A Business Intelligence Model for SMEs Based on Tacit Knowledge

This paper proposes a specific model of business intelligence in relation with SMEs practices, culture and competitive environment. This model is based on the mobilization of corporate tacit knowledge and informal information, aiming at interpreting anticipatory environmental information and assist strategic decision making. An empirical survey assessing the existing business intelligence practices in 20 French SMEs has identified seven necessary acceptance conditions of a business intelligence project as well as a managerial tool allowing tacit knowledge traceability.business intelligence; tacit knowledge; SMEs; sense-making

Risque d'explosion de l'Italie, l'un des trois initiateurs de l'Europe ? Application de la méthode Puzzle© à un cas macroéconomique

Le but du présent texte est de présenter la méthode Puzzle® pour l'exploitation des signaux faibles . Elle résulte des travaux de recherche d'une équipe du laboratoire CERAG-CNRS, université Pierre Mendès France, et a fait l'objet d'un grand nombre d'applications en entreprises ainsi que dans des ministères. Pour " faire plus vivant " nous avons choisi d'adopter une forme narrative et de présenter une fiction concernant la Chine. Cependant toutes les informations mentionnées sont exactes et leurs références sont précisées entre parenthèses.Risque ; explosion de l'Italie ;initiateurs de l'Europe ; Application de la méthode Puzzle© ;cas macroéconomique

Facteurs de risque lors de la conduite d'un projet de mise en place d'un dispositif de veille anticipative dans plusieurs organismes du secteur public

Le présent article s'intéresse aux facteurs de risque susceptibles d'advenir lors de la conduite de projets de mise en place d'un dispositif de veille anticipative stratégique. Sur la base d'une recherche action/intervention au sein de plusieurs organismes du secteur public, les chercheurs ont confronté, plusieurs des facteurs déjà identifiés dans des études antérieures concernant les risques des projets de SI et de veille à ceux rencontrés lors de leur intervention. L'objectif de cette confrontation est d'une part l'identification de facteurs de risques des projets de veille identiques à ceux des projets de SI et d'autre part, l'identification de facteurs de risques spécifiques aux projets de veille. L'intérêt de l'article d'un point de vu théorique est d'avoir fait émerger quatre hypothèses de nouveaux facteurs de risque qui sont autant de pistes de recherche. Il s'agit du mode de communication en face à face, du soutien du " middle management ", du choix du moment de mise en place du projet et du choix du chef de projet. D'un point de vu managérial, cette recherche permet de construire un début de connaissances actionnables permettant de faire de recommandations fondées à un chef de projet de veille démarrant sa tâche dans un tel contexte.Projet de SI, Veille anticipative stratégique, facteur de risque, secteur public, recherche action/intervention

IL-6: A Janus-like factor in abdominal aortic aneurysm disease

AbstractBackground and aimsAn abdominal aortic aneurysm (AAA) is part of the atherosclerotic spectrum of diseases. The disease is hallmarked by a comprehensive localized inflammatory response with striking IL-6 hyperexpression. IL-6 is a multifaceted cytokine that, depending on the context, acts as a pro- or anti-inflammatory factor. In this study, we explore a putative role for IL-6 in AAA disease.MethodsELISA’s, Western blot analysis, real time PCR and array analysis were used to investigate IL-6 expression and signaling in aneurysm wall samples from patients undergoing elective AAA repair. A role for IL-6 in AAA disease was tested through IL-6 neutralization experiments (neutralizing antibody) in the elastase model of AAA disease.ResultsWe confirmed an extreme disparity in aortic wall IL-6 content between AAA and atherosclerotic disease (median [5th–95th percentile] aortic wall IL-6 content: 281.6 [0.0–1820.8] (AAA) vs. 1.9 [0.0–37.8] μg/g protein (atherosclerotic aorta), (p < 0.001). Array analysis followed by pathway analysis showed that IL-6 hyper-expression is followed by increased IL-6 signaling (p < 0.000039), an observation confirmed by higher aneurysm wall pSTAT3 levels, and SOCS1 and SOCS3 mRNA expression, (p < 0.018).Remarkably, preventive IL-6 neutralization i.e. treatment started one day prior to the elastase-induction resulted in >40% 7-day mortality due to aortic rupture. In contrast, delayed IL-6 neutralization (i.e. neutralization started at day 4 after elastase induction) did not result in ruptures, and quenched AAA growth (p < 0.021).ConclusionsAAA disease is characterized by increased IL-6 signaling. In the context of the elastase model of AAA disease, IL-6 appears a multi-faceted factor, protective upon acute injury, but negatively involved in the perpetuation of the disease process

Bi-allelic GAD1 variants cause a neonatal onset syndromic developmental and epileptic encephalopathy.

Developmental and epileptic encephalopathies are a heterogeneous group of early-onset epilepsy syndromes dramatically impairing neurodevelopment. Modern genomic technologies have revealed a number of monogenic origins and opened the door to therapeutic hopes. Here we describe a new syndromic developmental and epileptic encephalopathy caused by bi-allelic loss-of-function variants in GAD1, as presented by 11 patients from six independent consanguineous families. Seizure onset occurred in the first 2 months of life in all patients. All 10 patients, from whom early disease history was available, presented with seizure onset in the first month of life, mainly consisting of epileptic spasms or myoclonic seizures. Early EEG showed suppression-burst or pattern of burst attenuation or hypsarrhythmia if only recorded in the post-neonatal period. Eight patients had joint contractures and/or pes equinovarus. Seven patients presented a cleft palate and two also had an omphalocele, reproducing the phenotype of the knockout Gad1-/- mouse model. Four patients died before 4 years of age. GAD1 encodes the glutamate decarboxylase enzyme GAD67, a critical actor of the γ-aminobutyric acid (GABA) metabolism as it catalyses the decarboxylation of glutamic acid to form GABA. Our findings evoke a novel syndrome related to GAD67 deficiency, characterized by the unique association of developmental and epileptic encephalopathies, cleft palate, joint contractures and/or omphalocele

Changes of bivalent chromatin coincide with increased expression of developmental genes in cancer

Bivalent (poised or paused) chromatin comprises activating and repressing histone modifications at the same location. This combination of epigenetic marks at promoter or enhancer regions keeps genes expressed at low levels but poised for rapid activation. Typically, DNA at bivalent promoters is only lowly methylated in normal cells, but frequently shows elevated methylation levels in cancer samples. Here, we developed a universal classifier built from chromatin data that can identify cancer samples solely from hypermethylation of bivalent chromatin. Tested on over 7,000 DNA methylation data sets from several cancer types, it reaches an AUC of 0.92. Although higher levels of DNA methylation are often associated with transcriptional silencing, counter-intuitive positive statistical dependencies between DNA methylation and expression levels have been recently reported for two cancer types. Here, we re-analyze combined expression and DNA methylation data sets, comprising over 5,000 samples, and demonstrate that the conjunction of hypermethylation of bivalent chromatin and up-regulation of the corresponding genes is a general phenomenon in cancer. This up-regulation affects many developmental genes and transcription factors, including dozens of homeobox genes and other genes implicated in cancer. Thus, we reason that the disturbance of bivalent chromatin may be intimately linked to tumorigenesis

Line-Up Elections: Parallel Voting with Shared Candidate Pool

We introduce the model of line-up elections which captures parallel or sequential single-winner elections with a shared candidate pool. The goal of a line-up election is to find a high-quality assignment of a set of candidates to a set of positions such that each position is filled by exactly one candidate and each candidate fills at most one position. A score for each candidate-position pair is given as part of the input, which expresses the qualification of the candidate to fill the position. We propose several voting rules for line-up elections and analyze them from an axiomatic and an empirical perspective using real-world data from the popular video game FIFA.Comment: Accepted to SAGT 202

Ocular lesions in hereditary hemorrhagic telangiectasia: genetics and clinical characteristics

Background: The aim of our study is to study the association between eye lesions in Hereditary Hemorrhagic Telangiectasia (HHT) and other signs of the disease, as well as to characterize its genetics. Methods: A cross-sectional study was conducted of a cohort of 206 patients studied in the HHT Unit of Hospital de Sierrallana, a reference centre for Spanish patients with HHT. Odds ratios for several symptoms or characteristics of HHT and ocular lesions were estimated using logistic regression adjusting for age and sex. Results: The ocular involvement was associated with being a carrier of a mutation for the ENG gene, that is, suffering from a type 1 HHT involvement (OR = 2.09; 95% CI [1.17–3.72]). p = 0.012). In contrast, patients with ocular lesions have less frequently mutated ACVRL1/ALK1 gene (OR = 0.52; 95% CI [0.30–3.88], p = 0.022). Conclusions: In conclusion, half of the patients with HHT in our study have ocular involvement. These eye lesions are associated with mutations in the ENG gene and ACVRL1/ALK1 gene. Thus, the ENG gene increases the risk of ocular lesions, while being a carrier of the mutated ACVRL1/ALK1 gene decreases said risk

ILAE Genetic Literacy Series: Postmorterm Genetic Testing in Sudden Unexpected Death in Epilepsy

A 24-year-old man with non-lesional bitemporal lobe epilepsy since age 16 years was found dead in bed around midday. He was last seen the previous night when he was witnessed to have a tonic–clonic seizure. Before his death, he was experiencing weekly focal impaired awareness seizures and up to two focal-to-bilateral tonic–clonic seizures each year. He had trialed several antiseizure medications and was on levetiracetam 1500 mg/day, lamotrigine 400 mg/day, and clobazam 10 mg/day at the time of death. Other than epilepsy, his medical history was unremarkable. Of note, he had an older brother with a history of febrile seizures and a paternal first cousin with epilepsy. No cause of death was identified following a comprehensive postmortem investigation. The coroner classified the death as “sudden unexpected death in epilepsy” (SUDEP), and it would qualify as “definite SUDEP” using the current definitions.1 This left the family with many questions unanswered; in particular, they wish to know what caused the death and whether it could happen to other family members. Could postmortem genetic testing identify a cause of death, provide closure to the family, and facilitate cascade genetic testing of first-degree family members who may be at risk of sudden death? While grieving family members struggle with uncertainty about the cause of death, we as clinicians also face similar uncertainties about genetic contributions to SUDEP, especially when the literature is sparse, and the utility of genetic testing is still being worked out. We aim to shed some light on this topic, highlighting areas where data is emerging but also areas where uncertainty remains, keeping our case in mind as we examine this clinically important area