1,775 research outputs found
Knowledge Exchange and the Trust Institution: a New Look at the Problem
In the knowledge economy, the search and exchange of knowledge is widely recognized as a key factor contributing to the creation and mobilization of company’s knowledge resources to maintain its competitive advantage. This study is devoted to identifying the role of interpersonal trust in the process of searching and sharing knowledge. Theoretical analysis shows that previously conducted studies in this research field are mainly focused on revealing the relationship between interpersonal trust and the willingness to use knowledge. This study is interested in the willingness to establish contact between economic actors for the purpose of knowledge exchange, and this becomes important when discontinuities in innovation result from a lack of knowledge exchange and interaction between stakeholders. The effects of two different types of interpersonal trust (cognition-based trust and affect-based trust) on willingness to share explicit and tacit knowledge between individuals have been separately examined and tested. The analysis conducted is based on data obtained from surveying 295 employees from large organizations in Penza, Russia. To validate the survey, a confirmatory factor analysis using structural equation modeling was undertaken to verify advanced causal hypotheses. To test the hypotheses, a multiple correlation-regression analysis was used. Results reveal that both types of interpersonal trust positively correlate with the willingness to share both explicit and implicit knowledge. Additionally, it has been established that the willingness to share tacit knowledge is more influenced by affect-based trust between individuals, while cognition-based trust is more significant in explaining the willingness to share explicit knowledge. The need to create favorable conditions within organizations to ensure the exchange of knowledge without constraints is highlighted
TonEBP/NFAT5 stimulates transcription of HSP70 in response to hypertonicity
While hyperosmolality of the kidney medulla is essential for urinary concentration, it imposes a great deal of stress. Cells in the renal medulla adapt to the stress of hypertonicity (hyperosmotic salt) by accumulating organic osmolytes. Tonicity-responsive enhancer (TonE) binding protein (TonEBP) (or NFAT5) stimulates transcription of transporters and a synthetic enzyme for the cellular accumulation of organic osmolytes. We found that dominant-negative TonEBP reduced expression of HSP70 as well as the transporters and enzyme. Near the major histocompatibility complex class III locus, there are three HSP70 genes named HSP70-1, HSP70-2, and HSC70t. While HSP70-1 and HSP70-2 were heat inducible, only HSP70-2 was induced by hypertonicity. In the 5' flanking region of the HSP70-2 gene, there are three sites for TonEBP binding. In cells transfected with a reporter plasmid containing this region, expression of luciferase was markedly stimulated in response to hypertonicity. Coexpression of the dominant-negative TonEBP reduced the luciferase expression. Mutating all three sites in the reporter plasmid led to a complete loss of induction by hypertonicity. Thus, TonEBP rather than heat shock factor stimulates transcription of the HSP70-2 gene in response to hypertonicity. We conclude that TonEBP is a master regulator of the renal medulla for cellular protection against high osmolality via organic osmolytes and molecular chaperones.open12
Equine rhinitis B viruses in horse fecal samples from the Middle East
published_or_final_versio
Polyphyletic origin of MERS coronaviruses and isolation of a novel clade A strain from dromedary camels in the United Arab Emirates
published_or_final_versio
Socioeconomic disparities in breast cancer survival: relation to stage at diagnosis, treatment and race
<p>Abstract</p> <p>Background</p> <p>Previous studies have documented lower breast cancer survival among women with lower socioeconomic status (SES) in the United States. In this study, I examined the extent to which socioeconomic disparity in breast cancer survival was explained by stage at diagnosis, treatment, race and rural/urban residence using the Surveillance, Epidemiology, and End Results (SEER) data.</p> <p>Methods</p> <p>Women diagnosed with breast cancer during 1998-2002 in the 13 SEER cancer registry areas were followed-up to the end of 2005. The association between an area-based measure of SES and cause-specific five-year survival was estimated using Cox regression models. Six models were used to assess the extent to which SES differences in survival were explained by clinical and demographical factors. The base model estimated the hazard ratio (HR) by SES only and then additional adjustments were made sequentially for: 1) age and year of diagnosis; 2) stage at diagnosis; 3) first course treatment; 4) race; and 5) rural/urban residence.</p> <p>Results</p> <p>An inverse association was found between SES and risk of dying from breast cancer (p < 0.0001). As area-level SES falls, HR rises (1.00 → 1.05 → 1.23 → 1.31) with the two lowest SES groups having statistically higher HRs. This SES differential completely disappeared after full adjustment for clinical and demographical factors (p = 0.20).</p> <p>Conclusion</p> <p>Stage at diagnosis, first course treatment and race explained most of the socioeconomic disparity in breast cancer survival. Targeted interventions to increase breast cancer screening and treatment coverage in patients with lower SES could reduce much of socioeconomic disparity.</p
Walks4work: Rationale and study design to investigate walking at lunchtime in the workplace setting
Background: Following recruitment of a private sector company, an 8week lunchtime walking intervention was implemented to examine the effect of the intervention on modifiable cardiovascular disease risk factors, and further to see if walking environment had any further effect on the cardiovascular disease risk factors. Methods. For phase 1 of the study participants were divided into three groups, two lunchtime walking intervention groups to walk around either an urban or natural environment twice a week during their lunch break over an 8week period. The third group was a waiting-list control who would be invited to join the walking groups after phase 1. In phase 2 all participants were encouraged to walk during their lunch break on self-selecting routes. Health checks were completed at baseline, end of phase 1 and end of phase 2 in order to measure the impact of the intervention on cardiovascular disease risk. The primary outcome variables of heart rate and heart rate variability were measured to assess autonomic function associated with cardiovascular disease. Secondary outcome variables (Body mass index, blood pressure, fitness, autonomic response to a stressor) related to cardiovascular disease were also measured. The efficacy of the intervention in increasing physical activity was objectively monitored throughout the 8-weeks using an accelerometer device. Discussion. The results of this study will help in developing interventions with low researcher input with high participant output that may be implemented in the workplace. If effective, this study will highlight the contribution that natural environments can make in the reduction of modifiable cardiovascular disease risk factors within the workplace. © 2012 Brown et al.; licensee BioMed Central Ltd
Ears of the Armadillo: Global Health Research and Neglected Diseases in Texas
Neglected tropical diseases (NTDs) have\ud
been recently identified as significant public\ud
health problems in Texas and elsewhere in\ud
the American South. A one-day forum on the\ud
landscape of research and development and\ud
the hidden burden of NTDs in Texas\ud
explored the next steps to coordinate advocacy,\ud
public health, and research into a\ud
cogent health policy framework for the\ud
American NTDs. It also highlighted how\ud
U.S.-funded global health research can serve\ud
to combat these health disparities in the\ud
United States, in addition to benefiting\ud
communities abroad
Epitaxial Bi2FeCrO6 Multiferroic Thin Films
We present here experimental results obtained on Bi2FeCrO6 (BFCO) epitaxial
films deposited by laser ablation directly on SrTiO3 substrates. It has been
theoretically predicted, by Baettig and Spaldin, using first-principles density
functional theory that BFCO is ferrimagnetic (with a magnetic moment of 2 Bohr
magneton per formula unit) and ferroelectric (with a polarization of ~80
microC/cm2 at 0K). The crystal structure has been investigated using X-ray
diffraction which shows that the films are epitaxial with a high crystallinity
and have a degree of orientation depending of the deposition conditions and
that is determined by the substrate crystal structure. Chemical analysis
carried out by X-ray Microanalysis and X-ray Photoelectron Spectroscopy (XPS)
indicates the correct cationic stoichiometry in the BFCO layer, namely
(Bi:Fe:Cr = 2:1:1). XPS depth profiling revealed that the oxidation state of Fe
and Cr ions in the film remains 3+ throughout the film thickness and that both
Fe and Cr ions are homogeneously distributed throughout the depth.
Cross-section high-resolution transmission electron microscopy images together
with selected area electron diffraction confirm the crystalline quality of the
epitaxial BFCO films with no identifiable foreign phase or inclusion. The
multiferroic character of BFCO is proven by ferroelectric and magnetic
measurements showing that the films exhibit ferroelectric and magnetic
hysteresis at room temperature. In addition, local piezoelectric measurements
carried out using piezoresponse force microscopy (PFM) show the presence of
ferroelectric domains and their switching at the sub-micron scale.Comment: Accepted for publication in Philosophical Magazine Letter
Rapid generation of human B-cell lymphomas via combined expression of Myc and Bcl2 and their use as a preclinical model for biological therapies
Although numerous mouse models of B-cell malignancy have been developed via the enforced expression of defined oncogenic lesions, the feasibility of generating lineage-defined human B-cell malignancies using mice reconstituted with modified human hematopoietic stem cells (HSCs) remains unclear. In fact, whether human cells can be transformed as readily as murine cells by simple oncogene combinations is a subject of considerable debate. Here, we describe the development of humanized mouse model of MYC/BCL2-driven ‘double-hit’ lymphoma. By engrafting human HSCs transduced with the oncogene combination into immunodeficient mice, we generate a fatal B malignancy with complete penetrance. This humanized-MYC/BCL2-model (hMB) accurately recapitulates the histopathological and clinical aspects of steroid-, chemotherapy- and rituximab-resistant human ‘double-hit’ lymphomas that involve the MYC and BCL2 loci. Notably, this model can serve as a platform for the evaluation of antibody-based therapeutics. As a proof of principle, we used this model to show that the anti-CD52 antibody alemtuzumab effectively eliminates lymphoma cells from the spleen, liver and peripheral blood, but not from the brain. The hMB humanized mouse model underscores the synergy of MYC and BCL2 in ‘double-hit’ lymphomas in human patients. Additionally, our findings highlight the utility of humanized mouse models in interrogating therapeutic approaches, particularly human-specific monoclonal antibodies.Kathy and Curt Marble Cancer Research FundSingapore-MIT Alliance for Research and TechnologyNational Institutes of Health (U.S.) (Grant R01-CA128803)Virginia and Daniel K. Ludwig Graduate FellowshipNational Institute of General Medical Sciences (U.S.) (Medical Scientist Training Program Grant T32GM007753)MIT School of Science (Cancer Research Fellowship
Viral Small Interfering RNAs Target Host Genes to Mediate Disease Symptoms in Plants
The Cucumber mosaic virus (CMV) Y-satellite RNA (Y-Sat) has a
small non-protein-coding RNA genome that induces yellowing symptoms in infected
Nicotiana tabacum (tobacco). How this RNA pathogen induces
such symptoms has been a longstanding question. We show that the yellowing
symptoms are a result of small interfering RNA (siRNA)-directed RNA silencing of
the chlorophyll biosynthetic gene, CHLI. The CHLI mRNA contains a 22-nucleotide
(nt) complementary sequence to the Y-Sat genome, and in Y-Sat-infected plants,
CHLI expression is dramatically down-regulated. Small RNA sequencing and
5′ RACE analyses confirmed that this 22-nt sequence was targeted for mRNA
cleavage by Y-Sat-derived siRNAs. Transformation of tobacco with a RNA
interference (RNAi) vector targeting CHLI induced Y-Sat-like symptoms. In
addition, the symptoms of Y-Sat infection can be completely prevented by
transforming tobacco with a silencing-resistant variant of the CHLI gene. These
results suggest that siRNA-directed silencing of CHLI is solely responsible for
the Y-Sat-induced symptoms. Furthermore, we demonstrate that two
Nicotiana species, which do not develop yellowing symptoms
upon Y-Sat infection, contain a single nucleotide polymorphism within the
siRNA-targeted CHLI sequence. This suggests that the previously observed species
specificity of Y-Sat-induced symptoms is due to natural sequence variation in
the CHLI gene, preventing CHLI silencing in species with a mismatch to the Y-Sat
siRNA. Taken together, these findings provide the first demonstration of small
RNA-mediated viral disease symptom production and offer an explanation of the
species specificity of the viral disease
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