In-utero pediatrics is a fetal general medicine for perinatal medicine redevelopment,with the main purpose of preventing and treating fetal diseases,which studies the early prevention,screening,diagnosis,and treatment of diseases from gametes,fertilized eggs,and embryos sequential to children,adolescents,adolescence,and even the entire life cycle.Medical ethics provides strong support for the normative development of this discipline.This paper summarized the formation and development of in-utero pediatrics,analyzed the vulnerability of service subjects within in-utero pediatrics,and sorted out their ethical issues in the prevention and control of birth defects,fetal intrauterine diagnosis and treatment,as well as multidisciplinary collaborative diagnosis and treatment.It was proposed that in-utero pediatrics should follow the medical principle of maternal and fetal interests first,the principle of respect,and the principle of no harm.Finally,suggestions for ethical review of clinical and research projects on in-utero pediatrics were proposed,including strengthening the advisory service role of the ethics committee in clinical practice,timely launching the guidelines of ethical review for clinical research,and enhancing the ethical awareness of medical staff.

Objective: To construct the mutants of ARID1A gene, which is an important component in human chromosomal remodeling complex Switch/Sucrose Non Fermentable (SWI/SNF), and identify their overexpression in liver cancer HepG2 cells. Methods: Overlap PCR was used to construct domain truncated mutantss pcDNA6-ARID1A/ΔARID and pcDNA6-ARID1A/ΔD UF3518 based on wild type plasmids pcDNA6-ARID1A. Lipofectionmethod was used to transfect the wild type and mutants into HepG2. Real-time PCR and western blotting were used to confirm the overexpression of ARID1A and the mutants. Results: SDS-PAGE and sequencingresult confirmed the successful construction of pcDNA6-ARID1A/ΔARID and pcDNA6-ARID1A/ΔDUF3518. Real-time PCR and western blottingresult confirmed the overexpression of both mRNA and protein of wild type ARID1A and ARID1A/ΔARID. The mRNA levels indicated that ARID1A/Δ DUF3518 were overexpressed, but the protein levels were quite low. Conclusions Functional domain truncated mutants of ARID1A were successfully constructed. Overexpression of wild type ARID1A and ARID1A/ΔARID in liver cancer HepG2 cells was successful. Loss of ARID1A/ΔDUF3518 protein suggest that DUF3518 may contribute to the protein structure stability.