NLM identifier NCT02254577.

No abstract

Objective-Given the importance of ET technique during assisted reproductive technology cycles, we evaluated the effect of embryo afterloading subsequent to placement of the ET catheter on pregnancy rates vs. a standard direct ET. Design-Retrospective cohort analysis. Setting-University-based assisted reproductive technology program.Patient(s)-Patients undergoing a fresh nondonor day 3 ET by a single provider over a 1-year period. Intervention(s)-None. Main Outcome Measure(s)-Clinical pregnancy.Result(s)-One hundred twenty-seven patients met inclusion criteria, and the overall pregnancy rate was 46.5%. There was no difference between the two groups with respect to age, basal FSH, or number of embryos transferred. The ET method used was at the discretion of the provider. There was no difference between the two groups in the presence of blood on the transfer catheter. However, there were significantly more transfer catheters with mucus contamination in the direct transfer group (25.58% vs. 5.95%). The clinical pregnancy rate in the group with ET using the afterloading technique was higher than in the direct ET group (52.4% vs. 34.9%). Conclusion(s)-There was a trend toward an increase in pregnancy rate when an embryo afterloading technique was used. A prospective randomized trial is needed to examine this issue. Technology reported an increase in live birth rates from 28% in 1996 to 32% in 2002 (1). This increase has been attributed to multiple factors including improved stimulation protocols (2-4), advances in embryology laboratory techniques (5), and improvement in ET techniques (6, 7). KeywordsEmbryo transfer is universally accepted as a crucial last step in any ART cycle. The importance of this step has been emphasized by the fact that different providers at the same institution may have disparate pregnancy rates after ET (8,9). Other variables affecting pregnancy include the ease of ET (7, 10, 11), presence or absence of blood on the transfer catheter (12), type of catheter used (13), technique used to perform the transfer (14-16), and experience of the physician (17).In the early 1990s, studies were first published on the use of a mock or "dummy" ET before the start of an IVF cycle (11,18). A mock ET allows the physician to choose the appropriate transfer catheter, measure the depth of the endometrial cavity, and anticipate potential problems at ET. However, a mock transfer remote from the actual ET is done under different circumstances and may not be reflective of actual conditions encountered on the day of ET. Sharif et al. (19) proposed to circumvent this problem by performing a mock ET immediately before the actual ET.To avoid additional trauma by the passage of two separate catheters, we began transferring embryos by an afterload technique, in which an empty catheter is placed at, or just past, the internal cervical os. The inner sheath is withdrawn, and a second inner sheath containing the embryos is passed. This gives the provider the benefit of an immediate mock transfer while minimizing mani...

Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant hereditary disorder characterized by multiple parathyroid, pancreatic, duodenal, and pituitary neuroendocrine tumors. Nonendocrine mesenchymal tumors, such as lipomas, collagenomas, and angiofibromas have also been reported. MEN1-associated neuroendocrine and some mesenchymal tumors have documented MEN1 gene alterations on chromosome 11q13. To test whether the MEN1 gene is involved in the pathogenesis of multiple smooth muscle tumors, we examined the 11q13 loss of heterozygosity (LOH) and clonality patterns in 15 leiomyomata of the esophagus, lung, and uterus from five patients with MEN1. Forty sporadic uterine leiomyomata were also studied for 11q13 LOH. LOH analysis was performed using four polymorphic DNA markers at the MEN1 gene locus; D11S480, PYGM, D11S449, and INT-2. The gene for multiple endocrine neoplasia type 1 (MEN1), an autosomal dominant tumor syndrome, has been mapped to chromosome 11q13 1 and recently identified. 2 The MEN1 gene is thought to act as a tumor suppressor based on the presence of inherited inactivating mutations in the constitutional DNA of affected family members accompanied by the loss of the wild-type allele in associated tumors. 2-4 Somatic inactivation of the MEN1 gene has been also documented in a subset of sporadic counterpart parathyroid, enteropancreatic, and pulmonary endocrine tumors, and mesenchymal tumors. 5 MEN1 patients typically present first with primary hyperparathyroidism resulting from multiple parathyroid tumors caused by MEN1 gene alterations. 6 Neuroendocrine tumors of the pancreas, duodenum, anterior pituitary gland, stomach, and lung are other tumors that are an integral part of MEN1. 7,8 Nonendocrine mesenchymal tumors, such as lipomas, angiofibromas, and collagenomas, have also been shown to be associated with MEN1 and MEN1 gene alterations. 8 -10 Leiomyomata have been occasionally documented in MEN1 patients, 8,[11][12][13][14] and loss of heterozygosity (LOH) at the MEN1 locus was recently shown in two esophageal leiomyomata from one MEN1 patient. 15 MEN1 gene inactivation in lung or uterine leiomyomata, however, has not been studied. To test whether MEN1 gene alterations are involved in the development of multiple smooth muscle tumors in MEN1 patients, we analyzed 15 leiomyomata from five patients with documented MEN1 germline mutations for LOH at the MEN1 gene locus. To assess whether MEN1 gene alterations are present in sporadic smooth muscle tumors, we analyzed 40 sporadic uterine leiomyomata for MEN1 gene deletion for comparison. Furthermore, to evaluate whether MEN1-associated leiomyomata arise as independent clonal events at different anatomical sites within an organ, the patterns of 11q13 LOH in different tumors from individual patients