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Background: Gestational diabetes mellitus (GDM) is one of the risk factors for postpartum urinary incontinence. Pelvic floor muscle training (PFMT) improves pelvic floor dysfunction in puerperal women, but patient compliance is low. Mobile Health (mHealth) is a promising solution. Objective: To investigate PFMT compliance and effects on pelvic floor muscles in GDM puerperal women guided by the mobile fitness app Keep. Methods: This randomized controlled trial included puerperal women with GDM (n = 72) who were delivered at a tertiary general hospital, selected from November 2021 to April 2022 using convenience sampling, and randomly divided into control (n = 36) and experimental (n = 36) groups. The control group performed PFMT based on routine postpartum PFMT training instruction. The experimental group performed PFMT based on Keep. Both groups had a 4-week intervention period. The PFMT compliance, International Consultation on Incontinence Questionnaire Short Form (ICIQ-SF), Pelvic Muscle Self-efficacy Scale, and the Knowledge, Attitude, Belief, and Practice (KAP) scores of PFMT in puerperal women in the groups were compared pre- and post-intervention. Pelvic floor surface electromyographic biofeedback was used to compare the post-intervention pelvic floor muscle strength between the two groups. Results: Compared with the control group, the test group had higher post-intervention maternal PFMT compliance, pelvic floor muscle strength, pelvic floor muscle self-efficacy, and KAP scores (p < 0.05); incontinence scores were lower (p < 0.05). Pelvic floor muscles in both groups recovered better post-intervention (p < 0.05). Conclusion: The Keep app can improve PFMT adherence, urinary incontinence, KAP scores, self-efficacy, and pelvic floor muscle strength in GDM puerperal women and promote pelvic floor rehabilitation after delivery. [ABSTRACT FROM AUTHOR]

Techniques to expand human hematopoietic stem cells ex-vivo could be beneficial to the fields of clinical hematopoietic stem cell transplantation and gene therapy targeted at hematopoietic stem cells. NUP98-HOXA10HD is a relatively newly discovered fusion gene that in mouse transplant experiments has been shown to increase numbers of hematopoietic stem cells. We evaluated whether this fusion gene could be used to expand engrafting human primitive CD34+ cells in an immunodeficient mouse model. Gene transfer was achieved using a lentiviral based vector. The engraftment of mobilized peripheral blood human CD34+ cells grown in culture for one week after gene transfer was evaluated 3–4 months after transplant and found to be 2–3 fold higher in the NUP98-HOXA10HD groups as compared to controls. These data suggest an expansive effect at least at the short term human repopulating cell level. Further evaluation in long term repopulating models and investment in a NUP98-HOXA10HD protein seems worthy of consideration. Additionally, the results here provide strong impetus to utilize NUP98-HOXA10HD as a tool to search for underlying genes and pathways involved in hematopoietic stem cell expansion that can be enhanced and have an even more potent expansive effect. [ABSTRACT FROM AUTHOR]

The safety of lentiviral (LV) vectors for gene therapy of genetic hematopoietic diseases would be considerably enhanced by the identification of a non-viral promoter capable of driving therapeutic levels of transgene expression in the target cell. Here, we tested the efficacy of the murine phosphoglycerate kinase (mPgk) promoter in a self-inactivating (SIN) LV vector to express canine CD18 in animals with canine leukocyte adhesion deficiency (CLAD) and in human LAD-1 CD34+ cells in NSG mice. Despite high transduction levels and high levels of CD18 expression per cell in CLAD CD34+ cells in vitro using the mPgk vector to drive canine CD18 expression, only two of five CLAD animals treated with ex vivo gene therapy achieved therapeutic levels of CD18+ neutrophils in vivo. Similarly, despite high transduction efficiency and high levels of CD18 expression in human LAD-1 CD34+ cells in vitro, the mPgk-hCD18 promoter resulted in a low percentage of CD45+/CD18+ cells and low levels of CD18 expression per neutrophil, when the transduced cells were transplanted into NSG mice. In contrast, human LAD-1 CD34+ cells transduced with a LV vector containing the viral MND promoter (MND-hCD18) and injected into NSG mice displayed a high percentage of CD45+/CD18+ cells and high levels of CD18 expression per neutrophil. These studies demonstrated that the mPgk promoter does not direct sufficient CD18 expression in neutrophils to replace a viral promoter for gene therapy of children with LAD-1. [ABSTRACT FROM AUTHOR]