Moshe Yaniv

Background: Meniscal injuries frequently accompany acute anterior cruciate ligament (ACL) tears, creating clinical dilemmas regarding optimal surgical timing. While delayed reconstruction increases risks of progressive meniscal damage, early intervention may interrupt natural healing capacity in the adolescent population. This study examines relationships between surgical timing, detailed tear characteristics, and meniscal healing patterns in adolescent ACL injuries. Methods: A retrospective cohort analysis of 55 adolescent patients (mean age: 14.9±1.9 y, range: 11.9 to 18; 63.6% male) undergoing arthroscopic ACL reconstruction (2015 to 2024) compared preoperative MRI findings with intraoperative meniscal evaluations. Individual meniscal tears (n=64) were characterized by anatomic location and morphologic configuration. Meniscal healing (absence of arthroscopically visible tears previously seen on MRI) was the primary outcome. Secondary analyses examined healing rates by location and surgical timing as a continuous variable. Multivariate logistic regression identified independent predictors. Results: Among 64 individual tears, 29 (45.3%) demonstrated spontaneous healing. Continuous timing analysis revealed healed tears averaged earlier surgery at 169.8±78.4 days versus persistent tears at 203.4±89.2 days (difference: 33.6 d, P =0.021). Medial meniscal tears showed significantly higher healing rates than lateral tears (60.0% vs. 27.6%, P =0.006). Multivariate analysis identified 3 independent predictors: medial location (OR: 3.9, 95% CI: 1.5-10.1, P =0.005), earlier surgical timing per day (OR: 0.994, 95% CI: 0.989-0.999, P =0.021), and posterior horn location (OR: 2.8, 95% CI: 1.1-7.2, P =0.031). Six new tears were identified at surgery (10.9% rate), with 5 occurring in patients with delayed surgery (>120 d from injury). Conclusion: This analysis demonstrates significant associations between surgical timing and meniscal healing in adolescent ACL injuries, with each day of delay associated with a 0.6% reduction in healing odds. These preliminary findings require validation in larger prospective studies before influencing treatment decisions but may inform patient counseling regarding expected outcomes. Level of Evidence: Level III—retrospective cohort study.

Supplementary Tables 2-3 from A Genomic Map of p53 Binding Sites Identifies Novel p53 Targets Involved in an Apoptotic Network

Supplementary Tables 2-3 from A Genomic Map of p53 Binding Sites Identifies Novel p53 Targets Involved in an Apoptotic Network

Supplementary Table 1 from A Genomic Map of p53 Binding Sites Identifies Novel p53 Targets Involved in an Apoptotic Network

Supplementary Table 1 from A Genomic Map of p53 Binding Sites Identifies Novel p53 Targets Involved in an Apoptotic Network

The transcriptional activity of the p53 protein is central to its role in tumor suppression. Identification of the complete repertoire of p53-regulated genes is critical for dissecting the complexity of the p53 network. Although several different approaches have been used to characterize the p53 genetic program, we still lack a comprehensive molecular understanding of how p53 prevents cancer. Using a computational approach, we generated a genome-wide map of p53 binding sites (p53BS) to identify novel p53 target genes. We show that the presence of nearby p53BS can identify new proapoptotic members of the Bcl2 family. We show that p53 binds to p53BS identified in the BCL-G/BCL2L14 gene and that induction of this gene contributes to p53-mediated apoptosis. We found that p53 activates the COL18A1 gene encoding the precursor for the antiangiogenic factor endostatin. We also show that p53 up-regulates the MAP4K4 gene and activates the c-Jun NH2-terminal kinase (JNK) pathway to drive apoptosis. Thus, unbiased mapping of the genomic landscape of p53BS provides a systematic and complementary approach to identify novel factors and connections in the p53 genetic network. Our study illustrates how systematic genomic approaches can identify binding sites that are functionally relevant for a p53 transcriptional program. The genetic link among p53, antiangiogenic factors, and the JNK signaling pathway adds new dimensions to understanding p53 function in highly connected genetic networks.

François Gros was a prominent French Molecular Biologist who made a major contribution to the discovery of messenger RNA in 1961. He pursued outstanding research on bacterial mRNA and its translation into proteins followed by pioneering work on muscle differentiation. I was lucky to be among his graduate students and owe much of my success in science to him. In this short text I will describe how the initial post-war studies of François guided him to discover the existence of short-lived RNA in bacteria, the messenger RNA containing the information for protein synthesis. I will also recount the influence he had on his students and their carrier in science.