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• A novel leakage model test system was proposed. • Deformation, uneven settlement and deterioration of the segment were simulated during service. • A non-linear growth trend in water leakage was observed. • Decreased contact stress and gasket aging aggravate leakage. With the increasing mileage and operation time of China's subsea tunnels, tunnels are entering a period of high disaster. Water leakage is one of the most common disasters. To study the mechanism of water leakage in subsea shield tunnels during the service period, a model test study was carried out by proposing a novel tunnel seepage leakage model test system in this paper. The system consists of a model frame, ground stress loading system, hydraulic pressure loading system, temperature control system, and monitoring system. Through 3D printing, the tunnel segments were innovatively made of resin. The process of uneven settlement, seawater erosion, joint deformation, gasket stress relaxation, and water leakage during the service period were successfully simulated by heating the model segments and local overloading. The test results showed that the joint deformation with service life could be approximately divided into three stages: non-linear rapid growth, linear growth, and non-linear slow growth. And the joint deformation and the aging of the gasket resulted in the decrease of the contact stress of the segment joint. Both exacerbated the leakage in the joint. By the time the service life reaches 16th year, the waterproofing performance no longer met the waterproofing standard for subsea tunnels. The developed test device and method are practical in predicting water surges in subsea tunnels during service life. This paper provides new insights into long-term waterproofing performance testing of shield tunnels under complex conditions. [ABSTRACT FROM AUTHOR]

Background: Previous studies have shown that individuals with schizophrenia have a greater risk for psoriasis than a typical person. This suggests that there might be a shared genetic etiology between the 2 conditions. We aimed to characterize the potential shared genetic susceptibility between schizophrenia and psoriasis using genome-wide marker genotype data., Methods: We obtained genetic data on individuals with psoriasis, schizophrenia and control individuals. We applied a marker-based coheritability estimation procedure, polygenic score analysis, a gene set enrichment test and a least absolute shrinkage and selection operator regression model to estimate the potential shared genetic etiology between the 2 diseases. We validated the results in independent schizophrenia and psoriasis cohorts from Singapore., Results: We included 1139 individuals with psoriasis, 744 with schizophrenia and 1678 controls in our analysis, and we validated the results in independent cohorts, including 441 individuals with psoriasis (and 2420 controls) and 1630 with schizophrenia (and 1860 controls). We estimated that a large fraction of schizophrenia and psoriasis risk could be attributed to common variants ( h 2 SNP = 29% ± 5.0%, p = 2.00 × 10 -8 ), with a coheritability estimate between the traits of 21%. We identified 5 variants within the human leukocyte antigen ( HLA ) gene region, which were most likely to be associated with both diseases and collectively conferred a significant risk effect (odds ratio of highest risk quartile = 6.03, p < 2.00 × 10 -16 ). We discovered that variants contributing most to the shared heritable component between psoriasis and schizophrenia were enriched in antigen processing and cell endoplasmic reticulum., Limitations: Our sample size was relatively small. The findings of 5 HLA gene variants were complicated by the complex structure in the HLA region., Conclusion: We found evidence for a shared genetic etiology between schizophrenia and psoriasis. The mechanism for this shared genetic basis likely involves immune and calcium signalling pathways.