17 beta estradiol/atrofija

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17 beta-estradiol treatment retards excitotoxic delayed degeneration in substantia nigra reticulata neurons.

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Estrogen treatment offers neuro-protection in animal experiments in which excitotoxic mechanisms destroy neurons. In a model of delayed neuronal degeneration that depends on excitotoxicity, we tested whether females had an altered susceptibility, and whether physiologic doses of estrogen

Low-dose 17-β-estradiol cream for vaginal atrophy in a cohort without prolapse: Serum levels and vaginal response including tissue biomarkers associated with tissue remodeling.

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OBJECTIVE Describe the effect of 50 mcg vaginal 17-β-estradiol (E2) cream on vaginal maturation, serum estrogen levels, atrophic symptoms, and biomarkers of oxidative stress and tissue remodeling in postmenopausal women without prolapse. METHODS Seventeen women, 65 years or older, applied

[DEGENERATION AND NECROSIS OF THE LIVER AND KIDNEY IN RATS AFTER THE ADMINISTRATION OF HIGH DOSES OF 17-BETA-ESTRADIOL AND ESTRIOL].

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Long-term effects of melatonin or 17 beta-estradiol on improving spatial memory performance in cognitively impaired, ovariectomized adult rats.

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Melatonin is an endogenously generated potent antioxidant. Our previous studies indicate that melatonin improved learning and memory deficits in APP695 transgenic mouse of Alzheimer's disease. An ovariectomized (OVX) rat model which is characterized by progressive memory deficits, central

Androgen and estrogen production in elderly men with gynecomastia and testicular atrophy after mumps orchitis.

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Gynecomastia developed in three men 1-30 yr after the occurrence of testicular atrophy due to mumps orchitis. At the time of study, these men were 63-68 yr of age. In these men the mean plasma production rate of testosterone was 816 microgram/24 h, a value 20% of that found in normal elderly men

The postnatal ontogeny of rat uterine glands and age-related effects of 17 beta-estradiol.

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In the uterus of the newborn rat, only the luminal epithelium is differentiated. Differentiation of musculature and glandular epithelium occurs postnatally, the latter originating as invaginations of the luminal epithelium into the stroma. Using unambiguous criteria for quantification of uterine

90-day feeding and one-generation reproduction study in Crl:CD BR rats with 17 beta-estradiol.

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Over the past several years, there has been increasing concern that chemicals and pesticides found in the environment may mimic endogenous estrogens, potentially producing adverse effects in wildlife and human populations. Because estrogenicity is one of the primary concerns, a 90-day/one-generation

Effect of growth factors on DNA labeling and cytoskeletal protein expression in 17-beta-estradiol and basic fibroblast growth factor pre-treated astrocyte cultures.

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Astrocytes react to all noxae which damage neurons. Their reactions include degeneration, hypertrophy, hyperplasia and fibre formation. Growth factors inducing proliferation and differentiation of both neurons and astrocytes in culture play a pivotal role in the dynamic flow of signaling molecules

Effect of 17-beta-estradiol on dopamine, serotonine and GABA striatal levels in 6-hydroxydopamine-treated rats.

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Intrastriatal injection (16microg) of the neurotoxic dopaminergic agent 6-hydroxydopamine (6-OHDA) in ovariectomized rats caused important reductions in striatal dopamine (DA) and serotonin (5-HT) levels and an increase in GABA content. Treatment of ovariectomized rats with estradiol (5 mg

Endocrine disrupting effects of low dose 17 β-estradiol (E2) on the Japanese quail (Coturnix japonica) were detected by modified one-generation reproduction study.

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Previously, we investigated endocrine disrupting effects of 17 β-estradiol (E(2)) on Japanese quail (Coturnix japonica) in the avian reproduction test according to the testing guidelines, in which new endpoints such as blood vitellogenin (VTG) concentration in parent quails and pathology of F(1)

Effects of dietary 17 beta-estradiol exposure on serum hormone concentrations and testicular parameters in male Crl:CD BR rats.

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A 90-day/one-generation reproduction study was conducted in male and female Crl:CD BR rats using dietary levels of 0, 0.05, 2.5, 10, and 50 ppm 17 beta-estradiol. The goals of this study were to set dose levels and evaluate several mechanistic endpoints for inclusion in multigeneration reproduction

17 beta-estradiol for postmenopausal estrogen replacement therapy.

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After physiological or surgical menopause, women are suddenly deficient in their main estrogenic hormone, 17 beta-estradiol. Only a very small amount of estradiol is still produced from adrenal precursors. More than 50 per cent of all postmenopausal women suffer for varying periods of time from the

2,3,7,8-Tetrachlorodibenzo-p-dioxin-induced thymic atrophy and lymphocyte stem cell alterations by mechanisms independent of the estrogen receptor.

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2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has both agonist and antagonist effects on estrogen-mediated activities and estrogen receptor (ER) levels in epithelial tissues following exposure. We previously demonstrated that TCDD alters bone marrow lymphocyte stem cells, including prothymocytes, as

A rehabilitation exercise program to remediate skeletal muscle atrophy in an estrogen-deficient organism may be ineffective.

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To determine rehabilitation exercise program effects under hormone deficient (ovariectomy or OVX) and hormone supplemented [OVX + 17-beta estradiol (E2)] conditions. Mature female rats (n = 123) were assigned to OVX or OVX + E2-supplemented groups. OVX and OVX + E2 groups were allocated to one of

Low-dose, vaginally administered estrogens may enhance local benefits of systemic therapy in the treatment of urogenital atrophy in postmenopausal women on hormone therapy.

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BACKGROUND When genital atrophy exists, systemic hormone therapy (HT) has a timing until to induce vaginal proliferation and symptomatic relieve. Thus, in order to obtain a prompt improvement, the association of local therapy acting on the genital epithelium to the systemic treatment should be

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