Gynecol Obstet Invest. 2004;58(3):140-4. Epub 2004 Jun 15.
Comparison of pregnancy outcomes of progesterone or progesterone + estradiol for luteal phase support in ICSI-ET cycles.
Gorkemli H, Ak D, Akyurek C, Aktan M, Duman S.
ART Unit of Selcuk University, Meram Faculty of Medicine, Konya, Turkey.
OBJECTIVE: To find out the effect of estradiol with progesterone for luteal phase support in IVF-ICSI cycles. MATERIALS AND METHODS: Patients were accepted for treatment in the ART unit of Selcuk University, Meram Faculty of Medicine, between January 2001 and March 2003. The study was done in a prospective manner. The age range of 252 women was 19-41 years and the total number of cycles was 310. All patients were treated with a long ovulation induction protocol. Patients were treated and divided into two groups in a randomized manner: group I used only 600 mg/day divided into three equal doses of micronized progesterone vaginally, and group II used transdermal estradiol 100 microg/day + 600 mg/day vaginal micronized progesterone. RESULTS: 310 ICSI cycles were carried out in 252 infertile couples between January 2001 and March 2003. From 22 of these cycles, oocytes were retrieved but no embryos were developed. In the remaining 288 cycles there were embryo transfers. All embryo development was achieved by ICSI treatment. In 148 out of 288 cycles, the luteal phase was supported only by vaginal micronized progesterone (group I). On the other hand, the remaining 140 cycles received vaginal micronized progesterone plus transdermal estradiol 100 microg/day (group II). The number of beta-hCG-positive results in group I and group II were 20 (13.5 %) and 54 (38.5%) respectively. CONCLUSION: Adding estradiol to progesterone for luteal phase support in ICSI-ET cycles may increase implantation and pregnancy rates. Copyright (c) 2004 S. Karger AG, Basel.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15205566&dopt=Abstract estradiol [PubMed - in process]
Eur J Pharm Biopharm. 2004 Jul;58(1):131-5.
Uptake of estradiol or progesterone into the CSF following intranasal and intravenous delivery in rats.
van den Berg MP, Verhoef JC, Romeijn SG, Merkus FW.
Department of Pharmaceutical Technology and Biopharmaceutics, Leiden/Amsterdam Centre for Drug Research, Leiden University, Leiden, The Netherlands.
The uptake of estradiol and progesterone into the cerebrospinal fluid (CSF) after intranasal and intravenous administration in rats was investigated. Each animal received estradiol intranasally (40 microg/rat) and by intravenous infusion (10 microg/rat) into the jugular vein using a vascular access port. Hereafter, the same set of rats was treated with progesterone intranasally (200 microg/rat) and by intravenous infusion (104 microg/rat). Following nasal delivery, both steroid hormones reach Cmax values in plasma and CSF at 15 min after administration. Intravenous infusion of estradiol and progesterone shows comparable plasma and CSF concentration-time profiles compared to the nasal route. For both hormones the AUCCSF/AUCplasma ratios (mean +/- SD) after intranasal delivery (estradiol 2.3 +/- 1.1%; progesterone 1.9 +/- 0.7%) do not differ significantly from the ratios shown after intravenous infusion (estradiol 2.0 +/- 0.6%; progesterone 2.2 +/- 0.8%). These results indicate that after nasal delivery estradiol and progesterone are rapidly absorbed into the systemic circulation, from where the non-protein bound hormones probably enter the CSF by crossing the blood-brain barrier. No extra direct nose-CSF transport could be demonstrated. Copyright 2004 Elsevier B.V.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15207546&dopt=Abstract estradiol [PubMed - in process]
FASEB J. 2004 Aug;18(11):1252-4. Epub 2004 Jun 18.
Estradiol induces proliferation of keratinocytes via a receptor mediated mechanism.
Verdier-Sevrain S, Yaar M, Cantatore J, Traish A, Gilchrest BA.
Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts 02118-2394, USA.
In this study, we investigated the effects of estradiol on the proliferation of neonatal keratinocytes, the expression of estrogen receptor isoforms, and the signaling mechanisms by which estradiol mediates cell growth. We demonstrate that estradiol binds neonatal keratinocytes with high affinity (Kd=5.2nM) and limited capacity (Bmax of 14.2fmol/mg of protein), confirming the presence of estrogen binding sites. Using specific antibodies, we demonstrate that keratinocytes express both estrogen receptor (ER)-alpha and ER-beta. At physiological concentrations, estradiol up-regulates the level of ER-alpha receptors in keratinocytes and induces keratinocyte proliferation. The proliferative effect of estradiol requires the availability of functional estrogen receptors, as it is abrogated by anti-estrogen administration. Estradiol effect on keratinocyte proliferation is most likely mediated in part by activation of a nongenomic, membrane-associated, signaling pathway involving activation of the extracellular signal regulated kinases 1 and 2 and in part by the genomic signaling pathway through activation of nuclear receptors.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15208259&dopt=Abstract estradiol [PubMed - in process]
Neurobiol Aging. 2004 Aug;25(7):925-33.
Androgen receptor mRNA is inversely regulated by testosterone and estradiol in adult mouse brain.
Kumar RC, Thakur MK.
Biochemistry & Molecular Biology Laboratory, Department of Zoology, Banaras Hindu University, Varanasi 221005, India.
Androgen receptor (AR) is expressed in different tissues including the brain and is under regulation by sex steroid hormones. It mediates the action of androgen which plays a key role in learning, memory, and other brain functions that deteriorate with increasing age. We have correlated the expression of AR mRNA with its promoter methylation and their regulation by testosterone and estradiol in the brain cortex of adult and old male and female mice. Results revealed that (i) AR mRNA expression was significantly higher in male than in female mice. (ii) In both sexes, AR mRNA level was down-regulated by testosterone in adult and old, but up-regulated by estradiol only in adult mice. (iii) Methylation of AR core promoter was increased by testosterone, but decreased by estradiol. These findings show that AR mRNA expression and its core promoter methylation are inversely regulated by testosterone and estradiol in the adult mice brain cortex. Such regulation of AR expression might influence androgen action during aging of the mice brain.
Ginecol Obstet Mex. 2003 Nov;71:600-4.
[Prognostic values of oestradiol/oocyte rate in ICSI patients]
[Article in Spanish]
Galache Vega P, Saucedo de la Llata E, Trevino Rodriguez A, Santos Haliscak R, Batiza Resendiz VA, Arenas Montezco L, Moraga Sanchez MR, Sepulveda Gonzalez J, Leal Almeida M, Rodriguez Pezino J, Garcia Villafana G, Hernandez Ayup S.
Instituto para el Estudio de la Concepcion Humana, Monterrey, NL.
OBJECTIVES: To analyze the pregnancy rate in women who underwent Intracytoplasmic Sperm Injection (ICSI) program depending of the oestradiol/oocyte index. STUDY DESIGN: Retrospective, comparative. MATERIAL AND METHODS: 332 patients were included. There were divided in three groups depending on the oestradiol/oocyte index: Group A:(100 pg/mL, group B: 101-250 pg/mL and group C: > 250 pg/mL). Therapeutic protocol. Down regulation with leuprolide acetate in late luteal phase protocol, COH with rec-FSH and / or HMG, ultrasonographic and estradiol blood levels were monitored; hCG application when > 3 follicles > 18 mm, oocyte retrieval performed 34 hours later. We analyzed: patient age, male age, number of follicles, estradiol serum levels at the day of hCG application, number of mature oocytes, oestradiol/oocyte index, fertilization rate, transferred embryos, transfer quality, catheter type and luteal support. Statistical analysis (SPSS 11) with chi square, ANOVA and Kruskall-Wallis was used. RESULTS: On having analyzed the number of metaphase II oocytes retrieval, oocytes fertilized and number of transferred embryos among three groups, the best results were obtained in group B. The differences among these variables were significant. (P = 0.014, p = 0.005 and p = 0.003, respectively). When the oestradiol/oocyte index was analyzed and the PR among groups (21.83, 36.62 and 17.80 %) we observed a significant difference (p = 0.003). CONCLUSION: It is convenient to monitor the oestradiol blood levels to offer schemes of COH less aggressive to improve the oocyte quality
Water Res. 2004 Jul;38(12):2918-26.
Behavior of pharmaceuticals, cosmetics and hormones in a sewage treatment plant.
Carballa M, Omil F, Lema JM, Llompart M, Garcia-Jares C, Rodriguez I, Gomez M, Ternes T.
Department of Chemical Engineering, School of Engineering, University of Santiago de Compostela, E-15782 Santiago de Compostela, Spain.
Two cosmetic ingredients (galaxolide, tonalide), eight pharmaceuticals (carbamazepine, diazepam, diclofenac, ibuprofen, naproxen, roxithromycin, sulfamethoxazole and iopromide) and three hormones (estrone, 17beta-estradiol and 17alpha-ethinylestradiol) have been surveyed along the different units of a municipal Sewage Treatment Plant (STP) in Galicia, NW Spain. Among all the substances considered, significant concentrations in the influent were only found for the two musks (galaxolide and tonalide), two anti-inflammatories (ibuprofen and naproxen), two natural estrogens (estrone, 17beta-estradiol), one antibiotic (sulfamethoxazole) and the X-ray contrast medium (iopromide), where the other compounds studied were below the limit of quantification. In the primary treatment, only the fragrances (30-50%) and 17beta-estradiol (20%) were partially removed. On the other hand, the aerobic treatment (activated sludges) caused an important reduction in all compounds detected, between 35% and 75%, with the exception of iopromide, which remained in the aqueous phase. The overall removal efficiencies within the STP ranged between 70-90% for the fragrances, 40-65% for the anti-inflammatories, around 65% for 17beta-estradiol and 60% for sulfamethoxazole. However, the concentration of estrone increased along the treatment due to the partial oxidation of 17beta-estradiol in the aeration tank.
Brain Res. 2004 Jul 23;1015(1-2):1-8.
Response of tyrosine hydroxylase and GTP cyclohydrolase I gene expression to estrogen in brain catecholaminergic regions varies with mode of administration.
Serova LI, Maharjan S, Huang A, Sun D, Kaley G, Sabban EL.
Department of Biochemistry and Molecular Biology, New York Medical College, Valhalla, NY 10595, USA.
The effect of different dose, mode and duration of estradiol administration was examined in the different brain catecholaminergic areas in ovariectomized (OVX) female rats. We determined changes in mRNA levels of tyrosine hydroxylase (TH), rate-limiting enzyme in catecholamine (CA) biosynthesis of GTP cyclohydrolase I (GTPCH), rate-limiting enzyme in biosynthesis as well as of tetrahydrobiopterin (BH4), and concentration of BH4, which is an essential cofactor for TH, tryptophan hydroxylase and nitric oxide synthase. Short-term administration of estradiol benzoate (EB) by five injections of 15 or 40 microg/kg 12 h apart led to increase in TH and GTPCH mRNA levels in dopaminergic and noradrenergic cell bodies of the ventral tegmental area (VTA), substantia nigra (SN), locus coeruleus (LC) and the nucleus of solitary tract (NTS) depending on dose of administration. Estrogen-elicited alterations in BH4 concentrations were mostly correlated with changes in GTPCH mRNA levels, except in SN. Long-term administration of estradiol by injections (EB: 25 microg/kg, 16 injections 26 h apart; 50 microg/kg, 16 injections 48 h apart) or pellets (0.1 mg 17 beta-estradiol, 14 days) were not very effective in modulating mRNA levels for both genes in most locations except the NTS. Long-term injections of EB elevated GTPCH mRNA levels throughout the NTS and in microvessels. Administration of estradiol by pellets led to decline of TH mRNA in rostral-medial and elevation in caudal parts of the NTS. Thus, estradiol has a complex and differential effect on TH and GTPCH gene expression in a tissue specific manner and depends on the mode of administration.
Sheng Li Xue Bao. 2004 Jun 25;56(3):379-83.
[Possible involvement of caveolin-1 in the inhibition of endothelin-1 induced proliferation of vascular smooth muscle cells by 17beta-estradiol]
[Article in Chinese]
Tan Z, Lin GP, Wang TH.
Department of Physiology, College of Basic Medical Sciences, Sun Yat-Sen University, Guangzhou 510089, China; E-mail: thwanzsums.edu.cn
The aim of the present study was to investigate the role of caveolin-1 in the inhibition of endothelin-1 induced proliferation of vascular smooth muscle cells (VSMCs) by 17beta-estradiol. In the cultured rat thoracic aortic VSMCs, proliferation of VSMCs was determined by using [(3)H]-thymidine incorporation and the expression of caveolin-1 protein was measured by immunofluorescence assays and Western blotting. The measurement demonstate VSMCs exposed to various concentrations of endothelin-1 (1-100 nmol/L) for 24 h induced an increase in [(3)H]-thymidine incorporation. Pretreament with various concentrations of 17beta-estradiol (0.1-10 nmol/L) for 24 h inhibited the proliferation effect of endothelin-1. Immunofluorescence assays showed that after 24 h treatment of VSMCs with endothelin-1 (100 nmol/L), the expression of caveolin-1 in VSMCs was significantly increased, whereas pretreament with 17beta-estradiol (10 nmol/L) for 24 h inhibited the effect. Western blotting results further proved that endothelin-1 inhibited and 17beta-estradiol increased the expression of caveolin-1 in VSMCs. These results demonstrate that 17beta-estradiol inhibits the VSMCs proliferation induced by endothelin-1, and that the effect of estradiol is probably mediated by caveolin-1.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15224154&dopt=Abstract estradiol [PubMed - in process]
J Steroid Biochem Mol Biol. 2004 May;89-90(1-5):371-4.
A combined treatment with 1alpha,25-dihydroxy-vitamin D3 and 17beta-estradiol reduces the expression of heat shock protein-32 (HSP-32) following cerebral cortical ischemia.
Losem-Heinrichs E, Gorg B, Schleicher A, Redecker C, Witte OW, Zilles K, Bidmon HJ.
C.&O. Vogt Institute of Brain Research, University St. 1, 40225 Dusseldorf, Germany.
1alpha,25-(OH)(2)-vitamin D(3) (1,25-D(3)) and 17beta-estradiol are both known to act neuroprotectively in certain experimental in vitro and in vivo settings and it has been noted that both steroids lead to an upregulation of certain neurotrophic factors. Here, we studied the effects of 1alpha,25-(OH)(2)-vitamin D(3) or 17beta-estradiol or their combined application on heat shock protein-32 (HSP-32) distribution after focal cortical ischemia using the well established photothrombosis model. Heat shock protein-32 is a well-established marker of the cerebral oxidative stress response and contributes to neuroprotection by metabolising cytotoxic free heme to carbon monoxide, iron and biliverdin. Photothrombotically lesioned rats were injected i.p. 1h after injury with either 1 microg 1alpha,25-(OH)(2)-vitamin D(3)/kg or 7 microg 17beta-estradiol/kg or a combination of both steroids. Groups of non-lesioned steroid-treated rats and lesioned, solvent-treated rats served as controls. In contrast to non-lesioned rats, in lesioned animals a significant increase in heat shock protein-32 expression occurred which was slightly, but non-significantly altered in the groups treated either with 1alpha,25-(OH)(2)-vitamin D(3) or 17beta-estradiol alone when compared to the solvent-treated control group. Only the combined treatment with 1alpha,25-(OH)(2)-vitamin D(3) and 17beta-estradiol resulted in a significant reduction of glial heat shock protein-32 immunoreactivity within the lesion-remote cortical areas supplied by the affected middle cerebral artery (MCA), indicating that both steroids act synergistically in a protective man
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