Leadership = Communication? The relations of leaders' communication styles with leadership styles, knowledge sharing and leadership outcomes

Purpose: The purpose of this study was to investigate the relations between leaders' communication styles and charismatic leadership, human-oriented leadership (leader's consideration), task-oriented leadership (leader's initiating structure), and leadership outcomes. Methodology: A survey was conducted among 279 employees of a governmental organization. The following six main communication styles were operationalized: verbal aggressiveness, expressiveness, preciseness, assuredness, supportiveness, and argumentativeness. Regression analyses were employed to test three main hypotheses. Findings: In line with expectations, the study showed that charismatic and human-oriented leadership are mainly communicative, while task-oriented leadership is significantly less communicative. The communication styles were strongly and differentially related to knowledge sharing behaviors, perceived leader performance, satisfaction with the leader, and subordinate's team commitment. Multiple regression analyses showed that the leadership styles mediated the relations between the communication styles and leadership outcomes. However, leader's preciseness explained variance in perceived leader performance and satisfaction with the leader above and beyond the leadership style variables. Implications: This study offers potentially invaluable input for leadership training programs by showing the importance of leader's supportiveness, assuredness, and preciseness when communicating with subordinates. Originality/value: Although one of the core elements of leadership is interpersonal communication, this study is one of the first to use a comprehensive communication styles instrument in the study of leadership. © 2009 The Author(s)

Spin 3/2 Baryons and Form Factors in AdS/QCD

We study the 5D Rarita-Schwinger fields to describe spin 3/2 baryons in AdS/QCD. We calculate the spectrum of spin 3/2 baryons (Delta resonances) and their form factors, together with meson-baryon couplings from AdS/QCD. The transition form-factors between Delta and nucleon are evaluated. Both pion and rho meson couplings have the same origin in the bulk and hence unified. The numerical values for the meson-baryon transition couplings are consistent with the values obtained from other methods. We also predict the numerical values of some new couplings associated with Delta resonances.Comment: 29 pages, 6 figure

Characterization of AKT independent effects of the synthetic AKT inhibitors SH-5 and SH-6 using an integrated approach combining transcriptomic profiling and signaling pathway perturbations

<p>Abstract</p> <p>Background</p> <p>Signal transduction processes mediated by phosphatidyl inositol phosphates affect a broad range of cellular processes such as cell cycle progression, migration and cell survival. The protein kinase AKT is one of the major effectors in this signaling network. Chronic AKT activation contributes to oncogenic transformation and tumor development. Therefore, analogs of phosphatidyl inositol phosphates (PIAs) were designed as new small drugs to block AKT activity for cancer treatment. Here we characterize the biological effects of the PIAs SH-5 and SH-6 in colorectal cancer cell lines.</p> <p>Methods</p> <p>Serum-starved or serum-supplemented human colorectal cancer cell lines SW480, HT29 and HCT116 were exposed to SH-5 and SH-6. AKT activation was determined by western blotting. Cell viability was assessed using a colorimetric XTT-based assay, apoptosis and cell cycle changes were monitored by FACS analysis. The dynamics of cell morphology alterations was evaluated by confocal and time-lapse microscopy. Transcriptional changes due to inhibitor treatment were analyzed using Affymetrix HG-U133A microarrays and RT-PCR.</p> <p>Results</p> <p>While the PIAs clearly reduce AKT phosphorylation in serum starved cells, we did not observe a significant reduction under serum supplemented conditions, giving us the opportunity to analyze AKT independent effects of these compounds. Both inhibitors induce broadly the same morphological alterations, in particular changes in cell shape and formation of intracellular vesicles. Moreover, we observed the induction of binucleated cells specifically in the SW480 cell line. Gene expression analysis revealed transcriptional alterations, which are mostly cell line specific. In accordance to the phenotype we found a gene group associated with mitosis and spindle organization down regulated in SW480 cells, but not in the other cell lines. A bioinformatics analysis using the Connectivity Map linked the gene expression pattern of the inhibitor treated SW480 cells to PKC signaling. Using confocal laser scanning microscopy and time lapse recording we identified a specific defect in the last step of the cytokinesis as responsible for the binucleation.</p> <p>Conclusions</p> <p>The PIAs SH-5 and SH-6 impinge on additional cellular targets apart from AKT in colorectal cancer cells. The effects are mostly cell line specific and have an influence at the outcome of the treatment. In view of potential clinical trials it will be necessary to take these diverse effects into consideration to optimize patient treatment.</p

Revisiting symmetries of lattice fermions via spin-flavor representation

Employing the spin-flavor representation, we investigate the structures of the doubler-mixing symmetries and the mechanisms of their spontaneous breakdown in four types of lattice fermion formulation. We first revisit the U(4)\timesU(4)A symmetries of the naive fermion with the vanishing bare mass m, and re-express them in terms of the spin-flavor representation. We apply the same method to the Wilson fermion, which possesses only the U(1) vector symmetry for general values of m. For a special value of m, however, there emerges an additional U(1) symmetry to be broken by pion condensation. We also explore two types of minimally doubled fermion, and discover a similar kind of symmetry enhancement and its spontaneous breakdown.Comment: 25 pages, no figure;v2 typos corrected;v3 Sec.2 is shortened. To appear in JHE

Healthism and the experiences of social, healthcare and self-stigma of women with higher weight

This study analyses how the discourse of healthism contributes to the social construction of weight stigma in women with higher-weight. In-depth semi-structured interviews were conducted with nine women who had undergone bariatric surgery and had lived with higher-weight during many years. A thematic analysis from a latent and constructionist perspective showed how the discourse of healthism was behind the experiences of stigma lived by the participants in the social and healthcare field. Even instances of self-stigma were found in our data. This study also illustrates how people influenced by healthism assumed individualism and the importance of body shape, core values of neoliberal consumer societies. In this way, people tended to blame women with higher-weight for their weight and to discriminate against for being far from the socially established ideal body. The findings can be useful to prevent weight stigmatization and to promote more appropriate and respectful strategies for obesity prevention and treatment

Noncoding deletions reveal a gene that is critical for intestinal function

Large-scale genome sequencing is poised to provide a substantial increase in the rate of discovery of disease-associated mutations, but the functional interpretation of such mutations remains challenging. Here we show that deletions of a sequence on human chromosome 16 that we term the intestine-critical region (ICR) cause intractable congenital diarrhoea in infants1,2. Reporter assays in transgenic mice show that the ICR contains a regulatory sequence that activates transcription during the development of the gastrointestinal system. Targeted deletion of the ICR in mice caused symptoms that recapitulated the human condition. Transcriptome analysis revealed that an unannotated open reading frame (Percc1) flanks the regulatory sequence, and the expression of this gene was lost in the developing gut of mice that lacked the ICR. Percc1-knockout mice displayed phenotypes similar to those observed upon ICR deletion in mice and patients, whereas an ICR-driven Percc1 transgene was sufficient to rescue the phenotypes found in mice that lacked the ICR. Together, our results identify a gene that is critical for intestinal function and underscore the need for targeted in vivo studies to interpret the growing number of clinical genetic findings that do not affect known protein-coding genes