Browsing
     by title


0-9 A B C D E F G H I J K L M N O P Q R S T U V W X Y Z

or enter first few letters:   
OK
Full Text
Peer Reviewed
See detailA novel cost-sensitive framework for customer churn predictive modeling
Correa Bahnsen, Alejandro UL; Aouada, Djamila UL; Ottersten, Björn UL

in Decision Analytics (2015), 2(5),

Customer churn predictive modeling deals with predicting the probability of a customer defecting using historical, behavioral and socio-economical information. This tool is of great benefit to ... [more ▼]

Customer churn predictive modeling deals with predicting the probability of a customer defecting using historical, behavioral and socio-economical information. This tool is of great benefit to subscription based companies allowing them to maximize the results of retention campaigns. The problem of churn predictive modeling has been widely studied by the data mining and machine learning communities. It is usually tackled by using classification algorithms in order to learn the different patterns of both the churners and non-churners. Nevertheless, current state-of-the-art classification algorithms are not well aligned with commercial goals, in the sense that, the models miss to include the real financial costs and benefits during the training and evaluation phases. In the case of churn, evaluating a model based on a traditional measure such as accuracy or predictive power, does not yield to the best results when measured by the actual financial cost, ie. investment per subscriber on a loyalty campaign and the financial impact of failing to detect a real churner versus wrongly predicting a non-churner as a churner. In this paper, we present a new cost-sensitive framework for customer churn predictive modeling. First we propose a new financial based measure for evaluating the effectiveness of a churn campaign taking into account the available portfolio of offers, their individual financial cost and probability of offer acceptance depending on the customer profile. Then, using a real-world churn dataset we compare different cost-insensitive and cost-sensitive classification algorithms and measure their effectiveness based on their predictive power and also the cost optimization. The results show that using a cost-sensitive approach yields to an increase in cost savings of up to 26.4% [less ▲]

Detailed reference viewed: 212 (5 UL)
Full Text
See detailNovel Double-Level-T-Gate Technology
Fox, Alfred; Mikulics, Martin; Hardtdegen, Hilde et al

in Conference Proceedings The 10th International Conference on Advanced Semiconductor devices and Microsystems (2014, October)

We developed a novel double-level-T-gate technology based on wet etching of a metal gate interlayer. With the help of this technological process we prepared T-gate feet with widths as small as 200 nm. The ... [more ▼]

We developed a novel double-level-T-gate technology based on wet etching of a metal gate interlayer. With the help of this technological process we prepared T-gate feet with widths as small as 200 nm. The major advantage of our process is its use of only standard optical lithography. It allows the fabrication of 100 nanometer size T-gates for transistors. High electron mobility transistors (HEMTs) were fabricated on an AlGaN/GaN/sapphire material structure with an original gate length Lg of 2 μm. Their cutoff frequency of 6 GHz was improved to 60 GHz by etching the gate to a 200 nm length double T-gate contact. [less ▲]

Detailed reference viewed: 107 (0 UL)
Full Text
Peer Reviewed
See detailNovel drug target identification for the treatment of dementia using multi-relational association mining
Nguyen, Thanh-Phuong UL; Priami, Corrado; Caberlotto, Laura

in Scientific Reports (2015), 5

Dementia is a neurodegenerative condition of the brain in which there is a progressive and permanent loss of cognitive and mental performance. Despite the fact that the number of people with dementia ... [more ▼]

Dementia is a neurodegenerative condition of the brain in which there is a progressive and permanent loss of cognitive and mental performance. Despite the fact that the number of people with dementia worldwide is steadily increasing and regardless of the advances in the molecular characterization of the disease, current medical treatments for dementia are purely symptomatic and hardly effective. We present a novel multi-relational association mining method that integrates the huge amount of scientific data accumulated in recent years to predict potential novel targets for innovative therapeutic treatment of dementia. Owing to the ability of processing large volumes of heterogeneous data, our method achieves a high performance and predicts numerous drug targets including several serine threonine kinase and a G-protein coupled receptor. The predicted drug targets are mainly functionally related to metabolism, cell surface receptor signaling pathways, immune response, apoptosis, and long-term memory. Among the highly represented kinase family and among the G-protein coupled receptors, DLG4 (PSD-95), and the bradikynin receptor 2 are highlighted also for their proposed role in memory and cognition, as described in previous studies. These novel putative targets hold promises for the development of novel therapeutic approaches for the treatment of dementia. [less ▲]

Detailed reference viewed: 186 (22 UL)
Full Text
Peer Reviewed
See detailA novel Eco-Driving Application to Reduce Energy Consumption of Electric Vehicles
Frank, Raphaël UL; Castignani, German UL; Schmitz, Raoul et al

in Proceedings of the 2nd International Conference on Connected Vehicles & Expo (ICCVE 2013) (2013, December)

Detailed reference viewed: 181 (5 UL)
Full Text
Peer Reviewed
See detailNovel efficient asynchronous cooperative co-evolutionary multi-objective algorithms
Nielsen, Sune Steinbjorn UL; Dorronsoro, Bernabé UL; Danoy, Grégoire UL et al

in Congress on Evolutionary Computation (CEC) (2012)

Detailed reference viewed: 174 (13 UL)
Full Text
Peer Reviewed
See detailA novel Fanconi anemia subtype associated with a dominant-negative mutation in RAD51
Ameziane, Najim; May, Patrick UL; Van de Vrugt, Henri J. et al

in Nature Communications (2015), 6(8829),

Fanconi anemia (FA) is a hereditary disease featuring hypersensitivity to DNA cross-linker-induced chromosomal instability in association with developmental abnormalities, bone marrow failure and a strong ... [more ▼]

Fanconi anemia (FA) is a hereditary disease featuring hypersensitivity to DNA cross-linker-induced chromosomal instability in association with developmental abnormalities, bone marrow failure and a strong predisposition to cancer. 17 FA disease genes have been reported, all of which act in a recessive mode of inheritance. Here we report on a de novo g.41022153G>A; p.Ala293Thr (NM_002875) missense mutation in one allele of the homologous recombination DNA repair gene RAD51 in an FA-like patient. This heterozygous mutation causes a novel FA subtype, “FA-R”, which appears to be the first subtype of FA caused by a dominant-negative mutation. The patient, who features microcephaly and mental retardation, has reached adulthood without the typical bone marrow failure and pediatric cancers. Together with the recent reports on RAD51-associated congenital mirror movement disorders our results point to an important role for RAD51-mediated homologous recombination in neurodevelopment, in addition to DNA repair and cancer susceptibility. [less ▲]

Detailed reference viewed: 190 (21 UL)
Full Text
Peer Reviewed
See detailA Novel Fast Process for Zn(O,S) Buffer Layers, Doped With Al and B and Deposited on CIGSSe Solar Cells
Hönes, C.; Hackenberg, J.; Keller, R. et al

in IEEE Journal of Photovoltaics (2017), 7

Detailed reference viewed: 127 (0 UL)
Full Text
Peer Reviewed
See detailNovel functional interaction between the plasma membrane Ca2+ pump 4b and the proapoptotic tumor suppressor Ras-associated factor 1 (RASSF1).
Armesilla, Angel L.; Williams, Judith C.; Buch, Mamta H. et al

in The Journal of biological chemistry (2004), 279(30), 31318-28

Plasma membrane calmodulin-dependent calcium ATPases (PMCAs) are enzymatic systems implicated in the extrusion of calcium from the cell. We and others have previously identified molecular interactions ... [more ▼]

Plasma membrane calmodulin-dependent calcium ATPases (PMCAs) are enzymatic systems implicated in the extrusion of calcium from the cell. We and others have previously identified molecular interactions between the cytoplasmic COOH-terminal end of PMCA and PDZ domain-containing proteins. These interactions suggested a new role for PMCA as a modulator of signal transduction pathways. The existence of other intracellular regions in the PMCA molecule prompted us to investigate the possible participation of other domains in interactions with different partner proteins. A two-hybrid screen of a human fetal heart cDNA library, using the region 652-840 of human PMCA4b (located in the catalytic, second intracellular loop) as bait, revealed a novel interaction between PMCA4b and the tumor suppressor RASSF1, a Ras effector protein involved in H-Ras-mediated apoptosis. Immunofluorescence co-localization, immunoprecipitation, and glutathione S-transferase pull-down experiments performed in mammalian cells provided further confirmation of the physical interaction between the two proteins. The interaction domain has been narrowed down to region 74-123 of RASSF1C (144-193 in RASSF1A) and 652-748 of human PMCA4b. The functionality of this interaction was demonstrated by the inhibition of the epidermal growth factor-dependent activation of the Erk pathway when PMCA4b and RASSF1 were co-expressed. This inhibition was abolished by blocking PMCA/RASSSF1 association with an excess of a green fluorescent protein fusion protein containing the region 50-123 of RASSF1C. This work describes a novel protein-protein interaction involving a domain of PMCA other than the COOH terminus. It suggests a function for PMCA4b as an organizer of macromolecular protein complexes, where PMCA4b could recruit diverse proteins through interaction with different domains. Furthermore, the functional association with RASSF1 indicates a role for PMCA4b in the modulation of Ras-mediated signaling. [less ▲]

Detailed reference viewed: 121 (0 UL)
Full Text
Peer Reviewed
See detailA novel GATA6 mutation in a child with congenital heart malformation and neonatal diabetes.
Eifes, Serge UL; Chudasama, Kishan K.; Molnes, Janne et al

in Clinical Case Reports (2013), 1(2), 86-90

Diabetes in neonates is a monogenetic disease and genetic analysis is warranted to allow best treatment, prognosis, and genetic counseling. Transcription factor mutations may have a variable expression ... [more ▼]

Diabetes in neonates is a monogenetic disease and genetic analysis is warranted to allow best treatment, prognosis, and genetic counseling. Transcription factor mutations may have a variable expression and different organs may be involved. [less ▲]

Detailed reference viewed: 102 (2 UL)
Full Text
Peer Reviewed
See detailA novel GDP-D-glucose phosphorylase involved in quality control of the nucleoside diphosphate sugar pool in Caenorhabditis elegans and mammals
Adler, Lital N.; Gomez, Tara A.; Clarke, Steven G. et al

in Journal of Biological Chemistry (2011), 286(24), 21511-23

The plant VTC2 gene encodes GDP-L-galactose phosphorylase, a rate-limiting enzyme in plant vitamin C biosynthesis. Genes encoding apparent orthologs of VTC2 exist in both mammals, which produce vitamin C ... [more ▼]

The plant VTC2 gene encodes GDP-L-galactose phosphorylase, a rate-limiting enzyme in plant vitamin C biosynthesis. Genes encoding apparent orthologs of VTC2 exist in both mammals, which produce vitamin C by a distinct metabolic pathway, and in the nematode worm Caenorhabditis elegans where vitamin C biosynthesis has not been demonstrated. We have now expressed cDNAs of the human and worm VTC2 homolog genes (C15orf58 and C10F3.4, respectively) and found that the purified proteins also display GDP-hexose phosphorylase activity. However, as opposed to the plant enzyme, the major reaction catalyzed by these enzymes is the phosphorolysis of GDP-D-glucose to GDP and D-glucose 1-phosphate. We detected activities with similar substrate specificity in worm and mouse tissue extracts. The highest expression of GDP-D-glucose phosphorylase was found in the nervous and male reproductive systems. A C. elegans C10F3.4 deletion strain was found to totally lack GDP-D-glucose phosphorylase activity; this activity was also found to be decreased in human HEK293T cells transfected with siRNAs against the human C15orf58 gene. These observations confirm the identification of the worm C10F3.4 and the human C15orf58 gene expression products as the GDP-D-glucose phosphorylases of these organisms. Significantly, we found an accumulation of GDP-D-glucose in the C10F3.4 mutant worms, suggesting that the GDP-D-glucose phosphorylase may function to remove GDP-D-glucose formed by GDP-D-mannose pyrophosphorylase, an enzyme that has previously been shown to lack specificity for its physiological D-mannose 1-phosphate substrate. We propose that such removal may prevent the misincorporation of glucosyl residues for mannosyl residues into the glycoconjugates of worms and mammals. [less ▲]

Detailed reference viewed: 201 (2 UL)
Full Text
Peer Reviewed
See detailA Novel Heap-based Pilot Assignment for Full Duplex Cell-Free Massive MIMO with Zero-Forcing
Nguyen, Van Hieu; Nguyen, van Dinh UL; Dobre, Octavia A. et al

in IEEE International Conference on Communications (2020, June 07)

This paper investigates the combined benefits of full-duplex (FD) and cell-free massive multiple-input multipleoutput (CF-mMIMO), where a large number of distributed access points (APs) having FD ... [more ▼]

This paper investigates the combined benefits of full-duplex (FD) and cell-free massive multiple-input multipleoutput (CF-mMIMO), where a large number of distributed access points (APs) having FD capability simultaneously serve numerous uplink and downlink user equipments (UEs) on the same time-frequency resources. To enable the incorporation of FD technology in CF-mMIMO systems, we propose a novel heapbased pilot assignment algorithm, which not only can mitigate the effects of pilot contamination but also reduce the involved computational complexity. Then, we formulate a robust design problem for spectral efficiency (SE) maximization in which the power control and AP-UE association are jointly optimized, resulting in a difficult mixed-integer nonconvex programming. To solve this problem, we derive a more tractable problem before developing a very simple iterative algorithm based on inner approximation method with polynomial computational complexity. Numerical results show that our proposed methods with realistic parameters significantly outperform the existing approaches in terms of the quality of channel estimate and SE. [less ▲]

Detailed reference viewed: 118 (29 UL)
Full Text
Peer Reviewed
See detailNovel HEMT layout: The RoundHEMT
Marso, Michel UL; Schimpf, K.; Fox, A. et al

in Electronics Letters (1995), 31(1995), 589-591

Detailed reference viewed: 90 (0 UL)
Full Text
Peer Reviewed
See detailA novel heterozygous OPA3 mutation located in the mitochondrial target sequence results in altered steady-state levels and fragmented mitochondrial network.
Grau, Tanja; Burbulla, Lena F.; Engl, Gertraud et al

in Journal of medical genetics (2013), 50(12), 848-58

BACKGROUND: Mutations in OPA3 have been reported in patients with autosomal dominant optic atrophy plus cataract and Costeff syndrome. Here, we report the results of a comprehensive study on OPA3 ... [more ▼]

BACKGROUND: Mutations in OPA3 have been reported in patients with autosomal dominant optic atrophy plus cataract and Costeff syndrome. Here, we report the results of a comprehensive study on OPA3 mutations, including the mutation spectrum and its prevalence in a large cohort of OPA1-negative autosomal dominant optic atrophy (ADOA) patients, the associated clinical phenotype and the functional characterisation of a newly identified OPA3 mutant. METHODS: Mutation analysis was carried out in a patient cohort of 121 independent ADOA patients. To characterise a novel OPA3 mutation, we analysed the mitochondrial import, steady-state levels and the mitochondrial localisation of the mutated protein in patients' fibroblasts. Furthermore, the morphology of mitochondria harbouring the mutated OPA3 was monitored. RESULTS: We identified four independent cases (representing families with multiple affected members) with OPA3 mutations. Besides the known p.Q105E mutation, we observed a novel insertion, c.10_11insCGCCCG/p.V3_G4insAP which is located in the mitochondrial presequence. Detailed functional analysis of mitochondria harbouring this novel mutation demonstrates a fragmented mitochondrial network with a decreased mitochondrial mass in patient fibroblasts. In addition, quantification of the OPA3 protein reveals decreased steady-state levels of the mutant protein compared with the native one. Comparison of the clinical phenotypes suggests that OPA3 mutations can additionally evoke hearing loss and by that extend the clinical manifestation of OPA3-associated optic atrophy. This finding is supported by expression analysis of OPA3 in murine cochlear tissue. CONCLUSIONS: In summary, our study provides new insights into the clinical spectrum and the pathogenesis of dominant optic atrophy caused by mutations in the OPA3 gene. [less ▲]

Detailed reference viewed: 130 (5 UL)
Peer Reviewed
See detailNovel homozygous p.E64D mutation in DJ1 in early onset Parkinson disease (PARK7).
Hering, Robert; Strauss, Karsten M.; Tao, Xiao et al

in Human mutation (2004), 24(4), 321-9

Mutations in the parkin gene have been identified as a common cause of autosomal recessive inherited Parkinson disease (PD) associated with early disease manifestation. However, based on linkage data ... [more ▼]

Mutations in the parkin gene have been identified as a common cause of autosomal recessive inherited Parkinson disease (PD) associated with early disease manifestation. However, based on linkage data, mutations in other genes contribute to the genetic heterogeneity of early-onset PD (EOPD). Recently, two mutations in the DJ1 gene were described as a second cause of autosomal recessive EOPD (PARK7). Analyzing the PARK7/DJ1 gene in 104 EOPD patients, we identified a third mutation, c.192G>C (p.E64D), associated with EOPD in a patient of Turkish ancestry and characterized the functional significance of this amino acid substitution. In the patient, a substantial reduction of dopamine uptake transporter (DAT) binding was found in the striatum using [(18)F]FP-CIT and PET, indicating a serious loss of presynaptic dopaminergic afferents. His sister, homozygous for E64D, was clinically unaffected but showed reduced dopamine uptake when compared with a clinically unaffected brother, who is heterozygous for E64D. We demonstrate by crystallography that the E64D mutation does not alter the structure of the DJ1 protein, however we observe a tendency towards decreased levels of the mutant protein when overexpressed in HEK293 or COS7 cells. Using immunocytochemistry in contrast to the homogenous nuclear and cytoplasmic staining in HEK293 cells overexpressing wild-type DJ1, about 5% of the cells expressing E64D and up to 80% of the cells expressing the recently described L166P mutation displayed a predominant nuclear localization of the mutant DJ1 protein. [less ▲]

Detailed reference viewed: 130 (2 UL)
Full Text
Peer Reviewed
See detailNovel human hepatic organoid model enables testing of drug-induced liver fibrosis in vitro.
Leite, Sofia B.; Roosens, Tiffany; El Taghdouini, Adil et al

in Biomaterials (2016), 78

Current models for in vitro fibrosis consist of simple mono-layer cultures of rodent hepatic stellate cells (HSC), ignoring the role of hepatocyte injury. We aimed to develop a method allowing the ... [more ▼]

Current models for in vitro fibrosis consist of simple mono-layer cultures of rodent hepatic stellate cells (HSC), ignoring the role of hepatocyte injury. We aimed to develop a method allowing the detection of hepatocyte-mediated and drug-induced liver fibrosis. We used HepaRG (Hep) and primary human HSCs cultured as 3D spheroids in 96-well plates. These resulting scaffold-free organoids were characterized for CYP induction, albumin secretion, and hepatocyte and HSC-specific gene expression by qPCR. The metabolic competence of the organoid over 21 days allows activation of HSCs in the organoid in a drug- and hepatocyte-dependent manner. After a single dose or repeated exposure for 14 days to the pro-fibrotic compounds Allyl alcohol and Methotrexate, hepatic organoids display fibrotic features such as HSC activation, collagen secretion and deposition. Acetaminophen was identified by these organoids as an inducer of hepatotoxic-mediated HSC activation which was confirmed in vivo in mice. This novel hepatic organoid culture model is the first that can detect hepatocyte-dependent and compound-induced HSC activation, thereby representing an important step forward towards in vitro compound testing for drug-induced liver fibrosis. [less ▲]

Detailed reference viewed: 117 (0 UL)
Peer Reviewed
See detailA novel immunofluorescent assay to investigate oxidative phosphorylation deficiency in mitochondrial myopathy: understanding mechanisms and improving diagnosis.
Rocha, Mariana C.; Grady, John P.; Grünewald, Anne UL et al

in Scientific reports (2015), 5

Oxidative phosphorylation defects in human tissues are often challenging to quantify due to a mosaic pattern of deficiency. Biochemical assays are difficult to interpret due to the varying enzyme ... [more ▼]

Oxidative phosphorylation defects in human tissues are often challenging to quantify due to a mosaic pattern of deficiency. Biochemical assays are difficult to interpret due to the varying enzyme deficiency levels found in individual cells. Histochemical analysis allows semi-quantitative assessment of complex II and complex IV activities, but there is no validated histochemical assay to assess complex I activity which is frequently affected in mitochondrial pathology. To help improve the diagnosis of mitochondrial disease and to study the mechanisms underlying mitochondrial abnormalities in disease, we have developed a quadruple immunofluorescent technique enabling the quantification of key respiratory chain subunits of complexes I and IV, together with an indicator of mitochondrial mass and a cell membrane marker. This assay gives precise and objective quantification of protein abundance in large numbers of individual muscle fibres. By assessing muscle biopsies from subjects with a range of different mitochondrial genetic defects we have demonstrated that specific genotypes exhibit distinct biochemical signatures in muscle, providing evidence for the diagnostic use of the technique, as well as insight into the underlying molecular pathology. Stringent testing for reproducibility and sensitivity confirms the potential value of the technique for mechanistic studies of disease and in the evaluation of therapeutic approaches. [less ▲]

Detailed reference viewed: 106 (21 UL)
Full Text
Peer Reviewed
See detailA novel immunomodulator, FTY-720 reverses existing cardiac hypertrophy and fibrosis from pressure overload by targeting NFAT (nuclear factor of activated T-cells) signaling and periostin.
Liu, Wei; Zi, Min; Tsui, Hoyee et al

in Circulation. Heart failure (2013), 6(4), 833-44

BACKGROUND: Hypertension or aortic stenosis causes pressure overload, which evokes hypertrophic myocardial growth. Sustained cardiac hypertrophy eventually progresses to heart failure. Growing evidence ... [more ▼]

BACKGROUND: Hypertension or aortic stenosis causes pressure overload, which evokes hypertrophic myocardial growth. Sustained cardiac hypertrophy eventually progresses to heart failure. Growing evidence indicates that restraining hypertrophy could be beneficial; here, we discovered that FTY-720, an immunomodulator for treating multiple sclerosis, can reverse existing cardiac hypertrophy/fibrosis. METHODS AND RESULTS: Male C57/Bl6 mice underwent transverse aortic constriction (TAC) for 1 week followed by FTY-720 treatment for 2 weeks under continuing TAC. Compared with vehicle-treated TAC hearts, FTY-720 significantly reduced ventricular mass, ameliorated fibrosis, and improved cardiac performance. Mechanistic studies led us to discover that FTY-720 appreciably inhibited nuclear factor of activated T-cells (NFAT) activity. Moreover, we found that in primary cardiomyocytes (rat and human) pertussis toxin (Gi-coupled receptor inhibitor) substantially blocked the antihypertrophic effect of FTY-720. This observation was confirmed in a mouse model of pressure overload. Interestingly, gene array analysis of TAC hearts revealed that FTY-720 profoundly decreased gene expression of a group of matricellular proteins, of which periostin was prominent. Analysis of periostin protein expression in TAC-myocardium, as well as in rat and human cardiac fibroblasts, confirmed the array data. Moreover, we found that FTY-720 treatment or knockdown of periostin protein was able to inhibit transforming growth factor-beta responsiveness and decrease collagen expression. CONCLUSIONS: FTY-720 alleviates existing cardiac hypertrophy/fibrosis through mechanisms involving negative regulation of NFAT activity in cardiomyocytes and reduction of periostin expression allowing for a more homeostatic extracellular compartment milieu. Together, FTY-720 or its analogues could be a promising new approach for treating hypertrophic/fibrotic heart disease. [less ▲]

Detailed reference viewed: 153 (0 UL)
See detailA Novel InAlAs/InGaAs Layer Structure for Monolithically Integrated Photoreceiver,
Hodel, U.; Orzati, A.; Marso, Michel UL et al

in Proc. 2000 Int. Conf. Indium Phosphide and Related Materials (2000)

Detailed reference viewed: 70 (0 UL)
See detailA Novel InGaAs Schottky-2DEG Diode
Marso, Michel UL; Kordoš, P.; Fox, A. et al

in Proceedings of the 5th International Conference on InP and Related Compounds, Paris, France (1993)

Detailed reference viewed: 109 (0 UL)
See detailNovel InP/GaInAs Photodetector for Integration in HEMT Circuits
Horstmann, M.; Marso, Michel UL; Schimpf, K. et al

in Proceedings of the 25th European Solid State Devices Research Conference, Den Haag, The Netherlands (1995)

Detailed reference viewed: 19 (0 UL)