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Objectives In view of the operational sea conditions of FPSO (Floating Production Storage and Offloading) ships in the South China Sea, this paper studies the optimization of the multi-point mooring system and side-by-side coupling system of FPSO ships and shuttle tankers. Methods ANSYS-AQWA software and the potential flow theory is used to conduct time-domain analysis, optimize the mooring line segments and proportions, as well as the position of the fairlead; and Fluent software is used to analyze the influence of the change of draft on the wind and current load when the two ships are abreast.Results The results show that a top section of 200 m of steel cable and a bottom section of 316 m of ship chain is the most suitable FPSO multi-point mooring structure for a water depth of 200 m. Maintaining tension on the side-by-side mooring line or increasing its weight can reduce the movement range of the shuttle tanker. After the position of the fairlead is moved to midship, the forces on the fender and mooring line become more uniform. When the weight of the alongside cable is 135 kg/m, the maximum and average values of the fender and alongside cable forces can be minimized.Conclusions The results of this study have reference value for better understanding the influence of mooring parameters on mooring line tension and its influence on the movement of the ship, and can be used to optimize the design of mooring schemes.

Structural variants are implicated in numerous diseases and make up the majority of varying nucleotides among human genomes. Here we describe an integrated set of eight structural variant classes comprising both balanced and unbalanced variants, which we constructed using short-read DNA sequencing data and statistically phased onto haplotype blocks in 26 human populations. Analysing this set, we identify numerous gene-intersecting structural variants exhibiting population stratification and describe naturally occurring homozygous gene knockouts that suggest the dispensability of a variety of human genes. We demonstrate that structural variants are enriched on haplotypes identified by genome-wide association studies and exhibit enrichment for expression quantitative trait loci. Additionally, we uncover appreciable levels of structural variant complexity at different scales, including genic loci subject to clusters of repeated rearrangement and complex structural variants with multiple breakpoints likely to have formed through individual mutational events. Our catalogue will enhance future studies into structural variant demography, functional impact and disease association.

[Objectives] In order to investigate the ultimate strength of CFRP-reinforced cracked stiffened panel in ship structure repair process,[Methods] in this paper,nonlinear finite element method is used to analyze the ultimate strength of CFRP-reinforced cracked stiffened panels subjected to axial compressive loads. Based on CFRP-reinforced cracked stiffened panel model,we compare the simulation results with the recorded test results,to verify the accuracy of the proposed method. By using double-side CFRP -reinforced cracked stiffened panel as the example,we study the ultimate strength of stiffened panel,and the peeling mechanism and the stress of the adhesive layer were analyzed.[Results] The results show that the ultimate strength of CFRP-reinforced cracked stiffened panels is significantly increased,and is close to the ultimate strength of stiffened panel with geometric initial defects;CFRP repairs the debonding of cracked stiffened panel after the ultimate strength is achieved.[Conclusions] The repair of the cracked stiffened panel by using CFRP can enhance the ultimate strength. It may provide guidance for the ships and offshore structure repair.

Genomic structural variants (SVs) are abundant in humans, differing from other forms of variation in extent, origin and functional impact. Despite progress in SV characterization, the nucleotide resolution architecture of most SVs remains unknown. We constructed a map of unbalanced SVs (that is, copy number variants) based on whole genome DNA sequencing data from 185 human genomes, integrating evidence from complementary SV discovery approaches with extensive experimental validations. Our map encompassed 22,025 deletions and 6,000 additional SVs, including insertions and tandem duplications. Most SVs (53%) were mapped to nucleotide resolution, which facilitated analysing their origin and functional impact. We examined numerous whole and partial gene deletions with a genotyping approach and observed a depletion of gene disruptions amongst high frequency deletions. Furthermore, we observed differences in the size spectra of SVs originating from distinct formation mechanisms, and constructed a map of SV hotspots formed by common mechanisms. Our analytical framework and SV map serves as a resource for sequencing-based association studies.