74 research outputs found

    Ensembles of probability estimation trees for customer churn prediction

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    Customer churn prediction is one of the most, important elements tents of a company's Customer Relationship Management, (CRM) strategy In tins study, two strategies are investigated to increase the lift. performance of ensemble classification models, i.e (1) using probability estimation trees (PETs) instead of standard decision trees as base classifiers; and (n) implementing alternative fusion rules based on lift weights lot the combination of ensemble member's outputs Experiments ale conducted lot font popular ensemble strategics on five real-life chin n data sets In general, the results demonstrate how lift performance can be substantially improved by using alternative base classifiers and fusion tides However: the effect vanes lot the (Idol cut ensemble strategies lit particular, the results indicate an increase of lift performance of (1) Bagging by implementing C4 4 base classifiets. (n) the Random Subspace Method (RSM) by using lift-weighted fusion rules, and (in) AdaBoost, by implementing both

    Qualitative Properties of Magnetic Fields in Scalar Field Cosmology

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    We study the qualitative properties of the class of spatially homogeneous Bianchi VI_o cosmological models containing a perfect fluid with a linear equation of state, a scalar field with an exponential potential and a uniform cosmic magnetic field, using dynamical systems techniques. We find that all models evolve away from an expanding massless scalar field model in which the matter and the magnetic field are negligible dynamically. We also find that for a particular range of parameter values the models evolve towards the usual power-law inflationary model (with no magnetic field) and, furthermore, we conclude that inflation is not fundamentally affected by the presence of a uniform primordial magnetic field. We investigate the physical properties of the Bianchi I magnetic field models in some detail.Comment: 12 pages, 2 figures in REVTeX format. to appear in Phys. Rev.

    Detection of paralytic shellfish toxins in mussels and oysters using the qualitative neogen lateral-flow immunoassay: an interlaboratory study

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    Paralytic shellfish toxins (PSTs) in bivalve molluscs represent a public health risk and are controlled via compliance with a regulatory limit of 0.8 mg saxitoxin (STX)center dot 2HCl equivalents per kilogram of shellfish meat (eq/kg). Shellfish industries would benefit from the use of rapid immunological screening tests for PSTs to be used for regulation, but to date none have been fully validated. An interlaboratory study involving 16 laboratories was performed to determine the suitability of the Neogen test to detect PSTs in mussels and oysters. Participants performed the standard protocol recommended by the manufacturer and a modified protocol with a conversion step to improve detection of gonyautoxin 1&4. The statistical analysis showed that the protocols had good homogeneity across all laboratories, with satisfactory repeatability, laboratory, and reproducibility variation near the regulatory level. The mean probability of detection (POD) at 0.8 mg STX center dot 2HCl eq/kg using the standard protocol in mussels and oysters was 0.966 and 0.997, respectively, and 0.968 and 0.966 using the modified protocol. The estimated LOD in mussels was 0.316 mg STX center dot 2HCl eq/kg with the standard and 0.682 mg STX center dot 2HCl eq/kg with the modified protocol, and 0.710 and 0.734 mg STX center dot 2HCl eq/kg for oysters, respectively. The Neogen test may be acceptable for regulatory purposes for oysters in accordance with European Commission directives in which the standard protocol provides, at the regulatory level, a probability of a negative response of 0.033 on 95% of occasions. Its use for mussels is less consistent at the regulatory level due to the wide prediction interval around the POD

    The genetic architecture of the human cerebral cortex

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    INTRODUCTION The cerebral cortex underlies our complex cognitive capabilities. Variations in human cortical surface area and thickness are associated with neurological, psychological, and behavioral traits and can be measured in vivo by magnetic resonance imaging (MRI). Studies in model organisms have identified genes that influence cortical structure, but little is known about common genetic variants that affect human cortical structure. RATIONALE To identify genetic variants associated with human cortical structure at both global and regional levels, we conducted a genome-wide association meta-analysis of brain MRI data from 51,665 individuals across 60 cohorts. We analyzed the surface area and average thickness of the whole cortex and 34 cortical regions with known functional specializations. RESULTS We identified 306 nominally genome-wide significant loci (P < 5 × 10−8) associated with cortical structure in a discovery sample of 33,992 participants of European ancestry. Of the 299 loci for which replication data were available, 241 loci influencing surface area and 14 influencing thickness remained significant after replication, with 199 loci passing multiple testing correction (P < 8.3 × 10−10; 187 influencing surface area and 12 influencing thickness). Common genetic variants explained 34% (SE = 3%) of the variation in total surface area and 26% (SE = 2%) in average thickness; surface area and thickness showed a negative genetic correlation (rG = −0.32, SE = 0.05, P = 6.5 × 10−12), which suggests that genetic influences have opposing effects on surface area and thickness. Bioinformatic analyses showed that total surface area is influenced by genetic variants that alter gene regulatory activity in neural progenitor cells during fetal development. By contrast, average thickness is influenced by active regulatory elements in adult brain samples, which may reflect processes that occur after mid-fetal development, such as myelination, branching, or pruning. When considered together, these results support the radial unit hypothesis that different developmental mechanisms promote surface area expansion and increases in thickness. To identify specific genetic influences on individual cortical regions, we controlled for global measures (total surface area or average thickness) in the regional analyses. After multiple testing correction, we identified 175 loci that influence regional surface area and 10 that influence regional thickness. Loci that affect regional surface area cluster near genes involved in the Wnt signaling pathway, which is known to influence areal identity. We observed significant positive genetic correlations and evidence of bidirectional causation of total surface area with both general cognitive functioning and educational attainment. We found additional positive genetic correlations between total surface area and Parkinson’s disease but did not find evidence of causation. Negative genetic correlations were evident between total surface area and insomnia, attention deficit hyperactivity disorder, depressive symptoms, major depressive disorder, and neuroticism. CONCLUSION This large-scale collaborative work enhances our understanding of the genetic architecture of the human cerebral cortex and its regional patterning. The highly polygenic architecture of the cortex suggests that distinct genes are involved in the development of specific cortical areas. Moreover, we find evidence that brain structure is a key phenotype along the causal pathway that leads from genetic variation to differences in general cognitive function

    A mathematical model of the eye lens epithelium of mammals that predicts cell density profiles in the ageing lens.

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    Purpose: To develop a mathematical model of the mammalian eye lens epithelium that is independent of the lens size and that accounts for the change in cell density from the anterior pole to the meridional rows at the lens equator. The model aims to predict the age dependent changes in cell density. Methods: Eye lenses were dissected, the epithelial flat mounted and then fixed and processed for immunofluoresence microscopy. Fluoresence signal were detected using either a Zeiss LSM 510 Meta or Leica SP5 scanning confocal microscope. Cell density measurements were made using DAPI and then bespoke software to segment images. Lenses from mice up to 2 years and from human donors from 20-90 years old were obtained with the required ethical, animal and human tissue authorisations. Results: The cellular distribution in the lens epithelium was measured in mouse, rat, rabbit, bovine and human lenses from the anterior pole of the lens to the meridional rows loacted at te lens equator. Measurements of cell proliferation (Ki67) and cell death (TUNEL) were also made. The epithelium was then modelled as a disk and an appropriate differential equation for the cell density distribution was solved. At any given time-point, this differential equation balances the pull-through due to fibre cell formation with net epithelial cell proliferation. Cell proliferation is concentrated in the peripheral region of the lens where the germinative zone is located, with only baseline proliferation rates observed in the central zone of the lens epithelium. The ratio of the per capita division rate for these two zones as predicted from the model was found to be equal to a recently measured gradient of matrix-bound FGF- 2 in the lens capsule. The model predicts that as the ratio of the proliferation parameter to the pull-through parameter declines, so the discrete peak in cell density found in the germinative zone will decay. Measurements of ageing mouse and human lens epithelial cell densities were used to affirm the predictive value of the model. Conclusions: We have developed a model of the mammalian lens epithelium that balances pull-through due to fibre cell formation with net cell proliferation. The model predicts the morphogen gradient that drives cell survival, cell proliferation and cell differentiation. It also successfully predicts the cell density changes that accompany ageing in the mouse lens. Commercial Relationships: Roy A. Quinlan, None; Junjie Wu, None; Weiju Wu, None; Chris Saunter, None; John Girkin, None Support: Fight for Sight (#1358) and Leverhulme Trust (RPG-2012- 554
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