Gynecology and obstetrics research : open journal最新文献

{"title":"Hyperuricemia as a Predictor of Perinatal Outcomes in Pregnancy Induced Hypertension","authors":"S. Khalil, S. H. Elshourbagy, Said Hamad, Essmat Hamdy Abo Zeid","doi":"10.17140/goroj-5-147","DOIUrl":"https://doi.org/10.17140/goroj-5-147","url":null,"abstract":"Copyright 2018 by Khalil SSH. This is an open-access article distributed under Creative Commons Attribution 4.0 International License (CC BY 4.0), which allows to copy, redistribute, remix, transform, and reproduce in any medium or format, even commercially, provided the original work is properly cited. cc Aim/Objective The aim of this study to determine the relationship between hyperuricemia and perinatal outcome in pregnancy induced hypertension. Material & Methods This prospective and observational study was carried out in the Department of Obstetrics & Gynecology of Tanta University. The study included (100) primigravida female patients in the third trimester (after 32 weeks gestation) with pregnancy induced hypertension .Serum uric acid assay was done then the patients were classified into three groups according to uric acid level; Group I (low hyperuricemia) uric acid below 25th percentile (<3.7 mg/dl ), group II (middle hyperuricemia) uric acid from 25th to 75th percentile (3.8 to 5.7 mg/dl ) and group III (high hyperuricemia) uric acid above 75th percentile (>5.8 mg/dl).","PeriodicalId":91488,"journal":{"name":"Gynecology and obstetrics research : open journal","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41945668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Developmental Environmental Exposure Alters the Epigenetic Features of Myometrial Stem Cells.","authors":"Qiwei Yang,&nbsp;Ayman Al-Hendy","doi":"10.17140/GOROJ-3-e005","DOIUrl":"https://doi.org/10.17140/GOROJ-3-e005","url":null,"abstract":"Uterine fibroids (UFs), are the most common pelvic tumors, occurring in 70-80% of all reproductive-aged women and are the leading indication for hysterectomy worldwide.1-3 Although UFs are benign tumors, they typically cause severe menstrual bleeding, pelvic pain, preterm labor, recurrent abortion, and infertility. Hysterectomy is currently the main treatment used in women who no longer desire childbearing.4-6 UFs are hormonally responsive to estradiol and progesterone as well as other steroid hormones, and regress after menopause.7 Although, the cause of UFs is largely unknown, several risk factors are linked to UF development, which include age, race and ethnicity, family history, body mass index (BMI), etc.7,8","PeriodicalId":91488,"journal":{"name":"Gynecology and obstetrics research : open journal","volume":"3 2","pages":"e1-e4"},"PeriodicalIF":0.0,"publicationDate":"2016-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5473610/pdf/nihms833932.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35098908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Developmental exposure to endocrine disrupting chemicals alters the epigenome: Identification of reprogrammed targets.","authors":"Lauren Prusinski,&nbsp;Ayman Al-Hendy,&nbsp;Qiwei Yang","doi":"10.17140/GOROJ-3-127","DOIUrl":"https://doi.org/10.17140/GOROJ-3-127","url":null,"abstract":"<p><p>Endocrine disruptions induced by environmental toxicants have placed an immense burden on society to properly diagnose, treat and attempt to alleviate symptoms and disease. Environmental exposures during critical periods of development can permanently reprogram normal physiological responses, thereby increasing susceptibility to disease later in life - a process known as developmental reprogramming. During development, organogenesis and tissue differentiation occur through a continuous series of tightly-regulated and precisely-timed molecular, biochemical and cellular events. Humans may encounter endocrine disrupting chemicals (EDCs) daily and during all stages of life, from conception and fetal development through adulthood and senescence. Though puberty and perimenopausal periods may be affected by endocrine disruption due to hormonal effects, prenatal and early postnatal windows are most critical for proper development due to rapid changes in system growth. Developmental reprogramming is shown to be caused by alterations in the epigenome. Development is the time when epigenetic programs are 'installed' on the genome by 'writers', such as histone methyltransferases (HMTs) and DNA methyltransferases (DNMTs), which add methyl groups to lysine and arginine residues on histone tails and to CpG sites in DNA, respectively. A number of environmental compounds, referred to as estrogenic endocrine disruptors (EEDs), are able to bind to estrogen receptors (ERs) and interfere with the normal cellular development in target tissues including the prostate and uterus. These EEDs, including diethylstilbestrol (DES), bisphenol A (BPA), and genistein (a phytoestrogen derived from soybeans), have been implicated in the malformation of reproductive organs and later development of disease. Due to the lack of fully understanding the underlying mechanisms of how environmental toxicants and their level of exposure affect the human genome, it can be challenging to create clear clinical guidance to address the potential health effects of lower-level exposures commonly experienced within the general population. In addition, human studies concerning environmental exposures are limited in feasibility by ethical concerns for human safety. Therefore, studies in animal models provide great opportunities to reveal links between early-life exposure to EDCs and related diseases. It has been shown that developmental exposure to EDCs, such as diethylstilbestrol (DES) and genistein, during reproductive tract development increases the incidence, multiplicity and overall size of uterine fibroids in the Eker rat model, concomitantly reprogramming estrogen-responsive gene expression. Importantly, EDC exposure represses enhancer of zeste 2 (EZH2) and reduces levels of the histone 3 lysine 27 trimethylation (H3K27me3) repressive mark through Estrogen receptor / Phosphatidylinositide 3-kinases / Protein kinase B non-genomic signaling in the developing uterus. More recent research id","PeriodicalId":91488,"journal":{"name":"Gynecology and obstetrics research : open journal","volume":"3 1","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2016-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.17140/GOROJ-3-127","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34331850","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential Co-Factor Role of Tobacco Specific Nitrosamine Exposures in the Pathogenesis of Fetal Alcohol Spectrum Disorder.","authors":"Valerie Zabala, Elizabeth Silbermann, Edward Re, Tomas Andreani, Ming Tong, Teresa Ramirez, Fusun Gundogan, Suzanne M de la Monte","doi":"10.17140/GOROJ-2-125","DOIUrl":"10.17140/GOROJ-2-125","url":null,"abstract":"<p><strong>Background: </strong>Cerebellar developmental abnormalities in Fetal Alcohol Spectrum Disorder (FASD) are linked to impairments in insulin signaling. However, co-morbid alcohol and tobacco abuses during pregnancy are common. Since smoking leads to tobacco specific Nitrosamine (NNK) exposures which have been shown to cause brain insulin resistance, we hypothesized that neurodevelopmental abnormalities in FASD could be mediated by ethanol and/or NNK.</p><p><strong>Methods: </strong>Long Evans rat pups were intraperitoneal (IP) administered ethanol (2 g/kg) on postnatal days (P) 2, 4, 6 and/or NNK (2 mg/kg) on P3, P5, and P7 to simulate third trimester human exposures. The Cerebellar function, histology, insulin and Insulin-like Growth Factor (IGF) signaling, and neuroglial protein expression were assessed.</p><p><strong>Results: </strong>Ethanol, NNK and ethanol+NNK groups had significant impairments in motor function (rotarod tests), abnormalities in cerebellar structure (Purkinje cell loss, simplification and irregularity of folia, and altered white matter), signaling through the insulin and IGF-1 receptors, IRS-1, Akt and GSK-3β, and reduced expression of several important neuroglial proteins. Despite similar functional effects, the mechanisms and severity of NNK and ethanol+NNK induced alterations in cerebellar protein expression differed from those of ethanol.</p><p><strong>Conclusions: </strong>Ethanol and NNK exert independent but overlapping adverse effects on cerebellar development, function, insulin signaling through cell survival, plasticity, metabolic pathways, and neuroglial protein expression. The results support the hypothesis that tobacco smoke exposure can serve as a co-factor mediating long-term effects on brain structure and function in FASD.</p>","PeriodicalId":91488,"journal":{"name":"Gynecology and obstetrics research : open journal","volume":"2 5","pages":"112-125"},"PeriodicalIF":0.0,"publicationDate":"2016-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5570438/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35303255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}