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Introduction: Vaginal laxity is a widespread and undertreated medical condition associated especially with vaginal parity. Aim: To evaluate the efficacy and safety of electroporation therapy treatment of vulvovaginal laxity by the Jett Plasma for Her II device. Methods: The Jett Plasma for Her II Study is a multicentric, prospective, randomized, single-blinded, and controlled study. Women presenting with vaginal laxity were randomized to receive electroporation therapy delivered to the vaginal tissue (active-82 patients) vs. therapy with zero intensity (placebo-9 patients). Results: A total of 91 subjects whose average age was 48.69 +- 10.89 were included. Due to the results of a one-way analysis of variance, it may be concluded that in the case of the vaginal laxity questionnaire (VLQ), there is a statistically significant difference between actively treated patients and the placebo group (F1,574 = 46.91; p < 0.001). In the case of the female sexual function index (FSFI), a one-way ANOVA test also showed a statistically significant difference between the actively treated patients and the placebo group (F1,278 = 7.97; p = 0.005). In the case of the incontinence impact questionnaire-7 (IIQ-7), a one-way ANOVA test showed a statistically significant difference between the actively treated patients and the placebo group (F1,384 = 15.51; p < 0.001). It confirms that improvement of vaginal laxity is conjoined with benefits in symptoms of urinary incontinence. Biopsy performed after the end of the treatment shows an increase in the vaginal mucosa thickness by an average of 100.04% in the active group. The treatment was well tolerated with no adverse events. No topical anesthetics were required. Conclusions: Treatments of vulvovaginal laxity by electroporation therapy achieved significant and sustainable 12-month effectiveness. Responses to the questionnaires also suggest subjective improvement in self-reported sexual function, incontinence, sexual satisfaction, and urogenital distress.

Mutations in IDH1 and IDH2 (encoding isocitrate dehydrogenase 1 and 2) drive the development of gliomas and other human malignancies. Mutant IDH1 induces epigenetic changes that promote tumorigenesis, but the scale and reversibility of these changes are unknown. Here, using human astrocyte and glioma tumorsphere systems, we generate a large-scale atlas of mutant-IDH1-induced epigenomic reprogramming. We characterize the reversibility of the alterations in DNA methylation, the histone landscape, and transcriptional reprogramming that occur following IDH1 mutation. We discover genome-wide coordinate changes in the localization and intensity of multiple histone marks and chromatin states. Mutant IDH1 establishes a CD24 + population with a proliferative advantage and stem-like transcriptional features. Strikingly, prolonged exposure to mutant IDH1 results in irreversible genomic and epigenetic alterations. Together, these observations provide unprecedented high-resolution molecular portraits of mutant-IDH1-dependent epigenomic reprogramming. These findings have substantial implications for understanding of mutant IDH function and for optimizing therapeutic approaches to targeting IDH-mutant tumors. This study uses human astrocytes and glioma tumorspheres to generate an atlas of mutant-IDH1-induced epigenomic reprogramming. The findings have implications for understanding mutant IDH function and for optimizing approaches to target IDH-mutant tumors.