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The complexity and variability of ocean waves make wave energy harvesting very challenging. Previous research has indicated that wave energy was mainly generated and transferred by wind, but the detailed correlation between wind and wave energy has not been discovered. Wave energy in the Gulf of Mexico (GoM) has high variability with distinct seasonal behavior. However, the underlying reasons for this unique behavior have not been discussed and discovered yet. In this paper, a computer animation-based dynamic visualization method was created to conduct exploratory and explanatory analyses of 36 years of meteorological data in the GoM from the WaveWatch III system to identify preliminary patterns and underlying reasons for the unique behavior of wave energy in the GoM. These preliminary patterns and underlying reasons were further analyzed using Energy Events and Breaks concepts. During both high and low levels wave energy periods, the detailed correlation between wave energy and the wind was analyzed and determined. High level wave power in the GoM was mainly generated by the local inland wind from northern weather patterns, while low level wave power was mainly generated by swells from the Caribbean and the Atlantic oceans, which entered the GoM through the two narrow pathways, the Straits of Yucatan and the Florida Straits. The results from this paper will also be able to help the design, placement, and operation of future wave energy converters to improve their efficiency in harvesting wave energy in the GoM. 

3D surface reconstruction usually begins with a point cloud and aims to build a representation of the object producing that point cloud. There are several algorithms to solve this problem, each with different priors over the point cloud, such as the type of object represented, or the method by which it was obtained. In this work, we focus on an algorithm called Non-Convex Hull (NCH), which reconstructs surfaces through a concept similar to the Medial Axis Transform. A new algorithm called Shrinking Planes is proposed to compute the NCH, based on the Shrinking Ball method with a few improvements. We prove that the new method can approximate surfaces to arbitrarily small error, and evaluate its performance on the surface reconstruction task. The new method maintains the same reconstruction quality as the Naïve Non-Convex Hull method, while achieving a large performance improvement. 

Abstract Glutaredoxins (GRXs) are small oxidoreductase enzymes that can reduce disulfide bonds in target proteins. The class III GRX gene family is unique to land plants, andArabidopsis thalianahas 21 class III GRXs, which remain largely uncharacterized. About 80% ofA. thalianaclass III GRXs are transcriptionally regulated by nitrate, and several recent studies have suggested roles for these GRXs in nitrogen signaling. Our objective was to functionally characterize two nitrate‐induced GRX genes,AtGRXS5andAtGRXS8, defining their roles in signaling and development in theA. thalianaroot. We demonstrated thatAtGRXS5andAtGRXS8are primarily expressed in root and shoot vasculature (phloem), and that the corresponding GRX proteins display nucleo‐cytosolic subcellular localization. Ectopic expression ofAtGRXS8in transgenic plants caused major alterations in root system architecture: Normal primary root development, but a near absence of lateral roots. RNA sequencing demonstrated that the roots ofAtGRXS8‐overexpressing plants show strongly reduced transcript abundance for many primary nitrate response genes, including the major high‐affinity nitrate transporters. Correspondingly, high‐affinity nitrate uptake and the transport of nitrate from roots to shoots are compromised inAtGRXS8‐overexpressing plants. Finally, we demonstrated that the AtGRXS8 protein can physically interact with the TGA1 and TGA4 transcription factors, which are central regulators of early transcriptional responses to nitrate inA. thalianaroots. Overall, these results suggest thatAtGRXS8acts to quench both transcriptional and developmental aspects of primary nitrate response, potentially by interfering with the activity of the TGA1 and TGA4 transcription factors.