Non-cavity-distorting fibroids negatively affect pregnancy rates after IVF.

Chronic pelvic pain (CPP) and bladder pain syndrome (BPS) can have a negative impact on quality of life. Neuromodulation has been suggested as a possible treatment for refractory pain. To assess the effectiveness of tibial and sacral nerve stimulation in the treatment of BPS and CPP. We searched until July 2012: the Cochrane Library, EMBASE (1980-2012), Medline (1950-2012), Web of knowledge (1900-2012), LILACS (1982-2012) and SIGLE (1990-2012) with no language restrictions. We manually searched through bibliographies and conference proceedings of the International Continence Society. Randomized and prospective quasi-randomized controlled studies vs. sham nerve stimulation treatment or usual care of patients with CPP and BPS who underwent sacral or tibial nerve stimulation were included. Any studies involving transcutaneous stimulation were excluded. The outcome was a cure or improvement in symptoms. Three studies with 169 patients treated with tibial nerve stimulation were included; two for CPP and one for BPS. There were improvements in pain, urinary and quality of life scores. There were no reported data for sacral nerve stimulation. There is scanty literature reporting variable success of posterior tibial nerve stimulation in improving pain, urinary symptoms and quality of life in CPP and BPS. In view of the dearth of quality literature, a large multi-centered clinical trial investigating the effectiveness of electrical nerve stimulation to treat BPS and CPP along with the cost-analysis of this treatment is recommended.

The advent of recombinant technology has made the production of modified proteins with desired properties possible. Corifollitropin alfa is a successful example of the first available long-acting, follicle stimulating hormone. Corifollitropin alfa has prolonged half-life and a slower absorption rate, but has the same receptor-binding and biological activity as recombinant FSH (rFSH). Its application is associated with the arrival of a novel simplified approach for controlled ovarian stimulation in IVF patients. Different studies have proven the efficiency of a single corifollitropin alfa dose to initiate and sustain multiple follicular development in a gonadotropin-releasing hormone antagonist protocol. Finally, corifollitropin alfa is well tolerated and is not correlated with serious adverse events, except for the slightly higher incidence of ovarian hyperstimulation syndrome compared with traditional management with recombinant FSH.

Ovarian response to follicle-stimulating hormone (FSH) action differs considerably among women; this has prompted researchers to determine which factors modify this response. The challenge is to identify the genes that affect the response to FSH stimulation by the application of pharmacogenetics to assisted reproduction techniques (ARTs). Recently, new insights have been gained in the investigation of the variability in the gene that encodes the FSH receptor (FSHR) gene or genes of the estrogen pathway. Several polymorphisms of the FSHR gene have been discovered, but Ser680Asn and Thr307Ala are the two most studied. The Ser680Asn polymorphism of the FSHR gene has been found to influence the ovarian response to FSH stimulation in women undergoing in vitro fertilization (IVF), and in women with the genotype Ser/Ser, the FSHR appears to be more resistant to FSH action. The clinical implications of this finding are highly important; the ultimate goal is to apply genetic markers as routine diagnostic tests before ovarian stimulation to predict ovarian response, determine the required FSH dose, and avoid the possible complications related to FSH stimulation.

The present study shows that the Gln27Gln genotype of β2-AR is the most predominant while the Glu27Glu is the least prevalent in our HF population. There was no difference in the prevalence of polymorphism Gln27Glu between HF patients and control subjects. However, the presence of Glu allele was associated with lower myocardial infarction rate.

We present a case series and literature review on the use of rescue human chorionic gonadotropin (hCG) in cases of empty follicle syndrome (EFS) after a gonadotropin-releasing hormone agonist (GnRHa) trigger. EFS was diagnosed after failure to collect any oocytes from one ovary. In such cases, a single dose of hCG was administered and the oocyte retrieval was repeated 36 h later. The main outcome measures were the number of mature oocytes (M2) and embryos (2PN), incidence of hospitalisation for severe ovarian hyperstimulation syndrome (OHSS) and clinical pregnancy when fresh embryo transfers occurred. Our population consisted of 322 patients, who had a GnRH agonist as oocyte maturation trigger (2-mg subcutaneous buserelin). Six patients (1.8%) developed EFS after the use of a GnRHa trigger. Mature oocytes were retrieved in 5 patients after the use of rescue hCG. One patient developed severe OHSS. Two patients had a fresh embryo transfer and one clinical pregnancy was reported. This is the first case series to report fresh embryo transfers and a clinical pregnancy with the use of rescue hCG after failure of the GnRHa trigger.

Previous microarray analyses of RNAs from 8-cell (8C) human embryos revealed a lack of cell cycle checkpoints and overexpression of core circadian oscillators and cell cycle drivers relative to pluripotent human stem cells [human embryonic stem cells/induced pluripotent stem (hES/iPS)] and fibroblasts, suggesting growth factor independence during early cleavage stages. To explore this possibility, we queried our combined microarray database for expression of 487 growth factors and receptors. Fifty-one gene elements were overdetected on the 8C arrays relative to hES/iPS cells, including 14 detected at least 80-fold higher, which annotated to multiple pathways: six cytokine family (CSF1R, IL2RG, IL3RA, IL4, IL17B, IL23R), four transforming growth factor beta (TGFB) family (BMP6, BMP15, GDF9, ENG), one fibroblast growth factor (FGF) family [FGF14(FH4)], one epidermal growth factor member (GAB1), plus CD36, and CLEC10A. 8C-specific gene elements were enriched (73%) for reported circadian-controlled genes in mouse tissues. High-level detection of CSF1R, ENG, IL23R, and IL3RA specifically on the 8C arrays suggests the embryo plays an active role in blocking immune rejection and is poised for trophectoderm development; robust detection of NRG1, GAB1, -2, GRB7, and FGF14(FHF4) indicates novel roles in early development in addition to their known roles in later development. Forty-four gene elements were underdetected on the 8C arrays, including 11 at least 80-fold under the pluripotent cells: two cytokines (IFITM1, TNFRSF8), five TGFBs (BMP7, LEFTY1, LEFTY2, TDGF1, TDGF3), two FGFs (FGF2, FGF receptor 1), plus ING5, and WNT6. The microarray detection patterns suggest that hES/iPS cells exhibit suppressed circadian competence, underexpression of early differentiation markers, and more robust expression of generic pluripotency genes, in keeping with an artificial state of continual uncommitted cell division. In contrast, gene expression patterns of the 8C embryo suggest that it is an independent circadian rhythm-competent equivalence group poised to signal its environment, defend against maternal immune rejection, and begin the rapid commitment events of early embryogenesis.

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