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David P. Mackinnon - One of the best experts on this subject based on the ideXlab platform.
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a bifactor approach to model multifaceted constructs in statistical mediation analysis
Educational and Psychological Measurement, 2018Co-Authors: Oscar Gonzalez, David P. MackinnonAbstract:Statistical mediation analysis allows researchers to identify the most important mediating constructs in the causal process studied. Identifying specific mediators is especially relevant when the hypothesized mediating construct consists of multiple related facets. The general definition of the construct and its facets might relate differently to an outcome. However, current methods do not allow researchers to study the relationships between general and specific aspects of a construct to an outcome simultaneously. This study proposes a bifactor measurement model for the mediating construct as a way to parse variance and represent the general aspect and specific facets of a construct simultaneously. Monte Carlo simulation results are presented to help determine the properties of Mediated Effect estimation when the mediator has a bifactor structure and a specific facet of a construct is the true mediator. This study also investigates the conditions when researchers can detect the Mediated Effect when the multidimensionality of the mediator is ignored and treated as unidimensional. Simulation results indicated that the mediation model with a bifactor mediator measurement model had unbiased and adequate power to detect the Mediated Effect with a sample size greater than 500 and medium a- and b-paths. Also, results indicate that parameter bias and detection of the Mediated Effect in both the data-generating model and the misspecified model varies as a function of the amount of facet variance represented in the mediation model. This study contributes to the largely unexplored area of measurement issues in statistical mediation analysis.
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comparing models of change to estimate the Mediated Effect in the pretest posttest control group design
Structural Equation Modeling, 2017Co-Authors: Matthew J Valente, David P. MackinnonAbstract:Models to assess mediation in the pretest-posttest control group design are understudied in the behavioral sciences even though it is the design of choice for evaluating experimental manipulations. The paper provides analytical comparisons of the four most commonly used models used to estimate the Mediated Effect in this design: Analysis of Covariance (ANCOVA), difference score, residualized change score, and cross-sectional model. Each of these models are fitted using a Latent Change Score specification and a simulation study assessed bias, Type I error, power, and confidence interval coverage of the four models. All but the ANCOVA model make stringent assumptions about the stability and cross-lagged relations of the mediator and outcome that may not be plausible in real-world applications. When these assumptions do not hold, Type I error and statistical power results suggest that only the ANCOVA model has good performance. The four models are applied to an empirical example.
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Bias, Type I Error Rates, and Statistical Power of a Latent Mediation Model in the Presence of Violations of Invariance.
Educational and psychological measurement, 2017Co-Authors: Margarita Olivera-aguilar, Samuel H. Rikoon, Oscar Gonzalez, Yasemin Kisbu-sakarya, David P. MackinnonAbstract:When testing a statistical mediation model, it is assumed that factorial measurement invariance holds for the mediating construct across levels of the independent variable X. The consequences of failing to address the violations of measurement invariance in mediation models are largely unknown. The purpose of the present study was to systematically examine the impact of mediator noninvariance on the Type I error rates, statistical power, and relative bias in parameter estimates of the Mediated Effect in the single mediator model. The results of a large simulation study indicated that, in general, the Mediated Effect was robust to violations of invariance in loadings. In contrast, most conditions with violations of intercept invariance exhibited severely positively biased Mediated Effects, Type I error rates above acceptable levels, and statistical power larger than in the invariant conditions. The implications of these results are discussed and recommendations are offered.
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the combined Effects of measurement error and omitting confounders in the single mediator model
Multivariate Behavioral Research, 2016Co-Authors: Matthew S Fritz, David A Kenny, David P. MackinnonAbstract:ABSTRACTMediation analysis requires a number of strong assumptions be met in order to make valid causal inferences. Failing to account for violations of these assumptions, such as not modeling measurement error or omitting a common cause of the Effects in the model, can bias the parameter estimates of the Mediated Effect. When the independent variable is perfectly reliable, for example when participants are randomly assigned to levels of treatment, measurement error in the mediator tends to underestimate the Mediated Effect, while the omission of a confounding variable of the mediator-to-outcome relation tends to overestimate the Mediated Effect. Violations of these two assumptions often co-occur, however, in which case the Mediated Effect could be overestimated, underestimated, or even, in very rare circumstances, unbiased. To explore the combined Effect of measurement error and omitted confounders in the same model, the Effect of each violation on the single-mediator model is first examined individually...
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RMediation: An R package for mediation analysis confidence intervals
Behavior research methods, 2011Co-Authors: Davood Tofighi, David P. MackinnonAbstract:This article describes the RMediation package,which offers various methods for building confidence intervals (CIs) for Mediated Effects. The Mediated Effect is the product of two regression coefficients. The distribution-of-the-product method has the best statistical performance of existing methods for building CIs for the Mediated Effect. RMediation produces CIs using methods based on the distribution of product, Monte Carlo simulations, and an asymptotic normal distribution. Furthermore, RMediation generates percentiles, quantiles, and the plot of the distribution and CI for the Mediated Effect. An existing program, called PRODCLIN, published in Behavior Research Methods, has been widely cited and used by researchers to build accurate CIs. PRODCLIN has several limitations: The program is somewhat cumbersome to access and yields no result for several cases. RMediation described herein is based on the widely available R software, includes several capabilities not available in PRODCLIN, and provides accurate results that PRODCLIN could not.
Hans-ulrich Häring - One of the best experts on this subject based on the ideXlab platform.
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leptin stimulates glucose transport and glycogen synthesis in c2c12 myotubes evidence for a pi3 kinase Mediated Effect
Diabetologia, 1997Co-Authors: Lucia Berti, Monika Kellerer, Edison Capp, Hans-ulrich HäringAbstract:It was recently shown that leptin impairs insulin signalling, i.e. insulin receptor autophosphorylation and insulin-receptor substrate (IRS)-1 phosphorylation in rat-1 fibroblasts, NIH3T3 cells and HepG2 cells. To evaluate whether leptin might impair the Effects of insulin in muscle tissue we studied the interaction of insulin and leptin in a muscle cell system, i.e. C2C12 myotubes. Preincubation of C2C12 cells with leptin (1-500 ng/ml) did not significantly affect insulin stimulated glucose transport and glycogen synthesis (1.8 to 2 fold stimulation); however, leptin by itself (1 ng/ml) was able to mimic approximately 80-90% of the insulin Effect on glucose transport and glycogen synthesis. Both glucose transport as well as glycogen synthesis were inhibited by the phosphatidylinositol-3 (PI3)-kinase inhibitor wortmannin and the protein kinase C inhibitor H7 while no Effect was observed with the S6-kinase inhibitor rapamycin. We determined whether the Effect of leptin occurs through activation of IRS-1 and PI3-kinase. Leptin did not stimulate PI3-kinase activity in IRS-1 immunoprecipitates; however, PI3-kinase activation could be demonstrated in p85 alpha immunoprecipitates (3.04 +/- 1.5 fold of basal). In summary the data provide the first evidence for a positive crosstalk between the signalling chain of the insulin receptor and the leptin receptor. Leptin mimics in C2C12 myotubes insulin Effects on glucose transport and glycogen synthesis most likely through activation of PI3-kinase. This Effect of leptin occurs independently of IRS-1 activation in C2C12 cells.
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leptin stimulates glucose transport and glycogen synthesis in c2c12 myotubes evidence for a pi3 kinase Mediated Effect
Diabetologia, 1997Co-Authors: Lucia Berti, Monika Kellerer, Edison Capp, Hans-ulrich HäringAbstract:It was recently shown that leptin impairs insulin signalling, i. e. insulin receptor autophosphorylation and insulin-receptor substrate (IRS)-1 phosphorylation in rat-1 fibroblasts, NIH3T3 cells and HepG2 cells. To evaluate whether leptin might impair the Effects of insulin in muscle tissue we studied the interaction of insulin and leptin in a muscle cell system, i. e. C2C12 myotubes. Preincubation of C2C12 cells with leptin (1–500 ng/ml) did not significantly affect insulin stimulated glucose transport and glycogen synthesis (1.8 to 2 fold stimulation); however, leptin by itself (1 ng/ml) was able to mimic approximately 80–90 % of the insulin Effect on glucose transport and glycogen synthesis. Both glucose transport as well as glycogen synthesis were inhibited by the phosphatidylinositol-3 (PI3)-kinase inhibitor wortmannin and the protein kinase C inhibitor H7 while no Effect was observed with the S6-kinase inhibitor rapamycin. We determined whether the Effect of leptin occurs through activation of IRS-1 and PI3-kinase. Leptin did not stimulate PI3-kinase activity in IRS-1 immunoprecipitates; however, PI3-kinase activation could be demonstrated in p85α immunoprecipitates (3.04 ± 1.5 fold of basal). In summary the data provide the first evidence for a positive crosstalk between the signalling chain of the insulin receptor and the leptin receptor. Leptin mimics in C2C12 myotubes insulin Effects on glucose transport and glycogen synthesis most likely through activation of PI3-kinase. This Effect of leptin occurs independently of IRS-1 activation in C2C12 cells. [Diabetologia (1997) 40: 606–609]
Tony Hunter - One of the best experts on this subject based on the ideXlab platform.
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essential role of tuberous sclerosis genes tsc1 and tsc2 in nf κb activation and cell survival
Cancer Cell, 2006Co-Authors: Sourav Ghosh, Carla V Rothlin, Pradeep Bist, Virginie Bottero, Ricardo G. Correa, Vinay Tergaonkar, Inder M. Verma, Tony HunterAbstract:Summary The TSC1-TSC2 complex has recently been implicated in cell survival responses. We observed that NF-κB signaling is attenuated in TSC1 - and TSC2 -deficient MEFs concomitant with reduced survival following DNA damage or TNFα stimulation. Reconstitution of TSC2 expression in TSC2 −/− MEFs rescued survival in an NF-κB activity-dependent manner. Furthermore, in TSC2 −/− MEFs, the rapamycin-Mediated inhibition of deregulated mTOR activity restored NF-κB activation and survival. This rapamycin-Mediated Effect was reversed by inhibition of NF-κB transcriptional activation or by inhibition of ERK1/2 MAP kinase or PI-3K pathways, which lie on signaling cascades that lead to NF-κB activation. These results provide evidence for a crosstalk between the TSC/Rheb/mTOR pathway and the NF-κB induction pathways and indicate that NF-κB functions as an important survival factor that regulates TSC2 -dependent cell survival.
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essential role of tuberous sclerosis genes tsc1 and tsc2 in nf κb activation and cell survival
Cancer Cell, 2006Co-Authors: Sourav Ghosh, Carla V Rothlin, Pradeep Bist, Virginie Bottero, Ricardo G. Correa, Vinay Tergaonkar, Inder M. Verma, Tony HunterAbstract:Summary The TSC1-TSC2 complex has recently been implicated in cell survival responses. We observed that NF-κB signaling is attenuated in TSC1 - and TSC2 -deficient MEFs concomitant with reduced survival following DNA damage or TNFα stimulation. Reconstitution of TSC2 expression in TSC2 −/− MEFs rescued survival in an NF-κB activity-dependent manner. Furthermore, in TSC2 −/− MEFs, the rapamycin-Mediated inhibition of deregulated mTOR activity restored NF-κB activation and survival. This rapamycin-Mediated Effect was reversed by inhibition of NF-κB transcriptional activation or by inhibition of ERK1/2 MAP kinase or PI-3K pathways, which lie on signaling cascades that lead to NF-κB activation. These results provide evidence for a crosstalk between the TSC/Rheb/mTOR pathway and the NF-κB induction pathways and indicate that NF-κB functions as an important survival factor that regulates TSC2 -dependent cell survival.
Lucia Berti - One of the best experts on this subject based on the ideXlab platform.
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leptin stimulates glucose transport and glycogen synthesis in c2c12 myotubes evidence for a pi3 kinase Mediated Effect
Diabetologia, 1997Co-Authors: Lucia Berti, Monika Kellerer, Edison Capp, Hans-ulrich HäringAbstract:It was recently shown that leptin impairs insulin signalling, i.e. insulin receptor autophosphorylation and insulin-receptor substrate (IRS)-1 phosphorylation in rat-1 fibroblasts, NIH3T3 cells and HepG2 cells. To evaluate whether leptin might impair the Effects of insulin in muscle tissue we studied the interaction of insulin and leptin in a muscle cell system, i.e. C2C12 myotubes. Preincubation of C2C12 cells with leptin (1-500 ng/ml) did not significantly affect insulin stimulated glucose transport and glycogen synthesis (1.8 to 2 fold stimulation); however, leptin by itself (1 ng/ml) was able to mimic approximately 80-90% of the insulin Effect on glucose transport and glycogen synthesis. Both glucose transport as well as glycogen synthesis were inhibited by the phosphatidylinositol-3 (PI3)-kinase inhibitor wortmannin and the protein kinase C inhibitor H7 while no Effect was observed with the S6-kinase inhibitor rapamycin. We determined whether the Effect of leptin occurs through activation of IRS-1 and PI3-kinase. Leptin did not stimulate PI3-kinase activity in IRS-1 immunoprecipitates; however, PI3-kinase activation could be demonstrated in p85 alpha immunoprecipitates (3.04 +/- 1.5 fold of basal). In summary the data provide the first evidence for a positive crosstalk between the signalling chain of the insulin receptor and the leptin receptor. Leptin mimics in C2C12 myotubes insulin Effects on glucose transport and glycogen synthesis most likely through activation of PI3-kinase. This Effect of leptin occurs independently of IRS-1 activation in C2C12 cells.
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leptin stimulates glucose transport and glycogen synthesis in c2c12 myotubes evidence for a pi3 kinase Mediated Effect
Diabetologia, 1997Co-Authors: Lucia Berti, Monika Kellerer, Edison Capp, Hans-ulrich HäringAbstract:It was recently shown that leptin impairs insulin signalling, i. e. insulin receptor autophosphorylation and insulin-receptor substrate (IRS)-1 phosphorylation in rat-1 fibroblasts, NIH3T3 cells and HepG2 cells. To evaluate whether leptin might impair the Effects of insulin in muscle tissue we studied the interaction of insulin and leptin in a muscle cell system, i. e. C2C12 myotubes. Preincubation of C2C12 cells with leptin (1–500 ng/ml) did not significantly affect insulin stimulated glucose transport and glycogen synthesis (1.8 to 2 fold stimulation); however, leptin by itself (1 ng/ml) was able to mimic approximately 80–90 % of the insulin Effect on glucose transport and glycogen synthesis. Both glucose transport as well as glycogen synthesis were inhibited by the phosphatidylinositol-3 (PI3)-kinase inhibitor wortmannin and the protein kinase C inhibitor H7 while no Effect was observed with the S6-kinase inhibitor rapamycin. We determined whether the Effect of leptin occurs through activation of IRS-1 and PI3-kinase. Leptin did not stimulate PI3-kinase activity in IRS-1 immunoprecipitates; however, PI3-kinase activation could be demonstrated in p85α immunoprecipitates (3.04 ± 1.5 fold of basal). In summary the data provide the first evidence for a positive crosstalk between the signalling chain of the insulin receptor and the leptin receptor. Leptin mimics in C2C12 myotubes insulin Effects on glucose transport and glycogen synthesis most likely through activation of PI3-kinase. This Effect of leptin occurs independently of IRS-1 activation in C2C12 cells. [Diabetologia (1997) 40: 606–609]
Sourav Ghosh - One of the best experts on this subject based on the ideXlab platform.
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essential role of tuberous sclerosis genes tsc1 and tsc2 in nf κb activation and cell survival
Cancer Cell, 2006Co-Authors: Sourav Ghosh, Carla V Rothlin, Pradeep Bist, Virginie Bottero, Ricardo G. Correa, Vinay Tergaonkar, Inder M. Verma, Tony HunterAbstract:Summary The TSC1-TSC2 complex has recently been implicated in cell survival responses. We observed that NF-κB signaling is attenuated in TSC1 - and TSC2 -deficient MEFs concomitant with reduced survival following DNA damage or TNFα stimulation. Reconstitution of TSC2 expression in TSC2 −/− MEFs rescued survival in an NF-κB activity-dependent manner. Furthermore, in TSC2 −/− MEFs, the rapamycin-Mediated inhibition of deregulated mTOR activity restored NF-κB activation and survival. This rapamycin-Mediated Effect was reversed by inhibition of NF-κB transcriptional activation or by inhibition of ERK1/2 MAP kinase or PI-3K pathways, which lie on signaling cascades that lead to NF-κB activation. These results provide evidence for a crosstalk between the TSC/Rheb/mTOR pathway and the NF-κB induction pathways and indicate that NF-κB functions as an important survival factor that regulates TSC2 -dependent cell survival.
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essential role of tuberous sclerosis genes tsc1 and tsc2 in nf κb activation and cell survival
Cancer Cell, 2006Co-Authors: Sourav Ghosh, Carla V Rothlin, Pradeep Bist, Virginie Bottero, Ricardo G. Correa, Vinay Tergaonkar, Inder M. Verma, Tony HunterAbstract:Summary The TSC1-TSC2 complex has recently been implicated in cell survival responses. We observed that NF-κB signaling is attenuated in TSC1 - and TSC2 -deficient MEFs concomitant with reduced survival following DNA damage or TNFα stimulation. Reconstitution of TSC2 expression in TSC2 −/− MEFs rescued survival in an NF-κB activity-dependent manner. Furthermore, in TSC2 −/− MEFs, the rapamycin-Mediated inhibition of deregulated mTOR activity restored NF-κB activation and survival. This rapamycin-Mediated Effect was reversed by inhibition of NF-κB transcriptional activation or by inhibition of ERK1/2 MAP kinase or PI-3K pathways, which lie on signaling cascades that lead to NF-κB activation. These results provide evidence for a crosstalk between the TSC/Rheb/mTOR pathway and the NF-κB induction pathways and indicate that NF-κB functions as an important survival factor that regulates TSC2 -dependent cell survival.
