The shift from outcrossing to predominantly selfing is one of the most common transitions in plant evolution. This evolutionary shift has received considerable attention from biologists; however, this work has almost exclusively been focused on animal-pollinated systems. Despite the seminal ecological and economic importance of wind-pollinated species, the mechanisms controlling the degree of outcrossing in wind-pollinated taxa remain poorly understood.
View Article and Find Full Text PDFMilitary members and female sex workers (FSWs) may be more likely to acquire or transmit HIV. Mapping HIV transmission across these high-risk populations and identifying behaviors associated with sexual network clustering are needed for effective HIV prevention approaches. A cross-sectional study recruited participants newly diagnosed with HIV among militaries, civilians, and FSWs in Zambia, Senegal, and Democratic Republic of the Congo (DRC).
View Article and Find Full Text PDFThe N-Myc transcription factor, encoded by MYCN, is a mechanistically validated, yet challenging, target for neuroblastoma (NB) therapy development. In normal neuronal progenitors, N-Myc undergoes rapid degradation, while, in MYCN-amplified NB cells, Aurora kinase A (Aurora-A) binds to and stabilizes N-Myc, resulting in elevated protein levels. Here, we demonstrate that targeted protein degradation of Aurora-A decreases N-Myc levels.
View Article and Find Full Text PDFPurpose: Postoperative pain is a major concern for patients undergoing ultrasound scalpel-assisted hemorrhoidectomy, potentially exacerbated by delayed wound healing. This study aimed to evaluate the impact of an intimate cleansing gel containing chlorhexidine, hyaluronic acid, and other anti-inflammatory agents (Antroclean Fisioderm) on postoperative pain, itching, and wound healing in patients who had undergone this procedure.
Methods: This multicenter observational case-control study involved a cohort of consecutive adult patients who underwent hemorrhoidectomy using an ultrasound device.
The APOBEC3 family of polynucleotide cytidine deaminases has diverse roles as viral restriction factors and oncogenic mutators. These enzymes convert cytidine to uridine in single-stranded (ss)DNA, inducing genomic mutations that promote drug resistance and tumor heterogeneity. Of the seven human APOBEC3 members, APOBEC3A (A3A) and APOBEC3B (A3B) are most implicated in driving pro-tumorigenic mutations.
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