Bacteriological following during fifteen years in social collective restauration

Pratiquée depuis 1985 en restauration collective sociale (restaurants sco laires), la méthode NORECOIN (normalisée, répétitive, codée et intégrée) a été appliquée à 128 restaurants au cours de la période de 1997-1999; l’échantillon est toujours le même depuis le début. Les résultats sont toujours excellents, dans la zone supérieure de la notation : 2,5 à 3 et sont même meilleurs que dans les périodes précédentes : les notes sont en effet : 2,71 à 2,99.Utilized since 1985 in social collective restauration (school restaurants), the NORECOIN method (normalized, repeatitive, coded and integrated) was applied to 128 restaurants during period 1 997- 1 999 ; sampling is always the same since the beginning. The results are always excellent, in the upper zone of notation : 2.5 to 3 and are even better than in the previous periods ; the notes are indeed : 2.17 to 2.99

Norecoin method in social collective restauration. Study during 3, 6 and 9 years

Après les premières études (1985, 1986-1987, 1988-1990), la méthode d’analyse NORECOIN (normalisée, répétitive, codée et intégrée) a été appliquée à 107 restaurants de restauration collective sociale (restaurants scolaires) au cours d’une nouvelle période : 1991-1993. Ont été à nouveau obtenus < 5% de plats cuisinés non conformes et < 10% de plats autres (entrées ou desserts) non conformes ou non satisfaisants. La note NORECOIN est, dans ce cas, comprise entre 2,5, et 3.After first studies (1985, 1986-1987, 1988-1990), the analysis method NORECOIN (normalized, repeatitive, coded and integrated) was applied for 107 restaurants of social collective restauration (school restaurants) during a new period: 1991-1993. Were yet obtained: < 5% of not conform cooked dishes and < 10% of other dishes (entrées or desserts) not conform or not satisfactory. In this case, the NORECOIN note ranged 2.5 to 3

NORECOIN method in social collective restauration. A new study during three years

Après une première étude (1985 - 1986 - 1987), la méthode d’analyse NORECOIN (normalisée, répétitive, codée et intégrée) a été appliquée à 96 restaurants de restauration collective sociale (restaurants scolaires) au cours d’une nouvelle période : 1988-1990. Ont été à nouveau obtenus < 5 % de plats cuisinés non conformes et < 10 % de plats autres (entrées ou desserts) non conformes ou non satisfaisants. La note NORECOIN est, dans ce cas, comprise entre 2,5 et 3.After a first study (1985 - 1986 - 1987) the analysis method NORECOIN (normalized, repeatitive, coded and integrated) was applied for 96 restaurants of social collective restauration (school restaurants) during a new period : 1988-1990. Were yet obtained : < 5 % of not conform cooked dishes and <10% of not conform or not satisfactory other dishes (entrées or desserts). In this case, the NORECOIN note ranged 2.5 to 3

Systematic comparison of digital maturity assessment models

ABSTRACT: Assessing the digital maturity of companies is essential to prepare for digital transformation in the context of Industry 4.0. Several digital maturity assessment models have emerged in the past few years to support this evaluation. One obstacle for companies is the impossibility of easily comparing themselves to one another quantitatively or qualitatively. This paper introduces a new way to compare digital maturity models through a quantitative framework that is compatible with a wide variety of models. Comparisons are performed in the space of the keywords used to characterize key performance indicators (KPIs) that are reverse engineered from the models. The matches are encoded in a keyword matrix that is used to automatically compute the match level of KPI pairs. The framework has been validated on 13 state-of-the-art maturity models whose analysis resulted in the identification of 451 KPIs characterized using 263 keywords structured according to 12 dimensions and 58 subdimensions

Digital maturity models: comparing manual and semi-automatic similarity assessment frameworks

The fourth industrial revolution is forcing companies to define their digital strategy, making it imperative that they assess their digital maturity as a basis for improvements. As a result, a variety of maturity models have emerged. However, it can be difficult to identify which one is most appropriate. This paper introduces a new methodology to compare a manual and a semi automatic framework for assessing the similarity of digital maturity models. It allows identifying the most adequate framework for comparing maturity models. Both frameworks have been designed to identify correspondences between KPIs. The analysis of the matches and the obtained results are then used to tune the semi-automatic framework. The proposed comparison methodology has been validated using two digital maturity models and shows that the semi-automatic framework provides good results in a very efficient manner. Several insights have been derived and will help to develop a new maturity model

Genetic risk of Parkinson disease and progression:: An analysis of 13 longitudinal cohorts.

OBJECTIVE: To determine if any association between previously identified alleles that confer risk for Parkinson disease and variables measuring disease progression. METHODS: We evaluated the association between 31 risk variants and variables measuring disease progression. A total of 23,423 visits by 4,307 patients of European ancestry from 13 longitudinal cohorts in Europe, North America, and Australia were analyzed. RESULTS: We confirmed the importance of GBA on phenotypes. GBA variants were associated with the development of daytime sleepiness (p.N370S: hazard ratio [HR] 3.28 [1.69-6.34]) and possible REM sleep behavior (p.T408M: odds ratio 6.48 [2.04-20.60]). We also replicated previously reported associations of GBA variants with motor/cognitive declines. The other genotype-phenotype associations include an intergenic variant near LRRK2 and the faster development of motor symptom (Hoehn and Yahr scale 3.0 HR 1.33 [1.16-1.52] for the C allele of rs76904798) and an intronic variant in PMVK and the development of wearing-off effects (HR 1.66 [1.19-2.31] for the C allele of rs114138760). Age at onset was associated with TMEM175 variant p.M393T (-0.72 [-1.21 to -0.23] in years), the C allele of rs199347 (intronic region of GPNMB, 0.70 [0.27-1.14]), and G allele of rs1106180 (intronic region of CCDC62, 0.62 [0.21-1.03]). CONCLUSIONS: This study provides evidence that alleles associated with Parkinson disease risk, in particular GBA variants, also contribute to the heterogeneity of multiple motor and nonmotor aspects. Accounting for genetic variability will be a useful factor in understanding disease course and in minimizing heterogeneity in clinical trials.The Intramural Research Program the National Institute on Aging (NIA, Z01-AG000949-02), Biogen Idec, and the Michael J Fox Foundation for Parkinson’s Researc

Differences in the Presentation and Progression of Parkinson's Disease by Sex.

BACKGROUND: Previous studies reported various symptoms of Parkinson's disease (PD) associated with sex. Some were conflicting or confirmed in only one study. OBJECTIVES: We examined sex associations to PD phenotypes cross-sectionally and longitudinally in large-scale data. METHODS: We tested 40 clinical phenotypes, using longitudinal, clinic-based patient cohorts, consisting of 5946 patients, with a median follow-up of 3.1 years. For continuous outcomes, we used linear regressions at baseline to test sex-associated differences in presentation, and linear mixed-effects models to test sex-associated differences in progression. For binomial outcomes, we used logistic regression models at baseline and Cox regression models for survival analyses. We adjusted for age, disease duration, and medication use. In the secondary analyses, data from 17 719 PD patients and 7588 non-PD participants from an online-only, self-assessment PD cohort were cross-sectionally evaluated to determine whether the sex-associated differences identified in the primary analyses were consistent and unique to PD. RESULTS: Female PD patients had a higher risk of developing dyskinesia early during the follow-up period, with a slower progression in activities of daily living difficulties, and a lower risk of developing cognitive impairments compared with male patients. The findings in the longitudinal, clinic-based cohorts were mostly consistent with the results of the online-only cohort. CONCLUSIONS: We observed sex-associated contributions to PD heterogeneity. These results highlight the necessity of future research to determine the underlying mechanisms and importance of personalized clinical management. © 2020 International Parkinson and Movement Disorder Society.This study was supported by the Intramural Research Program the National Institute on Aging (NIA, Z01-AG000949-02), Biogen Idec, and the Michael J Fox Foundation for Parkinson’s Research

Regulatory sites for splicing in human basal ganglia are enriched for disease-relevant information

Genome-wide association studies have generated an increasing number of common genetic variants associated with neurological and psychiatric disease risk. An improved understanding of the genetic control of gene expression in human brain is vital considering this is the likely modus operandum for many causal variants. However, human brain sampling complexities limit the explanatory power of brain-related expression quantitative trait loci (eQTL) and allele-specific expression (ASE) signals. We address this, using paired genomic and transcriptomic data from putamen and substantia nigra from 117 human brains, interrogating regulation at different RNA processing stages and uncovering novel transcripts. We identify disease-relevant regulatory loci, find that splicing eQTLs are enriched for regulatory information of neuron-specific genes, that ASEs provide cell-specific regulatory information with evidence for cellular specificity, and that incomplete annotation of the brain transcriptome limits interpretation of risk loci for neuropsychiatric disease. This resource of regulatory data is accessible through our web server, http://braineacv2.inf.um.es/

Identification of novel risk loci, causal insights, and heritable risk for Parkinson's disease: a meta-analysis of genome-wide association studies

Background Genome-wide association studies (GWAS) in Parkinson's disease have increased the scope of biological knowledge about the disease over the past decade. We aimed to use the largest aggregate of GWAS data to identify novel risk loci and gain further insight into the causes of Parkinson's disease. Methods We did a meta-analysis of 17 datasets from Parkinson's disease GWAS available from European ancestry samples to nominate novel loci for disease risk. These datasets incorporated all available data. We then used these data to estimate heritable risk and develop predictive models of this heritability. We also used large gene expression and methylation resources to examine possible functional consequences as well as tissue, cell type, and biological pathway enrichments for the identified risk factors. Additionally, we examined shared genetic risk between Parkinson's disease and other phenotypes of interest via genetic correlations followed by Mendelian randomisation. Findings Between Oct 1, 2017, and Aug 9, 2018, we analysed 7·8 million single nucleotide polymorphisms in 37 688 cases, 18 618 UK Biobank proxy-cases (ie, individuals who do not have Parkinson's disease but have a first degree relative that does), and 1·4 million controls. We identified 90 independent genome-wide significant risk signals across 78 genomic regions, including 38 novel independent risk signals in 37 loci. These 90 variants explained 16–36% of the heritable risk of Parkinson's disease depending on prevalence. Integrating methylation and expression data within a Mendelian randomisation framework identified putatively associated genes at 70 risk signals underlying GWAS loci for follow-up functional studies. Tissue-specific expression enrichment analyses suggested Parkinson's disease loci were heavily brain-enriched, with specific neuronal cell types being implicated from single cell data. We found significant genetic correlations with brain volumes (false discovery rate-adjusted p=0·0035 for intracranial volume, p=0·024 for putamen volume), smoking status (p=0·024), and educational attainment (p=0·038). Mendelian randomisation between cognitive performance and Parkinson's disease risk showed a robust association (p=8·00 × 10−7). Interpretation These data provide the most comprehensive survey of genetic risk within Parkinson's disease to date, to the best of our knowledge, by revealing many additional Parkinson's disease risk loci, providing a biological context for these risk factors, and showing that a considerable genetic component of this disease remains unidentified. These associations derived from European ancestry datasets will need to be followed-up with more diverse data. Funding The National Institute on Aging at the National Institutes of Health (USA), The Michael J Fox Foundation, and The Parkinson's Foundation (see appendix for full list of funding sources)

Rare and low-frequency coding variants alter human adult height

Height is a highly heritable, classic polygenic trait with ~700 common associated variants identified so far through genome - wide association studies . Here , we report 83 height - associated coding variants with lower minor allele frequenc ies ( range of 0.1 - 4.8% ) and effects of up to 2 16 cm /allele ( e.g. in IHH , STC2 , AR and CRISPLD2 ) , >10 times the average effect of common variants . In functional follow - up studies, rare height - increasing alleles of STC2 (+1 - 2 cm/allele) compromise d proteolytic inhibition of PAPP - A and increased cleavage of IGFBP - 4 in vitro , resulting in higher bioavailability of insulin - like growth factors . The se 83 height - associated variants overlap genes mutated in monogenic growth disorders and highlight new biological candidates ( e.g. ADAMTS3, IL11RA, NOX4 ) and pathways ( e.g . proteoglycan/ glycosaminoglycan synthesis ) involved in growth . Our results demonstrate that sufficiently large sample sizes can uncover rare and low - frequency variants of moderate to large effect associated with polygenic human phenotypes , and that these variants implicate relevant genes and pathways