Toward understanding inter-organizational knowledge transfer needs in SMEs:insight from a UK investigation

Purpose - External knowledge is generally believed to be of prime importance to small to medium-sized enterprises (SMEs). However, a review of the literature shows that no empirical research has looked at knowledge management issues at the inter-organizational level in SMEs. This paper seeks to report on an empirical investigation with UK SMEs in the service sector to identify their needs and practices regarding inter-organizational knowledge transfer, and thus provide empirical evidence to support the above belief. Design/methodology/approach - A two-tier methodology (i.e. using both questionnaire survey and interview approaches) is deployed to address the main research objectives. A questionnaire survey of SMEs is carried out to investigate their current inter-organizational knowledge transfer situation and managers' perception on various relevant issues. Then 12 face-to-face interviews with SME managers are conducted to further validate key findings drawn from the questionnaire survey. Findings - The empirical evidence collected from the survey and interviews confirms the general belief that external knowledge is of prime importance for SMEs, and demonstrates that SMEs have very strong needs for external knowledge and inter-organizational knowledge transfer. Research limitations/implications - The findings provide very strong underpinning for further theoretical research on inter-organizational knowledge transfer in SMEs. However, this study has certain limitations: its results may not be applicable to other industrial sectors or the same sector in other countries; or to micro or large companies; nor does it involve cross-cultural issues. Originality/value - By adopting a two-tier research methodology, this study provides more reliable understanding and knowledge on SMEs' inter-organizational knowledge transfer needs and practices, and fills the gap that exists in the empirical investigations on the subject. © Emerald Group Publishing Limited.

An insight into the activation mechanism of the calcatonin-gene-related peptide receptor

The calcitonin-gene- related peptide (CGRP) receptor is unique among G-protein coupled receptors (GPCRs) as it consists of at least three proteins: calcitonin receptor like receptor (CLR), receptor activity modifying protein (RAMP)1 and receptor component protein (RCP). An endogenous agonist for this curious receptor is aCGRP, which is a sensory nerve-derived peptide made up of 37 amino acids. aCGRP acts as a potent vasodilator having pronounced effects on arterioles and capillaries. Understanding the pharmacodynamics of the CGRP receptor may have pharmaceutical benefit as the receptor has been associated with the onset of migraines and implicated in Raynauds syndrome. The primary aim of this thesis was to identify functionally important residues in the extracellular face of the CGRP receptor. Three areas of interest were selected including the extreme N-terminus of the CLR, extracellular loop 1 (ECL1) of the CLR and its associated transmembrane (TM) regions, and finally extracellular loop 3 (ECL3) of the CLR and its juxtamembrane regions. A site-directed mutagenesis (SDM) strategy was used to investigate these regions, primarily substituting the innate residues of CLR with alanine and assessing the mutation on multiple criteria including a functional cAMP assay, cell-surface expression, total expression, agonist-mediated internalisation and aCGRP binding. The results are interpreted and discussed taking into consideration contemporary concepts surrounding Secretin-like GPCRs. Moreover, the thesis also contains details of RAMP purification. Overall the thesis provides novel data that furthers insight into the complex phenomenon of CGRP receptor activation. Site-directed mutants have been identified that affect aCGRP binding, receptor signal transduction, the CLR/RAMP1 interface and the integrity of the protein complex structure.

Threlfall v ECD Insight Ltd and others 2012

Case law report - online

Hypercapnia induces cleavage and nuclear localization of RelB protein, giving insight into CO2 sensing and signaling

Carbon dioxide (CO(2)) is increasingly being appreciated as an intracellular signaling molecule that affects inflammatory and immune responses. Elevated arterial CO(2) (hypercapnia) is encountered in a range of clinical conditions, including chronic obstructive pulmonary disease, and as a consequence of therapeutic ventilation in acute respiratory distress syndrome. In patients suffering from this syndrome, therapeutic hypoventilation strategy designed to reduce mechanical damage to the lungs is accompanied by systemic hypercapnia and associated acidosis, which are associated with improved patient outcome. However, the molecular mechanisms underlying the beneficial effects of hypercapnia and the relative contribution of elevated CO(2) or associated acidosis to this response remain poorly understood. Recently, a role for the non-canonical NF-?B pathway has been postulated to be important in signaling the cellular transcriptional response to CO(2). In this study, we demonstrate that in cells exposed to elevated CO(2), the NF-?B family member RelB was cleaved to a lower molecular weight form and translocated to the nucleus in both mouse embryonic fibroblasts and human pulmonary epithelial cells (A549). Furthermore, elevated nuclear RelB was observed in vivo and correlated with hypercapnia-induced protection against LPS-induced lung injury. Hypercapnia-induced RelB processing was sensitive to proteasomal inhibition by MG-132 but was independent of the activity of glycogen synthase kinase 3ß or MALT-1, both of which have been previously shown to mediate RelB processing. Taken together, these data demonstrate that RelB is a CO(2)-sensitive NF-?B family member that may contribute to the beneficial effects of hypercapnia in inflammatory diseases of the lung.