Modeling Commercial Processes and Customer Behaviors to Estimate

We propose a formal model for estimating the diffusion rate of a new product on a coherent market. Our approach is based on a discrete probabilistic modeling of customer behaviors and of commercial processes.Diffusion of innovation, diffusion rate, marketing, customer behavior, product diffusion

Modeling Commercial Processes and Customer Behaviors to Estimate

We propose a formal model for estimating the diffusion rate of a new product on a coherent market. Our approach is based on a discrete probabilistic modeling of customer behaviors and of commercial processes

Modeling Commercial Processes and Customer Behaviors to Estimate the Diffusion Rate of New Products

We propose a formal model for describing commercial processes and customer behaviors in order to estimate the diffusion rate of new products among time

Priorities for service improvement in personality disorder in Australia: Perspectives of consumers, carers and clinicians

Background: Improvements to service provision for personality disorder has been predominately explored through the perspectives of clinicians, with limited understanding of the views of consumers and carers. The aim of the present study was to understand the priorities for service improvement through multiple perspectives.Method: Twelve roundtables, with a total of 53 consumers, clinicians, and carers, discussed how organisations could improve service provision for people with personality disorder and completed a questionnaire on current and optimal service provision. Inductive thematic analysis was used to identify the priorities for service improvement and we aimed to identify differences between what participants currently receive and what they believe to be optimal.Results: Four priorities were identified: 1) increasing consumer, carer and peer involvement in care, 2) re-orienting approaches to service provision, 3) improving access and accessibility of treatment, and 4) building the capacity of services. Participants were more likely to receive individual or group treatment alone, yet believed combined individual and group treatment to be optimal. Significantly more participants believed that long-term treatment was optimal.Conclusion: A shift in focus from establishing a consistent approach to servicing, to focusing on holistic care which involves consumers and carers in care is required

Entangled quantum tunneling of two-component Bose-Einstein condensates

We examine the quantum tunneling process in Bose condensates of two interacting species trapped in a double well configuration. We discover the condition under which particles of different species can tunnel as pairs through the potential barrier between two wells in opposition directions. This novel form of tunneling is due to the interspecies interaction that eliminates the self- trapping effect. The correlated motion of tunneling atoms leads to the generation of quantum entanglement between two macroscopically coherent systems.Comment: 4 pages, 3 figure

Quasi-spin Model for Macroscopic Quantum Tunnelling between Two Coupled Bose-Einstein Condensates

The macroscopic quantum tunneling between two coupled Bose-Einstein condensates (BEC) (radio-frequency coupled two-component BECs or two BECs confined in a double-well potential) is mapped onto the tunneling of an uniaxial spin with an applied magnetic field. The tunneling exponent is calculated with an imaginary-time path-integral method. In the limit of low barrier, the dependence of tunneling exponent on the system parameters is obtained, and the crossover temperature from thermal regime to quantum regime is estimated. The detailed information about the tunnelling will give help to control population conversion between coupled BECs and realize quantum computation with coupled BECs.Comment: 20 pages, 4 figures, accepted by Phys.Rev.

Identification and Functional Characterization of G6PC2 Coding Variants Influencing Glycemic Traits Define an Effector Transcript at the G6PC2-ABCB11 Locus

Genome wide association studies (GWAS) for fasting glucose (FG) and insulin (FI) have identified common variant signals which explain 4.8% and 1.2% of trait variance, respectively. It is hypothesized that low-frequency and rare variants could contribute substantially to unexplained genetic variance. To test this, we analyzed exome-array data from up to 33,231 non-diabetic individuals of European ancestry. We found exome-wide significant (P<5×10-7) evidence for two loci not previously highlighted by common variant GWAS: GLP1R (p.Ala316Thr, minor allele frequency (MAF)=1.5%) influencing FG levels, and URB2 (p.Glu594Val, MAF = 0.1%) influencing FI levels. Coding variant associations can highlight potential effector genes at (non-coding) GWAS signals. At the G6PC2/ABCB11 locus, we identified multiple coding variants in G6PC2 (p.Val219Leu, p.His177Tyr, and p.Tyr207Ser) influencing FG levels, conditionally independent of each other and the non-coding GWAS signal. In vitro assays demonstrate that these associated coding alleles result in reduced protein abundance via proteasomal degradation, establishing G6PC2 as an effector gene at this locus. Reconciliation of single-variant associations and functional effects was only possible when haplotype phase was considered. In contrast to earlier reports suggesting that, paradoxically, glucose-raising alleles at this locus are protective against type 2 diabetes (T2D), the p.Val219Leu G6PC2 variant displayed a modest but directionally consistent association with T2D risk. Coding variant associations for glycemic traits in GWAS signals highlight PCSK1, RREB1, and ZHX3 as likely effector transcripts. These coding variant association signals do not have a major impact on the trait variance explained, but they do provide valuable biological insights

Loss-of-function mutations in UDP-Glucose 6-Dehydrogenase cause recessive developmental epileptic encephalopathy

Developmental epileptic encephalopathies are devastating disorders characterized by intractable epileptic seizures and developmental delay. Here, we report an allelic series of germline recessive mutations in UGDH in 36 cases from 25 families presenting with epileptic encephalopathy with developmental delay and hypotonia. UGDH encodes an oxidoreductase that converts UDP-glucose to UDP-glucuronic acid, a key component of specific proteoglycans and glycolipids. Consistent with being loss-of-function alleles, we show using patients’ primary fibroblasts and biochemical assays, that these mutations either impair UGDH stability, oligomerization, or enzymatic activity. In vitro, patient-derived cerebral organoids are smaller with a reduced number of proliferating neuronal progenitors while mutant ugdh zebrafish do not phenocopy the human disease. Our study defines UGDH as a key player for the production of extracellular matrix components that are essential for human brain development. Based on the incidence of variants observed, UGDH mutations are likely to be a frequent cause of recessive epileptic encephalopathy