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Vrije Universiteit Amsterdam

1. Verhoeven, M.O. Menopause, menopausal therapies and asymmetric dimethylarginine, an emerging cardiovascular risk factor .

Degree: 2007, Vrije Universiteit Amsterdam

Oestrogenen en asymmetrische dimethylarginine Hart- en vaatziekten (HVZ) vormen de belangrijkste doodsoorzaak in de Westerse wereld. Premenopauzale vrouwen hebben een lager risico op HVZ dan mannen van dezelfde leeftijd, maar na de menopauze neemt de kans op HVZ bij vrouwen snel toe. Door de eierstokken geproduceerde hormonen (oestrogenen en progestagenen) spelen waarschijnlijk een rol bij de bescherming van premenopauzale vrouwen tegen HVZ en mogelijk kan toediening van deze hormonen na de menopauze vrouwen enigszins beschermen tegen de versnelde toename van het risico van HVZ. Asymmetrische dimethylarginine (ADMA) is een stof die door het lichaam zelf wordt gemaakt. Een hoge concentratie van ADMA vermindert een goed functioneren van de bloedvaten en leidt tot een verhoogde kans op HVZ. Of ADMA ook een rol speelt bij de verhoogde kans op HVZ na de menopauze is nog niet eerder onderzocht. Dit proefschrift behandeld het onderzoek naar de relatie tussen oestrogenen en aan oestrogeen verwante stoffen en ADMA bij vrouwen van middelbare leeftijd. Er werd gekeken naar de invloed van de menopauze en naar de effecten van verschillende (hormonale) menopauzale therapieën op ADMA concentraties. De voornaamste bevinding was dat hogere oestrogeen concentraties gepaard gaan met lagere ADMA concentraties. Het ADMA verlagende effect van oestrogeensuppletie was groter bij orale toediening dan bij gebruik van pleisters of spray en bovendien afhankelijk van de gebruikte oestrogeen/progestageen combinatie. Hoewel dit onderzoek laat zien dat vrouwelijke geslachtshormonen ADMA spiegels in gunstige zin beïnvloeden, moeten de klinische consequenties hiervan nog nader onderzocht worden.

Subjects/Keywords: Menopausal therapy and asymmetric dimethylarginine; Menopause; Menopausal therapies; asymmetric dimethylarginine; cardiovascular risk factor; (o)estradiol

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Verhoeven, M. O. (2007). Menopause, menopausal therapies and asymmetric dimethylarginine, an emerging cardiovascular risk factor . (Doctoral Dissertation). Vrije Universiteit Amsterdam. Retrieved from http://hdl.handle.net/1871/12930

Chicago Manual of Style (16th Edition):

Verhoeven, M O. “Menopause, menopausal therapies and asymmetric dimethylarginine, an emerging cardiovascular risk factor .” 2007. Doctoral Dissertation, Vrije Universiteit Amsterdam. Accessed December 06, 2019. http://hdl.handle.net/1871/12930.

MLA Handbook (7th Edition):

Verhoeven, M O. “Menopause, menopausal therapies and asymmetric dimethylarginine, an emerging cardiovascular risk factor .” 2007. Web. 06 Dec 2019.

Vancouver:

Verhoeven MO. Menopause, menopausal therapies and asymmetric dimethylarginine, an emerging cardiovascular risk factor . [Internet] [Doctoral dissertation]. Vrije Universiteit Amsterdam; 2007. [cited 2019 Dec 06]. Available from: http://hdl.handle.net/1871/12930.

Council of Science Editors:

Verhoeven MO. Menopause, menopausal therapies and asymmetric dimethylarginine, an emerging cardiovascular risk factor . [Doctoral Dissertation]. Vrije Universiteit Amsterdam; 2007. Available from: http://hdl.handle.net/1871/12930


University of Florida

2. Singh, Meharvan, 1967-. The Role of estradiol as a neurotrophomodulatory substance for basal forebrain cholinergic neurons of the female Sprague-Dawley rat.

Degree: 1994, University of Florida

Subjects/Keywords: Brain; Cholinergics; Estrogens; Hippocampus; Learning; Messenger RNA; Neurons; Ovariectomy; Rats; Receptors; Brain  – physiology ( mesh ); Brain-Derived Neurotrophic Factor  – metabolism ( mesh ); Choline  – metabolism ( mesh ); Choline O-Acetyltransferase  – metabolism ( mesh ); Department of Pharmacodynamics thesis Ph.D ( mesh ); Estradiol  – pharmacology ( mesh ); Estradiol  – physiology ( mesh ); Learning ( mesh ); Memory ( mesh ); Nerve Growth Factors  – metabolism ( mesh ); Rats, Sprague-Dawley ( mesh ); Research ( mesh )

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Singh, Meharvan, 1. (1994). The Role of estradiol as a neurotrophomodulatory substance for basal forebrain cholinergic neurons of the female Sprague-Dawley rat. (Thesis). University of Florida. Retrieved from http://ufdc.ufl.edu/AA00011788

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Singh, Meharvan, 1967-. “The Role of estradiol as a neurotrophomodulatory substance for basal forebrain cholinergic neurons of the female Sprague-Dawley rat.” 1994. Thesis, University of Florida. Accessed December 06, 2019. http://ufdc.ufl.edu/AA00011788.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Singh, Meharvan, 1967-. “The Role of estradiol as a neurotrophomodulatory substance for basal forebrain cholinergic neurons of the female Sprague-Dawley rat.” 1994. Web. 06 Dec 2019.

Vancouver:

Singh, Meharvan 1. The Role of estradiol as a neurotrophomodulatory substance for basal forebrain cholinergic neurons of the female Sprague-Dawley rat. [Internet] [Thesis]. University of Florida; 1994. [cited 2019 Dec 06]. Available from: http://ufdc.ufl.edu/AA00011788.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Singh, Meharvan 1. The Role of estradiol as a neurotrophomodulatory substance for basal forebrain cholinergic neurons of the female Sprague-Dawley rat. [Thesis]. University of Florida; 1994. Available from: http://ufdc.ufl.edu/AA00011788

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

3. Karman, Bethany. Toxicity of TCDD in the mouse antral follicle.

Degree: PhD, 5274, 2012, University of Illinois – Urbana-Champaign

The persistent environmental contaminant, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a potent ovarian toxicant. These studies were designed to characterize the actions of TCDD on steroidogenesis, growth, and atresia of intact mouse antral follicles in vitro. Interestingly, TCDD has been shown to act mainly through binding to the aryl hydrocarbon receptor (AHR) in other tissues, and the AHR has been identified as an important factor in ovarian function. Thus, these studies were also designed to test the hypothesis that TCDD activates the AHR in antral follicles. Specifically, these studies were designed to test the hypothesis that TCDD exposure leads to decreased sex hormone production/secretion by antral follicles as well as decreased growth of antral follicles in vitro. Mouse antral follicles were exposed for 96 hours to a series of TCDD doses previously shown to have effects on ovarian tissues and cells in culture and to encompass environmentally relevant and pharmacological exposures (0.1-100nM). The results indicate that TCDD decreases progesterone (P), androstenedione (A4), testosterone (T), and estradiol (E2) levels in a dose response manner without altering growth of antral follicles. The 1nM dose of TCDD consistently lowered all four hormones measured. Thus, this dose was chosen to study more closely the mechanism of TCDD toxicity in the antral follicle. Interestingly, the addition of pregnenolone substrate (10μM) restores hormone levels to control levels, suggesting that TCDD has actions upstream of progesterone production. Thus, the next goal of these studies was to determine the mechanism by which TCDD inhibits steroidogenesis and whether this occurs in a time dependent manner. Specifically, experiments were designed to compare the effects of 48 and 96 hours TCDD exposure on hormone production/secretion, steroidogenic enzymes, atresia ratings, expression of members of the apoptotic pathway, and expression of the AHR and cytochrome P450, family 1, subfamily b, polypeptide 1 (Cyp1b1). TCDD exposure for 48 hours increased levels of A4, without changing HSD3B1 protein, HSD17B1 protein, estrone (E1), T or E2 levels. Further, TCDD did not alter atresia rating, but it did down-regulate the AHR protein compared to vehicle. TCDD exposure for 96 hours decreased transcript levels for Cyp11a1, Cyp17a1, Hsd17b1, and Cyp19a1, but increased Hsd3b1 transcript. TCDD exposure particularly lowered both Hsd17b1 transcript and HSD17B1 protein. However, TCDD exposure did not affect levels of E1 in the media. The down regulation of the AHR protein in TCDD exposed follicles persisted and Cyp1b1 transcripts were increased by 3-4 fold. Interestingly, levels of the proapototic factor, BCL2-associated X protein (Bax) were significantly reduced without affecting atresia ratings in antral follicles following TCDD exposure, suggesting an altered apoptotic pathway in exposed antral follicles. Finally, because Cyp1b1 is an important enzyme that is implicated in both biotransformation of TCDD and also in E2… Advisors/Committee Members: Flaws, Jodi A. (advisor), Flaws, Jodi A. (Committee Chair), Bahr, Janice M. (committee member), Bunick, David (committee member), Nardulli, Ann M. (committee member), Tischkau, Shelley Ann (committee member).

Subjects/Keywords: ovary; antral follicle; aryl hydrocarbon receptor; proliferation; apoptosis; atresia; steroidogenesis; Estradiol 17-beta-dehydrogenase 1 (HSD17B1); catechol-o-methyltransferase (COMT); embryonic ovary; kinesin family member 11 (Kif11); X-inactive specific transcript (Xist); female germ cells; mouse; 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)

…x28;17-beta) dehydrogenase 1 (HSD17B1) to estradiol-17β (E2), or… …ovulation, decreased circulating estradiol levels (E2), early reproductive senescence… …x29; HSD17B1 ESTRONE (E1) CYP19A1 17β-ESTRADIOL (E2) CYP19A1… …in the 2-, 4-, and 16[alpha ]-hydroxylation of 17[beta ]estradiol… …mechanisms involving estradiol regulation and responsiveness. Biol Reprod 76, 1062-1070. Beischlag… 

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Karman, B. (2012). Toxicity of TCDD in the mouse antral follicle. (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/34311

Chicago Manual of Style (16th Edition):

Karman, Bethany. “Toxicity of TCDD in the mouse antral follicle.” 2012. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed December 06, 2019. http://hdl.handle.net/2142/34311.

MLA Handbook (7th Edition):

Karman, Bethany. “Toxicity of TCDD in the mouse antral follicle.” 2012. Web. 06 Dec 2019.

Vancouver:

Karman B. Toxicity of TCDD in the mouse antral follicle. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2012. [cited 2019 Dec 06]. Available from: http://hdl.handle.net/2142/34311.

Council of Science Editors:

Karman B. Toxicity of TCDD in the mouse antral follicle. [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2012. Available from: http://hdl.handle.net/2142/34311

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