Gynecology And Womens Health

Grand Rapids, MI, United States

Gynecology And Womens Health

Grand Rapids, MI, United States
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Morelli S.S.,Gynecology and Womens Health | Goldsmith L.T.,Gynecology and Womens Health
Biology of Reproduction | Year: 2013

Human endometrium has the remarkable ability to regenerate all cellular compartments with every menstrual cycle; the cellular source remains unknown. The objective of the present study was to determine whether the bone marrow (BM) is a source of multiple endometrial cell types using a murine BM transplant model. BM cells were harvested from transgenic donor mice that ubiquitously express green fluorescent protein (GFP) and were injected into lethally irradiated, syngeneic female recipient mice. Recipients with successful hematopoietic reconstitution were sacrificed at 3, 5, 9, and 12 mo posttransplant, after which hysterectomy was performed. Numbers of GFP-positive, CD45-positive, and CD45-negative cells in the endometrial stromal and epithelial compartments were determined. In the stromal compartment, BM-derived cells (BMDCs) were detectable as early as 3 mo posttransplant, and the BM remained a long-term contributor of nonhematopoietic endometrial cells. Nonhematopoietic endometrial cells comprised 47.3%-72.2% of total BMDCs in the stromal compartment at 12 mo posttransplant. In contrast, BMDCs were not detected in the glandular or luminal epithelial compartments until 12 mo posttransplant. These data demonstrate that the BM is a significant source of nonhematopoietic endometrial stromal compartment cells and contributes to a much lesser extent to the epithelial compartments. That BM is a source of nonhematopoietic cells in the endometrial stromal and epithelial compartments provides a potential mechanism by which monthly regeneration of the endometrium may occur. © 2013 by the Society for the Study of Reproduction, Inc.

Heller D.S.,Gynecology and Womens Health | Cracchiolo B.,Gynecology and Womens Health
Journal of Minimally Invasive Gynecology | Year: 2014

The risk of occult malignancy being present at the time of uterine morcellation has been estimated to be about 1%. Dissemination of both benign and malignant disease may occur after morcellation, leading to a variety of peritoneal nodules. These lesions are reviewed. © 2014 AAGL.

Wang B.,Gynecology and Reproductive science | Parobchak N.,Gynecology and Reproductive science | Rosen M.,Gynecology and Reproductive science | Roche N.,Gynecology and Womens Health | Rosen T.,Gynecology and Reproductive science
Journal of Clinical Endocrinology and Metabolism | Year: 2014

Context: Progesterone (P4)contributes to the maintenance of human pregnancy, in part by inhibiting activity of the human pro-labor genes CRH and cyclooxygenase-2 (COX-2). However, the molecular mechanisms underlying the action of P4 remain poorly defined. We have shown that in human placenta, the constitutively activated noncanonical nuclear factor (NF)-κB pathway positively regulates CRH and COX-2, which is further stimulated by glucocorticoid receptor signaling. Objective: We investigated the role of P4 receptor (PR) in the regulation of nuclear activity of v-rel avian reticuloendotheliosis viral oncogene homolog B (RelB)/NF-κB2 and, in turn, expression of placental CRH and COX-2. Methods: We used a variety of techniques including gene silencing, ectopic expression, chromatin immunoprecipitation, Western blot, quantitative RT-PCR, and immunohistochemical staining assays in human placental tissues and primary culture of human cytotrophoblast. Results: We identified PR isoform-A (PR-A) as the only isoform of PR produced in human placenta. PR-A levels were lower in term placenta than in midterm placenta. Depletion of PR-A by short interfering RNA derepressed inhibition of CRH and COX-2 by P4 and the synthetic progestin 17α- hydroxyprogesterone caproate. Overexpression of PR-A inhibited transcription of CRH and COX-2, which was further downregulated by treatment with P4 or 17α-hydroxyprogesterone caproate. Such an inhibition was mediated by a negative functional interaction of PR-A with the activity of RelB/NF-κB2. Conclusion: P4 inhibits the pro-labor genesCRHand COX-2 via PR-A repression of the noncanonical NF-κB signaling in human placenta. Characterization of these pathways may identify potential drug targets for prevention of preterm birth. Copyright © 2014 by the Endocrine Society.

Mitwally M.F.,Gynecology and Womens Health | Diamond M.P.,Wayne State University | Abuzeid M.,Michigan State University
Fertility and Sterility | Year: 2010

Objective: To study the outcome of IVF-ET in women who used vaginal P (vaginal P4) versus those who used P in oil via IM injection (IM-P4) for luteal support. Design: Retrospective cohort. Setting: Tertiary referral infertility center. Patient(s): A cohort of 544 women. Intervention(s): In 145 women, vaginal P4 was used, while in 399 women, IM-P4 was used for luteal support. Main Outcome Measure(s): The primary outcome was ongoing pregnancy rate. Secondary outcomes included other IVF-ET outcomes: rates of clinical pregnancy and pregnancy loss (chemical and miscarriage) and serum P levels during the luteal phase and early pregnancy. Result(s): Women who used vaginal P4 for luteal support had ongoing pregnancy rates (odds ratio [OR], 1.0675; 95% confidence interval [CI], 0.7587-1.5020) and rates of total pregnancy loss (OR, 1.0775; 95% CI, 0.7383-1.5727) that were not statistically different from those who used IM-P4. During the luteal phase, women who used vaginal P4 had mean serum P levels that were not statistically different from those who used IM-P4. However, during early pregnancy, mean P levels in pregnant women who used vaginal P4 were statistically significantly higher. Conclusion(s): In women undergoing IVF-ET according to the GnRH agonist long protocol, luteal support with vaginal P4 was associated with treatment outcomes that were no different from those associated with IM-P4 luteal support. © 2010 American Society for Reproductive Medicine.

Bibee K.P.,University of Washington | Illsley N.P.,Gynecology and Womens Health | Moley K.H.,University of Washington
Reproductive Sciences | Year: 2011

Glucose transport from the maternal to fetal side of the placenta is critical for fetal growth and development due to the absence of fetal gluconeogenesis. Human GLUT9, existing as 2 isoforms, is a novel member of the transporter family. This study investigated the localization and relative expression levels of these isoforms in the human term placenta from both control and diabetic patients. Placenta samples were collected from normal pregnancies and those complicated by maternal diabetes (White classifications A1, A2, and B). Antibodies specific for the different isoforms were used to detect expression. Both forms of the protein are expressed in syncytiotrophoblast cells. Subcellular fractionation revealed an asymmetrical expression pattern with GLUT9a on basal membranes, whereas GLUT9b localizes to microvillus membranes. Expression of both isoforms is significantly increased in placental tissue from diabetic pregnancies. Altered expression of GLUT9 in the placenta may play a role in the fetal pathophysiology associated with diabetes-complicated pregnancies. © The Author(s) 2011.

Seungdamrong A.,Gynecology and Womens Health
Seminars in Reproductive Medicine | Year: 2016

Subclinical hypothyroidism has been found to be associated with adverse reproductive outcomes, such as infertility, miscarriage, preterm birth, and complications of pregnancy. Multiple studies have investigated the relationships between thyroid function, thyroid antibodies, fertility, and pregnancy. Thyroid autoimmunity is the most common cause of hypothyroidism in iodine-sufficient locations. Thyroid antibodies have been associated with adverse reproductive outcomes such as miscarriage and infertility. Debate exists regarding the method of identification of thyroid dysfunction in pregnancy, which can be conducted by targeted screening or by universal screening. Multiple professional societies have issued recommendations for the evaluation and treatment of thyroid dysfunction and pregnancy. Copyright ©, Thieme Medical Publishers. All rights reserved.

Illsley N.P.,Gynecology and Womens Health | Caniggia I.,Samuel Lunenfeld Research Institute | Zamudio S.,Gynecology and Womens Health
International Journal of Developmental Biology | Year: 2010

Insufficient oxygen leads to the cessation of growth in favor of cellular survival. Our unique model of high-altitude human pregnancy indicates that hypoxia-induced reductions in fetal growth occur at higher levels of oxygen than previously described. Fetal PO2 is surprisingly high and fetal oxygen consumption unaffected by high altitude, whereas fetal glucose delivery and consumption decrease. Placental delivery of energy-generating substrates to the fetus is thus altered by mild hypoxia, resulting in maintained fetal oxygenation but a relative fetal hypoglyce- mia. Our data point to this altered mix of substrates as a potential initiating factor in reduced fetal growth, since oxygen delivery is adequate. These data support the existence, in the placenta, of metabolic reprogramming mechanisms, previously documented in tumor cells, whereby HIF-1 stimulates reductions in mitochondrial oxygen consumption at the cost of increased glucose consumption. Decreased oxygen consumption is not due to substrate (oxygen) limitation but rather results from active inhibition of mitochondrial oxygen utilization. We suggest that under hypoxic conditions, metabolic reprogramming in the placenta decreases mitochondrial oxygen consumption and increases anerobic glucose consumption, altering the mix of energy-generating substrates available for transfer to the fetus. Increased oxygen is available to support the fetus, but at the cost of less glucose availability, leading to a hypoglycemia-mediated decrease in fetal growth. Our data suggest that metabolic reprogramming may be an initiating step in the progression to more severe forms of fetal growth restriction and points to the placenta as the pivotal source of fetal programming in response to an adverse intrauterine environment. © 2009 UBC Press.

Di Stefano V.,Gynecology and Reproductive science | Wang B.,Gynecology and Reproductive science | Parobchak N.,Gynecology and Reproductive science | Roche N.,Gynecology and Womens Health | Rosen T.,Gynecology and Reproductive science
Science Signaling | Year: 2015

Corticotropin-releasing hormone (CRH) produced in the placenta may be part of a clock that regulates the length of human gestation. Maternal plasma CRH abundance exponentially increases as pregnancy advances. Glucocorticoid stimulates CRH expression in full-term human placenta by promoting noncanonical (RelB/p52 heterodimer-mediated) nuclear factor kB (NF-kB) pathway activity. Using dexamethasone to mimic glucocorticoid exposure, we found that an epigenetic switch mediated the glucocorticoid-induced expression of CRH as gestation advances. The amount of acetylated histone H3 lysine 9 (H3K9) associated with the CRH promoter was greater in cytotrophoblasts from full-term placenta than in those from midterm placenta. Knocking down the lysine acetyltransferase CBP reduced H3K9 histone acetylation and prevented dexamethasone-induced CRH expression. Unexpectedly, knocking down the histone deacetylase HDAC1 or pharmacologically inhibiting type I and II HDACs also decreased the expression of CRH yet increased the acetylation of H3K9 and other histone regions. Both CBP and HDAC1 bound at the CRH promoter in a complex with the RelB/p52 heterodimer in a mutually dependent manner; knocking down any one factor in the complex prevented binding of the others as well as the dexamethasone-induced CRH expression. Our results suggest that glucocorticoids induce a transcription complex consisting of RelB/p52, CBP, and HDAC1 that triggers a dynamic acetylation-mediated epigenetic change to induce CRH expression in full-term human placenta.

Shwayder J.M.,Gynecology and Womens Health
Obstetrics and Gynecology | Year: 2010

The malpractice environment has adversely influenced physicians' practice patterns. Although liability reform has had a positive effect in several states, recent court decisions finding statutory damage caps unconstitutional threaten ongoing adoption of effective liability reform.59 The threat of medical liability is always present in obstetrics and gynecology. Practicing contemporary, evidence-based medicine with compassion and excellent communication is both best for patient care and the best way to avoid an allegation of negligence. If an adverse event occurs, open communication, empathizing with patients, and addressing accountability and remediation may prevent a liability claim. However, if a suit occurs, the best defense comprises contemporaneous, comprehensive, and accurate documentation. © 2010 by The American College of Obstetricians and Gynecologists. Published by Lippincott Williams & Wilkins.

Nyholm J.L.,Gynecology and Womens Health | Schleiss M.R.,University of Minnesota
International Journal of Women's Health | Year: 2010

Human cytomegalovirus (CMV) infection is the most common cause of perinatal viral infection in the developed world, resulting in approximately 40,000 congenitally infected infants in the United States each year. Congenital CMV infection can produce varying degrees of neurodevelopmental disabilities. The significant impact of congenital CMV has led the Institute of Medicine to rank development of a CMV vaccine as a top priority. Vaccine development has been ongoing; however no licensed CMV vaccine is currently available. Treatment of pregnant women with CMV hyperimmune globulin has shown promising results, but has not been studied in randomized controlled trials. Education on methods to prevent CMV transmission, particularly among young women of child-bearing age, should continue until a CMV vaccine becomes available. The epidemiology, clinical manifestations, prevention strategies, and treatment of CMV infections are reviewed. © 2010 Nyholm and Schleiss.

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