), the focus of this article is to provide some of the initial foundation work for the broader theoretical framework of how authentic leaders influence follower attitudes, behaviors, and performance. Here, we draw from positive organizational behavior, trust, hope, emotion, identification, and identity theories to describe the processes by which authentic leaders exert their influence on followers’ attitudes and behaviors. Research propositions based on the proposed theoretical model and implications for future theory building and research are presented

“Can you see the real me?” A self-based model of authentic leader and follower development

To address present and future leadership needs, a model of authentic leader and follower development is proposed and examined with respect to its relationship to veritable, sustainable follower performance. The developmental processes of leader and follower self-awareness and self-regulation are emphasized. The influence of the leader’s and followers’ personal histories and trigger events are considered as antecedents of authentic leadership and followership, as well as the reciprocal effects with an inclusive, ethical, caring and strength-based organizational climate. Positive modeling is viewed as a primary means whereby leaders develop authentic followers. Posited outcomes of authentic leader–follower relationships include heightened levels of follower trust in the leader, engagement, workplace well-being and veritable, sustainable performance. Testable propositions and directions for exploring them are presented and discussed

Fall 1970

How Water Moves in the Soil by Walter H. Gardner (page 3) Editorial (9) Turf Bulletin\u27s Photo Quiz by Fred Cheney (9) Public Relations by Marlin Ball (10) Turf Bulletin\u27s Photo Quiz Answer (11) Climate in the \u2770\u27s by James E. Newman (12) Know Your Seed--Ideas about Seed Quality by A.S. Carter (15)Seed Prices and Handling by Dwight M. Brown (16) Factors influencing Effectiveness of Two Surfactants on Water Repellent Soils by M.A. Mustafa and J. Letey (21

The Art of Hegel's Aesthetics. Hegelian Philosophy and the Perspectives of Art History

This volume explores one of modernity’s most profound and far-reaching philosophies of art: the Vorlesungen über die Ästhetik, delivered by Georg Friedrich Wilhelm Hegel in the 1820s. The book has two overriding objectives: first, to ask how Hegel’s work illuminates specific periods and artworks in light of contemporary art-historical discussions; second, to explore how art history helps us make better sense and use of Hegelian aesthetics. In bringing together a range of internationally acclaimed critical voices, the volume establishes an important disciplinary bridge between aesthetics and art history. Given the recent resurgence of interest in ‘global’ art history, and calls for more comparative approaches to ‘visual culture’, contributors ask what role Hegel has played within the field – and what role he could play in the future. What can a historical treatment of art accomplish? How should we explain the ‘need’ for certain artistic forms at different historical junctures? Has art history been ‘Hegelian’ without fully acknowledging it? Indeed, have art historians shirked some of the fundamental questions that Hegel raised

The medical student

The Medical Student was published from 1888-1921 by the students of Boston University School of Medicine

Brain Research to Ameliorate Impaired Neurodevelopment - Home-based Intervention Trial (BRAIN-HIT)

<p>Abstract</p> <p>Background</p> <p>This randomized controlled trial aims to evaluate the effects of an early developmental intervention program on the development of young children in low- and low-middle-income countries who are at risk for neurodevelopmental disability because of birth asphyxia. A group of children without perinatal complications are evaluated in the same protocol to compare the effects of early developmental intervention in healthy infants in the same communities. Birth asphyxia is the leading specific cause of neonatal mortality in low- and low-middle-income countries and is also the main cause of neonatal and long-term morbidity including mental retardation, cerebral palsy, and other neurodevelopmental disorders. Mortality and morbidity from birth asphyxia disproportionately affect more infants in low- and low-middle-income countries, particularly those from the lowest socioeconomic groups. There is evidence that relatively inexpensive programs of early developmental intervention, delivered during home visit by parent trainers, are capable of improving neurodevelopment in infants following brain insult due to birth asphyxia.</p> <p>Methods/Design</p> <p>This trial is a block-randomized controlled trial that has enrolled 174 children with birth asphyxia and 257 without perinatal complications, comparing early developmental intervention plus health and safety counseling to the control intervention receiving health and safety counseling only, in sites in India, Pakistan, and Zambia. The interventions are delivered in home visits every two weeks by parent trainers from 2 weeks after birth until age 36 months. The primary outcome of the trial is cognitive development, and secondary outcomes include social-emotional and motor development. Child, parent, and family characteristics and number of home visits completed are evaluated as moderating factors.</p> <p>Discussion</p> <p>The trial is supervised by a trial steering committee, and an independent data monitoring committee monitors the trial. Findings from this trial have the potential to inform about strategies for reducing neurodevelopmental disabilities in at-risk young children in low and middle income countries.</p> <p>Trial Registration</p> <p>Clinicaltrials.gov NCT00639184</p

Two Dot1 isoforms in Saccharomyces cerevisiae as a result of leaky scanning by the ribosome

Dot1 is a conserved histone methyltransferase that methylates histone H3 on lysine 79. We previously observed that in Saccharomyces cerevisiae, a single DOT1 gene encodes two Dot1 protein species. Here, we show that the relative abundance of the two isoforms changed under nutrient-limiting conditions. A mutagenesis approach showed that the two Dot1 isoforms are produced from two alternative translation start sites as a result of leaky scanning by the ribosome. The leaky scanning was not affected by the 5′- or 3′-untranslated regions of DOT1, indicating that translation initiation is determined by the DOT1 coding sequence. Construction of yeast strains expressing either one of the isoforms showed that both were sufficient for Dot1’s role in global H3K79 methylation and telomeric gene silencing. However, the absence of the long isoform of Dot1 altered the resistance of yeast cells to the chitin-binding drug Calcofluor White, suggesting that the two Dot1 isoforms have a differential function in cell wall biogenesis

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts