Assessing Maturity Requirements for Implementing and Using Product Lifecycle Management

Product lifecycle management (PLM) is a systematic and holistic way to approach challenges that exist in managing product related information along products’ lifecycle from product design to its disposal. There is an established set of information management approaches that address important subsets of lifecycle information management challenges, e.g. product data management (PDM), ERP and CRM. Common feature to PLM processes is that their implementation requires changes in organization, systems, conventions, and importantly, skills and capabilities. The aim of this paper is to discuss the issue of PLM implementation and how it can be aided with capability maturity assessment. Empirical part of the paper points out how capability maturity assessment can be conducted and how it is applicable in different stages of implementing and developing PLM

Evidence of Inbreeding Depression on Human Height

WOS:000306840400001Peer reviewe

Different Approaches of the PLM Maturity Concept and Their Use Domains – Analysis of the State of the Art

Part 3: PLM MaturityInternational audienceProduct lifecycle management (PLM) implementation and adoption involves extensive changes in both intra- and inter-organizational practices. Various maturity approaches, for instance based on CMM (Capability maturity modeling) principles, can be used to make the implementation of PLM a better approachable and a more carefully planned and coordinated process. However, there are a number of different types of current approaches which can be thought to fall under the concept of PLM maturity. The aim of this paper is to investigate, analyze and categorize the various existing PLM maturity approaches to get an organized picture of the models and their background presumptions, as well as their potential use domains, and to facilitate their proper use to better implement PLM in different industry contexts

In vitro protein digestion and carbohydrate colon fermentation of microbial biomass samples from bacterial, filamentous fungus and yeast sources

This study evaluated the nutritional quality of different microbial biomass samples by assessing their protein digestibility and carbohydrate fermentability in the colon using in vitro methods. Four microbial samples were produced: one hydrogen-oxidizing bacterial strain (Nocardioides nitrophenolicus KGS-27), two strains of filamentous fungi (Rhizopus oligosporus and Paecilomyces variotii), and one yeast strain (Rhodotorula babjevae). The microorganisms were grown in bioreactors, harvested and dried before analysis. The commercial fungal product Quorn was used as a reference. The protein digestibility of the microbial samples was analysed using the INFOGEST in vitro model, followed by quantification of N-terminal amine groups. An in vitro faecal fermentation experiment was also performed to evaluate the degradation of carbohydrates in microbial biomass samples and formation of short-chain fatty acids (SCFA). The fungal biomass samples had higher protein hydrolysis (60-75%) than the bacterial sample (12%) and Quorn (45%), while the yeast biomass had the highest protein digestibility (85%). Heat-treatment of the biomass significantly reduced its protein digestibility. Total dietary fibre (DF) content of fungal biomass was 31 – 43%(DW), mostly insoluble, whereas the bacterial biomass contained mainly soluble DF (total DF: 25.7%, of which 23.5% were soluble and 2.2% insoluble). After 24 h of colonic in vitro fermentation, SCFA production from the biomass of Paecilomyces, Quorn and Rhodotorula was similar to that of wheat bran, while 17% and 32% less SCFA were produced from the biomass of Rhizopus and the bacterial strain, respectively. Further studies are needed to clarify the reasons for the observed differences in protein digestibility and DF fermentability, especially regarding the cell wall structures and role of post-processing

Genetic Determinants of Height Growth Assessed Longitudinally from Infancy to Adulthood in the Northern Finland Birth Cohort 1966

Recent genome-wide association (GWA) studies have identified dozens of common variants associated with adult height. However, it is unknown how these variants influence height growth during childhood. We derived peak height velocity in infancy (PHV1) and puberty (PHV2) and timing of pubertal height growth spurt from parametric growth curves fitted to longitudinal height growth data to test their association with known height variants. The study consisted of N = 3,538 singletons from the prospective Northern Finland Birth Cohort 1966 with genotype data and frequent height measurements (on average 20 measurements per person) from 0–20 years. Twenty-six of the 48 variants tested associated with adult height (p<0.05, adjusted for sex and principal components) in this sample, all in the same direction as in previous GWA scans. Seven SNPs in or near the genes HHIP, DLEU7, UQCC, SF3B4/SV2A, LCORL, and HIST1H1D associated with PHV1 and five SNPs in or near SOCS2, SF3B4/SV2A, C17orf67, CABLES1, and DOT1L with PHV2 (p<0.05). We formally tested variants for interaction with age (infancy versus puberty) and found biologically meaningful evidence for an age-dependent effect for the SNP in SOCS2 (p = 0.0030) and for the SNP in HHIP (p = 0.045). We did not have similar prior evidence for the association between height variants and timing of pubertal height growth spurt as we had for PHVs, and none of the associations were statistically significant after correction for multiple testing. The fact that in this sample, less than half of the variants associated with adult height had a measurable effect on PHV1 or PHV2 is likely to reflect limited power to detect these associations in this dataset. Our study is the first genetic association analysis on longitudinal height growth in a prospective cohort from birth to adulthood and gives grounding for future research on the genetic regulation of human height during different periods of growth.University Hospital Oulu, BiocenterAcademy of Finland (project grant 104781)Academy of Finland (project grant 120315)Academy of Finland. Center of Excellence in Complex Disease GeneticsUniversity of OuluNational Heart, Lung, and Blood Institute (grant 5R01HL087679-02 through the STAMPEED program (1RL1MH083268-01))Sixth Framework Programme (European Commission) (ENGAGE project grant agreement HEALTH-F4-2007-201413)Medical Research Council (Great Britain) (studentship grant G0500539)Medical Research Council (Great Britain) (centre grant G0600705)Wellcome Trust (project grant GR069224)Research Councils U

FTO genotype is associated with phenotypic variability of body mass index

There is evidence across several species for genetic control of phenotypic variation of complex traits, such that the variance among phenotypes is genotype dependent. Understanding genetic control of variability is important in evolutionary biology, agricultural selection programmes and human medicine, yet for complex traits, no individual genetic variants associated with variance, as opposed to the mean, have been identified. Here we perform a meta-analysis of genome-wide association studies of phenotypic variation using ∼170,000 samples on height and body mass index (BMI) in human populations. We report evidence that the single nucleotide polymorphism (SNP) rs7202116 at the FTO gene locus, which is known to be associated with obesity (as measured by mean BMI for each rs7202116 genotype), is also associated with phenotypic variability. We show that the results are not due to scale effects or other artefacts, and find no other experiment-wise significant evidence for effects on variability, either at loci other than FTO for BMI or at any locus for height. The difference in variance for BMI among individuals with opposite homozygous genotypes at the FTO locus is approximately 7%, corresponding to a difference of ∼0.5 kilograms in the standard deviation of weight. Our results indicate that genetic variants can be discovered that are associated with variability, and that between-person variability in obesity can partly be explained by the genotype at the FTO locus. The results are consistent with reported FTO by environment interactions for BMI, possibly mediated by DNA methylation. Our BMI results for other SNPs and our height results for all SNPs suggest that most genetic variants, including those that influence mean height or mean BMI, are not associated with phenotypic variance, or that their effects on variability are too small to detect even with samples sizes greater than 100,000

Genome-wide meta-analysis identifies 11 new loci for anthropometric traits and provides insights into genetic architecture

<p>Approaches exploiting trait distribution extremes may be used to identify loci associated with common traits, but it is unknown whether these loci are generalizable to the broader population. In a genome-wide search for loci associated with the upper versus the lower 5th percentiles of body mass index, height and waist-to-hip ratio, as well as clinical classes of obesity, including up to 263,407 individuals of European ancestry, we identified 4 new loci (IGFBP4, H6PD, RSRC1 and PPP2R2A) influencing height detected in the distribution tails and 7 new loci (HNF4G, RPTOR, GNAT2, MRPS33P4, ADCY9, HS6ST3 and ZZZ3) for clinical classes of obesity. Further, we find a large overlap in genetic structure and the distribution of variants between traits based on extremes and the general population and little etiological heterogeneity between obesity subgroups.</p>