• Journal of Aquaculture
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• v.6 no.2
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• pp.125-132
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• 1993

To determine the effective dose of $17\beta-estradiol$ on the production of all female populations of Nile tilapia, Oreochromis niloticus, the first feeding-stage larvae were fed 0, 60, 120, 240 and 480 ppm of $17\beta-estradiol$ in the diet for 30 days. Rates of sex reversal, survival and growth of each treated group were analyzed. Effects of 3 different treatment durations, 10, 20 and 30 days, treated with 480 ppm $17\beta-estradiol$ in the diet to produce all females, were also evaluated. The incidence of female fish were clearly dose and time dependent. The female induction rate of 0, 60, 120, 240 and 480 ppm were 47.5, 86.4, 91.3, 97.0 and $100\%$, respectively. Female induction rates of 480 ppm treated for 10, 20 and 30 days were 64.2, 84.3 and $100\%$ respectively. The survival rate of each treated group was not different from the control, and the growth rates of the treatment groups decreased as the treatment duration and the concentration of the estrogen hormone increased.

• Korean Journal of Veterinary Service
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• v.31 no.4
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• pp.457-463
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• 2008

The sex steroid hormone estradiol-$17{\beta}(E_2)$ mediate their biological effects on development, differentiation and maintenance of reproductive tract and other target tissue through gene regulation by nuclear steroid receptors. Although the importance of $E_2$ in many physiological process has been reported, but little is known about the effects of $E_2$ on primary cultured chicken hepatocyte. therefore, in the present study, we have examined the effect of $E_2$ on cell proliferation and it's related signal cascades. $E_2$ increase $[^3H]$-thymidine incorporation in time-(${\leq}8hr$) and dose-($10^{-10}M$)dependent manner and treatment of $E_2$ increased the phosphorylation of p44/43 MAPKs(p44/42 mitogen-activated protein kinase) and JNK(c-Jun N-terminal kinase) in a time dependent manner. In addition, PD98059(p44/42 blocker, $10^{-5}M$), SP600125(JNK blocker, $10^{-6}M$) blocked the estrogen-induced increase in $[^3H]$-thymidine incorporation. In conclusion, $E_2$ stimulates the proliferation of primary cultured chicken hepatocytes and this action is mediated by p44/42 MAPKs and JNK signal transduction pathway.

• Korean Journal of Animal Reproduction
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• v.27 no.4
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• pp.281-285
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• 2003

This study was carried out to find out the changes on serum concentrations of estradiol-17$\beta$, progesterone in primiparous Duroc, Landrace and Yorkshire sows weaned at 7 or 21 days. Also, we compared the litter size at birth and weaning among the breeds weaned after lactation for 7 or 21 days. The estradiol-17$\beta$ concentrations among the breeds were 6.9∼8.8 pg/ml and 6.4∼8.8 pg/ml after lactation for 7 or 21 days, respectively. The progesterone concentrations ranged from 0.3 ng/ml to 1.6 ng/ml. Duroc sow showed higher progesterone concentration compared with Landrace and Yorkshire sows weaned after lactation for 7 or 21 days. Also, we found out that litter size at birth and weaning, respectively, did not show any differences between day 7 and day 21 of lactation. From the facts mentioned above, it was suggested that very early weaning systems could work with no apparent adverse effect on prolificacy.

• The Journal of Korean Medicine
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• v.21 no.4
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• pp.9-15
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• 2000

Objective : The aim of this study was to investigate the neuroprotection effect of estrogen on brain atrophy following cerebral infarction. Method : All animals in this study were classified into 4 groups; ovariectomy group (OVXgroup), cerebral infarction group (INF group), combination ovariectomy and cerebral infarction group (OVX + INF group), and naturally intact group for control data (NOR group). Cerebral infarction was made by Chen's method with some modification. Ovariectomy was performed by Wayforth's method. Experimental data for each group was collected at 15 days, month, 3 months, and 6 months after starting observation. Serum $17{\beta}-estradiol(E2)$ was determined by radioimmunoassay. Brain volume was measured and calculated with image analysis. Each brain was sliced at intervals of 2mm in chamber after 30 min of freezing in refregerater. Cerebral volume was obtained by sum of volume of each slice level, which was mean $area{\;}{\times}{\;}2mm$. Results : Cerebral ischemia was found to decrease the serum concentration of $17{\beta}-{\;}estradiol(E2)$ and to inhibit the physiologically conpensatary function of the ovariectomized rats. Also we found that deprivation of estrogen have resulted in more severe cerebral atrophy followed by cerebral infarction. Conclusion : It is suggested that estrogen has a neuroprotection effect on cerebral atrophy following cerebral infarction.

• Korean Journal of Animal Reproduction
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• v.22 no.1
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• pp.29-34
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• 1998

Jugular plasma concentrations of luteinizing hormone, prolactin, estradiol-17\ulcorner and 13, 14-dihydro-15-keto-prostaglandin-F2봬(PGFM) were meausred prepartum during the last 12 days of pregnancy, at parturition, then 1 day after parturition in 16 goats. Plasma samples were analyzed for luteinizing hormone(LH), estradiol-17\ulcorner(E2), prolactin(PRL) and prostagladin F2봬(PGF2봬) concentrations by radioimmunoassay. 1. The concentrations of plasma luteinizing hormone in Korean native goats remained fairly constant(0.20 0.02\ulcorner0.38 0.04 mlu/ml) from 12 days prepartum to 1 postpartum but the concentrations of plasma prolactin rose slightly from 1 day prepartum. 2. The estradiol-17\ulcorner concentrations increased rapidly after day 1 before partum, reaching a peak at parturition(74.8 77.5 pg/ml), and falling to 63.8 2.8 pg/ml at day 1 postpartum. 3. Starting at 323.2 69.6 twelve days before parturition, the concentrations of plasma prostaglandin F2봬 rose during the 1 day preceeding parturition(650.7봬57.8 pg/ml) and peaked at 1081.4 164.9 on the day of parturition. At day 1 postpartum, the concentrations of PGF2봬 decreased to 425.3 60.4 pg/ml. Finally, these results show that changes in prostaglandin F2봬 concentrations before parturition were closely related to changes in estradiol-17\ulcorner concnetrations, but after parturition they remained elevated whereas estradiol-17\ulcorner concentrations fell abruptly.

• Animal cells and systems
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• v.4 no.1
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• pp.71-76
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• 2000

The aim of this study was to investigate expression patterns of the prolactin (PRL) and c-fos genes by 17$\beta$-estradiol (17$\beta$-E) and stress in the mouse pituitary. In the pituitary, the levels of PRL mRNA were found high with some fluctuation at 30, 50, and 90 min whereas the levels of PRL mRNA were low at 120 min when ovariectomized female mice were injected with 17$\beta$-E or vehicle. PRL mRNA levels began to increase again at 4 h and remained high up to 24 h only in the 17$\beta$-E- treated mice. The overall changes in c-fos mRNA by 17$\beta$-E were very similar to those in PRL mRNA in the pituitary. Subsequent study revealed that these high initial levels of PRL and c-fos mRNAs were caused by stress during Injection, not by 17$\beta$-E, since vehicle injection alone into the ovariectomized mice could increase the levels of PRL and c-fos mRNAs. The stress-induced elevations of PRL and c-fos mRNAs were inhibited by bromocriptin, a dopamine agonist, suggesting that the dopaminergic system is involved in the action route of injection stress. In addition, the induced levels of c-fos mRNA by 17$\beta$-E and stress in the pituitary were very low compared with those in the uterus. The time course changes in c-fos mRNA level were different between the pituitary and uterus. Taken together, these data indicate that PRL and c-tos gene expression in the pituitary are regulated by 17$\beta$-E and stress in a parallel manner, supporting the notion that c-Fos plays a role in regulation of PRL gene expression.

• 한국생물공학회:학술대회논문집
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• 2005.04a
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• pp.88-92
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• 2005

Aptamer is the single-stranded oligonucleotide which binds to various target molecules such as proteins, peptides, lipids and small organic molecules with high affinity and specificity. DNA aptamers specific for the $17{\beta}-estradiol$ were selected by SELEX (Systematic Evolution of Ligands by EXponential enrichment) process from a random DNA library. These DNA aptamers have a high affinity to $17{\beta}-estradiol$ as an endocrine disrupting chemical. Nanowell and $200{\mu}m$ gold electrode were used as substrate for DNA aptamer immobilization and electrochemical analysis. Especially, nanowell gold electrode was fabricated by e-beam lithography. The size of single nanowell is 130nm and 40,000 nanowells were deposited on one gold electrode. The immobilization method was based on the interaction between the biotinylated aptamer and streptavidin deposited on gold electrode previously. Immobilization procedure was optimized by surface plasma resonance (SPR) and electrochemical analysis. After the immobilization of DNA aptamer on streptavidin modified gold electrode, $17{\beta}-estradiol$ solution was treated on aptamer immobilized gold electrode. The current of gold electrode was decreased by the binding of $17{\beta}-estradiol$ to DNA aptamer immobilized on gold electrode. However, in negative control experiments of 1-aminoanthraquinone and 2-methoxynaphthalene, the current was rarely decreased. And more sensitive data was obtained from nanowell gold electrode comparing with $200{\mu}m$ gold electrode.

• Korean Journal of Veterinary Research
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• v.26 no.1
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• pp.31-37
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• 1986

The present study has been carried out to elucidate the antiestrogenic effects of tamoxifen on RNA and protein synthesis in uteri of immature rats. Immature female Sprague-Dawley rats were allocated into 4 groups and injected with $5{\mu}g$ of estradiol-$17{\beta}$, $50{\mu}g$ of tamoxifen, a combination of both, or vehicle only subcutaneously three times with an interval of 24 hours respectively. The specific activities of $^3H$-uridine incorporation into uterine RNA and those of $^3H$-leucine incorporation into uterine protein were measured before and 1, 3, 6, 12, 24, 48 and 72 hours after the above treatments. The results obtained were summarized as follows; 1. Tamoxifen itself increased RNA synthesis an hour after treatment(169.18% of control), but it's specific activity was reduced to control level after 3 hours. Tamoxifen inhibited significantly (p<0.01) the activity of RNA synthesis of estradiol-$17{\beta}$. 2. The increasing rate of protein synthesis was lower in tamoxifen treated group than that in estradiol-$17{\beta}$ treated group. While the rate was steadily increased up to 357.4% of control by estradiol-$17{\beta}$ in 72 hours, tamoxifen itself failed to increase the rate after 24 hours and significantly (p<0.01) inhibited the activity of estradiol-$17{\beta}$(-167.4%).

• Applied Biological Chemistry
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• v.49 no.3
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• pp.196-201
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• 2006

Vitellogenin, which is found in the serum of female and male fishes exposed to environmental endocrine disrupter or estrogen hormone, is used as a biomarker for environmental contamination with an endocrine disrupter. In order to produce antibody against vitellogenin, a synthetic peptide for partial vitellogenin was injected into rabbits. In addition, by using ion exchange chromatography on DE-52, vitellogenin was purified from the serum of carp induced with $17{\beta}$-estradiol. Polyclonal antibody against purified vitellogenin reacted well with vitellogenin in the serum of carp induced with $17{\beta}$-estradiol and the serum of female carp, whereas polyclonal antibody against the vitellogenin peptide did not react with proteins in those samples. This may indicate that vitellogenin proteins, covalently modified largely, could not be detected by Western blotting with the polyclonal antibody against the synthetic vitellogenin peptide.

• Korean Journal of Veterinary Research
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• v.25 no.2
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• pp.187-195
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• 1985

The Present study has been carried out to elucidate the antiestrogenic effects of tamoxifen in uteri of immature rats. Immature female Sprague-Dawley rats were allocated into 4, groups and injected with $5{\mu}g$ of estradiol-$17{\beta}$, $50{\mu}g$ of tamoxifen, a combination of both or vehicle only subcutaneously three times after an interval of 24 hours respectively. The concentrations, of cytosol estradiol receptor in uterus were measured by DCC method before and 1, 3, 6, 12, 24, 48 and 72 hours after the above treatments and those of nuclear estradiol were measured by protamine exchange method 72 hours and those of nuclear estradiol were measured by protamine exchange method 72 hours after the above treatments. The results obtained were summarized as follows: 1. The binding affinity of tamoxifen to estradiol receptor in uterine cytosol was lower than that of estradiol-$17{\beta}$, accordingly the translocation of estradiol receptor into the nucleus was found to be delayed. 2. Tamoxifen caused the retention of estradiol receptor in nucleus over 24 hours and inhibited the replenishment of the receptor from nucleus to cytosol in uterus.