Developing Leadership for Creative Efforts: A Preface

Michael D. Mumford is the George Lynn Cross distinguished research professor of psychology at the University of Oklahoma where he directs the Center for Applied Social Research. He received his doctoral degree from the University of Georgia in 1983 in the fields of industrial and organizational psychology and psychometrics. He is a fellow of the American Psychological Association (Divisions 3, 5, 10, 14), the Society for Industrial and Organizational Psychology, and the American Psychological Society. He has written more than 270 articles on leadership, creativity, innovation, planning, and ethics. He has served as senior editor of The Leadership Quarterly, and he sits on the editorial boards of the Creativity Research Journal, The Journal of Creative Behavior, IEEE Transactions on Engineering Management, and Ethics and Behavior, among other journals. He has served as principal investor on grants totaling more than US$30 million from the National Science Foundation, The National Institute of Health, the Department of Defense, the Department of Labor, and the Department of State. He is a recipient of the Society for Industrial and Organizational Psychology’s M. Scott Myers Award for Applied Research in the Workplace.Yeshttps://us.sagepub.com/en-us/nam/manuscript-submission-guideline

Hydraulic resistance to overland flow on surfaces with partially submerged vegetation

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/96239/1/wrcr13661.pd

Modify the redefined: strategic human resource development maturity at a crossroads

This integrative literature review reports on strategic human resource development (SHRD) models that examine the strategic embeddedness of HRD (SHRD maturity) in organizations. A review and critique of all existing SHRD models is provided, exemplifying their limitations and building upon their strengths to inform a modified SHRD framework. The latter suggests an enhanced set of strategic components to assess SHRD maturity. This paper further outlines how SHRD aspirations can be practiced within complex, dynamic, and continually changing business and economic environments. The SHRD literature is advanced by new insights on how HRD scholars and practitioners could assess and enhance the maturity of their HRD interventions in the context of constantly changing (dynamic) environments. The modified SHRD framework further contributes to the academic literature with its enhanced set of strategic characteristics, as well as with its SHRD pointers, all of which can offer a better evaluation of SHRD maturity during periods of business and economic complexity and uncertainty

Severe Biallelic Loss-of-function Mutations in Nicotinamide Mononucleotide Adenylyltransferase 2 (NMNAT2) in Two Fetuses with Fetal Akinesia Deformation Sequence

The three nicotinamide mononucleotide adenylyltransferase (NMNAT) family members synthesize the electron carrier nicotinamide adenine dinucleotide (NAD+) and are essential for cellular metabolism. In mammalian axons, NMNAT activity appears to be required for axon survival and is predominantly provided by NMNAT2. NMNAT2 has recently been shown to also function as a chaperone to aid in the refolding of misfolded proteins. Nmnat2 deficiency in mice, or in its ortholog dNmnat in Drosophila, results in axon outgrowth and survival defects. Peripheral nerve axons in NMNAT2-deficient mice fail to extend and innervate targets, and skeletal muscle is severely underdeveloped. In addition, removing NMNAT2 from established axons initiates axon death by Wallerian degeneration. We report here on two stillborn siblings with fetal akinesia deformation sequence (FADS), severely reduced skeletal muscle mass and hydrops fetalis. Clinical exome sequencing identified compound heterozygous NMNAT2 variant alleles in both cases. Both protein variants are incapable of supporting axon survival in mouse primary neuron cultures when overexpressed. In vitro assays demonstrate altered protein stability and/or defects in NAD+ synthesis and chaperone functions. Thus, both patient NMNAT2 alleles are null or severely hypo-morphic. These data indicate a previously unknown role for NMNAT2 in human neurological development and provide the first direct molecular evidence to support the involvement of Wallerian degeneration in a human axonal disorder.Funding for the project comes from the NIH (R.W.S. R01NS085023; R.G.Z. R56NS095893), the UK Medical Research Council grant (J.G. MR/N004582/1), the John and Lucille van Geest Foundation (M.C.) and the Taishan Scholar Project of Shandong Province, China (R.G.Z.)

Neurotoxin-mediated potent activation of the axon degeneration regulator SARM1

Axon loss underlies symptom onset and progression in many neurodegenerative disorders. Axon degeneration in injury and disease is promoted by activation of the nicotinamide adenine dinucleotide (NAD)-consuming enzyme SARM1. Here, we report a novel activator of SARM1, a metabolite of the pesticide and neurotoxin vacor. Removal of SARM1 completely rescues mouse neurons from vacor-induced neuron and axon death in vitro and in vivo. We present the crystal structure the Drosophila SARM1 regulatory domain complexed with this activator, the vacor metabolite VMN, which as the most potent activator yet know is likely to support drug development for human SARM1 and NMNAT2 disorders. This study indicates the mechanism of neurotoxicity and pesticide action by vacor, raises important questions about other pyridines in wider use today, provides important new tools for drug discovery, and demonstrates that removing SARM1 can robustly block programmed axon death induced by toxicity as well as genetic mutation

Regulation of cell survival by sphingosine-1-phosphate receptor S1P1 via reciprocal ERK-dependent suppression of bim and PI-3-kinase/protein kinase C-mediated upregulation of Mcl-1

Although the ability of bioactive lipid sphingosine-1-phosphate (S1P) to positively regulate anti-apoptotic/pro-survival responses by binding to S1P1 is well known, the molecular mechanisms remain unclear. Here we demonstrate that expression of S1P1 renders CCL39 lung fibroblasts resistant to apoptosis following growth factor withdrawal. Resistance to apoptosis was associated with attenuated accumulation of pro-apoptotic BH3-only protein Bim. However, although blockade of extracellular signal-regulated kinase (ERK) activation could reverse S1P1-mediated suppression of Bim accumulation, inhibition of caspase-3 cleavage was unaffected. Instead S1P1-mediated inhibition of caspase-3 cleavage was reversed by inhibition of phosphatidylinositol-3-kinase (PI3K) and protein kinase C (PKC), which had no effect on S1P1 regulation of Bim. However, S1P1 suppression of caspase-3 was associated with increased expression of anti-apoptotic protein Mcl-1, the expression of which was also reduced by inhibition of PI3K and PKC. A role for the induction of Mcl-1 in regulating endogenous S1P receptor-dependent pro-survival responses in human umbilical vein endothelial cells was confirmed using S1P receptor agonist FTY720-phosphate (FTY720P). FTY720P induced a transient accumulation of Mcl-1 that was associated with a delayed onset of caspase-3 cleavage following growth factor withdrawal, whereas Mcl-1 knockdown was sufficient to enhance caspase-3 cleavage even in the presence of FTY720P. Consistent with a pro-survival role of S1P1 in disease, analysis of tissue microarrays from ER+ breast cancer patients revealed a significant correlation between S1P1 expression and tumour cell survival. In these tumours, S1P1 expression and cancer cell survival were correlated with increased activation of ERK, but not the PI3K/PKB pathway. In summary, pro-survival/anti-apoptotic signalling from S1P1 is intimately linked to its ability to promote the accumulation of pro-survival protein Mcl-1 and downregulation of pro-apoptotic BH3-only protein Bim via distinct signalling pathways. However, the functional importance of each pathway is dependent on the specific cellular context

Self Assessment in Insects: Honeybee Queens Know Their Own Strength

Contests mediate access to reproductive opportunities in almost all species of animals. An important aspect of the evolution of contests is the reduction of the costs incurred during intra-specific encounters to a minimum. However, escalated fights are commonly lethal in some species like the honeybee, Apis mellifera. By experimentally reducing honeybee queens' fighting abilities, we demonstrate that they refrain from engaging in lethal contests that typically characterize their reproductive dominance behavior and coexist peacefully within a colony. This suggests that weak queens exploit an alternative reproductive strategy and provides an explanation for rare occurrences of queen cohabitation in nature. Our results further indicate that self-assessment, but not mutual assessment of fighting ability occurs prior to and during the agonistic encounters