Valuing seafood attributes: stated choice model

This study applied brand choice model and stated preference data collected in French context by means of choice experiment to investigate value of intrinsic and extrinsic attributes of various fresh seafood species. The estimated models show that the extrinsic attributes (i.e. product forms, production method, and product origin) and intrinsic attributes (i.e. seafood species: salmon, cod, mussels, ect.) were significant determinants of consumer choice of seafood for their household consumption. Consumers assigned a significantly higher value for domestic and wild catch product. However, a deeper look into the market structure we revealed that only 39.5% of the sample is willing to pay a premium price for domestic and wild catch items in general. Salmon, cod, and saithe were evaluated relatively highest valued products while oyster, pangasius, and crab are lowest valued items. Market shares of the species in segments and entire market were predicted and appeared closely to actual market shares. The segment membership probability was estimated by the model and then regressed on demographic to give good suggestions for managers

Market structure and segments for seafood: A stated preference approach

Demand structure and market segmentation for seafood have been investigated intensively. However, most the researches so far applied traditional demand analysis and descriptive segmentation approach by separated models. The traditional demand analysis assuming consumer homogeneity, behavior consistence, and using aggregate data may result biased estimation, while the segmentation based on descriptive approach has results less accessible and actionable. We the first used discrete choice model and stated preference data to simultaneously estimate the demand structure and segments for twelve seafood species in French context. The four-latent segments model have the best fit to the data and demand elasticities estimated are comparable to those in the traditional studies but provide more efficient and actionable guidance for practitioners. Consistence with previous seafood demand study we found that elasticities of high valued fish such as salmon, tuna, cod, sole, and shrimp are price elastic while low valued species like mussels, oyster, and pangasius are inelastic. Moreover, latent class model revealed that 39.5% of the sample are not price sensitive, 29.6% moderate sensitive, 20.3% sensitive, and 10.6% are very sensitive. Similarly, we investigated deeper for particular species and uncovered demand structure of each species. For instance, only 30.9% of consumers are price elastic for salmon, while 39.5% and 29.6% of the sample are inelastic and moderate elastic for this species, respectively. We also regressed the segment membership probabilities on the consumer characteristics to give better segment description and provide efficient guidance for seafood producers and marketers

Sixteen new lung function signals identified through 1000 Genomes Project reference panel imputation

Lung function measures are used in the diagnosis of chronic obstructive pulmonary disease. In 38,199 European ancestry individuals, we studied genome-wide association of forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and FEV1/FVC with 1000 Genomes Project (phase 1)-imputed genotypes and followed up top associations in 54,550 Europeans. We identify 14 novel loci (P <5 x 10(-8)) in or near ENSA, RNU5F-1, KCNS3, AK097794, ASTN2, LHX3, CCDC91, TBX3, TRIP11, RIN3, TEKT5, LTBP4, MN1 and AP1S2, and two novel signals at known loci NPNT and GPR126, providing a basis for new understanding of the genetic determinants of these traits and pulmonary diseases in which they are altered.Peer reviewe

Multi-ancestry genome-wide association analyses improve resolution of genes and pathways influencing lung function and chronic obstructive pulmonary disease risk

Lung-function impairment underlies chronic obstructive pulmonary disease (COPD) and predicts mortality. In the largest multi-ancestry genome-wide association meta-analysis of lung function to date, comprising 580,869 participants, we identified 1,020 independent association signals implicating 559 genes supported by ≥2 criteria from a systematic variant-to-gene mapping framework. These genes were enriched in 29 pathways. Individual variants showed heterogeneity across ancestries, age and smoking groups, and collectively as a genetic risk score showed strong association with COPD across ancestry groups. We undertook phenome-wide association studies for selected associated variants as well as trait and pathway-specific genetic risk scores to infer possible consequences of intervening in pathways underlying lung function. We highlight new putative causal variants, genes, proteins and pathways, including those targeted by existing drugs. These findings bring us closer to understanding the mechanisms underlying lung function and COPD, and should inform functional genomics experiments and potentially future COPD therapies

Identification of genetic variants associated with Huntington's disease progression: a genome-wide association study

Background Huntington's disease is caused by a CAG repeat expansion in the huntingtin gene, HTT. Age at onset has been used as a quantitative phenotype in genetic analysis looking for Huntington's disease modifiers, but is hard to define and not always available. Therefore, we aimed to generate a novel measure of disease progression and to identify genetic markers associated with this progression measure. Methods We generated a progression score on the basis of principal component analysis of prospectively acquired longitudinal changes in motor, cognitive, and imaging measures in the 218 indivduals in the TRACK-HD cohort of Huntington's disease gene mutation carriers (data collected 2008–11). We generated a parallel progression score using data from 1773 previously genotyped participants from the European Huntington's Disease Network REGISTRY study of Huntington's disease mutation carriers (data collected 2003–13). We did a genome-wide association analyses in terms of progression for 216 TRACK-HD participants and 1773 REGISTRY participants, then a meta-analysis of these results was undertaken. Findings Longitudinal motor, cognitive, and imaging scores were correlated with each other in TRACK-HD participants, justifying use of a single, cross-domain measure of disease progression in both studies. The TRACK-HD and REGISTRY progression measures were correlated with each other (r=0·674), and with age at onset (TRACK-HD, r=0·315; REGISTRY, r=0·234). The meta-analysis of progression in TRACK-HD and REGISTRY gave a genome-wide significant signal (p=1·12 × 10−10) on chromosome 5 spanning three genes: MSH3, DHFR, and MTRNR2L2. The genes in this locus were associated with progression in TRACK-HD (MSH3 p=2·94 × 10−8 DHFR p=8·37 × 10−7 MTRNR2L2 p=2·15 × 10−9) and to a lesser extent in REGISTRY (MSH3 p=9·36 × 10−4 DHFR p=8·45 × 10−4 MTRNR2L2 p=1·20 × 10−3). The lead single nucleotide polymorphism (SNP) in TRACK-HD (rs557874766) was genome-wide significant in the meta-analysis (p=1·58 × 10−8), and encodes an aminoacid change (Pro67Ala) in MSH3. In TRACK-HD, each copy of the minor allele at this SNP was associated with a 0·4 units per year (95% CI 0·16–0·66) reduction in the rate of change of the Unified Huntington's Disease Rating Scale (UHDRS) Total Motor Score, and a reduction of 0·12 units per year (95% CI 0·06–0·18) in the rate of change of UHDRS Total Functional Capacity score. These associations remained significant after adjusting for age of onset. Interpretation The multidomain progression measure in TRACK-HD was associated with a functional variant that was genome-wide significant in our meta-analysis. The association in only 216 participants implies that the progression measure is a sensitive reflection of disease burden, that the effect size at this locus is large, or both. Knockout of Msh3 reduces somatic expansion in Huntington's disease mouse models, suggesting this mechanism as an area for future therapeutic investigation