This study aimed to investigate the effect of auxiliary Kirschner wire (K-wire) technique in the closed reduction of children with Gartland type III supracondylar humerus fractures by comparing with manual reduction alone. Retrospective analysis was performed on the clinical data of 68 cases of supracondylar humerus fractures. Thirty-six patients received closed reduction and percutaneous fixation with auxiliary K-wire technique (group A). Thirty-two patients received conventional manual reduction and percutaneous pin fixation (Group B). In group A, the average operation time was 20.5 ± 8.5 minutes, the average frequency of intraoperative radiographic observations was 4.3 ± 1.1, the average fracture healing time was 6.2 ± 1.8 weeks, and the complication rate was 3/36, 8.3%. The mean operation time was 36.1 ± 10.2 minutes, the average frequency of intraoperative radiography was 8.9 + 1.7 times, the average fracture healing time was (6.1 ± 1.6) weeks, and the complication rate was 2/32, 6.3%. The operation time in group A was significantly shorter than that in group B. The difference between the 2 groups was statistically significant ( P = .012). The frequency of radiography in group A was significantly less than that in group B ( P = .001). Compared with manual reduction, auxiliary K-wire technology can significantly shorten the operation time, reduce the radiant quantity of the surgeon, improve the efficiency of closed reduction of children with Gartland type III supracondylar humerus fractures, and reduce the risk of developing postoperative complications. And meanwhile, there is no significant effect on the imaging and functional outcomes of affected extremities, which is worthy of respect.

Objective: Pulmonary atresia (PA) is a rare type of complex cyanotic congenital heart defect characterized primarily by an undeveloped pulmonary valve or pulmonary artery. Therefore, defining a disease-causing gene mutation in a pulmonary atresia family is a possible method of genetic counseling, future prenatal diagnosis, and therapeutic approaches for pulmonary atresia. Methods: Blood samples were collected from six PA family members, and genomic DNA was extracted using the QIAamp DNA Blood Mini Kit. Gene detection was performed using a second-generation sequencing gene panel. Results: Genetic testing results indicated that a heterozygous mutation originating from maternal inheritance was detected in the BMPR2 gene of the proband's genomic DNA. The pathogenic gene was c.2804C>T (p. A935V). The mutation was also detected in the genomic DNA of the proband's elder brother (III-1), but not in other family members. Conclusion: To the best of our knowledge, this is the first study to report the BMPR2 variant responsible for pulmonary atresia. The frequency of the c.2804C>T (p. A935V) mutation detected in this family is extremely low in the normal population (1/246048). The mutation was highly conserved among different species. Sorting intolerant from tolerant (SIFT) predicts it to be a harmful mutation.