This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

Vertebrate replication forks arrested at an interstrand DNA crosslink (ICL) can engage the Fanconi anemia (FA) pathway of ICL repair. The FANCP product, SLX4, binds the FANCQ/XPF/ERCC4-ERCC1 endonuclease, which incises bidirectionally arrested forks to 'unhook' the ICL. The resulting double strand break (DSB) is repaired by homologous recombination (HR). Whether this mechanism operates at replication blocks other than ICLs is unknown. Here, we study the role of mammalian SLX4 in HR triggered by a site-specific, chromosomal DNA-protein replication fork barrier formed by the Escherichia coli-derived Tus/Ter complex. We identify an SLX4-XPF-mediated step that is required for Tus/Ter-induced HR but not for HR induced by a replication-independent DSB. We additionally identify a requirement for SLX4-XPF in DSB-induced 'long tract' gene conversion, a replicative HR pathway related to break-induced replication. Our work suggests that Tus/Ter-induced HR recapitulates the incision step of replication-coupled ICL repair, and that the full FA mechanism can process DNA-protein barriers for HR.

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INTRODUCTION: The aim of this study is to assess the safety and feasibility of Indocyanine Green (ICG) dye in patients with adnexal torsion. Our hypothesis is that the use of ICG dye will aid in the surgical determination of tissue viability, ultimately preventing the resection of salvageable ovaries. METHODS: An IRB approved pilot study is currently enrolling patients 18-45 years old with suspected adnexal torsion in a multicentered tertiary care hospital setting. During laparoscopy, the involved adnexa is untwisted and ICG dye is injected intravenously. The untwisted ovary is then observed. Adnexal tissue demonstrating perfusion is preserved and patients are followed postoperatively with anti-Mullerian hormone level and ultrasound. Non-perfused tissue is resected and histologically evaluated for necrosis. RESULTS: Eleven patients with suspected adnexal torsion were enrolled, of which eight had surgically confirmed torsion. Six women demonstrated perfusion with the use of ICG dye even though three of these patients had minimal or no flow on preoperative ultrasound. The remaining 2/8 patients with confirmed torsion failed to demonstrate perfusion with the ICG dye and oophorectomies were performed. One of these patients had confirmed histologic necrosis. There have been no adverse events. CONCLUSION: The use of intravenous ICG dye appears to be a safe and valuable adjunct in the surgical management of adnexal torsion. This may be particularly helpful in patients with diminished adnexal perfusion on preoperative ultrasound. Further research is recommended to determine the generalized role of ICG dye in patients with adnexal torsion.

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