12 research outputs found

    Mitigation of plasma-wall interactions with low-Z powders in DIII-D high confinement plasmas

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    Experiments with low-Z powder injection in DIII-D high confinement discharges demonstrated increased divertor dissipation and detachment while maintaining good core energy confinement. Lithium (Li), boron (B), and boron nitride (BN) powders were injected in high-confinement mode plasmas (Ip=I_p=1 MA, Bt=B_t=2 T, PNB=P_{NB}=6 MW, ⟨ne⟩=3.6−5.0⋅1019\langle n_e\rangle=3.6-5.0\cdot10^{19} m−3^{-3}) into the upper small-angle slot (SAS) divertor for 2-s intervals at constant rates of 3-204 mg/s. The multi-species BN powders at a rate of 54 mg/s showed the most substantial increase in divertor neutral compression by more than an order of magnitude and lasting detachment with minor degradation of the stored magnetic energy WmhdW_{mhd} by 5%. Rates of 204 mg/s of boron nitride powder further reduce ELM-fluxes on the divertor but also cause a drop in confinement performance by 24% due to the onset of an n=2n=2 tearing mode. The application of powders also showed a substantial improvement of wall conditions manifesting in reduced wall fueling source and intrinsic carbon and oxygen content in response to the cumulative injection of non-recycling materials. The results suggest that low-Z powder injection, including mixed element compounds, is a promising new core-edge compatible technique that simultaneously enables divertor detachment and improves wall conditions during high confinement operation

    A manually annotated Actinidia chinensis var. chinensis (kiwifruit) genome highlights the challenges associated with draft genomes and gene prediction in plants

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    Most published genome sequences are drafts, and most are dominated by computational gene prediction. Draft genomes typically incorporate considerable sequence data that are not assigned to chromosomes, and predicted genes without quality confidence measures. The current Actinidia chinensis (kiwifruit) 'Hongyang' draft genome has 164\ua0Mb of sequences unassigned to pseudo-chromosomes, and omissions have been identified in the gene models

    Parkinson's disease -synuclein mutations exhibit defective axonal transport in cultured neurons

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    ?-Synuclein is a major protein constituent of Lewy bodies and mutations in ?-synuclein cause familial autosomal dominant Parkinson's disease. One explanation for the formation of perikaryal and neuritic aggregates of ?-synuclein, which is a presynaptic protein, is that the mutations disrupt ?-synuclein transport and lead to its proximal accumulation. We found that mutant forms of ?-synuclein, either associated with Parkinson's disease (A30P or A53T) or mimicking defined serine, but not tyrosine, phosphorylation states exhibit reduced axonal transport following transfection into cultured neurons. Furthermore, transfection of A30P, but not wild-type, ?-synuclein results in accumulation of the protein proximal to the cell body. We propose that the reduced axonal transport exhibited by the Parkinson's disease-associated ?-synuclein mutants examined in this study might contribute to perikaryal accumulation of ?-synuclein and hence Lewy body formation and neuritic abnormalities in diseased brai

    Mitigation of plasma-wall interactions with low-Z powders in DIII-D high confinement plasmas

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    International audienceExperiments with low-Z powder injection in DIII-D high confinement discharges demonstrated increased divertor dissipation and detachment while maintaining good core energy confinement. Lithium (Li), boron (B), and boron nitride (BN) powders were injected in high-confinement mode plasmas (Ip=I_p=1 MA, Bt=B_t=2 T, PNB=P_{NB}=6 MW, ⟨ne⟩=3.6−5.0⋅1019\langle n_e\rangle=3.6-5.0\cdot10^{19} m−3^{-3}) into the upper small-angle slot (SAS) divertor for 2-s intervals at constant rates of 3-204 mg/s. The multi-species BN powders at a rate of 54 mg/s showed the most substantial increase in divertor neutral compression by more than an order of magnitude and lasting detachment with minor degradation of the stored magnetic energy WmhdW_{mhd} by 5%. Rates of 204 mg/s of boron nitride powder further reduce ELM-fluxes on the divertor but also cause a drop in confinement performance by 24% due to the onset of an n=2n=2 tearing mode. The application of powders also showed a substantial improvement of wall conditions manifesting in reduced wall fueling source and intrinsic carbon and oxygen content in response to the cumulative injection of non-recycling materials. The results suggest that low-Z powder injection, including mixed element compounds, is a promising new core-edge compatible technique that simultaneously enables divertor detachment and improves wall conditions during high confinement operation

    The C9orf72 protein interacts with Rab1a and the ULK1 complex to regulate initiation of autophagy

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    A GGGGCC hexanucleotide repeat expansion in the C9orf72 gene is the most common genetic cause of amyotrophic lateral sclerosis and frontotemporal dementia (C9ALS/FTD). C9orf72 encodes two C9orf72 protein isoforms of unclear function. Reduced levels of C9orf72 expression have been reported in C9ALS/FTD patients, and although C9orf72 haploinsufficiency has been proposed to contribute to C9ALS/FTD, its significance is not yet clear. Here, we report that C9orf72 interacts with Rab1a and the Unc-51-like kinase 1 (ULK1) autophagy initiation complex. As a Rab1a effector, C9orf72 controls initiation of autophagy by regulating the Rab1a-dependent trafficking of the ULK1 autophagy initiation complex to the phagophore. Accordingly, reduction of C9orf72 expression in cell lines and primary neurons attenuated autophagy and caused accumulation of p62-positive puncta reminiscent of the p62 pathology observed in C9ALS/FTD patients. Finally, basal levels of autophagy were markedly reduced in C9ALS/FTD patient-derived iNeurons. Thus, our data identify C9orf72 as a novel Rab1a effector in the regulation of autophagy and indicate that C9orf72 haploinsufficiency and associated reductions in autophagy might be the underlying cause of C9ALS/FTD-associated p62 pathology
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