“Brick & Mortar” Education and “Real World” Experience: Assessing HRM Alumni Perceptions of their Early Professional Development

In this research we examined the extent to which three distinct human resource management (HRM) undergraduate programs provide coverage of the 13 core content areas specified by the Society for Human Resource Management (SHRM) and explored the usefulness of various ways of learning including their undergraduate coursework, an internship, and previous work experience as related to early professional development. Based on perceptions of HRM alumni, the findings reveal that the three curricula provided significant differences in levels of proficiency in seven of the core areas and in perceived usefulness of the learning methods. Implications for HRM curriculum development and students’ professional development are discussed

The Impact of Passing the Professional in Human Resources Exam on Early Career Success for Undergraduates Entering the Human Resource Field

This study investigates the impact of passing the Professional in Human Resources (PHR) certification exam on the early career success of recent college graduates. Data were gathered from alumni of three Midwestern universities who earned an undergraduate degree in business administration (i.e., BBA) with a major in human resources. The survey was designed to measure early career success indicators including finding a job in the HR field, starting salary, and number of promotions. Results reveal that the probability of one’s first job after graduation being in human resources was significantly greater for those who had passed the PHR exam compared with those who did not pass or did not take the exam. Passing the PHR exam was not associated with significant differences in starting salary or early career promotions. Implications, study strengths and limitations, and suggestions for future research are discussed

In Solidarity

This edition of Next Page is a departure from our usual question and answer format with a featured campus reader. Instead, we asked speakers who participated in the College’s recent Student Solidarity Rally (March 1, 2017) to recommend readings that might further our understanding of the topics on which they spoke

Whale call data for the North Pacific : November 1995 through July 1999 occurrence of calling whales and source locations from SOSUS and other acoustic systems

May also be cited as: WHOI-00-02Calls of blue whales (Balaenoptera musculus), fin whales (Balaenoptera physalus), and humpback whales (Megaptera novaeangliae) were identified in the data from U.S. Navy Sound Surveilance System (SOSUS) and other hydrophone arrays. These data on calling whales from November 1995 through July 1999 have been listed here for four offshore, deep-water Regions along continental margins of the North and Northeast Pacific. The occurrence of calling whales was monitored during two-day periods each week. Call data recorded from each array identified species, call occurrence, variation, received beam, and relative numbers of calling whales. This allowed assessment of seasonal distribution of calls for the different species, and provided locations for sources received at multiple arrays. Blue whale tonal sounds were distributed widely, received most in the NW Region, with a peak in occurrence in the fall. Fin whale "20-Hz" repetitive pulse sequences were received from whales grouped in local areas in all Regions, with a peak in occurrence in midwinter. Humpback songs were received from December through May particularly in the SE Region. The offshore listening systems allowed basin-wide monitoring of the seasonal distribution of these callng whales.Funding was provided by the Office Naval Research under Grant No. N00014-96-1-1130, SERDP and CNO N45

Characterization of early disease status in treatment-naive male paediatric patients with Fabry disease enrolled in a randomized clinical trial.

Trial designThis analysis characterizes the degree of early organ involvement in a cohort of oligo-symptomatic untreated young patients with Fabry disease enrolled in an ongoing randomized, open-label, parallel-group, phase 3B clinical trial.MethodsMales aged 5-18 years with complete α-galactosidase A deficiency, without symptoms of major organ damage, were enrolled in a phase 3B trial evaluating two doses of agalsidase beta. Baseline disease characteristics of 31 eligible patients (median age 12 years) were studied, including cellular globotriaosylceramide (GL-3) accumulation in skin (n = 31) and kidney biopsy (n = 6; median age 15 years; range 13-17 years), renal function, and glycolipid levels (plasma, urine).ResultsPlasma and urinary GL-3 levels were abnormal in 25 of 30 and 31 of 31 patients, respectively. Plasma lyso-GL-3 was elevated in all patients. GL-3 accumulation was documented in superficial skin capillary endothelial cells (23/31 patients) and deep vessel endothelial cells (23/29 patients). The mean glomerular filtration rate (GFR), measured by plasma disappearance of iohexol, was 118.1 mL/min/1.73 m(2) (range 90.4-161.0 mL/min/1.73 m(2)) and the median urinary albumin/creatinine ratio was 10 mg/g (range 4.0-27.0 mg/g). On electron microscopy, renal biopsy revealed GL-3 accumulation in all glomerular cell types (podocytes and parietal, endothelial, and mesangial cells), as well as in peritubular capillary and non-capillary endothelial, interstitial, vascular smooth muscle, and distal tubules/collecting duct cells. Lesions indicative of early Fabry arteriopathy and segmental effacement of podocyte foot processes were found in all 6 patients.ConclusionsThese data reveal that in this small cohort of children with Fabry disease, histological evidence of GL-3 accumulation, and cellular and vascular injury are present in renal tissues at very early stages of the disease, and are noted before onset of microalbuminuria and development of clinically significant renal events (e.g. reduced GFR). These data give additional support to the consideration of early initiation of enzyme replacement therapy, potentially improving long-term outcome.Trial registrationClinicalTrials.gov NCT00701415

Pathogenic forms of tau inhibit kinesin-dependent axonal transport through a mechanism involving activation of axonal phosphotransferases

© The Author(s), 2011. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Journal of Neuroscience 31 (2011): 9858-9868, doi:10.1523/JNEUROSCI.0560-11.2011.Aggregated filamentous forms of hyperphosphorylated tau (a microtubule-associated protein) represent pathological hallmarks of Alzheimer's disease (AD) and other tauopathies. While axonal transport dysfunction is thought to represent a primary pathogenic factor in AD and other neurodegenerative diseases, the direct molecular link between pathogenic forms of tau and deficits in axonal transport remain unclear. Recently, we demonstrated that filamentous, but not soluble, forms of wild-type tau inhibit anterograde, kinesin-based fast axonal transport (FAT) by activating axonal protein phosphatase 1 (PP1) and glycogen synthase kinase 3 (GSK3), independent of microtubule binding. Here, we demonstrate that amino acids 2–18 of tau, comprising a phosphatase-activating domain (PAD), are necessary and sufficient for activation of this pathway in axoplasms isolated from squid giant axons. Various pathogenic forms of tau displaying increased exposure of PAD inhibited anterograde FAT in squid axoplasm. Importantly, immunohistochemical studies using a novel PAD-specific monoclonal antibody in human postmortem tissue indicated that increased PAD exposure represents an early pathogenic event in AD that closely associates in time with AT8 immunoreactivity, an early marker of pathological tau. We propose a model of pathogenesis in which disease-associated changes in tau conformation lead to increased exposure of PAD, activation of PP1-GSK3, and inhibition of FAT. Results from these studies reveal a novel role for tau in modulating axonal phosphotransferases and provide a molecular basis for a toxic gain-of-function associated with pathogenic forms of tau.This work was supported by NIH Grants T32 AG020506-07 (N.M.K.); AG09466 (L.I.B.); and NS23868, NS23320, and NS41170 (S.T.B.); as well as 2007/2008 MBL Summer Research Fellowships and an ALS/CVS Therapy Alliance grant (G.M.)