FDI Effects on National Competitiveness: A Cluster Approach

Despite the close relationship between the activities of multinational enterprises (MNEs) and the competitiveness of host countries, few studies have linked these two subjects from a global perspective. Combining Porter's approach and the work accomplished by international business economists provides a powerful analytical tool with which to review the recent empirical and theoretical literature on the effects of foreign direct investment (FDI) on national competitiveness. The contention is that FDI can indeed be a source of competitiveness but that previous studies have neglected the role of location, in particular the role of clustering on the absorptive capacity of the host State. The aim of this paper is to provide a comprehensive conceptual framework for assessing the effects of FDI on competitiveness to guide policy-makers as well as further researc

Device-independent security of quantum cryptography against collective attacks

We present the optimal collective attack on a Quantum Key Distribution (QKD) protocol in the "device-independent" security scenario, where no assumptions are made about the way the QKD devices work or on what quantum system they operate. Our main result is a tight bound on the Holevo information between one of the authorized parties and the eavesdropper, as a function of the amount of violation of a Bell-type inequality.Comment: 5 pages, 1 figure. v2: minor modification

Standards for the diagnosis and management of Complex Regional Pain Syndrome: Results of a European Pain Federation task force

Background: Complex Regional Pain Syndrome is a painful and disabling post-traumatic primary pain disorder. Acute and chronic CRPS are major clinical challenges. In Europe progress is hampered by significant heterogeneity in clinical practice. We sought to establish standards for the diagnosis and management of CPRS. Methods: The European Pain Federation established a pan-European task force of experts in CRPS who followed a four-stage consensus challenge process to produce mandatory quality standards worded as grammatically imperative (must-do) statements. Results: We developed 17 standards in 8 areas of care. There are 2 standards in diagnosis, 1 in multi-disciplinary care, 1 on assessment, 3 for care pathways, 1 on information and education, 4 in pain management, 3 in physical rehabilitation, and 2 on distress management. The standards are presented, summarised, and their generation and consequences discussed. Also presented are domains of practice for which no agreement on a standard could be reached. Areas of research needed to improve the validity and uptake of these standards are discussed. Conclusion: The European Pain Federation task force present 17 standards of the diagnosis and management of CPRS for use in Europe. These are considered achievable for most countries, and aspirational for a minority of countries depending on their healthcare resource and structures.Significance: This position statement summarizes expert opinion on acceptable standards for CRPS care in Europe

Device-independent quantum key distribution secure against collective attacks

Device-independent quantum key distribution (DIQKD) represents a relaxation of the security assumptions made in usual quantum key distribution (QKD). As in usual QKD, the security of DIQKD follows from the laws of quantum physics, but contrary to usual QKD, it does not rely on any assumptions about the internal working of the quantum devices used in the protocol. We present here in detail the security proof for a DIQKD protocol introduced in [Phys. Rev. Lett. 98, 230501 (2008)]. This proof exploits the full structure of quantum theory (as opposed to other proofs that exploit the no-signalling principle only), but only holds again collective attacks, where the eavesdropper is assumed to act on the quantum systems of the honest parties independently and identically at each round of the protocol (although she can act coherently on her systems at any time). The security of any DIQKD protocol necessarily relies on the violation of a Bell inequality. We discuss the issue of loopholes in Bell experiments in this context.Comment: 25 pages, 3 figure

New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk.

Levels of circulating glucose are tightly regulated. To identify new loci influencing glycemic traits, we performed meta-analyses of 21 genome-wide association studies informative for fasting glucose, fasting insulin and indices of beta-cell function (HOMA-B) and insulin resistance (HOMA-IR) in up to 46,186 nondiabetic participants. Follow-up of 25 loci in up to 76,558 additional subjects identified 16 loci associated with fasting glucose and HOMA-B and two loci associated with fasting insulin and HOMA-IR. These include nine loci newly associated with fasting glucose (in or near ADCY5, MADD, ADRA2A, CRY2, FADS1, GLIS3, SLC2A2, PROX1 and C2CD4B) and one influencing fasting insulin and HOMA-IR (near IGF1). We also demonstrated association of ADCY5, PROX1, GCK, GCKR and DGKB-TMEM195 with type 2 diabetes. Within these loci, likely biological candidate genes influence signal transduction, cell proliferation, development, glucose-sensing and circadian regulation. Our results demonstrate that genetic studies of glycemic traits can identify type 2 diabetes risk loci, as well as loci containing gene variants that are associated with a modest elevation in glucose levels but are not associated with overt diabetes

New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk

Levels of circulating glucose are tightly regulated. To identify new loci influencing glycemic traits, we performed meta-analyses of 21 genome-wide association studies informative for fasting glucose, fasting insulin and indices of beta-cell function (HOMA-B) and insulin resistance (HOMA-IR) in up to 46,186 nondiabetic participants. Follow-up of 25 loci in up to 76,558 additional subjects identified 16 loci associated with fasting glucose and HOMA-B and two loci associated with fasting insulin and HOMA-IR. These include nine loci newly associated with fasting glucose (in or near ADCY5, MADD, ADRA2A, CRY2, FADS1, GLIS3, SLC2A2, PROX1 and C2CD4B) and one influencing fasting insulin and HOMA-IR (near IGF1). We also demonstrated association of ADCY5, PROX1, GCK, GCKR and DGKB-TMEM195 with type 2 diabetes. Within these loci, likely biological candidate genes influence signal transduction, cell proliferation, development, glucose-sensing and circadian regulation. Our results demonstrate that genetic studies of glycemic traits can identify type 2 diabetes risk loci, as well as loci containing gene variants that are associated with a modest elevation in glucose levels but are not associated with overt diabetes

A genome-wide association search for type 2 diabetes genes in African Americans.

African Americans are disproportionately affected by type 2 diabetes (T2DM) yet few studies have examined T2DM using genome-wide association approaches in this ethnicity. The aim of this study was to identify genes associated with T2DM in the African American population. We performed a Genome Wide Association Study (GWAS) using the Affymetrix 6.0 array in 965 African-American cases with T2DM and end-stage renal disease (T2DM-ESRD) and 1029 population-based controls. The most significant SNPs (n = 550 independent loci) were genotyped in a replication cohort and 122 SNPs (n = 98 independent loci) were further tested through genotyping three additional validation cohorts followed by meta-analysis in all five cohorts totaling 3,132 cases and 3,317 controls. Twelve SNPs had evidence of association in the GWAS (P<0.0071), were directionally consistent in the Replication cohort and were associated with T2DM in subjects without nephropathy (P<0.05). Meta-analysis in all cases and controls revealed a single SNP reaching genome-wide significance (P<2.5×10(-8)). SNP rs7560163 (P = 7.0×10(-9), OR (95% CI) = 0.75 (0.67-0.84)) is located intergenically between RND3 and RBM43. Four additional loci (rs7542900, rs4659485, rs2722769 and rs7107217) were associated with T2DM (P<0.05) and reached more nominal levels of significance (P<2.5×10(-5)) in the overall analysis and may represent novel loci that contribute to T2DM. We have identified novel T2DM-susceptibility variants in the African-American population. Notably, T2DM risk was associated with the major allele and implies an interesting genetic architecture in this population. These results suggest that multiple loci underlie T2DM susceptibility in the African-American population and that these loci are distinct from those identified in other ethnic populations

Heart 'omics' in AGEing (HOMAGE): design, research objectives and characteristics of the common database.

Heart failure is common in older people and its prevalence is increasing. The Heart 'omics' in AGEing (HOMAGE) project aims to provide a biomarker approach that will improve the early diagnosis of heart failure. A large clinical database, based on (1) prospective population studies or (2) cross-sectional, prospective studies or randomized controlled trials (RCTs) of patients at risk for or with overt cardiovascular disease will be constructed to determine most promising 'omics'-based biomarkers to identify the risk of developing heart failure and/or comorbidities. Population studies, patient cohorts and RCTs are eligible for inclusion in the common database, if they received ethical approval to obtain and share data and have baseline information on cardiovascular risk factors. Currently, the HOMAGE database includes 43,065 subjects, from 20 studies in eight European countries, including healthy subjects from three population studies in France, Belgium and Italy (n  =  7,124), patients with heart failure (n  =  4,312) from four cohorts in the UK, Spain and Switzerland and patients at high risk for cardiovascular disease (n  =  31,629) in 13 cohorts. It is anticipated that more partners will join the consortium and enlarge the pooled data. This large merged database will be a useful resource with which to identify candidate biomarkers that play a role in the mechanism underlying the onset and progression of heart failure