361 research outputs found

    Land reclamation using reservoir sediments in Tigray, northern Ethiopia

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    Accelerated soil erosion leads to sedimentation in reservoirs and a decline in their life span. As many reservoirs in northern Ethiopia are dry at the end of the dry season, we were able to evaluate the potential of using reservoir sediments for land reclamation. Stripped land from which construction material for the reservoirs had been excavated was covered with 0, 15 and 30 cm of sediment and planted with a local garlic cultivar (Allium sativum). The applied reservoir sediments had low to medium organic C and total N contents and were high in available P and exchangeable cations. The yield of garlic increased with additional available water and the application of sediments. The results show that total biomass and bulb yield were three times higher on the reclaimed plots than on the control ones (11.7 t/ha vs. 3.6 t/ha for the biomass; 7.7 t/ha vs. 2.0 t/ha for the yield). When sediment transport and labour costs were taken into account, plots with 15 cm of sediments had in the first cropping season a cost-benefit ratio of 3, whilst those with 30 cm had a cost-benefit ratio of 0.9. This study demonstrates that the use of relatively small quantities of reservoir sediments is an economically viable strategy for land reclamation. The result can be improvement in income for resource-poor farmers by as much as 76%, and the life expectancy of the reservoirs is also increased

    Simulation and experimental verification of W-band finite frequency selective surfaces on infinite background with 3D full wave solver NSPWMLFMA

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    We present the design, processing and testing of a W-band finite by infinite and a finite by finite Grounded Frequency Selective Surfaces (FSSs) on infinite background. The 3D full wave solver Nondirective Stable Plane Wave Multilevel Fast Multipole Algorithm (NSPWMLFMA) is used to simulate the FSSs. As NSPWMLFMA solver improves the complexity matrix-vector product in an iterative solver from O(N(2)) to O(N log N) which enables the solver to simulate finite arrays with faster execution time and manageable memory requirements. The simulation results were verified by comparing them with the experimental results. The comparisons demonstrate the accuracy of the NSPWMLFMA solver. We fabricated the corresponding FSS arrays on quartz substrate with photolithographic etching techniques and characterized the vector S-parameters with a free space Millimeter Wave Vector Network Analyzer (MVNA)

    C9orf72-derived arginine-containing dipeptide repeats associate with axonal transport machinery and impede microtubule-based motility

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    A hexanucleotide repeat expansion in the C9orf72 gene is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). How this mutation leads to these neurodegenerative diseases remains unclear. Here, we show using patient stem cell-derived motor neurons that the repeat expansion impairs microtubule-based transport, a process critical for neuronal survival. Cargo transport defects are recapitulated by treating neurons from healthy individuals with proline-arginine and glycine-arginine dipeptide repeats (DPRs) produced from the repeat expansion. Both arginine-rich DPRs similarly inhibit axonal trafficking in adult Drosophila neurons in vivo. Physical interaction studies demonstrate that arginine-rich DPRs associate with motor complexes and the unstructured tubulin tails of microtubules. Single-molecule imaging reveals that microtubule-bound arginine-rich DPRs directly impede translocation of purified dynein and kinesin-1 motor complexes. Collectively, our study implicates inhibitory interactions of arginine-rich DPRs with axonal transport machinery in C9orf72-associated ALS/FTD and thereby points to potential therapeutic strategies.</p

    C9orf72-derived arginine-containing dipeptide repeats associate with axonal transport machinery and impede microtubule-based motility

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    A hexanucleotide repeat expansion in the C9orf72 gene is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). How this mutation leads to these neurodegenerative diseases remains unclear. Here, we show using patient stem cell-derived motor neurons that the repeat expansion impairs microtubule-based transport, a process critical for neuronal survival. Cargo transport defects are recapitulated by treating neurons from healthy individuals with proline-arginine and glycine-arginine dipeptide repeats (DPRs) produced from the repeat expansion. Both arginine-rich DPRs similarly inhibit axonal trafficking in adult Drosophila neurons in vivo. Physical interaction studies demonstrate that arginine-rich DPRs associate with motor complexes and the unstructured tubulin tails of microtubules. Single-molecule imaging reveals that microtubule-bound arginine-rich DPRs directly impede translocation of purified dynein and kinesin-1 motor complexes. Collectively, our study implicates inhibitory interactions of arginine-rich DPRs with axonal transport machinery in C9orf72-associated ALS/FTD and thereby points to potential therapeutic strategies.</p
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