• Clinical and Experimental Reproductive Medicine
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• v.29 no.4
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• pp.251-258
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• 2002

Objective : The aim of this study was to evaluate the outcomes of the GnRH antagonist (Cetrotide) minimal stimulation protocol comparing with GnRH agonist combined long step down stimulation protocol in PCOS patients. Materials and Method: From Apr 2001 to May 2002, 22 patients (22 cycles) were performed in controlled ovarian hyperstimulation using by GnRH antagonist and GnRH agonist for PCOS patients. GnRH antagonist (Cetrotide) combined minimal stimulation protocol was administered in 10 patients (10 cycles, Study Group) and GnRH agonist long step down stimulation protocol was administered in 12 patients (12 cycles, Control Group). We compared the pregnancy rate/cycle, total FSH (A)/cycle, Retrieved oocyte/cycle, the incidence of ovarian hyperstimulation syndrome, multiple pregnancy rate between the two groups. Student-t test were used to determine statistical significance. Statistical significance was defined as p<0.05. Results: Group of GnRH antagonist (Cetrorelix) minimal stimulation protocol produced fewer oocytes (6.4 versus 16.3 oocytes/cycle) using a lower dose of FSH (22.2 versus 36.1 Ample/cycle) and none developed OHSS and multiple pregnancy. Although the trends were in favour of the GnRH antagonist (Cetrorelix) protocol, the differences did not reach statistical significance. This was probably due to small sample size. Conclusion: The use of GnRH antagonist reduce the risk of ovarian hyperstimulation and multiple pregnancy. We suggest that GnRH antagonist might be alternative controlled ovarian hyperstimulation method, especially in PCOS patients who will be ovarian high response.

• Asian-Australasian Journal of Animal Sciences
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• v.11 no.1
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• pp.78-83
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• 1998

The objective of this study was to investigate the responsiveness of hypophysis and gonads to synthetic GnRH among prepubertal buffalo heifers at 12 months of age. Peripheral plasma FSH, LH, estradiol and progesterone level were measured in blood samples collected at 1 hr before and up to 18 days subsequent to the administration of $200{\mu}g$ GnRH (n=6) or saline (n=6) in Murrah buffalo heifers. The pretreatment peripheral plasma FSH, LH, estradiol and progesterone among GnRH treated heifers were $7.35{\pm}0.45ng/ml$, $1.08{\pm}0.3ng/ml$, $22.93{\pm}1.06pg/ml$ and $0.27{\pm}0.04ng/ml$ respectively. A quick elevation (p < 0.01) of FSH and LH within five min of GnRH administration was observed in all geifers. Although the peak FSH $(89.57{\pm}23.43ng/ml)$ and LH $(7.52{\pm}3.08ng/ml)$ reached by 10 min of GnRH administration, yet the animals differed both in terms of their amplitude response of FSH and LH release as well as in terms of time which animals took to exhiit maximum response to GnRH administration. The GnRH administration did not cause alteration in plasma estradiol and progesterone level. The present study suggests that the pituitary of 12 month buffalo heifers has capacity to synthesize and store of gonadotropin and have developed receptors for GnRH for a spike of gonadotropin release.

• Journal of Veterinary Clinics
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• v.20 no.2
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• pp.212-219
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• 2003

The effect of GnRH and/or hCG on the implantation, pregnancy, and the concentration of plasma estradiol and progesterone were studied in pregnant rats. GnRH 50, or 100ug and/or hCG 50 or 100 IU were administered once on day 2 or 9 of gestation, respectively. Rats were autopsied on days 8 or 16. Administration of GnRH on day 2 did not induce the prevention of implantation and termination of pregnancy but was able to induce termination of pregnancy administering on day 9. Administration of hCG induced delayed implantation on day 2 and termination of pregnancy on day 2 and 9. Administration of GnRH concomitant with hCG had no effect on prevention of implantation on day 2 but induced termination of pregnancy with a very increased fetal resorption on day 2 and with a moderate increased fetal resorption on day 9. Administration of GnRH concomitant with hCG on day 2 induced more increased termination of pregnancy compared to injection of GnRH or HCG and opposite result was observed on day 9. Plasma estradiol and progesterone concentrations by administering GnRH and/or hCG had no effect on the termination of pregnancy the pregnant rats.

• BMB Reports
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• v.45 no.10
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• pp.554-559
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• 2012

Oligosaccharide modification by N-acetylglucosaminyltransferase-V (GnT-V), a glycosyltransferase encoded by the Mgat5 gene that catalyzes the formation of ${\beta}1$,6GlcNAc (N-acetylglucosamine) branches on N-glycans, is thought to be associated with cancer growth and metastasis. Overexpression of GnT-V in cancer cells enhances the signaling of growth factors such as epidermal growth factor by increasing galectin-3 binding to polylactosamine structures on receptor N-glycans. In contrast, GnT-V deficient mice are born healthy and lack ${\beta}1$,6GlcNAc branches on N-glycans, but develop immunological disorders due to T-cell dysfunction at 12-20 months of age. We have developed Mgat5 transgenic (Tg) mice (GnT-V Tg mice) using a ${\beta}$-actin promoter and found characteristic phenotypes in skin, liver, and T cells in the mice. Although the GnT-V Tg mice do not develop spontaneous cancers in any organs, there are differences in the response to external stimuli between wild-type and GnT-V Tg mice. These changes are similar to those seen in cancer progression but are unexpected in some aspects. In this review, we summarize what is known about GnT-V functions in skin and liver cells as a means to understand the physiological roles of GnT-V in mice.

• Journal of Veterinary Clinics
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• v.3 no.1
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• pp.227-233
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• 1986

A total of 600 Holstein cows in Chonnam province was examined to make a diagnosis on the ovarian follicular cyst. By clinical signs and rectal examination, 57 cows were found to have ovarian follicular cyst. Attempts were made to treat the cows which had ovarian follicular cyst with GnRH, HCG respectively. The results obtained were summarized as follows : 1. The rates of estreous induction with GnRH or HCG were 91.4%, 77.2%, respectively. The GnRH treated group was showed significantly higher than HCG treated group. The mean days from the GnRH or HCG treated to estrum were 25.1 and 23.5 days, respectively. 2. The Conception rates with GnRH or HCG treatment were 78.2% and 76.5％, respectively. 3. Services per conception with GnRH or HCG treatment were 1.5 and 2.1 respectively. 4, Days from GnRH or HCG treatment to concept were 38.2 and 45.8 days, respectively. 5. Intramuscular injection with GnRH and intraovarian injection with HCG were revealed the most effective routes in all the other routes.

• Development and Reproduction
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• v.7 no.1
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• pp.49-56
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• 2003

There have been reports that administrated high-dose gonadotropin-releasing hormone-agonist(GnRH-Ag) suppresses endogenous gonadotropin production and inhibits function of ovary. In human IVF-ET program, however, GnRH-Ag is employed in large amounts during superovulation induction resulting to luteal phase defects which must be supported with progesterone. To elucidate the reason of luteal phase defects by GnRH-Ag, the aim of this study was to investigate the apoptosis changes in the ovary and the hormonal changes in the serum after GnRH-Ag and PMSG administration in adult mice in a method similar to human superovualtion induction. GnRH-Ag(10 ${\mu}$g) or saline was injected every 12h beginning 48h prior to PMSG injection until 48h at)or PMSG injection when blood sampling and ovary collection was performed. In results, the ovary weight in the GnRH-Ag only injection group was significantly lower when compared with the other two groups, PMSG only or PMSC + GnRH-Ag injection. The ratio of preantral follicles in the ovary are increased in the GnRH-Ag only group, while the ratio of antral follicles are decreased and the corpus luteum ratio is increased in the PMSG + GnRH-Ag group. The proportion of all follicles showing apoptosis in the GnRH-Ag only in.iection group was seen to be more than twice the proportion seen in the PMSC only injection group, and such increased apoptosis is decreased after addition of PMSC. The serum levels of both estradiol and progesterone were significantly lower in the CnRH-hg only group compared to those in the other two groups. When the administration of GnRH-Ag were followed by PMSG in;ection, however, estradiol concentration was completely recovered compared to the serum level of PMSG group, but not progesterone level. In conclusion the use of GnRH-Ag in human IVF-ET program may induce the apoptosis and the suppression of hormone production by ovary leading to luteal phase defects, thus adequate progesterone support seems to be necessary against them.

• The Korean Journal of Pharmacology
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• v.30 no.1
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• pp.19-28
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• 1994

The effects of gonadoropin-releasing hormone (GnRH) and ovarian steroid hormones on the release of luteinizing hormone (LH) and its subunit mRNA levels were investigated in anterior pituitary cells in culture. LH concentration was measured by a specific radioimmunoassay and mRNA levels of u and $LH{\beta}$ subunits by RNA slot blot hybridization assay. GnRH stimulated LH release in a dose-dependent manner from cultured pituitary cells. However, the basal LH release in the absence of GnRH was not changed during the course of 24h culture, strongly suggesting that release of LH is directly controlled by GnRH. The treatment of the pituitary cells with GnRH increased $LH{\beta}$ subunit mRNA levels in a dose-dependent manner, reaching the maximum with $2\;{\times}\;10^{-10}M$ GnRH while no significant increase in ${\alpha}$ subunit mRNA levels was observed after GnRH treatment. Estradiol did not augment GnRH-induced LH release while progesterone augmented GnRH-induced LH release in a dose-dependent manner at the level of pituitary. However, estradiol and progesterone increased basal and GnRH-induced $LH{\beta}$ subunit mRNA levels in a dose-dependent manner. The treatment of estrogen antagonist, LYI17018 blocked the effect of estradiol on GnRH-induced $LH{\beta}$ subunit mRNA levels in a dose-dependent manner while progesterone antagonist, Ru486 tended to block the effect of progesterone on GnRH-induced $LH{\beta}$ subunit mRNA levels. It is therefore suggested that GnRH Playa a major role in LH release and subunit biosynthesis by influencing the steady state $LH{\beta}$ subunit mRNA loves and ovarian steroid hormones modulate subunit biosynthesis via directly acting on pituitary gonadotropes.

• The Korean Journal of Zoology
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• v.37 no.3
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• pp.311-317
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• 1994

Seasonal variations of GnRH were investigated by immunohlstochemicsl technique in three species of frog, Rona niEromaculutu, R. dvbowskii 8nd R. mgosa with different ovulation period in order to examine the relationship between GnRH expression and reproductive function. In all three species of frog, the intensity of GnRH immunoreactivitv and the number of GnRH neurons in the brawn were relatively high in frogs at the pre-ovulation period and markedly increased at the ovulation period. Those were then decreased after ovulation and further lowered during early hibernation period. These results indicate that GnRH experssion is closely related to specific phases of annual reproductive cycle in frog.

• The Korean Journal of Pharmacology
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• v.23 no.2
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• pp.57-75
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• 1987

Two modalities of gonadotropin secretion, pulsatile gonadotropin and preovulatory gonadotropin surge, have been identified in the mammals. Pulsatile gonadotropin secretion is modulated by the pulsatile pattern of GnRH release and complex ovarian steroid feedback actions. The neural mechansim that regulates the pulsatile release of GnRH in the hypothalamus is called "GnRH pulse generator". Ovarian steroids, estradiol and progesterone, appear to exert thier feedback effects both directly on the pituitary to modulate gonadotropin release and on a hypothalamic site to modulate GnRH release; estradiol primarily affects the amplitude while progesterone decreases the frequency of the pulsatile GnRH. Steroid hormones are known to affect catecholamine transmission in brain. MBH-POA is richly innervated by NE systems and close apposition of NE terminals and GnRH cell bodies occurs in the MBH as well as in the POA. NE normally facilitates pulsatile LH release by acting through ${\alpha}-receptor$ mechanism. However, precise nature of facilitative role of NE transmission in maintaining pulsatile LH has not been clearly understood. Close apposition of DA and GnRH terminals in ME might permit DA to influence GnRH release. Action of DA transmission probably is mediated by axo-axonic contacts between GnRH and DA fibers in the ME. Dopamine transmission does not normally regulate pulsatile LH release, but under certain conditions, increased DA transmission inhibit LH pulse. Endogenous opioid acts to suppress the secretion of GnRH into hypophysial portal circulation, thereby inhibiting gonadotropin secretion. However, an interaction between endogenenous opioid peptides and gonadotropin release is a complex one which involves ovarian hormones as well. LH secretion appears to be most suppressed by endogenenous opioids during the luteal phase, at a time of elevated progesterone secretion. The arcuate nucleus contains not only cell bodies for GnRH and ${\beta}-endorphin$ but also a dense aborization of fibers suggesting that GnRH release is changed by the interactions between GnRH and ${\beta}-endorphin$ cell bodies within the arcuate nucleus. The frequency and amplitude of pulsatile LH release seem to be increased during the preovulatory gonadotropin surge. Estradiol exerts positive feedback action on the hypothalamo-pituitary axis to trigger preovulatory LH surge. GnRH is also crucial hormonal stimulus for preovulatory LH surge. It is unlikely, however, that increased secretion of GnRH during the preovulatory gonadotropin surge represents an obligatory neural signal for generation of the LH discharge in primates including human. Modulation of preovulatory LH surge by catecholamines has been studied almost exclusively in rats. NE and E may be involved in distinct way to accumulate GnRH in the MBH and its release into the hypophysial portal system during the critical period for LH surge on proestrus in rats. However, the mechanisms whereby augmented adrenergic transmission may facilitate the formation and accumulation of GnRH in the ME-ARC nerve terminals before the LH surge have not been clearly understood.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.32 no.3
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• pp.266-270
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• 1999

Two forms of gonadotropin releasing hormone (GnRH) are identified in the brain of adult mature spotted sea bass (Lateolabrax sp.) by immunohistochemical methods. Salmon GnRH immunoreactive (sGnRH-ir) cell bodies were distributed in the olfactory bulb, ventral telencephalon and preoptic region. Immunoreactive fibers were observed in the vicinity of the brain including the olfactory bulbs, the telencephalon, the optic nerve, the optic tectum, the cerebellum, the medulla oblongata and rostral spinal cord. In most cases, these fibers did not form well defined bundles. However, there was a clear continuum of immunoreactive fibers, extending from the olfactory bulbs to the pituitary. cGnRH-II-ir cell bodies were only found in olfactory bulbs. However, the distribution of cGnRH-II-ir fibers was basically similar to that of sGnRH-ir fibers except for the absence of their continuity between the olfactory bulbs and the pituitary. These data suggest that sGnRH and cGnRH-II are endogenous peptides and indicate the presence of multiple neuroendocrine functions in the brain of the spotted sea bass. It seems that sGnRH not only regulates GTH secretion but also functions as a neurotransmitter, whereas cGnRH-II functions only as a neurotransmitter.