The Effective Use of Multimedia Distance Learning Technology: The Role of Technology Self-Efficacy, Attitudes, Reliability, Use and Distance in a Global Multimedia Distance Learning Classroom

According to the 1999 ASTD State of the Industry Report, the use of multimedia distance learning (MDL) technology for training delivery has increased substantially over the past few years. However, few empirical studies have been conducted that rigorously examine the factors that determine the effectiveness of MDL courses. In this study, we examine participants’ technology self-efficacy and attitudes toward technology (measured before/after training), and perceptions of technology reliability, effective use, and distance (measured after training) as antecedents to ratings of training effectiveness (general effectiveness, specific effectiveness, learning effectiveness; measured after training) in an international HRM course. In a sample of 52 participants from four countries we hypothesize that technology self-efficacy will affect participants’ attitudes toward technology; attitudes toward technology will affect participants’ perceptions of training effectiveness. In addition, we hypothesize that technology reliability and effective use will affect participants’ perceptions of classroom distance; distance perceptions will affect participants’ perceptions of training effectiveness. Finally, we hypothesize that both technology attitudes and distance perceptions will be related to participants’ perceptions of training effectiveness controlling for technology self-efficacy, reliability, and effective use. The results indicate that attitudes toward technology completely/partially mediated the relationship between technology self-efficacy and the three measures of effectiveness. Distance perceptions completely/partially mediated the relationship between technology reliability and effectiveness. Effective technology use was not significantly related to effectiveness. Finally, attitudes toward technology and distance perceptions explained a significant or marginally significant amount of variance in the effectiveness measures after controlling for technology self-efficacy, reliability, and effective use

The University of New Hampshire Engaged Scholars Academy: Instilling in Faculty Principles of Effective Partnership

Over the last decade, the University of New Hampshire (UNH) has promoted mutually beneficial partnerships between faculty and community partners vis-à-vis the Engaged Scholars Academy (ESA), a faculty development program aimed at enhancing faculty understanding of the principles of partnership and engaged scholarship. This research seeks to determine whether and how the ESA has impacted faculty-community partnerships around engaged scholarship. Findings suggest that Engaged Scholar Academy participants – as compared to non-participants – have a deeper understanding of the principles of partnership, are more likely to feel their scholarship is enhanced, spend more time with partners, engage their partners throughout the process of inquiry, and focus more on sustaining partnership outcomes

Hedge fund incentives, management commitment and survivorship

Management ownership in hedge funds sends conflicting signals—signals which reduce investors’ perception of survivorship risk. We document that decisions on management ownership are purposely self-selected. Such decisions are most likely motivated by unique incentive mechanisms imbedded in hedge funds. We examine the impact of managerial ownership decisions on fund survivorship risk by accounting for unobserved fund manager motivations that affect both ownership decisions and survivorship risk. Our findings suggest that the conventional argument that having management commitment can reduce survival risk (and therefore align the interests between managers and investors) is significantly overstated. These results are robust to using alternative ownership measures and controlling for different samples

Opera Theatre Gala presents Cupid: Friend or FOE

Kennesaw State University School of Music presents Opera Theater Gala, Cupid: Friend or FOE.https://digitalcommons.kennesaw.edu/musicprograms/1394/thumbnail.jp

Finding Complex Biological Relationships in Recent PubMed Articles Using Bio-LDA

The overwhelming amount of available scholarly literature in the life sciences poses significant challenges to scientists wishing to keep up with important developments related to their research, but also provides a useful resource for the discovery of recent information concerning genes, diseases, compounds and the interactions between them. In this paper, we describe an algorithm called Bio-LDA that uses extracted biological terminology to automatically identify latent topics, and provides a variety of measures to uncover putative relations among topics and bio-terms. Relationships identified using those approaches are combined with existing data in life science datasets to provide additional insight. Three case studies demonstrate the utility of the Bio-LDA model, including association predication, association search and connectivity map generation. This combined approach offers new opportunities for knowledge discovery in many areas of biology including target identification, lead hopping and drug repurposing.Comment: 14 pages, 8 figures, 10 table

Inhibition of ERK activation enhances the repair of double-stranded breaks via non-homologous end joining by increasing DNA-PKcs activation

AbstractNon-homologous end joining (NHEJ) is one of the major pathways that repairs double-stranded DNA breaks (DSBs). Activation of DNA-PK is required for NHEJ. However, the mechanism leading to DNA-PKcs activation remains incompletely understood. We provide evidence here that the MEK–ERK pathway plays a role in DNA-PKcs-mediated NHEJ. In comparison to the vehicle control (DMSO), etoposide (ETOP)-induced DSBs in MCF7 cells were more rapidly repaired in the presence of U0126, a specific MEK inhibitor, based on the reduction of γH2AX and tail moments. Additionally, U0126 increased reactivation of luciferase activity, which resulted from the repair of restriction enzyme-cleaved DSBs. Furthermore, while inhibition of ERK activation using the dominant-negative MEK1K97M accelerated the repair of DSBs, enforcing ERK activation with the constitutively active MEK1Q56P reduced DSB repair. In line with MEK activating ERK1 and ERK2 kinases, knockdown of either ERK1 or ERK2 increased DSB repair. Consistent with the activation of DNA-PKcs being required for NHEJ, we demonstrated that inhibition of ERK activation using U0126, MEK1K97M, and knockdown of ERK1 or ERK2 enhanced ETOP-induced activation of DNA-PKcs. Conversely, enforcing ERK activation by MEK1Q56P reduced ETOP-initiated DNA-PKcs activation. Taken together, we demonstrate that ERK reduces NHEJ-mediated repair of DSBs via attenuation of DNA-PKcs activation

Common reduction of the Raf kinase inhibitory protein in clear cell renal cell carcinoma

Despite the recent progress in our understanding of clear cell renal cell carcinomas (ccRCCs), the etiology of ccRCC remains unclear. We reported here a prevailing reduction of the raf kinase inhibitory protein (RKIP) in ccRCC. In our examination of more than 600 ccRCC patients by western blot and immunohistochemistry, RKIP was significantly reduced in 80% of tumors. Inhibition of RKIP transcription in ccRCC occurs to greater levels than VHL transcription based on the quantification analysis of their transcripts in six large datasets of DNA microarray available in Oncomine™ with the median rank of suppression being 582 and 2343 for RKIP and VHL, respectively. Collectively, the magnitude of RKIP reduction and the levels of its downregulation match those of VHL. Furthermore, RKIP displays tumor suppressing activity in ccRCC. While modulation of RKIP expression did not affect the proliferation of A498 and 786-0 ccRCC cells and neither their ability to form xenograft tumors in NOD/SCID mice, ectopic expression or knockdown of RKIP inhibited or enhanced A498 and 786-0 ccRCC cell invasion, respectively. This was associated with robust changes in vimentin expression, a marker of EMT. Taken together, we demonstrate here that downregulation of RKIP occurs frequently at a rate that reaches that of VHL, suggesting RKIP being a critical tumor suppressor for ccRCC. This is consistent with RKIP being a tumor suppressor for other cancers

A Multi-Scale Approach to Study Biochemical and Biophysical Aspects of Resveratrol on Diesel Exhaust Particle-Human Primary Lung Cell Interaction

Diesel exhaust particles (DEPs) are major air pollutants that lead to numerous human disorders, especially pulmonary diseases, partly through the induction of oxidative stress. Resveratrol is a polyphenol that ameliorates the production of reactive oxygen species (ROS) and delays aging-related processes. Herein we studied the cytoprotective effect of resveratrol on DEP-exposed human lung cells in a factorial experimental design. This work investigates biophysical features including cellular compositions and biomechanical properties, which were measured at the single-cell level using confocal Raman microspectroscopy (RM) and atomic force microscopy (AFM), respectively. Principal component analysis (PCA), hierarchical cluster analysis (HCA) and partial least square regression (PLS) analysis were applied to analyze Raman spectra with and without resveratrol protection. The health status of individual cells could be effectively predicted using an index derived from characteristic Raman spectral peak (e.g., 1006 cm−1) based on PLS model. AFM measurements indicated that cellular adhesion force was greatly reduced, while Young’s modulus was highly elevated in resveratrol treated DEP-exposed cells. Anti-oxidant resveratrol reduced DEP-induced ROS production and suppressed releases of several cytokines and chemokines. These findings suggest resveratrol may enhance resistance of human lung cells (e.g., SAEC) to air pollutants (e.g. DEPs)

IQGAP2, A candidate tumour suppressor of prostate tumorigenesis

AbstractLoss of IQGAP2 contributes to the tumorigenesis of hepatocellular carcinoma and gastric cancer. However, whether IQGAP2 also suppresses prostate tumorigenesis remains unclear. We report here that IQGAP2 is a candidate tumour suppressor of prostate cancer (PC). Elevated IQGAP2 was detected in prostatic intraepithelial neoplasia (PIN), early stages of PCs (Gleason score ≤3), and androgen-dependent LNCaP PC cells. However, IQGAP2 was expressed at substantially reduced levels not only in prostate glands and non-tumorigenic BPH-1 prostate epithelial cells but also in advanced (Gleason score 4 or 5) and androgen-independent PCs. Furthermore, xenograft tumours that were derived from stem-like DU145 cells displayed advanced features and lower levels of IQGAP2 in comparison to xenograft tumours that were produced from non stem-like DU145 cells. Collectively, these results suggest that IQGAP2 functions in the surveillance of prostate tumorigenesis. Consistent with this concept, ectopic IQGAP2 reduced the proliferation of DU145, PC3, and 293T cells as well as the invasion ability of DU145 cells. While ectopic IQGAP2 up-regulated E-cadherin in DU145 and PC3 cells, knockdown of IQGAP2 reduced E-cadherin expression. In primary PC and DU145 cells-derived xenograft tumours, the majority of tumours with high levels of IQGAP2 were strongly-positive for E-cadherin. Therefore, IQGAP2 may suppress PC tumorigenesis, at least in part, by up-regulation of E-cadherin. Mechanistically, overexpression of IQGAP2 significantly reduced AKT activation in DU145 cells and inhibition of AKT activation upregulated E-cadherin, suggesting that IQGAP2 increases E-cadherin expression by inhibiting AKT activation. Taken together, we demonstrate here that IQGAP2 is a candidate tumour suppressor of PC

A life of data: Characteristics and challenges of very long term self-tracking for health and wellness

As self-tracking has evolved from a niche movement to a mass-market phenomenon, it has become possible for people to track a broad range of activities and vital parameters over years, even decades. The associated opportunities, as well as the challenges, have had very little research attention so far. With the phenomenon of long-term tracking becoming widespread and important, we have identified its key characteristics by drawing on work from UbiComp, HCI, and health informatics. We identify important differences between long- and short-term tracking, and discuss consequences for the tracking process. Going beyond previous models for short-term tracking, we now present a model for long-term tracking, integrating its distinctive characteristics in purposeful and incidental tracking. Finally, we present major topics for future research