First application of data assimilation-based control to fusion plasma

ORCID　0000-0001-7597-0683Magnetic fusion plasmas, which are complex systems comprising numerous interacting elements, have large uncertainties. Therefore, future fusion reactors require prediction-based advanced control systems with an adaptive system model and control estimation robust to uncertainties in the model and observations. To address this challenge, we introduced a control approach based on data assimilation (DA), which describes the system model adaptation and control estimation based on the state probability distribution. The first implementation of a DA-based control system was achieved at the Large Helical Device to control the high temperature plasma. The experimental results indicate that the control system enhanced the predictive capability using real-time observations and adjusted the electron cyclotron heating power for a target temperature. The DA-based control system provides a flexible platform for advanced control in future fusion reactors.journal articl

Copper-Induced Deregulation of microRNA Expression in the Zebrafish Olfactory System

Although environmental trace metals, such as copper (Cu), can disrupt normal olfactory function in fish, the underlying molecular mechanisms of metal-induced olfactory injury have not been elucidated. Current research has suggested the involvement of epigenetic modifications. To address this hypothesis, we analyzed microRNA (miRNA) profiles in the olfactory system of Cu-exposed zebrafish. Our data revealed 2, 10, and 28 differentially expressed miRNAs in a dose–response manner corresponding to three increasing Cu concentrations. Numerous deregulated miRNAs were involved in neurogenesis (e.g., let-7, miR-7a, miR-128, and miR-138), indicating a role for Cu-mediated toxicity via interference with neurogenesis processes. Putative gene targets of deregulated miRNAs were identified when interrogating our previously published microarray database, including those involved in cell growth and proliferation, cell death, and cell morphology. Moreover, several miRNAs (e.g., miR-203a, miR-199*, miR-16a, miR-16c, and miR-25) may contribute to decreased mRNA levels of their host genes involved in olfactory signal transduction pathways and other critical neurological processes via a post-transcriptional mechanism. Our findings provide novel insight into the epigenetic regulatory mechanisms of metal-induced neurotoxicity of the fish olfactory system and identify novel miRNA biomarkers of metal exposures

5) セボフルレン麻酔のてんかん焦点脳波に及ぼす影響（I.一般演題, 第35回新潟麻酔懇話会 第14回新潟ショックと蘇生・集中治療研究会）

departmental bulletin pape

Copper-Induced Deregulation of microRNA Expression in the Zebrafish Olfactory System

Although environmental trace metals, such as copper (Cu), can disrupt normal olfactory function in fish, the underlying molecular mechanisms of metal-induced olfactory injury have not been elucidated. Current research has suggested the involvement of epigenetic modifications. To address this hypothesis, we analyzed microRNA (miRNA) profiles in the olfactory system of Cu-exposed zebrafish. Our data revealed 2, 10, and 28 differentially expressed miRNAs in a dose–response manner corresponding to three increasing Cu concentrations. Numerous deregulated miRNAs were involved in neurogenesis (e.g., let-7, miR-7a, miR-128, and miR-138), indicating a role for Cu-mediated toxicity via interference with neurogenesis processes. Putative gene targets of deregulated miRNAs were identified when interrogating our previously published microarray database, including those involved in cell growth and proliferation, cell death, and cell morphology. Moreover, several miRNAs (e.g., miR-203a, miR-199*, miR-16a, miR-16c, and miR-25) may contribute to decreased mRNA levels of their host genes involved in olfactory signal transduction pathways and other critical neurological processes via a post-transcriptional mechanism. Our findings provide novel insight into the epigenetic regulatory mechanisms of metal-induced neurotoxicity of the fish olfactory system and identify novel miRNA biomarkers of metal exposures

Copper-Induced Deregulation of microRNA Expression in the Zebrafish Olfactory System

Although environmental trace metals, such as copper (Cu), can disrupt normal olfactory function in fish, the underlying molecular mechanisms of metal-induced olfactory injury have not been elucidated. Current research has suggested the involvement of epigenetic modifications. To address this hypothesis, we analyzed microRNA (miRNA) profiles in the olfactory system of Cu-exposed zebrafish. Our data revealed 2, 10, and 28 differentially expressed miRNAs in a dose–response manner corresponding to three increasing Cu concentrations. Numerous deregulated miRNAs were involved in neurogenesis (e.g., let-7, miR-7a, miR-128, and miR-138), indicating a role for Cu-mediated toxicity via interference with neurogenesis processes. Putative gene targets of deregulated miRNAs were identified when interrogating our previously published microarray database, including those involved in cell growth and proliferation, cell death, and cell morphology. Moreover, several miRNAs (e.g., miR-203a, miR-199*, miR-16a, miR-16c, and miR-25) may contribute to decreased mRNA levels of their host genes involved in olfactory signal transduction pathways and other critical neurological processes via a post-transcriptional mechanism. Our findings provide novel insight into the epigenetic regulatory mechanisms of metal-induced neurotoxicity of the fish olfactory system and identify novel miRNA biomarkers of metal exposures

Copper-Induced Deregulation of microRNA Expression in the Zebrafish Olfactory System

Although environmental trace metals, such as copper (Cu), can disrupt normal olfactory function in fish, the underlying molecular mechanisms of metal-induced olfactory injury have not been elucidated. Current research has suggested the involvement of epigenetic modifications. To address this hypothesis, we analyzed microRNA (miRNA) profiles in the olfactory system of Cu-exposed zebrafish. Our data revealed 2, 10, and 28 differentially expressed miRNAs in a dose–response manner corresponding to three increasing Cu concentrations. Numerous deregulated miRNAs were involved in neurogenesis (e.g., let-7, miR-7a, miR-128, and miR-138), indicating a role for Cu-mediated toxicity via interference with neurogenesis processes. Putative gene targets of deregulated miRNAs were identified when interrogating our previously published microarray database, including those involved in cell growth and proliferation, cell death, and cell morphology. Moreover, several miRNAs (e.g., miR-203a, miR-199*, miR-16a, miR-16c, and miR-25) may contribute to decreased mRNA levels of their host genes involved in olfactory signal transduction pathways and other critical neurological processes via a post-transcriptional mechanism. Our findings provide novel insight into the epigenetic regulatory mechanisms of metal-induced neurotoxicity of the fish olfactory system and identify novel miRNA biomarkers of metal exposures

Copper-Induced Deregulation of microRNA Expression in the Zebrafish Olfactory System

Although environmental trace metals, such as copper (Cu), can disrupt normal olfactory function in fish, the underlying molecular mechanisms of metal-induced olfactory injury have not been elucidated. Current research has suggested the involvement of epigenetic modifications. To address this hypothesis, we analyzed microRNA (miRNA) profiles in the olfactory system of Cu-exposed zebrafish. Our data revealed 2, 10, and 28 differentially expressed miRNAs in a dose–response manner corresponding to three increasing Cu concentrations. Numerous deregulated miRNAs were involved in neurogenesis (e.g., let-7, miR-7a, miR-128, and miR-138), indicating a role for Cu-mediated toxicity via interference with neurogenesis processes. Putative gene targets of deregulated miRNAs were identified when interrogating our previously published microarray database, including those involved in cell growth and proliferation, cell death, and cell morphology. Moreover, several miRNAs (e.g., miR-203a, miR-199*, miR-16a, miR-16c, and miR-25) may contribute to decreased mRNA levels of their host genes involved in olfactory signal transduction pathways and other critical neurological processes via a post-transcriptional mechanism. Our findings provide novel insight into the epigenetic regulatory mechanisms of metal-induced neurotoxicity of the fish olfactory system and identify novel miRNA biomarkers of metal exposures

Flow diagram illustrating the experimental design and analysis.

<p>Neonatal mice were treated from postnatal day five (P5) to P9 as described and RNA was analyzed as shown. Abbreviation: molecular signatures database (MSigDB).</p

Categorized Gene Set Enrichment Analysis (GSEA) data to contrast the effects of morphine detected using three separate gene set collections.

<p>Individual GSEA data points from Tables <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0123047#pone.0123047.t002" target="_blank">2</a>–<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0123047#pone.0123047.t006" target="_blank">6</a> were assigned to basic biological function categories and the counts for each category were divided by the total for each gene set collection (Reactome, dark gray; GO:C5, light gray; Biocarta, white). This illustrates the relative agreement between gene set collections used to detect differential gene expression after neonatal morphine treatment.</p

Reactome MS5-responsive Gene sets.

<p>Gene sets (Reactome) with mRNAs affected by neonatal morphine (MS5). Alphabetical order.</p><p>Reactome MS5-responsive Gene sets.</p