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Objective: The aim of this study was to investigate the value of genetic testing using exome sequencing (ES) in oligohydramnios pregnancies with or without other structural abnormalities. Materials and methods: A total of 110 singleton pregnancies complicated by oligohydramnios were enrolled, including 52 of isolated oligohydramnios and 58 of non-isolated oligohydramnios. All fetal samples were first tested by quantitative fluorescent polymerase chain reaction (QF-PCR) and followed by chromosomal microarray analysis (CMA). Those with normal CMA were informed of the option of trio ES. Results: QF-PCR detected chromosomal abnormality in 4 cases (4/110, 3.6%), including 1 of XXY, 1 of XYY and 2 of triploidy. The remaining 106 cases were tested by CMA, with pathogenic copy number variations (CNVs) detected in 5 cases (5/106, 4.7%), and uniparental disomy (UPD) in 2 cases (2/106, 1.9%). As an option for cases with a normal CMA, ES was accepted by 12 non-isolated cases, and pathogenic or likely pathogenic variants were detected in 5, involving the following genes: PBX1, FREM2, PKHD1 and BBS2, with a 41.7% (5/12) diagnostic rate. Conclusion: We provided further evidence of using advanced genetic approaches for oligohydramnios pregnancy. Non-isolated oligohydramnios increases the risk of having monogenetic conditions.

The implementation of expressway toll-free policy during holidays in China has caused serious congestion and frequent accidents on expressways. Many studies have explored the policy’s macroscopic outcome and its countermeasures for policy managers, while limited attention has been paid to the influence mechanism of the policy on the individuals’ travel behavior, especially the mode choice behavior. More insight into the dynamic effects of individuals reacting to policy measure is needed. This study aims at analyzing the adaption progress of the individual’s mode choice behavior and estimating the time-varying influence of the traffic policy on the mode split. With assumptions travelers’ adapting behavior conform to the inertia and myopia principles, a Logit dynamic evolutionary model for mode choice is proposed. A unique globally stable equilibrium state for the model is derived with the strict mathematical analysis. As an application, the influence of the expressway toll-free policy on mode split is evaluated. The travel cost structure, the sensitivity of the travel distance and traffic supply, and the evolutionary dynamics of the mode split are analyzed in scenarios with and without the expressway toll-free policy. The result indicates that travel distance and network’s total supply amount remarkably affect the implementation effect of the policy.

CC chemokine receptor 4 (CCR4) is a kind of G-protein-coupled receptor, which plays a pivotal role in allergic inflammation. The interaction between 2-(2-(4-chloro-phenyl)-5-{[(naphthalen-1-ylmethyl)-carbamoyl]-methyl}-4-oxo-thiazolidin-3-yl)-N-(3-morpholin-4-yl-propyl)-acetamide (S009) and the N-terminal extracellular tail (ML40) of CCR4 has been validated to be high affinity by capillary zone electrophoresis (CZE). The S009 is a known CCR4 antagonist. Now, a series of new thiourea derivatives have been synthesized. Compared with positive control S009, they were screened using ML40 as target by CZE to find some new drugs for allergic inflammation diseases. The synthesized compounds XJH-5, XJH-4, XJH-17 and XJH-1 displayed the interaction with ML40, but XJH-9, XJH-10, XJH-11, XJH-12, XJH-13, XJH-14, XJH-3, XJH-8, XJH-6, XJH-7, XJH-15, XJH-16 and XJH-2 did not bind to ML40. Both qualification and quantification characterizations of the binding were determined. The affinity of the four compounds was valued by the binding constant, which was similar with the results of chemotactic experiments. The established CEZ method is capable of sensitive and fast screening for a series of lactam analogs in the drug discovery for allergic inflammation diseases. Keywords: Capillary zone electrophoresis, CCR4 antagonist, 2-(2-(4-chloro-phenyl)-5-{[(naphthalen-1-ylmethyl)-carbamoyl]-methyl}-4-oxo-thiazolidin-3-yl)-N-(3-morpholin-4-yl-propyl)-acetamide, Interactions, Structural modification