Prolonged second stage of labor in delivery using epidural analgesia is a risk factor for postpartum urinary retention.

AIM: To determine the postpartum urinary retention rate and risk factors after delivery using epidural analgesia. METHODS: This single-center retrospective study targeted 341 women who gave birth after at least 37 weeks of gestation from April to August 2021; from this cohort, 208 patients were examined. The postpartum urinary retention rate was compared between the no epidural analgesia group (n = 107) and epidural analgesia group (n = 101). Subsequently, risk factors for postpartum urinary retention were investigated in the epidural analgesia group. RESULTS: After adjustment by propensity score matching for age, body mass index, being primiparous, and labor induction as covariates, the analysis of the incidence of postpartum urinary retention revealed that the epidural analgesia group exhibited a significantly higher postpartum urinary retention rate than the no epidural analgesia group (30% vs. 11%, p = 0.02). The investigation results regarding risk factors for postpartum urinary retention in the epidural analgesia group obtained through a univariate analysis showed that being primiparous and having a prolonged second stage of labor were significantly correlated with postpartum urinary retention. Multivariate analysis indicated that a prolonged second stage of labor was an independent risk factor for postpartum urinary retention (p = 0.03; odds ratio: 3.18; 95% confidence interval: 1.08-9.77). All patients recovered from postpartum urinary retention by day 4. CONCLUSIONS: The postpartum urinary retention rate after delivery using epidural analgesia was 25.7%. In the case of epidural analgesia deliveries, a prolonged second stage of labor was an independent risk factor for postpartum urinary retention.

An Integrated Genomic Approach Identifies HOXC8 as an Upstream Regulator in Ovarian Endometrioma.

PURPOSE: To identify the upstream regulators (URs) involved in the onset and pathogenesis of ovarian endometrioma. METHODS: Recently, a method called Significance-based Modules Integrating the Transcriptome and Epigenome (SMITE) that uses transcriptome data in combination with publicly available data for identifying URs of cellular processes has been developed. Here, we used SMITE with transcriptome data from ovarian endometrioma stromal cells (ovESCs) and eutopic endometrium stromal cells (euESCs) in combination with publicly available gene regulatory network data. To confirm the URs identified by SMITE, we developed a Boolean network simulation to see if correcting aberrant expressions of the identified genes could restore the entire gene expression profile of ovESCs to a profile similar to that of euESCs. We then established euESCs overexpressing the identified gene and characterized them by cell function assays and transcriptome analysis. RESULTS: SMITE identified 12 potential URs in ovarian endometrioma that were confirmed by the Boolean simulation. One of the URs, HOXC8, was confirmed to be overexpressed in ovESCs. HOXC8 overexpression significantly enhanced cell proliferation, migration, adhesion, and fibrotic activities, and altered expression statuses of the genes involved in transforming growth factor (TGF)-ß signaling. HOXC8 overexpression also increased the expression levels of phosphorylated SMAD2/SMAD3. The increased adhesion and fibrosis activities by HOXC8 were significantly inhibited by E-616452, a selective inhibitor of TGF-ß receptor type I kinases. MAIN CONCLUSIONS: Integrated genomic approaches identified HOXC8 as an UR in ovarian endometrioma. The pathological features of ovarian endometrioma including cell proliferation, adhesion, and fibrosis were induced by HOXC8 and its subsequent activation of TGF-ß signaling.

Fibrosis and adipogenesis originate from a common mesenchymal progenitor in skeletal muscle.

Accumulation of adipocytes and collagen type-I-producing cells (fibrosis) is observed in muscular dystrophies. The origin of these cells had been largely unknown, but recently we identified mesenchymal progenitors positive for platelet-derived growth factor receptor alpha (PDGFRα) as the origin of adipocytes in skeletal muscle. However, the origin of muscle fibrosis remains largely unknown. In this study, clonal analyses show that PDGFRα(+) cells also differentiate into collagen type-I-producing cells. In fact, PDGFRα(+) cells accumulated in fibrotic areas of the diaphragm in the mdx mouse, a model of Duchenne muscular dystrophy. Furthermore, mRNA of fibrosis markers was expressed exclusively in the PDGFRα(+) cell fraction in the mdx diaphragm. Importantly, TGF-ß isoforms, known as potent profibrotic cytokines, induced expression of markers of fibrosis in PDGFRα(+) cells but not in myogenic cells. Transplantation studies revealed that fibrogenic PDGFRα(+) cells mainly derived from pre-existing PDGFRα(+) cells and that the contribution of PDGFRα(-) cells and circulating cells was limited. These results indicate that mesenchymal progenitors are the main origin of not only fat accumulation but also fibrosis in skeletal muscle.