Background: Premature ovarian insufficiency (POI) is a challenging disease, with limited treatment options at the moment. Umbilical cord blood mesenchymal stem cells (UCMSCs) have demonstrated promising regenerative abilities in several diseases including POI. Materials and Method: A pre-clinical murine case versus vehicle control randomized study. Two experiments ran in parallel in each of the three groups. The first was to prove the ability of UCMSCs in restoring ovarian functions. The second was to prove improved fertility. A total of 36 mice were randomly assigned; 6 mice into each of 3 groups for two experiments. Group 1 (control), group 2 (sham chemotherapy), group 3 (stem cells). Results: In the first experiment, post-UCMSCs treatment (group 3) showed signs of restored ovarian function in the form of increased ovarian weight and estrogen-dependent organs (liver, uterus), increased follicular number, and a significant decrease in FSH serum levels (p < 0.05) compared to group 2, and anti-Mullerian hormone (AMH) serum levels increased (p < 0.05) in group 3 versus group 2. Immuno-histochemistry analysis demonstrated a higher expression of AMH, follicle stimulating hormone receptor (FSHR) and Inhibin A in the growing follicles of group 3 versus group 2. In the second experiment, post-UCMSCs treatment (group 3) pregnancy rates were higher than group 2, however, they were still lower than group 1. Conclusion: We demonstrated the ability of UCMSCs to restore fertility in female cancer survivors with POI and as another source of stem cells with therapeutic potentials.

Summary To better understand outcomes in postpartum patients who receive peripartum anaesthetic interventions, we aimed to assess quality of recovery metrics following childbirth in a UK‐based multicentre cohort study. This study was performed during a 2‐week period in October 2021 to assess in‐ and outpatient post‐delivery recovery at 1 and 30 days postpartum. The following outcomes were reported: obstetric quality of recovery 10‐item measure (ObsQoR‐10); EuroQoL (EQ‐5D‐5L) survey; global health visual analogue scale; postpartum pain scores at rest and movement; length of hospital stay; readmission rates; and self‐reported complications. In total, 1638 patients were recruited and responses analysed from 1631 (99.6%) and 1282 patients (80%) at one and 30 days postpartum, respectively. Median (IQR [range]) length of stay postpartum was 39.3 (28.5–61.0 [17.7–513.4]), 40.3 (28.5–59.1 [17.8–220.9]), and 35.9 (27.1–54.1 [17.9–188.4]) h following caesarean, instrumental and vaginal deliveries, respectively. Median (IQR [range]) ObsQoR‐10 score was 75 ([62–86] 4–100) on day 1, with the lowest ObsQoR‐10 scores (worst recovery) reported by patients undergoing caesarean delivery. Of the 1282 patients, complications within the first 30 days postpartum were reported by 252 (19.7%) of all patients. Readmission to hospital within 30 days of discharge occurred in 69 patients (5.4%), with 49 (3%) for maternal reasons. These data can be used to inform patients regarding expected recovery trajectories; facilitate optimal discharge planning; and identify populations that may benefit most from targeted interventions to improve postpartum recovery experience.

Uterine fibroids (UFs) are benign smooth muscle neoplasms affecting up to 70% of reproductive age women. Treatment of symptomatic UFs places a significant economic burden on the US health-care system. Several specific genetic abnormalities have been described as etiologic factors of UFs, suggesting that a low DNA damage repair capacity may be involved in the formation of UF. In this study, we used human fibroid and adjacent myometrial tissues, as well as an in vitro cell culture model, to evaluate the expression of MutS homolog 2 (MSH2), which encodes a protein belongs to the mismatch repair system. In addition, we deciphered the mechanism by which polycomb repressive complex 2 protein, EZH2, deregulates MSH2 in UFs. The RNA expression analysis demonstrated the deregulation of MSH2 expression in UF tissues in comparison to its adjacent myometrium. Notably, protein levels of MSH2 were upregulated in 90% of fibroid tissues (9 of 10) as compared to matched adjacent myometrial tissues. Human fibroid primary cells treated with 3-deazaneplanocin A (DZNep), chemical inhibitor of EZH2, exhibited a significant increase in MSH2 expression (P < .05). Overexpression of EZH2 using an adenoviral vector approach significantly downregulated the expression of MSH2 (P < .05). Chromatin immunoprecipitation assay demonstrated that enrichment of H3K27me3 in promoter regions of MSH2 was significantly decreased in DZNep-treated fibroid cells as compared to vehicle control. These data suggest that EZH2-H3K27me3 regulatory mechanism dynamically changes the expression levels of DNA mismatch repair gene MSH2, through epigenetic mark H3K27me3. MSH2 may be considered as a marker for early detection of UFs.

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