• Development and Reproduction
• /
• v.4 no.2
• /
• pp.231-236
• /
• 2000

Recent studies have clearly shown that the expression of genes for gonadotropin-releasing hormone (GnRH) and its receptor in the rat reproductive organs including ovary, testis, placenta uterus and mammary gland. Moreover, luteinizing hormone (LH) classically known to be a main target product of GnRH in anterior pituitary has been found in rat gonads. These findings suggested the presence of local circuit composed of GnRH and LH in the rat gonads. The present study was undertaken to elucidate whether the genes for LH and its receptor are expressed in rat mammary gland. Expression of LH and its receptor genes in the rat mammary gland was demonstrated by reverse transcription-polymerase chain reaction (RT-PCR) and specific LH radioimmunoassay (RIA). The LH${\beta}$ transcripts in the mammary gland from cycling rats contained the pituitary type of LH${\beta}$ exons 1~3 encoding the entire LH${\beta}$ polypeptide but lacked the rat testis-specific LH${\beta}$ exon(s). Presence of ${\alpha}$ -subunit transcripts in the rat mammary gland were determined by RT-PCR. The cDNA fragments encoding exons 2~7 of rat LH receptor transcripts were amplified in both rat ovary and mammary gland samples. We could detect the GnRH expression in mammary gland from cycling virgin rats, and this result disagreed with previous report that mammary GnRH expression is occured in lactating rats only. Considerable amounts of immunoreactive LH molecules with good RIA parallelism in standard curve were detected in crude extracts from the rat mammary gland, indicating that the immunoreactive LH materials in the gland might be identical to authentic pituitary LH. To our knowledge, the present study demonstrated for the first time the expression of LH subunits and LH receptor in the rat mammary gland. Our findings suggested that the mammary gland might be the novel source and target of LH and the mammary LH could be act as a local regulator with auto-and/or paracrine manner under the regulation of local GnRH.

• Clinical and Experimental Reproductive Medicine
• /
• v.25 no.2
• /
• pp.199-205
• /
• 1998

The present study was performed to analyze the expression of LH genes in the rat ovary. Expression of LH subunit genes in the rat ovary was demonstrated by amplification of ovarian RNA by RT-PCR. The ovarian $LH_\beta$ transcripts contained at least two parts of the published cDNA structure, the pituitary exons 1, 2 and 3 and the part of testicular ex on 1 in the major trancripts form in rat testis. Using RIA, significant amount of LH-like molecules were detected in crude ovarian extracts, and the competition curves with increasing amount of tissue extracts were parallel with those of standard peptide, indicating that the ovarian immunoreactive LH-like material is similar to authentic pituitary LH molecule. The administration of PMSG to immature rats resulted in a sharp decrease of the ovarian LH contents after 24 h post-injection. In conclusion, these findings demonstrate that genes for LH subunits are expressed in the rat ovary, and suggest that LH can playa central role in regulation of female reproduction with both endocrine (by pituitary LH) and auto- and/or para-crine (by ovarian LH) manner.

• Clinical and Experimental Reproductive Medicine
• /
• v.26 no.2
• /
• pp.157-161
• /
• 1999

Recent studies clearly demonstrated that the novel expression of LH gene in the rat testis, and suggested the local action of the LH-like molecule. The present study was performed to analyze the expression of LH genes in the rat accessory reproductive organs. Expression of LH subunit genes in the rat uterus and epididymis was demonstrated by reverse transcription-polymerase chain reaction (RT-PCR) and specific LH radioimmunoassay (RIA). The $LH_{beta}$ transcripts in these organs contained the published cDNA structure, the pituitary type exons 1-3, which encoded the entire $LH_{beta}$ polypeptide. Presence of the transcripts for the ${\alpha}$-subunit in the rat reproductive tissues were also confirmed by RT-PCR. In the LH RIA, significant levels of LH were detected in crude extracts from the rat ovary, uterus and epididymis. The competition curves with increasing amount of tissue extracts were parallel with those of standard peptide, indicating that the immunoreactive LH-like materials in these tissues are similar to authentic pituitary LH molecule. In rat epididymis, the highest amount of immunoreactive LH was detected in corpus area. Our findings demonstrated that the genes for LH subunits are expressed in the rat accessory reproductive organs, and suggested that these extrapituitary LH may act as a local regulator with auto and/or paracrine manner.

• The Korean Journal of Pharmacology
• /
• v.32 no.3
• /
• pp.347-355
• /
• 1996

We examined the effects of EGTA and verapamil on phorbol ester-and forskolin-stimulated LH releases and $LH{\beta}$ subunit mRNA levels in order to verify the role of extracellular $Ca^{++}$ on PKC- or cAMP-induced increases in LH release and $LH{\beta}$ subunit mRNA levels in cultured anterior pituitary cells of rat. Forskolin-stimulated $LH{\beta}$ subunit mRNA levels as well as LH release were all suppressed by prevention of $Ca^{++}$ mobilization from extracellular environment, after the treatment of EGTA as a $Ca^{++}$ chelator or verapamil as a $Ca^{++}$ channel blocker. PMA-stimulated $LH{\beta}$ subunit mRNA levels were also suppressed by the treatment of EGTA and verapamil, while PMA-induced LH release was not affected. From the present study, it is, therefore, suggested that PKC activation and cAMP elevation all stimulate $LH{\beta}$ subunit mRNA levels and these are extracellular $Ca^{++}$-dependent. However, LH releases by PKC activation and cAMP increase seem to be different each other. LH release by PKC activation is thought to be independent of extracellular $Ca^{++}$. On the other hand, cAMP stimulated-LH release is thought to be dependent on the entry of extracellular $Ca^{++}$.

• The Korean Journal of Pharmacology
• /
• v.29 no.2
• /
• pp.225-235
• /
• 1993

Pituitary LH release has been known to be regulated by the hypothalamic gonadotropin releasing hormone (GnRH) and the gonadal steroid hormones. In addition, neurotransmitters and neuropeptides are actively involved in the control of LH secretion. The alteration in LH release might reflect changes in biosynthesis and/or posttranslational processing of LH. However, little is known about the mechanism by which biosynthesis of LH subunits is regulated, especially at the level of transcription. In order to investigate if ovarian steroid hormones regulate the LH subunit gene expression, ${\alpha}\;and\;LH{\beta}$ steady state mRNA levels were determined in anterior pituitaries of ovariectomized rats. Serum LH concentrations and pituitary LH concentrations were increased markedly with time after ovariectomy. ${\alpha}\;and\;LH{\beta}$ subunit mRNA levels after ovariectomy were increased in a parallel manner with serum LH concentrations and pituitary LH contents, the rise in $LH{\beta}$ subunit mRNA levels being more prominent than the rise in ${\alpha}\;subunit$ mRNA. ${\alpha}\;and\;LH{\beta}$ subunit mRNA levels in ovariectomized rats were negatively regulated by the continuous treatment of ovarian steriod hormones for $1{\sim}4\;days$ and $LH{\beta}\;subunit$ mRNA seemed to be more sensitive to negative feedback of estradiol than progesterone. Treatment of estrogen antagonist, LY117018 or progesterone antagonist, RU486 significantly restroed LH subunit mRNA levels as well as LH release which were suppressed by estradiol or progesterone treatment. These results suggest that ovarian steroids negatively regulate the LH synthesis at the pretranslational level by modulating the steady state levels of ${\alpha}\;and\;LH{\beta}\;subunit$ mRNA and $LH{\beta}\;subunit$ mRNA seemed to be more sensitive to negative feedback action of estradiol than progesterone.

• Clinical and Experimental Reproductive Medicine
• /
• v.26 no.3
• /
• pp.377-381
• /
• 1999

Objectives: Recent studies, including our own, demonstrated that the novel expression of LH gene in rat gonads and uterus, indicating that the local production and action of the LH-like molecule. In the present study, we investigated whether human uterus also expresses the LH gene. Design: Reverse transcription-polymerase chain reaction (RT-PCR) amplified the cDNA fragments coding $LH_{\beta}$ polypeptide from human endometrium but not from myometrium. Presence of the transcripts for the ${\alpha}$-subunit in human endometrium was also confirmed by RT-PCR. Results: Transcripts for $LH_{\beta}$ subunit were detected in endometrial samples from women with endometriosis. The gene for LH/hCG receptor was expressed in both endometrium and myometrium, showing good agreement with previous studies. Increased level of $LH_{\beta}$ transcript was determined in the endometrium from follicular phase compared to that from luteal phase. Conclusion: Taken together, our findings demonstrated that 1) the genes for LH subunits and LH/hCG receptor are expressed in human uterus, 2) the uterine LH expression was changed during menstrual cycle, suggesting that the uterine LH may playa local role in the control of uterine physiology and function(s).

• Magazine of the Korean Society of Agricultural Engineers
• /
• v.41 no.3
• /
• pp.41-50
• /
• 1999

Derivatio of reasonable design floods was attempted by comparative analysis of design floods derived by Generalized Extreme Value(GEV) distribution using methods of L-moments and LH-moments for the annual maximum series at ten watersheds along Han, Nagdong. Geum, Yeongsan and Seomjin river systems, LH-coefficient of variation, LH-skewness and Lh-kurtosis were calcualted by KH-moment ration respectively. Paramenters were estimated by the Method of LH-Moments, Design floods obtained by Method of LH-Moments using different methods for plotting positionsi n GEV distribution and design floods were compared with those obtained using the Method of L-Moments by the Relative Mean Errors(RME) and Relative Absolute Errors(RAE). The results was found that design floods derived by the method of L-Moments and LH-Moments using Cunnane plotting position formula in the GEV distribution are much closer to those of the observed data in comparison with those obtained by methods of L-moments and LH-moments using the other formula for plotting positions from the viewpoint of Relative Mean Errors and Relative Absolute Errors. In viewpoint of the fact that hydrqulic structures including dams and levees are genrally using design floods with the return period of two hundred years or so, design floods derived by LH-Moments are seemed to be more reasonable than those of L-Moments in the GEV distribution.

• Clinical and Experimental Reproductive Medicine
• /
• v.7 no.1_2
• /
• pp.3-10
• /
• 1980

Pituitary gonadotropes, as target cells, exhibit cyclic changes in terms of LH and FSH release in synchrony with the estradiol levels. The ultimate release is determined by the relative size of the two pools of gonadotropins, which is regulated by the two controllers: LH-RH and estradiol. LH-RH appears to serve as a primary drive on the gonadotrope, stimulating gonadotropin synthesis, storage, and release. Estradiol amplifies the action of LH-RH and induces the development of a self-priming effect of LH-RH except that it impedes LH-RH mediated gonadotropin release. Negative and positive feedback action of estradiol is revealed to operate by different mechanisms. The pituitary capacity increases severalfold from early to late follicular phase, which is considered to be prerequisite for the development of mid-cycle surge. CNS-hypothalamic dopamine, norepinephrine, and prostaglandins, as well as LH-RH, are involved in the negative and positive feedback effects of estradiol. The possible mechanisms in the triggering of LH-RH release for the initiation of midcycle LH-RH surge are considered.

• Proceedings of the Korean Society of Propulsion Engineers Conference
• /
• 1997.04a
• /
• pp.215-220
• /
• 1997

본 연구는 추진제 연소관 내부에 도포 되는 내열재 라이닝 공정을 최적화하기 위해 라이너 Premix 반응성을 실험하고 그결과를 토대로 Premix 저장조건을 설정하였다. HX-계열의 Bonding agent를 사용하는 LH-2, LH-5, LH-6 라이너를 선택하여 각각 20, 30, $40^{\circ}C$하에서 5주간 저장후 경화제와 경화촉매를 주입하고 초기점도를 측정하여 반응성을 예측하였다. 그 결과 Bonding agent로 HX-868을 사용하는 LH-5, LH-6 라이너가 HX-752를 사용하는 LH-2보다 반응성이 빠르며, 경화제와 경화촉매로 DDI와 T-12를 사용하는 LH-5 라이너가 IPDI와 $Fe(AA)_3$를 사용하는 LH-6 라이너 보다 반응성이 빠르게 나타났다. 이러한 저장온도와 기간에 따른 반응성을 토대로 공정 적용시 급격한 점도 상승에 의한 작업의 불안정성을 피하기 위해 일정 점도를 초과하지 않는 라이너 Premix 저장조건을 설정하였고, 향후에는 Bonding agent로. HX-868을 사용하는 LH-5, LH-6 라이너는 보다 공정성이 양호한 HX-752로 바꾸어 주는 것이 바람직 할 것이다.

• Clinical and Experimental Reproductive Medicine
• /
• v.18 no.1
• /
• pp.13-21
• /
• 1991

To investigate the factors that affect the fertilization and cleavage rates of mature oocytes, 44 patients undergoing controlled ovarian hyperstimulation(COH) with FSH/hMG/hCG regimen for IVF - ET were analyzed. During follicular phase, serum LH levels were measured by radioimmunoassay and bioassay. Based on the mean follicular immunoactive LH(i-LH) and bioactive LH(b-LH) levels, patients were divided into 3 groups, respectively. There were no significant differences in basal serum FSH levels on menstrual cycle day 3, serum estradiol($E_2$) and progesterone ($P_4$) levels on the day of hCG administration, and the numbers of follicles aspirated and oocytes retrieved among groups. In relation to the mean follicular i-LH levels, the fertilization and cleavage rates of mature oocytes did not show a significant difference among groups. However, in groups with higher mean follicular b-LH levels, the fertilization and cleavage rates were reduced significantly. During late follicular phase, day-to-day variance in b-LH levels was not significant, but there was a significant difference among groups. There was no significant correlation between serum P. and b-LH levels. These data suggest that the fertilization and cleavage rates of mature oocytes are adversely affected by the raised mean follicular b-LH levels, and monitoring of serum b-LH levels is more useful in COH when compared with i-LH. It appears that the reduced rates are not due to the attenuated endogenous LH surge.