Background : This experiment was conducted to select GAP applying seed disinfectants in Astragalus membranaceus and Platycodon grandiflorum. Methods and Results : We carried out the chemical efficacy and injury test. For the efficacy test, we investigated fungal detection rate by seed disinfectants and for the chemical injury, we investigated germination rate and emergence rate by seed disinfectants in reference amount and fold amount. These experiments carried out two times. The results obtained are as follows. In the experiment for seed disinfectants selection of Astragalus membranaceus, all tested chemicals such as Tebuconazole emulsifiable concentrate(EC), Thiophanate-methyl + Triflumizole wettable powder(WP), Prochloraz copper chloride complex+Tebuconazole suspension concentrate(SC), Prochloraz emulsifiable concentrate(EC), Fludioxonil wetting liquid(WL) and Hexaconazol+Prochloraz emulsifiable concentrate(EC) had control value of 80% or above against seed contaminated fungi. However two chemicals such as Tebuconazole EC and Prochloraz copper chloride complex+Tebuconazole SC and two chemicals such as Prochloraz EC and Hexaconazol+Prochloraz EC exhibited chemical injury significantly in reference amount and in fold amount respectively, compared to non treated control. In the case of seed disinfectants selection of Platycodon grandiflorum, Prochloraz copper chloride complex+Tebuconazole SC, Prochloraz EC and Hexaconazol+Prochloraz EC had control value of above 80% against seed contaminated fungi except Thiophanate-methyl+Triflumizole WP and Fludioxonil WL. However Hexaconazol+Prochloraz EC and Prochloraz copper chloride complex+Tebuconazole SC exhibited chemical injury significantly in reference amount and in fold amount respectively, compared to non treated control. Conclusion : From the above results, we finally selected three items of seed disinfectants including Thiophanate-methyl+Triflumizole WP and Fludioxonil WL in Astragalus membranaceus and Prochloraz emulsion in Platycodon grandiflorum.

Background: We evaluated the effect of ulinastatin on paw withdrawal threshold (PWT), IL-6, and IL-10 in SD rats after spinal nerve ligation (SNL). Methods: Group C received N/S and Group E received ulinastatin IV for three days following SNL. PWT, IL-6, and IL-10 were measured on the 3rd, 5th, and 7th day. Results: Group E showed higher PWT compared to group C. IL-6 was lower in group E than in group C. No differences in IL-10 were observed between group C and group E. Conclusion: Ulinastatin increased the PWT and its effect appears to be involved with IL-6, not IL-10.

The Egr family of zinc finger transcription factors consisting of 4 members (Egr1 to Egr4) regulates critical genetic programs involved in cellular growth, differentiation, and function. They are co-ex-pressed in many different tissues, suggesting that they may have some redundant functions. While it is clear that estrogen regulates Egr1 in estrogen sensitive breast cancer cells, function of Egr1 and mechanisms by which estrogen (E2) and/or progesterone (P4) regulates Egr1 in uterus still remain unexplored. Thus, we have examined regulatory mechanisms by which Egr1 is regulated in the uterus and abnormal uterine phenotypes of Egr1(－/－) mice. Eight-week-old female mice were ovariectomized (OVX) and rested for a week. Uteri of OVX mice treated with various concentrations of E2 and/or other hormones were collected at 2 h after hormone treatment unless otherwise indicated. ICI 182,780 [estrogen receptor (ER) antagonist] or RU486 [progesterone receptor (PR) antagonist] was injected to OVX mice 30 min prior to hormone treatments. OVX Egr1(+/+) and Egr1(－/－) mice were treated with E2 and/or P4 to examine expression patterns of genes important for estrogen responses, and steroid hormone-induced cell proliferation in the uterus. Collected uteri were utilized for RT-PCR, realtime RT-PCR, Western blotting and histological analyses. Egr1 mRNA was rapidly induced with the highest level at 2h after E2 treatment and gradually deceased to basal levels at 12 h. Pretreatment of ICI 182,780 significantly reduced E2-induced increase of Egr1. However, an agonist for GPR30, a membrane estrogen receptor failed to induce mRNA expression of Egr1, suggesting that E2-dependent Egr1 transcription is mainly regulated via nuclear estrogen receptor, ER. P4 effectively dampened E2-dependent Egr1 transcription and its antagonistic effects were partially interfered with RU486 pretreatment. Histological analyses with BrdU incorporation experiments showed that vascular permeability (an early estrogen response) but not cell proliferation (a late response) was significantly impaired in the uteri of E2 treated OVX Egr1(－/－) mice. Interestingly, some genes involved in early estrogen responses such as Bip and HIF-1a but not those in late responses are dysregulated in uteri of Egr1(－/－) mice. Collectively, our results show that E2 transiently induces Egr1 via activation of nuclear ER. P4 antagonizes E2-dependent Egr1 regulation via PR. Impaired early estrogenic responses in Egr1(－/－) uteri could be due to aberrant gene expression affected by loss of Egr1 which act as a master regulator of estrogen actions in the uterus.-ex

In particular, maternal prostacyclin (PGI2) is critical for embryo implantation and the action of PGI2 is not mediated via its G protein-coupled membrane receptor, IP, but its nuclear receptor, peroxisome proliferator-activated receptor δ (PPARδ). Recently, several studies have shown that PGI2 enhances blastocyst development and/or hatching rate in vitro, and subsequently implantation and live birth rates in mice. However, the mechanism by which PGI2 improves preimplantation embryo development in vitro remains unclear. Using molecular, pharmacologic and genetic approaches, we show that PGI2-induced PPARδ activation accelerates blastocyst hatching in mice. mRNAs for PPARδ, RXRs (heterodimeric partners of PPARδ) and PGI2 synthase are temporally induced after zygotic gene activation and their expression reaches maximum levels at the blastocyst stage, suggesting that functional complex of PPARδ can be formed in the blastocyst. Carbaprostacyclin (cPGI, a stable analogue of PGI2) and GW501516 (a PPARδ selective agonist) significantly accelerated blastocyst hatching but did not increase total cell number of cultured blastocysts. Whereas U51605 (a PGIS inhibitor) interfered with blastocyst hatching, GW501516 restored U51605-induced retarded hatching. In contrast to improvement of blastocyst hatching by PPARδ agonists, PPAR antagonists significantly inhibited blastocyst hatching. Furthermore, deletion of PPARδ at early stages of preimplantation mouse embryos caused delay of blastocyst hatching, but did not impair blastocyst development. Taken together, PGI2-induced PPARδ activation accelerates blastocyst hatching in mice.