[Objective]To reconstruct anterior cruciate ligament (ACL) by using ligament advanced reinforcement system(LARS),and to investigate the integration of LARS artificial ligament with bone interface in the animals with regard to imageology, biomechanics and histology.[Method]Twenty-four Boer goats were randomly divided into three groups. The animal mode of ACL reconstruction was established by clinical ACL reconstruction system. Gross observation was made, and histological, imageological and biomechanical changes were observed at 4, 8 and 12 weeks after surgery, respectively. Statistical analysis was performed.[Result](1)At 4 weeks after surgery,ligament-bone interface had great amount of loose bindweb and infiltration of chronic inflammation cells. At 8 weeks after surgery, there was new bone formation. Part of samples had Sharpey fibers. At 12 weeks after surgery, Sharpey fibers.and a large number of fibroblasts were noted in the interface between LARS artificial ligament and bone interface. But calcified cartilage was not founded.(2)The imageology examination for group 3 was made at 4, 8 and 12 weeks after surgery. The data were analyzed statistically by the image processing software of eflime,and there was evident statistical difference (P0.05 ) .[Conclusion]After ACL reconstruction by LARS artificial ligament, indirect connection developed via Sharpey fibers in bone tunnel at the end of LARS artificial ligament and bone interface. The integration of LARS artificial ligament with bone interface has been improved and its intensity is increased.

Objective:To investigate the clinical and genetic characteristics of peroxisome D-bifunctional protein deficiency (PDBPD) associated with HSD17B4 mutation. Methods:The clinical and genetic characteristics of 2 cases of PDBPD in August 2020, at Children′s Hospital Affiliated to Nanjing Medical University caused by HSD17B4 gene mutation were retrospectively analyzed. Results:Male proband and his sister suffered from neonatal epilepsy, psychomotor development disorders, ataxia, myasthenia, hearing impairment, and foot deformity.The very long chain fatty acids in serum were normal, and brain magnetic resonance imaging (MRI) showed bilateral cerebellar hemisphere atrophy.Electromyography suggested changes in the myoelectricity of multiple peripheral neurogenic lesions.Auditory evoked potential displayed severe bilateral sensorineural hearing loss.Exome sequencing identified compound heterozygous mutations (c.1171G > C, c.686-2A>T) in HSD17B4.The clinical diagnosis was PDBPD, aged 8 and 14 years, respectively. Conclusions:Two cases of HSD17B4 mutation-induced PDBPD were first reported in Chinese mainland, which was in line with its typical clinical manifestations.The newly discovered c. 1171G> C and c. 686-2A>T mutations enriched the HSD17B4 mutation spectrum.