Background: It is necessary to evaluate the effects of competency-based training (CBT) model in the clinical training of new nurses, to provide insights to the management of nurses. Methods: We searched PubMed, EMBASE, Cochrane Library, Web of Science, China National Knowledge Infrastructure (CNKI), China Science and Technology Journal Database, Wanfang and Weipu Databases for the randomized controlled trials (RCTs) on the application effect of CBT in new nurse training up to December 15, 2021. Two investigators independently screened the literature, extracted the data and evaluated the quality of the literatures. RevMan 5.3 software was used for meta-analysis. Results: A total of 7 RCTs involving 639 new nurses were included. Meta-analyses indicated that CBT improved the ability of clinical nursing care [SMD = 1.52, 95%CI (0.13~2.90), P = 0.03], critical thinking and innovation[SMD = 0.69, 95%CI (0.43~0.95), P<0.001], interpersonal communication[SMD = 0.74, 95%CI (0.51~0.97), P<0.001], professional construction and development[SMD = 1.92, 95%CI (1.41~2.42), P<0.001], level of comprehensive knowledge[SMD = 1.20, 95%CI (0.63~1.76), P<0.001] and level of good personal traits[SMD = 1.89, 95%CI (1.27~2.50), P0.05). Conclusions: CBT is beneficial for improving the competency of newly recruited nurses. More RCTs from different population and regions are needed to further elucidate the role of CBT in nurse management.

Chronic hepatitis B (CHB) is a major global health issue. The role of rare genetic variants in CHB has not been elucidated. We aimed to identify rare allelic variants predisposing to CHB. We performed exome sequencing in 50 CHB patients who had no identifiable risk factors for CHB and 40 controls who were healthy and hepatitis B surface antibody-positive, but had never received hepatitis B vaccination. We selected six rare variant alleles and followed up their association with disease status by Sanger sequencing in a case-control study comprising 1,728 CHB patients and 1,636 healthy controls. The latter had either not been immunized with hepatitis B vaccine or had uncertain vaccination status. Our results showed that transmembrane protein 2 p.Ser1254Asn, interferon alpha 2 p.Ala120Thr, its regulator NLR family member X1 p.Arg707Cys, and complement component 2 p.Glu318Asp were associated with CHB, with P values of <1.0 × 10−7, 2.76 × 10−5, 5.08 × 10−5, 2.78 × 10−4 and odds ratios (ORs) of 2.45, 4.08, 2.34, and 1.97, respectively. The combined P value was <2.0 × 10−16. As there has been no indication of immunological functions for the associated gene, transmembrane protein 2 , we further studied its expression by immunohistochemistry, real-time polymerase chain reaction, and western blotting. Our results showed that it was strongly expressed by healthy hepatocytes, but its expression was reduced in liver tissues with CHB, hepatitis B viral (HBV) genome-containing HepG2.2.15 cells, as compared with healthy liver tissues and non-HBV genome-containing HepG2 cells ( P = 0.022 and 0.0036, respectively). Conclusion : We identified four missense mutations associated with CHB, our results providing evidence for rare inborn genetic defects that contribute to increased host susceptibility to CHB.

TYK2 variants can impact disease onset or progression. In our previous study, we identified abnormal splicing that happened near rs781536408 in the TYK2 gene. The purpose of this research was to examine the effect of the mutation on alternative splicing in vivo and in vitro. Whole exome sequencing was performed to identify the mutations followed by bidirectional Sanger sequencing. Then the minigene analysis was carried out based on HeLa and HEK293T cell lines. The results showed that rs781536408 (c.2395G>A, p.G799R) was homozygous in the patient, but heterozygous in parents. PCR amplification confirmed the abnormal splicing in the somatic cells of the patients, but not in the parents. Sanger sequencing results showed that there was a skipping of exon18 near the mutation. For minigene analysis, there was no difference between the wild-type and the mutant type in the two minigene construction strategies, indicating that mutation c.2395G>A had no effect on splicing in vitro. Combining the results of in vivo, we speculated that the effect of the mutation on splicing was not absolute, but rather in degree.