Faculty Research Incentives and Business School Health: A New Perspective for Marketing

Prior research has heavily debated the value of academic research of faculty to the business schools that employ them. We study, conceptually and empirically (by surveying faculty and interviewing (associate) deans), the role of the faculty research incentive system in business school health. We find that higher research health is congruent with higher teaching quality, stronger resource support, and stronger external stakeholder support. R-quality of research (i.e., rigor) contributes more strongly to research health than research quantity, while q-quality of research (i.e., relevance) contributes positively to teaching quality and external stakeholder support. We also find that research task incentives are misaligned: (1) in faculty evaluations, the number of publications receives too much weight, while creativity, literacy, practical relevance, and awards receive too little weight; and (2) the faculty feels that they are insufficiently compensated, while (associate) deans feel faculty is compensated too much for its research. These incentive misalignments are largest in schools that perform the worst on research and business school health overall. We explore improvements that business schools and faculty can introduce

Academic Research in Marketing and Business School Health

Academic research in marketing is of key importance to the health of business schools. However, there has been considerable debate in recent years whether academic research in marketing, and business in general, delivers enough on this promise. Our goal is to add a coherent and novel faculty management perspective to this debate. We identify three limiters in the faculty management system that restrict the impact academic research in marketing may have on business school health: (1) the imperfect metrics used to evaluate marketing academics that focus primarily on quantity, (2) the weak professional alignment betwee

Faculty Research Incentives and Business School Health: A New Perspective from and for Marketing

Grounded in sociological agency theory, the authors study the role of the faculty research incentive system in the academic research conducted at business schools and business school health. The authors surveyed 234 marketing professors and completed 22 interviews with 14 (associate) deans and 8 external institution stakeholders. They find that research quantity contributes to the research health of the school, but not to other aspects of business school health. r-quality of research (i.e., rigor) contributes more strongly to the research health of the school than research quantity. q-quality (i.e., practical importance) of research does not contribute to the research health of the school but contributes positively to teaching health and several other dimensions of business school health. Faculty research incentives are misaligned: (1) when monitoring research faculty, the number of publications receives too much weight, while creativity, literacy, relevance, and awards receive too little weight; and (2) on average, faculty feels that they are insufficiently compensated for their research, while (associate) deans feel they are compensated too much for their research. These incentive misalignments are largest in schools that perform the worst on research (r- and q-) quality. The authors explore how business schools and faculty can remedy these misalignments

Choice in Computer-Mediated Environments

In the last several years, the increased diffusion of computer andtelecommunications technologies in businesses and homes has produced newways for organizations to connect with their customers. These computermediated environments (CMEs) such as the World Wide Web raise new researchquestions. In this paper, we examine the potential research issuesassociated with CMEs in five areas: (1) decision processes, (2) advertisingand communications, (3) brand choice, (4) brand communities, and (5)pricing.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47229/1/11002_2004_Article_138117.pd

LAT Onboard Science: Gamma-Ray Burst Identification

The main goal of the Large Area Telescope (LAT) onboard science program is to provide quick identification and localization of Gamma Ray Bursts (GRB) onboard the LAT for follow-up observations by other observatories. The GRB identification and localization algorithm will provide celestial coordinates with an error region that will be distributed via the Gamma ray burst Coordinate Network (GCN). We present results that show our sensitivity to bursts as characterized using Monte Carlo simulations of the GLAST observatory. We describe and characterize the method of onboard track determination and the GRB identification and localization algorithm. Onboard track determination is considerably different than in the onground case, resulting in a substantially altered point spread function. The algorithm contains tunable parameters which may be adjusted after launch when real bursts characteristics at very high energies have been identified

Concentration Independent Modulation of Local Micromechanics in a Fibrin Gel

Methods for tuning extracellular matrix (ECM) mechanics in 3D cell culture that rely on increasing the concentration of either protein or cross-linking molecules fail to control important parameters such as pore size, ligand density, and molecular diffusivity. Alternatively, ECM stiffness can be modulated independently from protein concentration by mechanically loading the ECM. We have developed a novel device for generating stiffness gradients in naturally derived ECMs, where stiffness is tuned by inducing strain, while local mechanical properties are directly determined by laser tweezers based active microrheology (AMR). Hydrogel substrates polymerized within 35 mm diameter Petri dishes are strained non-uniformly by the precise rotation of an embedded cylindrical post, and exhibit a position-dependent stiffness with little to no modulation of local mesh geometry. Here we present the device in the context of fibrin hydrogels. First AMR is used to directly measure local micromechanics in unstrained hydrogels of increasing fibrin concentration. Changes in stiffness are then mapped within our device, where fibrin concentration is held constant. Fluorescence confocal imaging and orbital particle tracking are used to quantify structural changes in fibrin on the micro and nano levels respectively. The micromechanical strain stiffening measured by microrheology is not accompanied by ECM microstructural changes under our applied loads, as measured by confocal microscopy. However, super-resolution orbital tracking reveals nanostructural straightening, lengthening, and reduced movement of fibrin fibers. Furthermore, we show that aortic smooth muscle cells cultured within our device are morphologically sensitive to the induced mechanical gradient. Our results demonstrate a powerful cell culture tool that can be used in the study of mechanical effects on cellular physiology in naturally derived 3D ECM tissues

VEGFR2 promotes central endothelial activation and the spread of pain in inflammatory arthritis

Chronic pain can develop in response to conditions such as inflammatory arthritis. The central mechanisms underlying the development and maintenance of chronic pain in humans are not well elucidated although there is evidence for a role of microglia and astrocytes. However in pre-clinical models of pain, including models of inflammatory arthritis, there is a wealth of evidence indicating roles for pathological glial reactivity within the CNS. In the spinal dorsal horn of rats with painful inflammatory arthritis we found both a significant increase in CD11b+ microglia-like cells and GFAP+ astrocytes associated with blood vessels, and the number of activated blood vessels expressing the adhesion molecule ICAM-1, indicating potential glio-vascular activation. Using pharmacological interventions targeting VEGFR2 in arthritic rats, to inhibit endothelial cell activation, the number of dorsal horn ICAM-1+ blood vessels, CD11b+ microglia and the development of secondary mechanical allodynia, an indicator of central sensitization, were all prevented. Targeting endothelial VEGFR2 by inducible Tie2-specific VEGFR2 knock-out also prevented secondary allodynia in mice and glio-vascular activation in the dorsal horn in response to inflammatory arthritis. Inhibition of VEGFR2 in vitro significantly blocked ICAM-1-dependent monocyte adhesion to brain microvascular endothelial cells, when stimulated with inflammatory mediators TNFa and VEGF-A165a. Taken together our findings suggest that a novel VEGFR2-mediated spinal cord gliovascular mechanism may promote peripheral CD11b+ circulating cell transmigration into the CNS parenchyma and contribute to the development of chronic pain in inflammatory arthritis. We hypothesise that preventing this glio-vascular activation and circulating cell translocation into the spinal cord could be a new therapeutic strategy for pain caused by rheumatoid arthritis