• Korean Journal of Ecology and Environment
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• v.36 no.1 s.102
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• pp.1-8
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• 2003

Growth, colony formation and microcystin production of 'low-toxic' Microcysits aeruginosa $K{\"{u}}tzing$ were examined in relation to the 'info-chemicals' released by zooplankton. Algae were cultured in a medium with or without filtered water taken from cultures of Daphnia magna Straus (300 ind./L) or Moina macrocopa Straus (500 ind./L), The growth of M. aeruginosa, based on cell number, was also significantly different from populations cultured in the media with and without filtered zooplankton water from the exponential growth phase. In the 6-day experiment, the growth pattern of M. aeruginosa cultured with ZCMF was clearly different to control with-out ZCMF. Mean number of cells/particle and particle bio-volume of M. aeruginosa increased significantly from the day 2 for the Daphnia-CMF or Moina-CMF treat-ments. Microcystin production was promoted showing from 18.7 to 55 ${\mu}g/g$-dry cell in the zooplankton treatments relative to the controls. At peaked level on day 4, the highest level of up to $70.5{\pm}16.8\;{\mu}g/g$-dry cell was observed in the D. magna treatment. This study suggested that 'info-chemicals' from zooplankton might induce the increase of algal growth rates, colony formation and microcystin production, these seem to be advantageous to the alga and thus as a grazing defense mechanism.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.8
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• pp.3581-3586
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• 2014

Aim: To investigate the effects of tetramethypyrazine (TMP) on proliferation and apoptosis of the human gastric carcinoma cell line 7901 and its possible mechanism of action. Methods: The viability of TMP-treated 7901 cells was measured with a 3-(4, 5-dimethyl-thiazol-2-yl)-2,5-diphenyltetrazolium bromide assay (MTT) and cell apoptosis was analyzed by flow cytometry. The distribution of cells in different phases of cell cycle after exposure of TMPs was analyzed with flow cytometry. To investigate the molecular mechanisms of TMP-mediated apoptosis, the expression of NF-${\kappa}Bp65$, cyclinD1 and p16 in SGC-7901 cells was analyzed by reverse transcription-polymerase chain reaction (RT-PCR) and western blotting. Results: TMP inhibited the proliferation of human gastric carcinoma cell line 7901 in dose and time dependent manners. Cell growth was suppressed by TMP at different concentrations (0.25, 0.5, 1.0, 2.0 mg/ml), the inhibition rate is 0.46%, 4.36%, 14.8%, 76.1% (48h) and 15.5%, 18.5%, 41.2%, 89.8% (72h) respectively. When the concentration of TMPs was 2.0mg/ml, G1-phase arrest in the SGC-7901 cells was significant based on the data for cell cycle distribution. RT-PCR demonstrated that NF-${\kappa}Bp65$ and cyclin D1 mRNA expression was significantly down-regulated in 7901 cells treated with 2.0 mg/ml TMP for 72h (p<0.05), while the p16 mRNA level was up-regulated (p<0.05). The protein expression of NF-${\kappa}Bp65$ and cyclin D1 decreased gradually with the increase in TMP concentration, compared with control cells (p<0.05), while expression of protein p16 was up-regulated (p<0.01). Conclusion: TMP exhibits significant anti-proliferative and pro-apoptotic effects on the human gastric carcinoma cell line SGC-7901. NF-${\kappa}Bp65$, cyclinD1 and p16 may also play important roles in the regulation mechanisms.

• 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.

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.6
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• pp.445-453
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• 2000

The present investigation tested the hypothesis that the activation of protein kinase G (PKG) leads to a phosphorylation of $Ca^{2+}-activated$ potassium channel $(K_{Ca}\;channel)$ and is involved in the activation of $K_{Ca}$ channel activity in cerebral arterial smooth muscle cells of the rabbit. Single-channel currents were recorded in cell-attached and inside-out patch configurations of patch-clamp techniques. Both molsidomine derivative 3-morpholinosydnonimine-N-ethylcarbamide $(SIN-1,\;50\;{\mu}M)$ and 8-(4-Chlorophenylthio)-guanosine-3',5'-cyclic monophosphate $(8-pCPT-cGMP,\;100\;{\mu}M),$ a membrane-permeable analogue of cGMP, increased the $K_{Ca}$ channel activity in the cell-attached patch configuration, and the effect was removed upon washout of the drugs. In inside-out patches, single-channel current amplitude was not changed by SIN-1 and 8-pCPT-cGMP. Application of ATP $(100\;{\mu}M),$ cGMP $(100\;{\mu}M),$ ATP+cGMP $(100\;{\mu}M\;each),$ PKG $(5\;U/{\mu}l),$ ATP $(100\;{\mu}M)+PKG\;(5\;U/{\mu}l),$ or cGMP $(100\;{\mu}M)+PKG\;(5\;U/{\mu}l)$ did not increase the channel activity. ATP $(100\;{\mu}M)+cGMP\;(100\;{\mu}M)+PKG\;(5\;U/{\mu}l)$ added directly to the intracellular phase of inside-out patches increased the channel activity with no changes in the conductance. The heat-inactivated PKG had no effect on the channel activity, and the effect of PKG was inhibited by 8-(4-Chlorophenylthio)-guanosine-3',5'-cyclic monophosphate, Rp-isomer $(Rp-pCPT-cGMP,\;100\;{\mu}M),$ a potent inhibitor of PKG or protein phosphatase 2A (PP2A, 1 U/ml). In the presence of okadaic acid (OA, 5 nM), PP2A had no effect on the channel activity. The $K_{Ca}$ channel activity spontaneously decayed to the control level upon washout of ATP, cGMP and PKG, and this was prevented by OA (5 nM) in the medium. These results suggest that the PKG-mediated phosphorylations of $K_{Ca}$ channels, or some associated proteins in the membrane patch increase the activity of the $K_{Ca}$ channel, and the activation may be associated with the vasodilating action.

• Journal of Acupuncture Research
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• v.17 no.2
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• pp.169-186
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• 2000

To study anti-cancer effect and molecular biological mechanism of bee venom for aqua-acupuncture, the effects of bee venom on cell viability, apoptosis, and cell cycle were analyzed using MTT assay, tryphan blue assay, [3H]thymidine release assay, flow cytometric analysis, activity of caspase-3 protease activity assay, and immunocytometric analysis of PCNA. To explore whether anti-cancer effects of bee venom are associated with the transcriptional control of gene expression, quantitative RT-PCR analysis of apoptosis- and cell cycle-related genes was performed. The obtained results are summarized as follows: 1. The MTT assay demonstrated that cell viability was decreased by bee venom in a dose-dependant manner. 2. Significant induction of apoptosis was identified using tryphan blue assay, [$^3H$]thymidine release assay, and flow cytometric analysis of sub $G_1$ fraction. 3. In analysis of caspase-3 protease activity, the activity had increased significantly, in a dose-dependant manner. 4. Quantitative RT-PCR analysis of the apoptosis-related genes showed that Bcl-2 and $Bcl-X_L$ were down-regulated whereas Bax was up-regulated by bee venom treatment. 5. In flow cytometric analysis of cell cycle and immunocytometric analysis of PCNA expression, cell numbers of $G_1$ phase was increased by a dose-dependant manner. 6. In quantitative RT-PCR analysis of the cell cycle-related genes, p21, p27, and p57 were increased, while Cyclin D1, CDK4, c-Myc, c-Fos, and Histone H3 were decreased. In contrast, there were no remarkable changes in expression levels of CDC2 and c-Jun.

• Analyses & Alternatives
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• v.2 no.2
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• pp.111-141
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• 2018

By the middle of 2018 there are signs of China's entry into a new period of development, characterized by a change in the old model: "market reforms-inner-party democratization - moderate foreign policy" to another: "market reforms - Xi Jinping personality cult - offensive foreign policy." This model contains the risks of arising of the contradiction between economic freedom and political-ideological rigidity which can lead to destabilization of the political life. However, in the current positive economic dynamics, these risks may come out, rather, in the medium and long term. Today, the political situation in China remains stable - despite growing dissatisfaction in scientific expert and educational circles due to increased control over the intellectual sphere by the authorities. The need for a new redistribution of power between central and provincial authorities could potentially disrupt political stability in the medium term, but, at the moment, is not a critical negative factor. The economic situation is positive-stable. Forecasts indicate a possible increase in China's GDP in 2018 at 6.5%. At the same time, there are negative expectations in connection with the Sino-US and potentially Sino-European "trade war". In the Chinese foreign policy, as a response to Western pressure, China increasingly uses the Russian direction of its diplomacy in the expanded version of Russia + SCO. The nuance here is seen in China's adjusted approach to the SCO: first of all, not as a mechanism for cooperation with Russia, but as an organization that allows using Russia's potential for pressure on the US in the Sino-US strategic rivalry. In the second half of 2018, the Chinese economy will continue to develop steadily, albeit with unresolved traditional problems (debts of provinces and state-owned enterprises, ineffective state sector, risks on the financial and real estate market). In politics, discontent with the cult of Xi will accumulate, but without real threats to its power. Weakening in economic opposition between China and the United States is possible due to Beijing's search for compromises on tariffs, intellectual property, trade deficit. To find such trade-offs, Xi will use the so-called. "Personal diplomacy" of direct contacts with Trump.

• Journal of Life Science
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• v.33 no.10
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• pp.767-775
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• 2023

Sulfasalazine is a disease-modifying antirheumatic abiotic agent. It is a derivative of aminosalicylic acid and has been used for the treatment of various inflammatory diseases, such as rheumatoid arthritis, ulcerative colitis, and Crohn's disease, since it was first synthesized in 1941 and approved as a medicine in the United States in 1950. However, its mechanism of action has not yet been clearly identified. In this study, the effects of sulfasalazine on cell survival, apoptosis, and cell cycle progression in macrophages, which are major immune cells that regulate inflammatory responses, were investigated using mouse macrophage RAW 264.7 cells. Sulfasalazine inhibited the viability of RAW 264.7 cells in a dose-dependent manner, starting at a concentration of 0.25 mM. Annexin-V staining was used to confirm that the decrease in cell viability was due to apoptosis, and the number of Annexin-V-positive cells increased significantly at a concentration of 0.25 mM or higher. The effect of sulfasalazine on the expression of key proteins that regulate the G0/G1 phase of the cell cycle was also investigated. Sulfasalazine treatment significantly increased the expression of the cyclin-dependent kinase inhibitors p21 and p27 in RAW 264.7 cells. Although sulfasalazine is frequently used as a control drug in studies on inflammatory diseases, such as inflammatory colitis and rheumatoid arthritis, studies on its effect on macrophages are very limited. Therefore, the results of this study are expected to provide vital information on the use of sulfasalazine as a disease treatment.

• The Korean Journal of Air & Space Law and Policy
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• v.31 no.2
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• pp.237-269
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• 2016

Asia-Pacific Space Cooperation Organization (APSCO) is the only intergovernmental space cooperation organization in Asia. Since its establishment to date, eight countries have signed the convention and become member states. South Korea participated actively in the preparatory phase of creating the organization, and one conference organized by AP-MCSTA which is the predecessor of APSCO was held in South Korea. However, after the APSCO Convention was opened for signature in 2005 to date, South Korea does not ratify the Convention and become a member. The rapid development of space commercialization and privatization, as well as the fastest growing commercial space market in Asia, provides opportunities for Asian countries to cooperate with each other in relevant space fields. And to participate in the existing cooperation framework (e.g., the APSCO) by the Asian space countries (e.g., South Korea) could be a proper choice. Even if the essential cooperation in particular space fields is challenging, joint space programs among different Asian countries for dealing with the common events can be initiated at the first steps. Since APSCO has learned the successful legal arrangements from ESA, the legal measures established by its Convention are believed to be qualified to ensure the achievement of benefits of different member states. For example, the regulation of the "fair return" principle confirms that the return of interests from the relevant programs is in proportion to the member's investment in the programs. Moreover, the distinguish of basic and optional activities intends to authorize the freedom of the members to choose programs to participate. And for the voting procedure, the acceptance of the "consensus" by the Council is in favor of protecting the member's interest when making decisions. However, political factors that are potential to block the participation of South Korea in APSCO are difficult to be ignored. A recent event is an announcement of deploying THAAD by South Korea, which causes tension between South Korea and China. The cooperation between these two states in space activities will be influenced. A long-standing barrier is that China acts as a non-member of the main international export control mechanism, i.e., the MTCR. The U.S takes this fact as the main reason to prevent South Korea to cooperate with China in developing space programs. Although the political factors that will block the participation of South Korea in APSCO are not easy to removed shortly, legal measures can be taken to reduce the political influence. More specifically, APSCO is recommended to ensure the achievement of commercial interests of different cooperation programs by regulating precisely the implementation of the "fair return" principle. Furthermore, APSCO is also suggested to contribute to managing the common regional events by sharing satellite data. And it is anticipated that these measures can effectively response the requirements of the rapid development of space commercialization and the increasing common needs of Asia, thereby to provide a platform for the further cooperation. In addition, in order to directly reduce the political influence, two legal measures are necessary to be taken: Firstly, to clarify the rights and responsibilities of the host state (i.e., China) as providing assistance, coordination and services to the management of the Organization to release the worries of the other member states that the host state will control the Organization's activities. And secondly, to illustrate that the cooperation in APSCO is for the non-military purpose (a narrow sense of "peaceful purpose") to reduce the political concerns. Regional cooperation in Asia regarding space affairs is considered to be a general trend in the future, so if the participation of South Korea in APSCO can be finally proved to be feasible, there will be an opportunity to discuss the creation of a comprehensive institutionalized framework for space cooperation in Asia.

• Journal of Life Science
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• v.18 no.1
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• pp.120-128
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• 2008

The death ligand tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)/ Apo1L is a cytokine that activates apoptosis through cell surface death receptors. TRAIL has sparked growing interest in oncology due to its reported ability to selectively trigger cancer cell death. Euphorbiae humifusae Wind has been used in traditional Oriental medicine as a folk remedy used for the treatment of cancer. However, the mechanism responsible for the anticancer effects of E. humifusae not clearly understood. Here, we show that treatment with subtoxic doses of water extract of E. humifusae (WEEH) in combination with TRAIL induces apoptosis in TRAIL-resistant human gastric carcinoma AGS cells. Combined treatment with WEEH and TRAIL induced chromatin condensation and sub-G1 phase DNA content. These indicators of apoptosis were correlated with the induction of caspase activity that resulted in the cleavage of poly (ADP-ribose) polymerase. Combined treatment also triggered the loss of mitochondrial membrane potential. Furthermore, co-treatment with WEEH and TRAIL down-regulated the protein levels of the anti-apoptotic proteins such as Bcl-2, Bcl-xL, XIAP and cIAP-1. Although more study will be needed to examine the detailed mechanisms, this combined treatment may offer an attractive strategy for safely treating gastric adenocarcinomas and the results provide important new insights into the possible molecular mechanisms of the anticancer activity of E. humifusae.

• Journal of Life Science
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• v.23 no.3
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• pp.389-398
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• 2013

Platycodin D is a major constituent of triterpene saponins, which is found in the root of Platycodon grandiflorum, Platycodi Radix, which is widely used in traditional Oriental medicine for the treatment of many chronic inflammatory diseases. Several pharmacological effects of this compound have been reported recently, such as anti-inflammation, immunogenicity, anti-adipogenesis, lowered cholesterol, and anti-cancer activity. However, the mechanism by which this action occurs is poorly understood. In this study, we found that platycodin D greatly increased the potential of the anti-proliferative effect in various cancer cell lines. Our data revealed that platycodin D treatment resulted in a time- and concentration-response growth inhibition of U937 cells by inducing apoptosis, as evidenced by the formation of apoptotic bodies, chromatin condensation, and the accumulation of cells in the sub-G1 phase. Apoptosis induction of U937 cells by platycodin D correlated with an increase in the Bax/Bcl-2 ratio and caused the down-regulation of IAP family members. In addition, platycodin D treatment resulted in proteolytic activation of caspase-3, the concomitant degradation of poly(ADP-ribose) polymerases, and the collapse of the mitochondria membrane potential (${\Delta}{\Psi}_m$). However, the cytotoxic effects induced by platycodin D treatment were significantly inhibited by z-DEVD-fmk, a caspase-3 inhibitor, which demonstrated the important role that caspase-3 played in the observed cytotoxic effect. These findings suggest that platycodin D may be a potential chemotherapeutic agent for use in the control of human leukemia U937 cells. These findings also provided important new insights into possible molecular mechanisms of the anti-cancer activity of platycodin D.