39 research outputs found

    Follicle Stimulating Hormone and Anti-Müllerian Hormone per Oocyte in Predicting in vitro Fertilization Pregnancy in High Responders: A Cohort Study

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    Background: Follicle stimulating hormone (FSH) and Anti-Müllerian hormone (AMH) are utilized to differentiate between good and poor response to controlled ovarian hyperstimulation. Their respective roles in defining functional ovarian reserve remain, however, to be elucidated. To better understand those we investigated AMH and FSH per oocyte retrieved (AMHo and FSHo). Methodology/Principal Findings: Three-hundred and ninety-six women, undergoing first in vitro fertilization cycles, were retrospectively evaluated. Women with oocyte yields.75 th percentile for their age group were identified as high responders. In a series of logistic regression analyses, AMHo and FSHo levels were then evaluated as predictive factors for pregnancy potential in high responders. Patients presented with a mean age of 38.065.0 years, mean baseline FSH of 11.868.7 mIU/mL and mean AMH of 1.662.1 ng/mL. Those 88 women, who qualified as high responders, showed mean FSH of 9.766.5 mIU/mL, AMH of 3.163.1 ng/mL and oocyte yields of 15.867.1. Baseline FSH and AMH did not predict pregnancy in high responders. However, a statistically significant association between FSHo and pregnancy was observed in high responders, both after univariate regression (p = 0.02) and when adjusted for age, percentage of usable embryos, and number of embryos transferred (p = 0.03). Rate of useable embryos also significantly affected pregnancy outcome independently of FSHo (p = 0.01). AMHo was also associated with clinical pregnancy chances in high responders (p = 0.03

    The mechanisms of skeletal muscle atrophy in response to transient knockdown of the vitamin D receptor in vivo

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    Objective Vitamin‐D deficiency is estimated to affect ∼40% of the world's population and has been associated with impaired muscle maintenance. Vitamin‐D exerts its actions through the Vitamin‐D‐receptor (VDR), the expression of which was recently confirmed in skeletal muscle, and its down‐regulation is linked to reduced muscle mass and functional decline. To identify potential mechanisms underlying muscle atrophy, we studied the impact of VDR knockdown (KD) on mature skeletal muscle in vivo, and myogenic regulation in vitro in C2C12 cells. Methods Male Wistar rats underwent in vivo electrotransfer (IVE) to knock down the VDR in hind‐limb tibialis anterior (TA) muscle for 10 days. Comprehensive metabolic and physiological analysis was undertaken to define the influence loss of the VDR on muscle fibre composition, protein synthesis, anabolic and catabolic signalling, mitochondrial phenotype, and gene expression. Finally, in vitro lentiviral transfection was used to induce sustained VDR‐KD in C2C12 cells to analyse myogenic regulation. Results Muscle VDR‐KD elicited atrophy through a reduction in total protein content, resulting in lower myofibre area. Activation of autophagic processes was observed, with no effect upon muscle protein synthesis or anabolic signalling. Furthermore, RNA‐Seq analysis identified systematic down‐regulation of multiple mitochondrial respiration related protein and genesets. Finally, in vitro VDR‐knockdown impaired myogenesis (cell cycling, differentiation and myotube formation). Conclusion Taken together, these data indicate a fundamental regulatory role of the VDR in the regulation of myogenesis and muscle mass; whereby it acts to maintain muscle mitochondrial function and limit autophagy. Joseph Bass completed his PhD in Medicine and Health in 2017 at The University of Nottingham, where he is currently a Research Fellow. Joe is interested in examining the mechanistic regulation of musculoskeletal health, particularly factors impacting muscle atrophy susceptibility.Additional co-authors: Nathaniel J. Szewczyk, Mark E. Cleasby, Philip J. Atherto

    A scoping review and thematic analysis of social and behavioural research among HIV-serodiscordant couples in high-income settings.

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    CAPRISA, 2015.Abstract available in pdf

    At-home urine estrone-3-glucuronide quantification predicts oocyte retrieval outcomes comparably with serum estradiol

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    Objective: To investigate the feasibility of monitoring urine estrone-3-glucuronide (E3G) with an at-home device during gonadotropin stimulation for in vitro fertilization and oocyte cryopreservation. Design: Prospective, observational cohort study. Setting: Private fertility clinic. Patient(s): Thirty patients undergoing stimulation with a gonadotropin-releasing hormone antagonist protocol for in vitro fertilization or oocyte cryopreservation. Intervention(s): Daily collection of the first urine in the morning during stimulation and analysis performed at home by each patient with the Mira Fertility Tracker. Main Outcome Measure(s): Primary outcomes were correlation of urine E3G and serum estradiol (E2) concentrations on the day of trigger to the number of total and metaphase 2 oocytes (MII). Secondary outcomes of interest were the correlation of matched E3G and E2 measurements and the daily trends of E3G and E2 during stimulation. Result(s): Both urine E3G and serum E2 concentrations on the day of trigger significantly correlated with retrieval outcomes to a similar extent, with E3G demonstrating slightly higher correlation to the number of MII oocytes than that demonstrated by E2 (r = 0.485 vs. 0.391, respectively). The Pearson correlation coefficient for matched E3G and E2 levels was 0.761. The correlation coefficients of determination for daily trends of E3G and E2 during stimulation were 0.7066 and 0.6102, respectively. Conclusion(s): Measured on the day of trigger, urine E3G monitoring during gonadotropin stimulation was comparable with serum E2 for predicting oocyte retrieval outcomes. Matched daily samples confirmed good correlation of urine E3G and serum E2. The option of at-home estrogen monitoring with devices such as Mira offers an alternative to traditional serum monitoring that may improve patient experience. Clinical Trial Registration Number: NCT05493202
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