The Experts below are selected from a list of 66 Experts worldwide ranked by ideXlab platform
Peter A. Hall - One of the best experts on this subject based on the ideXlab platform.
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Contextual cues as modifiers of cTBS effects on indulgent eating.
Brain stimulation, 2019Co-Authors: Adrian B. Safati, Peter A. HallAbstract:Abstract Background Prior studies have found that continuous theta burst stimulation (cTBS) targeting the left dlPFC results in reliable increases in consumption of calorie-dense food items. However, it is not known to what extent such effects are modified by cues in the immediate eating environment. Tempting environments (i.e., those saturated with appetitive eating cues) may lead to more reliance on cognitive control networks involving the dlPFC, thereby enhancing cTBS effects on indulgent eating. Objective/Hypothesis The objective was to examine the extent to which cTBS effects on indulgent eating would be modified by contextual cues. It was hypothesized that cTBS effects would be stronger in the presence of facilitating cues. Methods Using a single-blinded between-subjects factorial design, 107 TMS-naive adults were randomly assigned to one of four conditions: 1) active cTBS + facilitating cues, 2) sham cTBS + facilitating cues, 3) active cTBS + inhibiting cues, 4) sham cTBS + inhibiting cues. Following stimulation participants completed a flanker paradigm and a taste test during which quantity consumed was assessed surreptitiously. Results Findings revealed a significant interaction between stimulation and cue type (F(1,102) = 6.235, p = .014), such that cTBS resulted in increased food consumption (compared to sham) in the presence of the facilitating cue but not in the presence of the inhibiting cue. Moderated mediational analyses showed selective mediation of cTBS effects on consumption through cTBS attenuation of flanker interference scores. Conclusions The effects of cTBS on indulgent eating are strengthened in the presence of facilitating cues. Methodologically speaking, facilitating cues may be a Functional Prerequisite for exploring cTBS effects on eating in the laboratory. Substantively, the findings also suggest that facilitating cues in the eating environment may amplify counter-intentional food indulgence in everyday life via cognitive control failure.
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Contextual cues as modifiers of cTBS effects on indulgent eating
2019Co-Authors: Adrian B. Safati, Peter A. HallAbstract:Abstract Background Prior studies have found that continuous theta burst stimulation (cTBS) targeting the left dlPFC results in reliable increases in consumption of calorie-dense food items. However, it is not known to what extent such effects are modified by cues in the immediate eating environment. Tempting environments (i.e., those saturated with appetitive eating cues) may lead to more reliance on cognitive control networks involving the dlPFC, thereby enhancing cTBS on eating. Objective/Hypothesis The objective was to examine the extent to which cTBS effects on eating would be modified by contextual cues. It was hypothesized that cTBS effects on eating would be stronger in the presence of facilitating cues. Methods Using a between-subjects factorial design, 107 adults were randomly assigned to one of four conditions: 1) active cTBS + facilitating cues, 2) sham cTBS + facilitating cues, 3) active cTBS + inhibiting cues, 4) sham cTBS + inhibiting cues. Following stimulation participants completed a flanker paradigm and a taste test during which quantity consumed was assessed surreptitiously. Results Findings revealed a significant interaction between stimulation and cue type (F(1,102)=6.235, p=.014), such that the effects of cTBS were stronger for those in the facilitating cue condition. Conclusions The effects of cTBS on eating are strengthened in the presence of facilitating cues. Methodologically speaking, facilitating cues may be a Functional Prerequisite for exploring cTBS effects on eating in the laboratory. Substantively, the findings also suggest that facilitating cues in the eating environment may amplify counter-intentional food indulgence in everyday life via cognitive control failure.
Toshinori Kinoshita - One of the best experts on this subject based on the ideXlab platform.
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Auxin Activates the Plasma Membrane H+-ATPase by Phosphorylation during Hypocotyl Elongation in Arabidopsis
Plant physiology, 2012Co-Authors: Koji Takahashi, Ken-ichiro Hayashi, Toshinori KinoshitaAbstract:The phytohormone auxin is a major regulator of diverse aspects of plant growth and development. The ubiquitin-ligase complex SCFTIR1/AFB (for Skp1-Cul1-F-box protein), which includes the TRANSPORT INHIBITOR RESPONSE1/AUXIN SIGNALING F-BOX (TIR1/AFB) auxin receptor family, has recently been demonstrated to be critical for auxin-mediated transcriptional regulation. Early-phase auxin-induced hypocotyl elongation, on the other hand, has long been explained by the acid-growth theory, for which proton extrusion by the plasma membrane H+-ATPase is a Functional Prerequisite. However, the mechanism by which auxin mediates H+-ATPase activation has yet to be elucidated. Here, we present direct evidence for H+-ATPase activation in etiolated hypocotyls of Arabidopsis (Arabidopsis thaliana) by auxin through phosphorylation of the penultimate threonine during early-phase hypocotyl elongation. Application of the natural auxin indole-3-acetic acid (IAA) to endogenous auxin-depleted hypocotyl sections induced phosphorylation of the penultimate threonine of the H+-ATPase and increased H+-ATPase activity without altering the amount of the enzyme. Changes in both the phosphorylation level of H+-ATPase and IAA-induced elongation were similarly concentration dependent. Furthermore, IAA-induced H+-ATPase phosphorylation occurred in a tir1-1 afb2-3 double mutant, which is severely defective in auxin-mediated transcriptional regulation. In addition, α-(phenylethyl-2-one)-IAA, the auxin antagonist specific for the nuclear auxin receptor TIR1/AFBs, had no effect on IAA-induced H+-ATPase phosphorylation. These results suggest that the TIR1/AFB auxin receptor family is not involved in auxin-induced H+-ATPase phosphorylation. Our results define the activation mechanism of H+-ATPase by auxin during early-phase hypocotyl elongation; this is the long-sought-after mechanism that is central to the acid-growth theory.
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Auxin Activates the Plasma Membrane H + -ATPase by Phosphorylation during Hypocotyl Elongation
2012Co-Authors: Koji Takahashi, Ken-ichiro Hayashi, Toshinori KinoshitaAbstract:the acid-growth theory, for which proton extrusion by the plasma membrane H + -ATPase is a Functional Prerequisite. However, the mechanism by which auxin mediates H + -ATPase activation has yet to be elucidated. Here, we present direct evidence for H + ATPase activation in etiolated hypocotyls of Arabidopsis (Arabidopsis thaliana) by auxin through phosphorylation of the penultimate threonine during early-phase hypocotyl elongation. Application of the natural auxin indole-3-acetic acid (IAA) to endogenous auxin-depleted hypocotyl sections induced phosphorylation of the penultimate threonine of the H + -ATPase and increased H + -ATPase activity without altering the amount of the enzyme. Changes in both the phosphorylation level of H + ATPase and IAA-induced elongation were similarly concentration dependent. Furthermore, IAA-induced H + -ATPase phosphorylation occurred in a tir1-1 afb2-3 double mutant, which is severely defective in auxin-mediated transcriptional regulation. In addition, a-(phenylethyl-2-one)-IAA, the auxin antagonist specific for the nuclear auxin receptor TIR1/AFBs, had no effect on IAA-induced H + -ATPase phosphorylation. These results suggest that the TIR1/AFB auxin receptor family is not involved in auxin-induced H + -ATPase phosphorylation. Our results define the activation mechanism of H + -ATPase by auxin during early-phase hypocotyl elongation; this is the long-sought-after mechanism that is central to the acid-growth theory.
Adrian B. Safati - One of the best experts on this subject based on the ideXlab platform.
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Contextual cues as modifiers of cTBS effects on indulgent eating.
Brain stimulation, 2019Co-Authors: Adrian B. Safati, Peter A. HallAbstract:Abstract Background Prior studies have found that continuous theta burst stimulation (cTBS) targeting the left dlPFC results in reliable increases in consumption of calorie-dense food items. However, it is not known to what extent such effects are modified by cues in the immediate eating environment. Tempting environments (i.e., those saturated with appetitive eating cues) may lead to more reliance on cognitive control networks involving the dlPFC, thereby enhancing cTBS effects on indulgent eating. Objective/Hypothesis The objective was to examine the extent to which cTBS effects on indulgent eating would be modified by contextual cues. It was hypothesized that cTBS effects would be stronger in the presence of facilitating cues. Methods Using a single-blinded between-subjects factorial design, 107 TMS-naive adults were randomly assigned to one of four conditions: 1) active cTBS + facilitating cues, 2) sham cTBS + facilitating cues, 3) active cTBS + inhibiting cues, 4) sham cTBS + inhibiting cues. Following stimulation participants completed a flanker paradigm and a taste test during which quantity consumed was assessed surreptitiously. Results Findings revealed a significant interaction between stimulation and cue type (F(1,102) = 6.235, p = .014), such that cTBS resulted in increased food consumption (compared to sham) in the presence of the facilitating cue but not in the presence of the inhibiting cue. Moderated mediational analyses showed selective mediation of cTBS effects on consumption through cTBS attenuation of flanker interference scores. Conclusions The effects of cTBS on indulgent eating are strengthened in the presence of facilitating cues. Methodologically speaking, facilitating cues may be a Functional Prerequisite for exploring cTBS effects on eating in the laboratory. Substantively, the findings also suggest that facilitating cues in the eating environment may amplify counter-intentional food indulgence in everyday life via cognitive control failure.
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Contextual cues as modifiers of cTBS effects on indulgent eating
2019Co-Authors: Adrian B. Safati, Peter A. HallAbstract:Abstract Background Prior studies have found that continuous theta burst stimulation (cTBS) targeting the left dlPFC results in reliable increases in consumption of calorie-dense food items. However, it is not known to what extent such effects are modified by cues in the immediate eating environment. Tempting environments (i.e., those saturated with appetitive eating cues) may lead to more reliance on cognitive control networks involving the dlPFC, thereby enhancing cTBS on eating. Objective/Hypothesis The objective was to examine the extent to which cTBS effects on eating would be modified by contextual cues. It was hypothesized that cTBS effects on eating would be stronger in the presence of facilitating cues. Methods Using a between-subjects factorial design, 107 adults were randomly assigned to one of four conditions: 1) active cTBS + facilitating cues, 2) sham cTBS + facilitating cues, 3) active cTBS + inhibiting cues, 4) sham cTBS + inhibiting cues. Following stimulation participants completed a flanker paradigm and a taste test during which quantity consumed was assessed surreptitiously. Results Findings revealed a significant interaction between stimulation and cue type (F(1,102)=6.235, p=.014), such that the effects of cTBS were stronger for those in the facilitating cue condition. Conclusions The effects of cTBS on eating are strengthened in the presence of facilitating cues. Methodologically speaking, facilitating cues may be a Functional Prerequisite for exploring cTBS effects on eating in the laboratory. Substantively, the findings also suggest that facilitating cues in the eating environment may amplify counter-intentional food indulgence in everyday life via cognitive control failure.
Koji Takahashi - One of the best experts on this subject based on the ideXlab platform.
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Auxin Activates the Plasma Membrane H+-ATPase by Phosphorylation during Hypocotyl Elongation in Arabidopsis
Plant physiology, 2012Co-Authors: Koji Takahashi, Ken-ichiro Hayashi, Toshinori KinoshitaAbstract:The phytohormone auxin is a major regulator of diverse aspects of plant growth and development. The ubiquitin-ligase complex SCFTIR1/AFB (for Skp1-Cul1-F-box protein), which includes the TRANSPORT INHIBITOR RESPONSE1/AUXIN SIGNALING F-BOX (TIR1/AFB) auxin receptor family, has recently been demonstrated to be critical for auxin-mediated transcriptional regulation. Early-phase auxin-induced hypocotyl elongation, on the other hand, has long been explained by the acid-growth theory, for which proton extrusion by the plasma membrane H+-ATPase is a Functional Prerequisite. However, the mechanism by which auxin mediates H+-ATPase activation has yet to be elucidated. Here, we present direct evidence for H+-ATPase activation in etiolated hypocotyls of Arabidopsis (Arabidopsis thaliana) by auxin through phosphorylation of the penultimate threonine during early-phase hypocotyl elongation. Application of the natural auxin indole-3-acetic acid (IAA) to endogenous auxin-depleted hypocotyl sections induced phosphorylation of the penultimate threonine of the H+-ATPase and increased H+-ATPase activity without altering the amount of the enzyme. Changes in both the phosphorylation level of H+-ATPase and IAA-induced elongation were similarly concentration dependent. Furthermore, IAA-induced H+-ATPase phosphorylation occurred in a tir1-1 afb2-3 double mutant, which is severely defective in auxin-mediated transcriptional regulation. In addition, α-(phenylethyl-2-one)-IAA, the auxin antagonist specific for the nuclear auxin receptor TIR1/AFBs, had no effect on IAA-induced H+-ATPase phosphorylation. These results suggest that the TIR1/AFB auxin receptor family is not involved in auxin-induced H+-ATPase phosphorylation. Our results define the activation mechanism of H+-ATPase by auxin during early-phase hypocotyl elongation; this is the long-sought-after mechanism that is central to the acid-growth theory.
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Auxin Activates the Plasma Membrane H + -ATPase by Phosphorylation during Hypocotyl Elongation
2012Co-Authors: Koji Takahashi, Ken-ichiro Hayashi, Toshinori KinoshitaAbstract:the acid-growth theory, for which proton extrusion by the plasma membrane H + -ATPase is a Functional Prerequisite. However, the mechanism by which auxin mediates H + -ATPase activation has yet to be elucidated. Here, we present direct evidence for H + ATPase activation in etiolated hypocotyls of Arabidopsis (Arabidopsis thaliana) by auxin through phosphorylation of the penultimate threonine during early-phase hypocotyl elongation. Application of the natural auxin indole-3-acetic acid (IAA) to endogenous auxin-depleted hypocotyl sections induced phosphorylation of the penultimate threonine of the H + -ATPase and increased H + -ATPase activity without altering the amount of the enzyme. Changes in both the phosphorylation level of H + ATPase and IAA-induced elongation were similarly concentration dependent. Furthermore, IAA-induced H + -ATPase phosphorylation occurred in a tir1-1 afb2-3 double mutant, which is severely defective in auxin-mediated transcriptional regulation. In addition, a-(phenylethyl-2-one)-IAA, the auxin antagonist specific for the nuclear auxin receptor TIR1/AFBs, had no effect on IAA-induced H + -ATPase phosphorylation. These results suggest that the TIR1/AFB auxin receptor family is not involved in auxin-induced H + -ATPase phosphorylation. Our results define the activation mechanism of H + -ATPase by auxin during early-phase hypocotyl elongation; this is the long-sought-after mechanism that is central to the acid-growth theory.
Ken-ichiro Hayashi - One of the best experts on this subject based on the ideXlab platform.
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Auxin Activates the Plasma Membrane H+-ATPase by Phosphorylation during Hypocotyl Elongation in Arabidopsis
Plant physiology, 2012Co-Authors: Koji Takahashi, Ken-ichiro Hayashi, Toshinori KinoshitaAbstract:The phytohormone auxin is a major regulator of diverse aspects of plant growth and development. The ubiquitin-ligase complex SCFTIR1/AFB (for Skp1-Cul1-F-box protein), which includes the TRANSPORT INHIBITOR RESPONSE1/AUXIN SIGNALING F-BOX (TIR1/AFB) auxin receptor family, has recently been demonstrated to be critical for auxin-mediated transcriptional regulation. Early-phase auxin-induced hypocotyl elongation, on the other hand, has long been explained by the acid-growth theory, for which proton extrusion by the plasma membrane H+-ATPase is a Functional Prerequisite. However, the mechanism by which auxin mediates H+-ATPase activation has yet to be elucidated. Here, we present direct evidence for H+-ATPase activation in etiolated hypocotyls of Arabidopsis (Arabidopsis thaliana) by auxin through phosphorylation of the penultimate threonine during early-phase hypocotyl elongation. Application of the natural auxin indole-3-acetic acid (IAA) to endogenous auxin-depleted hypocotyl sections induced phosphorylation of the penultimate threonine of the H+-ATPase and increased H+-ATPase activity without altering the amount of the enzyme. Changes in both the phosphorylation level of H+-ATPase and IAA-induced elongation were similarly concentration dependent. Furthermore, IAA-induced H+-ATPase phosphorylation occurred in a tir1-1 afb2-3 double mutant, which is severely defective in auxin-mediated transcriptional regulation. In addition, α-(phenylethyl-2-one)-IAA, the auxin antagonist specific for the nuclear auxin receptor TIR1/AFBs, had no effect on IAA-induced H+-ATPase phosphorylation. These results suggest that the TIR1/AFB auxin receptor family is not involved in auxin-induced H+-ATPase phosphorylation. Our results define the activation mechanism of H+-ATPase by auxin during early-phase hypocotyl elongation; this is the long-sought-after mechanism that is central to the acid-growth theory.
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Auxin Activates the Plasma Membrane H + -ATPase by Phosphorylation during Hypocotyl Elongation
2012Co-Authors: Koji Takahashi, Ken-ichiro Hayashi, Toshinori KinoshitaAbstract:the acid-growth theory, for which proton extrusion by the plasma membrane H + -ATPase is a Functional Prerequisite. However, the mechanism by which auxin mediates H + -ATPase activation has yet to be elucidated. Here, we present direct evidence for H + ATPase activation in etiolated hypocotyls of Arabidopsis (Arabidopsis thaliana) by auxin through phosphorylation of the penultimate threonine during early-phase hypocotyl elongation. Application of the natural auxin indole-3-acetic acid (IAA) to endogenous auxin-depleted hypocotyl sections induced phosphorylation of the penultimate threonine of the H + -ATPase and increased H + -ATPase activity without altering the amount of the enzyme. Changes in both the phosphorylation level of H + ATPase and IAA-induced elongation were similarly concentration dependent. Furthermore, IAA-induced H + -ATPase phosphorylation occurred in a tir1-1 afb2-3 double mutant, which is severely defective in auxin-mediated transcriptional regulation. In addition, a-(phenylethyl-2-one)-IAA, the auxin antagonist specific for the nuclear auxin receptor TIR1/AFBs, had no effect on IAA-induced H + -ATPase phosphorylation. These results suggest that the TIR1/AFB auxin receptor family is not involved in auxin-induced H + -ATPase phosphorylation. Our results define the activation mechanism of H + -ATPase by auxin during early-phase hypocotyl elongation; this is the long-sought-after mechanism that is central to the acid-growth theory.
