No abstract

miR-93 was increased in PCOS granulosa cells and targeted CDKN1A to promote proliferation and cell cycle progression. Insulin could upregulate the expression of miR-93 and stimulate cell proliferation. This might provide a new insight into the dysfunction of granulosa cells in PCOS.

Objectives. To evaluate pregnancy outcomes and its determinants in women with polycystic ovary syndrome (PCOS). Methods. Two-hundred and twenty pregnant PCOS and 594 healthy women were followed from early pregnancy. Incidences of gestational diabetes mellitus (GDM), pregnancy-induced hypertension (PIH), preterm birth, twinning, and fetal growth restriction (FGR) were determined. Results. The incidence of GDM was notably higher among all PCOS combined (54.9%; OR: 2.9, 95% CI: 2.0–4.1) and PCOS subgroups, whether they conceived spontaneously (51.5%; OR: 3.3, 95% CI: 2.0–5.4), or via IVF-ET or ovarian stimulation, compared with controls (14.3%; P < 0.001). The incidence of PIH was also higher among all PCOS (10.4%; OR: 2.2, 95% CI: 1.1–4.4) and the subgroup conceiving spontaneously (11.8%; OR: 2.6, 95% CI: 1.1–6.2; P < 0.001) but not for those conceiving with IVF-ET (9.1%) or ovarian stimulation (9.4%). Lean women with PCOS (BMI <24 kg/m2) had higher incidences of GDM (51.1% versus 14.5%; OR: 5.6, 95% CI: 3.4–9.0) and PIH (8.9% versus 3.2%; OR: 3.0, 95% CI: 1.3–7.1) than lean controls. PCOS woemn with normal glucose tolerance had higher risk for PIH than their comparable control group (OR: 4.0, 95% CI: 1.3–11.7). Conclusion. This study suggested that PCOS is an independent risk factor for the development of GDM and PIH. This trial is registered with ChiCTR-RCC-11001824.

No abstract

Gonadal soma-derived factor (gsdf) is reported to be a male initiator in medaka based on loss- and gain- of function via targeted disruption, or transgenic over-expression. However, little is known about how gsdf promotes undifferentiated gonad entry into male pathways or prevents entry into the female pathway. We utilized a visible folliculogenesis system with a reporter cassette of dual-color fluorescence expression to identify difference between oocyte development from wildtype and gsdf deficiency medaka. A red fluorescent protein (RFP) is driven by a major component of the synaptonemal complex (SYCP3) promoter which enables RFP expression solely in oocytes after the onset of meiosis, and a histone 2b-EGFP fused protein (H2BEGFP) under the control of an elongation factor (EF1α) promoter, wildly used as a mitotic reporter of cell cycle. This mitosis-meiosis visible switch revealed that early meiotic oocytes present in gsdf deficiency were more than those in wildtype ovaries, corresponding to the decrease of inhibin expression detected by real-time qPCR analysis, suggesting gsdf is tightly involved in the process of medaka oocyte development at early stage.