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Human capital sourcing is a major determinant of firm effectiveness. We develop logic that favors a specialized sourcing strategy in which organizations emphasize one type of sourcing, focusing either on developing or acquiring human capital, as opposed to a balanced approach. We then identify characteristics and capabilities that lead firms to adopt one sourcing type over another. Additionally, we examine whether aligning sourcing decisions with organizational characteristics and capabilities relates to better performance. We use panel regression to examine how sourcing decisions ultimately impact performance. Results suggest that specialized sourcing relates to improved performance more strongly than does a balanced approach, that certain organizational capabilities are advantageous for specific types of sourcing, and that aligning sourcing strategy with organizational fit partially relates to greater organizational performance. [ABSTRACT FROM AUTHOR]

Market-based instruments are increasingly seen as an option for policy-makers to achieve the environmental and economic outcomes that society demands. The attitudes of farmers towards the concept of producing environmental services on farms and what they would need to be paid for such services were explored in a study of 45 farmers in the Walgett Shire of north-west NSW. To contractually manage and maintain parcels of their land for conservation inperpetuity, participants reported that they would need to be paid $25/ha for 'basic' grazing country, $53/ha for country considered to be 'special' grazing country (e.g. riparian zone, unique topography, wildlife corridors), and $206/ha for cropping country. While farmers were receptive to the concept of becoming involved in payments for the production of environmental services, factors such as age, land value, concerns about the environment, the role of government, and the binding nature of in-perpetuity contractual arrangements, affected their willingness to participate. [ABSTRACT FROM AUTHOR]

The article explores the potential benefits of developing comprehensive approaches for estimating the economic and social value of emerging and established university innovations. Topics include the role of colleges and universities in the creation and dissemination of innovations that affect the knowledge economy, directions in the valuation of university entrepreneurship, and recommendations for future research.

Hyperplastic Polyposis (HPPS) is a poorly characterized syndrome that increases colorectal cancer (CRC) risk. We aimed to provide a molecular classification of HPPS. We obtained 282 tumours from 32 putative HPPS patients with ≥ 10 hyperplastic polyps (HPs); some patients also had adenomas and CRCs. We found no good evidence of microsatellite instability (MSI) in our samples. The epithelium of HPs was monoclonal. Somatic BRAF mutations occurred in two-thirds of our patients' HPs, and KRAS2 mutations in 10%; both mutations were more common in younger cases. The respective mutation frequencies in a set of 'sporadic' HPs were 18% and 10%. Importantly, the putative HPPS patients generally fell into two readily defined groups, one set whose polyps had BRAF mutations, and another set whose polyps had KRAS2 mutations. The most plausible explanation for this observation is that there exist different forms of inherited predisposition to HPPS, and that these determine whether polyps follow a BRAF or KRAS2 pathway. Most adenomas and CRCs from our putative HPPS patients had 'classical' morphology and few of these lesions had BRAF or KRAS2 mutations. These findings suggest that tumourigenesis in HPPS does not necessarily follow the 'serrated' pathway. Although current definitions of HPPS are sub-optimal, we suggest that diagnosis could benefit from molecular analysis. Specifically, testing BRAF and KRAS2 mutations, and perhaps MSI, in multiple polyps could help to distinguish HPPS from sporadic HPs. We propose a specific model which would have diagnosed five more of our cases as HPPS compared with the WHO clinical criteria. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Presents a study which undertook a genomewide screen of 11 families segregating multiple leiomyomatosis (ML) to detect the localization of the ML gene. Subjects and methods; Results; Discussion.

Classifying behavior patterns in mouse models of neurological, psychiatric and neurodevelopmental disorders is critical for understanding disease causality and treatment. However, complete characterization of behavior is time-intensive, prone to subjective scoring, and often requires specialized equipment. Although several reports describe automated home-cage monitoring and individual task scoring methods, we report the first open source, comprehensive toolbox for automating the scoring of several common behavior tasks used by the neuroscience community. We show this new toolbox is robust and achieves equal or better consistency when compared to manual scoring methods. We use this toolbox to study the alterations in behavior that occur following blast-induced traumatic brain injury (bTBI), and study if these behavior patterns are altered following genetic deletion of the transcription factor Ets-like kinase 1 (Elk-1). Due to the role of Elk-1 in neuronal survival and proposed role in synaptic plasticity, we hypothesized that Elk-1 deletion would improve some neurobehavioral deficits, while impairing others, following blast exposure. In Elk-1 knockout animals, deficits in open field, spatial object recognition and elevated zero maze performance after blast exposure disappeared, while new significant deficits appeared in spatial and associative memory. These are the first data suggesting a molecular mediator of anxiety deficits following blast-induced traumatic brain injury, and represent the utility of the broad screening tool we developed. More broadly, we envision this open-source toolbox will provide a more consistent and rapid analysis of behavior across many neurological diseases, promoting the rapid discovery of novel pathways mediating disease progression and treatment.

The loading conditions used in some current in vivo and in vitro blast-induced neurotrauma models may not be representative of real-world blast conditions. To address these limitations, we developed a compressed-gas driven shock tube with different driven lengths that can generate Friedlander-type blasts. The shock tube can generate overpressures up to 650 kPa with durations between 0.3 and 1.1 ms using compressed helium driver gas, and peak overpressures up to 450 kPa with durations between 0.6 and 3 ms using compressed nitrogen. This device is used for short duration blast overpressure loading for small animal in vivo injury models, and contrasts the more frequently used long duration/high impulse blast overpressures in the literature. We also developed a new apparatus that is used with the shock tube to recreate the in vivo intracranial overpressure response for loading in vitro culture preparations. The receiver device surrounds the culture with materials of similar impedance to facilitate the propagation of a single overpressure pulse through the tissue. This method prevents pressure waves reflecting off the tissue that can cause unrealistic deformation and injury. The receiver performance was characterized using the longest helium-driven shock tube, and produced in-fluid overpressures up to 1500 kPa at the location where a culture would be placed. This response was well correlated with the overpressure conditions from the shock tube (R2 = 0.97). Finite element models of the shock tube and receiver were developed and validated to better elucidate the mechanics of this methodology. A demonstration exposing a culture to the loading conditions created by this system suggest tissue strains less than 5% for all pressure levels simulated, which was well below functional deficit thresholds for strain rates less than 50 s-1. This novel system is not limited to a specific type of culture model and can be modified to reproduce more complex pressure pulses.

Due to the prominent role of improvised explosive devices (IEDs) in wounding patterns of U.S. war-fighters in Iraq and Afghanistan, blast injury has risen to a new level of importance and is recognized to be a major cause of injuries to the brain. However, an injury risk-function for microscopic, macroscopic, behavioral, and neurological deficits has yet to be defined. While operational blast injuries can be very complex and thus difficult to analyze, a simplified blast injury model would facilitate studies correlating biological outcomes with blast biomechanics to define tolerance criteria. Blast-induced traumatic brain injury (bTBI) results from the translation of a shock wave in air, such as that produced by an IED, into a pressure wave within the skull-brain complex. Our blast injury methodology recapitulates this phenomenon in vitro, allowing for control of the injury biomechanics via a compressed-gas shock tube used in conjunction with a custom-designed, fluid-filled receiver that contains the living culture. The receiver converts the air shock wave into a fast-rising pressure transient with minimal reflections, mimicking the intracranial pressure history in blast. We have developed an organotypic hippocampal slice culture model that exhibits cell death when exposed to a 530  17.7 kPa peak overpressure with a 1.026 ± 0.017 ms duration and 190 ± 10.7 kPa-ms impulse in-air. We have also injured a simplified in vitro model of the blood-brain barrier, which exhibits disrupted integrity immediately following exposure to 581  10.0 kPa peak overpressure with a 1.067 ms ± 0.006 ms duration and 222 ± 6.9 kPa-ms impulse in-air. To better prevent and treat bTBI, both the initiating biomechanics and the ensuing pathobiology must be understood in greater detail. A well-characterized, in vitro model of bTBI, in conjunction with animal models, will be a powerful tool for developing strategies to mitigate the risks of bTBI.

Two quantitative, automated methods for the determination of C reactive protein (CRP) were compared: turbidimetry (Cobas Fara II, Roche, Welwyn Garden City, UK) and fluorescence polarisation TDx, Abbott, Wokingham, UK). One hundred and twenty routine serum samples submitted for measurement of CRP were tested using both procedures. The results were compared using regression line analysis and showed a high degree of correlation (r2 = 0.99, X coefficient = 1.01, constant = 0.11). C reactive protein can be accurately measured using the automated turbidimetric method which can be recommended as an alternative to fluorescence polarisation. [ABSTRACT FROM PUBLISHER]

Background: Compound heterozygosity for missense variants of the base excision repair (BER) gene MYH has been linked to inheritance of multiple colorectal adenomas or carcinoma in a single UK family. Colorectal adenomas From affected individuals displayed an excess of somatic G:C→T:A transversions in the adenomatous polyposis coli (APC) gene, consistent with a BER defect. Methods: 157 unrelated UK patients with multiple (3 to 115) colorectal adenomas were screened for germ line mutations in MYH and subsets were screened for the related BER genes, MTH1 and OGG1. Adenomas from patients harbouring pathogenic MYH germ line mutations were tested for somatic APC mutations and loss of heterozygosity at MYH. Clinicopathological and molecular data were compared between patients with and without MYH mutations. Results: Fourteen (9%) patients harboured germ line MYH variants, with 8 (5%) having biallelic, pathogenic mutations. Both nonsense and protein truncating MYH mutations were found. Missense variants Y165C and G382D were the most frequent alterations observed. Patients with biallelic MYH mutations had more polyps than carriers of single mutations or MYH wild-type patients (medians, 55 v 3 v 7, respectively; p < 0.01). Four out of 28 (29%) patients with 15 to 115 adenomas had biallelic MYH mutations. All somatic APC mutations identified in such patients were the expected somatic G:C-→T:A transversions. No clearly pathogenic MTH1 or OGG1 germ line mutations were identified. Conclusions: The data provide strong evidence to show that individuals with two allelic MYH mutations are predisposed to a multiple adenoma phenotype. Progression to colorectal carcinoma occurs in some cases. [ABSTRACT FROM AUTHOR]