• Journal of the Korea Institute of Information and Communication Engineering
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• v.17 no.4
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• pp.971-980
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• 2013

System performance improvement through the concentrated residual dispersion per span (RDPS) in special transmission fiber spans in optical transmission links with dispersion management (DM) for wavelength division multiplexed (WDM) transmission is investigated through the comparison with the performance in optical transmission links with uniform RDPS in every fiber spans. It is confirmed that, in optical links with RDPS of 0 ps/nm uniformly distributed in the rest fiber spans, if RDPS of 300 ps/nm and 1,320 ps/nm are concentrated in 5th-13th fiber spans and 6th-13th fiber spans, respectively, then the best performance is obtained. It is also confirmed that optimal net residual dispersion (NRD) controlled by precompensation and postcompensation are 10 ps/nm and -10 ps/nm, respectively, in all two cases, and the effective launching power range below 1 dB eye opening penalty (EOP) in the concentrated RDPS of 300 ps/nm and 1,320 ps/nm are improved by 2 dB and 6 dB than optical transmission links with the uniformly distributed RDPS, respectively.

• The Journal of Korean Institute of Communications and Information Sciences
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• v.40 no.8
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• pp.1507-1514
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• 2015

Non-orthogonal multiple access (NOMA) is a promising candidate for 5G networks. NOMA achieves superior spectral efficiency than conventional orthogonal multiple access (OMA), as in NOMA multiple users uses the same time and frequency resources. Multiple-input-multiple-output (MIMO) is one another promising technique that can enhance system performance. In this paper we present a spectral and energy efficient multiple antenna based NOMA scheme, known as spatially modulated NOMA. In the proposed scheme the cell edge users are multiplexed in spatial domain, which means the information to cell edge users is conveyed using the transmit antenna indices. In NOMA the performance of cell edge users are deeply effected as it treats signals of others as noise. The proposed scheme achieves superior spectral efficiency than the conventional NOMA. The number of decoding steps involved in decoding NOMA signal reduces by one as cell edge user is multiplexed in spatial domain. The proposed scheme is more energy efficient as compare to conventional NOMA. All of the three gains high spectral, energy efficiency and one step reduction in decoding comes at cost of multiple transmit antennas at base station.

• The Journal of Korean Institute of Communications and Information Sciences
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• v.32 no.10C
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• pp.1032-1041
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• 2007

The global navigation satellite system (GNSS), which is the core technique for the location based service, adopts the direct sequence/spread spectrum (DS/SS) as its modulation method. The success of a DS/SS system depends on the synchronization between the received and locally generated pseudo noise (PN) signals. As a step in the synchronization process, the tacking scheme performs fine adjustment to bring the phase difference between the two PN signals to zero. The most widely used tracking scheme is the delay locked loop with early minus late discriminator (EL-DLL). In the ideal case, the EL-DLL is the best estimator among various DLL. However, in the band-limited multipath environment, the EL-DLL has tracking bias. In this paper, the timing offset range of correlation function is divided into advanced offset range (AOR) and delayed offset range (DOR) centering around the correct synchronization time point. The tracking bias results from the following two reasons: symmetry distortion between correlation values in AOR and DOR, and mismatch between the time point corresponding to the maximum correlation value and the synchronization time point. The former and latter are named as the type I and type II tracking bias, respectively. In this paper, when the receiver has finite bandwidth in the presence of multipath signals, it is shown that the type II tracking bias becomes a more dominant error factor than the type I tracking bias, and the correlation values in AOR are not almost changed. Exploiting these characteristics, we propose a novel tracking bias mitigation scheme and demonstrate that the tracking accuracy of the proposed scheme is higher than that of the conventional scheme, both in the presence and absence of noise.

• Herbal Formula Science
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• v.16 no.2
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• pp.205-217
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• 2008

Objectives : We investigated the effects of Herba Ephedrae and Rhizoma Amorphophalli on high fat diet induced obese male mice. Methods : 8 weeks old, high fat diet induced obese male mice were divided into 5 groups: C57BL/6 normal control, obese vehicle control, GGEx55 (Herba Ephedrae), GGEx61 (Rhizoma Amorphophalli), GGEx62 (Herba Ephedrae + Rhizoma Amorphophalli). After mice were treated with GGEx for 8 weeks, we measured body weight gain, food intake, feeding efficiency ratio, rectal temperature, fat weight, plasma leptin and lipid levels. We also took micro-computerized axial tomography (micro-CT) on the mice. Results : 1. GGEx55 and GGEx62 groups significantly decreased body weight gain and feeding efficiency ratio compared with vehicle control. But they significantly increased rectal temperature. 2. Plasma total cholesterol and LDL-cholesterol concentrations were significantly increased by GGEx55 groups, whereas were significantly decreased by GGEx62 groups compared with vehicle control. 3. GGEx55 and GGEx62 groups significantly decreased total, subcutaneous and visceral fat as well as fat areas in micro-CT analysis of abdomen compared with vehicle control. 4. Plasma GOT and GPT concentrations were significantly increased by GGEx55 groups compared with vehicle control. Conclusions : These results demonstrate that GGEx55 and GGEx62 effectively reduces body weight gain, feeding efficiency ratio in high fat diet induced obese mice, leading to the modulation of obesity. In addition, GGEx55 and GGEx62 decreases visceral adipose tissue mass and improves plasma lipids, suggesting that GGEx55 and GGEx62 may act as a therapeutic agent for obesity.

• The Korean Journal of Pain
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• v.22 no.1
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• pp.16-20
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• 2009

Background: Zaprinast is an inhibitor of phosphodiesterase 5, 6 and 9. Phosphodiesterase inhibitors could produce anti-nociceptive effects by promoting the accumulation of cGMP. We hypothesized that intrathecal zaprinast could attenuate the allodynia induced by chronic constriction injury of the sciatic nerve in rat. Methods: Sprague-Dawley rats were prepared with four loose ligations of the left sciatic nerve just proximal to the trifurcation into the sural, peroneal and tibial nerve branches. Tactile allodynia was measured by applying von Frey filaments to the lesioned hindpaw. The thresholds for the withdrawal responses were assessed. Zaprinast ($3-100{\mu}g$) was administered intrathecally by the direct lumbar puncture method to obtain the dose-response curve and the 50% effective dose ($ED_{50}$). Measurements were taken before and 15, 30, 45, 60, 90, 120, and 180 min after the intrathecal doses of zaprinast. The side effects were also observed. Results: Intrathecal zaprinast resulted in a dose-dependent antiallodynic effect. The maximal effects occurred within 15-30 min and then they gradually decreased down to the baseline level over time in all the groups. There was a dose dependent increase in the magnitude and duration of the effect. The $ED_{50}$ value was $17.4{\mu}g$ (95% confidence intervals; $14.7-20.5{\mu}g$). No severe motor weakness or sedation was observed in any of the rats. Conclusions: Intrathecally administered zaprinast produced a dose-dependent antiallodynic effect in the chronic constriction injury neuropathic pain model. These findings suggest that spinal phosphodiesterase 5, 6 and 9 may play an important role in the modulation of neuropathic pain.

• Development and Reproduction
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• v.13 no.4
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• pp.297-303
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• 2009

Implantation of blastocyst into the uterine endometrium is established by the existence of histologically and functionally prepared uterine endometrium. Doc-1, an oral cancer suppressor gene, is expressed under the control of steroid hormones and has been suggested as a proliferation regulator of endometrial cells. However, the role is not much clear and in this study we examined the expression modulation of Doc-1 in decidualizing cells in vitro. In vitro decidualization was performed in endometrial stroma cells using progesterone and estrogen. Until 24 hr after decidual induction the proliferation of stroma cell was significantly increased but decreased after then. On the other hand, most of the cells differentiated into decidual cell after 48 hr of induction. The Doc-1 protein was co-localized in a specific deciudal cells and colocalization rate was increased in a parallel manner with the induction time. Based on these results, it is suggested that Doc-1 expression is under the control of both steroid hormones and decidual signals, and Doc-1 protein is involved in suppression of the proliferation of decidualizing cells.

• 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.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.1
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• pp.25-33
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• 2016

Ion channels in carcinoma and their roles in cell proliferation are drawing attention. Intracellular $Ca^{2+}$ ($[Ca^{2+}]_i$)-dependent signaling affects the fate of cancer cells. Here we investigate the role of $Ca^{2+}$-activated $K^+$ channel (SK4) in head and neck squamous cell carcinoma cells (HNSCCs) of dif-ferent cell lines; SNU-1076, OSC-19 and HN5. Treatment with $1{\mu}M$ ionomycin induced cell death in all the three cell lines. Whole-cell patch clamp study suggested common expressions of $Ca^{2+}$-activated $Cl^-$ channels (Ano-1) and $Ca^{2+}$-activated nonselective cation channels (CAN). 1-EBIO, an activator of SK4, induced outward $K^+$ current (ISK4) in SNU-1076 and OSC-19. In HN5, ISK4 was not observed or negligible. The 1-EBIO-induced current was abolished by TRAM-34, a selective SK4 blocker. Interestingly, the ionomycin-induced cell death was effectively prevented by 1-EBIO in SNU-1076 and OSC-19, and the rescue effect was annihilated by combined TRAM-34. Con-sistent with the lower level of ISK4, the rescue by 1-EBIO was least effective in HN5. The results newly demonstrate the role of SK4 in the fate of HNSCCs under the $Ca^{2+}$ overloaded condition. Pharmacological modulation of SK4 might provide an intriguing novel tool for the anti-cancer strategy in HNSCC.

• Journal of Veterinary Clinics
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• v.18 no.4
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• pp.418-423
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• 2001

To investigate the modulation of nerve growth factor (NGF) during corneal epithelial wound healing and the effect of topical NGF on corneal epithelial wound healing in dogs. An axial epithelial defect was created in the right eye using 6mm axial corneal mechanical debridement while the left served as an unwounded control. The tears were collected from both eyes during 1 week and the corneal epithelium was processed for the measurement of NGF at day 0 and 7. The NGF content of tears and corneal epithelium was determined by enzyme-linked immunosorbent assay. In another experiment, the animals were divided into 3 groups. The right eyes in each group were treated every six hours with 200 ug/ml of recombinant human (rh) NGF, murine NGF, or 600 ug/ml of anti-NGF blocking antibody. The left eye of each animal was treated with bovine serum albumin (BSA) to serve as controls. Wound healing was analyzed using NIH image software. Tear NGF was markedly increased in the wounded eyes, relative to tears from control eyes during the early healing period. The NGF content of the corneal epithelium was elevated in the wounded eye (p=0.024). Time to wound closure and rate of epithelial migration were not significantly different between the NGF treated or the NGF antibody treated, and the control BSA treated eyes. Corneal epithelial wounding increased NGF content only on the wounded side during the early healing period. Neither topical recombinant human or murine NGF affected corneal epithelial wound healing in the normal dog.