Start-ups in entrepreneurial ecosystems: the role of relational capacity

Purpose: Entrepreneurial ecosystems provide the context for start-ups to access resources. The authors investigate the reliance of start-ups on their entrepreneurial ecosystem and the driving factors behind the proportion of local actors (belonging to their entrepreneurial ecosystem) within their overall set of relationships (their business ecosystem). Recognizing the limited relational capacity of firms, the authors focus on three differentiating firm characteristics: size, age and innovation of firms. Design/methodology/approach: The authors developed a sample of 163 start-ups located in the entrepreneurial ecosystem of Toulouse, France. The authors investigated the characteristics of their relationship sets using regression analysis. Findings: The results confirm that age is inversely related to the proportion of a start-up's relationships located in its entrepreneurial ecosystem. More surprisingly, for older start-ups, the authors also highlight the presence of a moderating effect of the start-up's size on the relationship between its degree of innovation and the proportion of its relationships in its entrepreneurial ecosystem: Larger and more innovative start-ups appear to rely more on their local entrepreneurial ecosystem. Originality/value: This research increases the understanding of the characteristics driving the interactions of start-ups with their entrepreneurial ecosystems by adopting a relational capacity approach. The authors introduce digital methods as an innovative approach for uncovering firms' ecosystems. Finally, from a practical point of view, the research should provide public authorities seeking to promote the link between local resources and the development of innovative start-ups in their regions with interesting insights

Rigidity of noncompact complete Bach-flat manifolds

Let $(M,g)$ be a noncompact complete Bach-flat manifold with positive Yamabe constant. We prove that $(M,g)$ is flat if $(M, g)$ has zero scalar curvature and sufficiently small $L_{2}$ bound of curvature tensor. When $(M, g)$ has nonconstant scalar curvature, we prove that $(M, g)$ is conformal to the flat space if $(M, g)$ has sufficiently small $L_2$ bound of curvature tensor and $L_{4/3}$ bound of scalar curvature.Comment: 10 pages, To appear J. Geom. Physic

Q-curvature Flow for GJMS Operators with Non-trivial Kernel

We investigate the prescribed Q-curvature flow for GJMS operators with non-trivial kernel on compact manifolds of even dimension. When the total Q-curvature is negative, we identify a conformally invariant condition on the nodal domains of functions in the kernel of the GJMS operator, allowing us to prove the global existence and the convergence of the flow to a metric which is conformal to the initial one, and having a prescribed Q-curvature. If the total Q-curvature is positive, we show that the flow blows up in finite time.Comment: 11 page

Mobile Geriatric Team Advice: Effect on Length of Hospital Stay in Older Adults

International audienc

La conférence expérimentale sommeil et travail à horaires atypiques : une mise en situation inédite de 5h à 13h

International audienceObjectifLes médecins du sommeil connaissent depuis longtemps les effets délétères du manque de sommeil en relation notamment avec le travail à horaires atypiques. En mai 2012 la Haute Autorité de santé a recommandé d‘informer les travailleurs et le CHSCT sur l’ensemble des risques identifiés. Cela a permis au Laboratoire du Sommeil en collaboration avec l’École des Mines d’Albi et la Société de médecine du travail Midi-Pyrénées d’initier une expérience innovante. Le but étant de placer l’assistance dans la situation de privation de sommeil d’un poste du matin pour sensibiliser les managers et les acteurs de prévention en entreprises (APE) aux conséquences du manque de sommeil sur la santé physique, mentale et sur la pénibilité. Nous avons élaboré des questionnaires d’évaluation soumis aux participants pendant les conférences et les siestes.MéthodesTreize conférences de spécialistes du sommeil, médecins du travail, psychologue, chef d’entreprise, sportif de haut niveau, enseignant-chercheur. Tout au long de la conférence, les participants répondent, par boîtiers électroniques interactifs, à 30 questions et tests de vigilance. Six ateliers sieste d’1 h sont organisés à partir de 6 h 30. Une pause repas à 9 h avec présentation de matériels de traitement des apnées du sommeil. Nous proposons dans cet article une analyse des réponses entre siesteurs/non-siesteurs (S/NS).RésultatsCent soixante-douze participants (70 % de femmes) : managers 15 %, APE 67 %. Vingt-deux pour cent se sont levés avant 3 h, 89 % ont dormi moins de 6 h, 28 % ont un score d’Epworth > 10. Près de 38 % font des journées de plus de 17 h, 23 % somnolent au volant, 34 % ronflent, 39 % ne font jamais la sieste, par manque de temps pour 49 %. Enfin, 42 % des participants ont ressenti une baisse de leur vigilance entre 7 et 9 h. Parmi les 49 candidats S, 37 % ont eu l’impression d’avoir dormi et 70 % d’avoir fait le vide. Après la pause, seulement 10 % des S ont ressenti une baisse de vigilance contre 30 % des NS (Chi2 = 13,52, p = 0,035).ConclusionNeuf participants sur 10 pensent que cette conférence contribuera à modifier leur pratique professionnelle. L’atelier sieste a eu un effet positif sur la vigilance. Dossier complet et vidéo sur http://eric.mullens.free.fr

Binding cooperativity of membrane adhesion receptors

The adhesion of cells is mediated by receptors and ligands anchored in apposing membranes. A central question is how to characterize the binding affinity of these membrane-anchored molecules. For soluble molecules, the binding affinity is typically quantified by the binding equilibrium constant K3D in the linear relation [RL] = K3D [R][L] between the volume concentration [RL] of bound complexes and the volume concentrations [R] and [L] of unbound molecules. For membrane-anchored molecules, it is often assumed by analogy that the area concentration of bound complexes [RL] is proportional to the product [R][L] of the area concentrations for the unbound receptor and ligand molecules. We show here (i) that this analogy is only valid for two planar membranes immobilized on rigid surfaces, and (ii) that the thermal roughness of flexible membranes leads to cooperative binding of receptors and ligands. In the case of flexible membranes, the area concentration [RL] of receptor-ligand bonds is proportional to the square of [R][L] for typical lengths and concentrations of receptors and ligands in cell adhesion zones. The cooperative binding helps to understand why different experimental methods for measuring the binding affinity of membrane-anchored molecules have led to values differing by several orders of magnitude.Comment: 9 pages, 4 figures; to appear in Soft Matte

Anti-Inflammatory Treatment with FTY720 Starting after Onset of Symptoms Reverses Synaptic Deficits in an AD Mouse Model

Therapeutic approaches providing effective medication for Alzheimer’s disease (AD) patients after disease onset are urgently needed. Previous studies in AD mouse models suggested that physical exercise or changed lifestyle can delay AD-related synaptic and memory dysfunctions when treatment started in juvenile animals long before onset of disease symptoms, while a pharmacological treatment that can reverse synaptic and memory deficits in AD mice was thus far not identified. Repurposing food and drug administration (FDA)-approved drugs for treatment of AD is a promising way to reduce the time to bring such medication into clinical practice. The sphingosine-1 phosphate analog fingolimod (FTY720) was approved recently for treatment of multiple sclerosis patients. Here, we addressed whether fingolimod rescues AD-related synaptic deficits and memory dysfunction in an amyloid precursor protein/presenilin-1 (APP/PS1) AD mouse model when medication starts after onset of symptoms (at five months). Male mice received intraperitoneal injections of fingolimod for one to two months starting at five to six months. This treatment rescued spine density as well as long-term potentiation in hippocampal cornu ammonis-1 (CA1) pyramidal neurons, that were both impaired in untreated APP/PS1 animals at six to seven months of age. Immunohistochemical analysis with markers of microgliosis (ionized calcium-binding adapter molecule 1; Iba1) and astrogliosis (glial fibrillary acid protein; GFAP) revealed that our fingolimod treatment regime strongly down regulated neuroinflammation in the hippocampus and neocortex of this AD model. These effects were accompanied by a moderate reduction of Aβ accumulation in hippocampus and neocortex. Our results suggest that fingolimod, when applied after onset of disease symptoms in an APP/PS1 mouse model, rescues synaptic pathology that is believed to underlie memory deficits in AD mice, and that this beneficial effect is mediated via anti-neuroinflammatory actions of the drug on microglia and astrocytes

Anti-Inflammatory Treatment with FTY720 Starting after Onset of Symptoms Reverses Synaptic Deficits in an AD Mouse Model

Therapeutic approaches providing effective medication for Alzheimer’s disease (AD) patients after disease onset are urgently needed. Previous studies in AD mouse models suggested that physical exercise or changed lifestyle can delay AD-related synaptic and memory dysfunctions when treatment started in juvenile animals long before onset of disease symptoms, while a pharmacological treatment that can reverse synaptic and memory deficits in AD mice was thus far not identified. Repurposing food and drug administration (FDA)-approved drugs for treatment of AD is a promising way to reduce the time to bring such medication into clinical practice. The sphingosine-1 phosphate analog fingolimod (FTY720) was approved recently for treatment of multiple sclerosis patients. Here, we addressed whether fingolimod rescues AD-related synaptic deficits and memory dysfunction in an amyloid precursor protein/presenilin-1 (APP/PS1) AD mouse model when medication starts after onset of symptoms (at five months). Male mice received intraperitoneal injections of fingolimod for one to two months starting at five to six months. This treatment rescued spine density as well as long-term potentiation in hippocampal cornu ammonis-1 (CA1) pyramidal neurons, that were both impaired in untreated APP/PS1 animals at six to seven months of age. Immunohistochemical analysis with markers of microgliosis (ionized calcium-binding adapter molecule 1; Iba1) and astrogliosis (glial fibrillary acid protein; GFAP) revealed that our fingolimod treatment regime strongly down regulated neuroinflammation in the hippocampus and neocortex of this AD model. These effects were accompanied by a moderate reduction of Aβ accumulation in hippocampus and neocortex. Our results suggest that fingolimod, when applied after onset of disease symptoms in an APP/PS1 mouse model, rescues synaptic pathology that is believed to underlie memory deficits in AD mice, and that this beneficial effect is mediated via anti-neuroinflammatory actions of the drug on microglia and astrocytes