On Antenna Orientation for Inter-Cell Interference Coordination in Cellular Network MIMO Systems

Sheu, Jeng-Shin,Lyu, Shin-Hong,Huang, Chuan-Yuan The Korea Institute of Information and Commucation 2016 Journal of communications and networks Vol.18 No.4

Next-generation (4G) systems are designed to support universal frequency reuse (UFR) to achieve best use of valuable spectra. However, it leads to undesirable interference level near cell borders. To control this, 4G systems adopt techniques, such as network multiple-input multiple-output (MIMO) and inter-cell interference coordination (ICIC), to improve cell-edge throughput. Network MIMO aims at mitigating inter-cell interference towards cell-edge users (CEUs) through multi-cell cooperation, where each collaborative base station serves both cell-center users (CCUs) and CEUs, including other cells' CEUs, under a power constraint. The present ICIC strategies cannot be directly applied to network MIMO because they were designed in absence of multi-cell coordination. In the presence of network MIMO, this paper investigates antenna orientations in ICIC and the method of power management. Results show that a proper antenna orientation can improve the cell-edge capacity and meantime lower the interference to CCUs. Capacity inconsistency between CCUs and CEUs is detrimental to mobile communications. Simulation results show that the proposed power management for ICIC in network MIMO systems can achieve a uniform data rate regardless users' position.

Spinal cytochrome P450c17 plays a key role in the development of neuropathic mechanical allodynia: Involvement of astrocyte sigma-1 receptors

Choi, Sheu-Ran,Roh, Dae-Hyun,Yoon, Seo-Yeon,Choi, Hoon-Seong,Kang, Suk-Yun,Han, Ho-Jae,Beitz, Alvin J.,Lee, Jang-Hern Elsevier 2019 NEUROPHARMACOLOGY - Vol.149 No.-

<P><B>Abstract</B></P> <P>While evidence indicates that sigma-1 receptors (Sig-1Rs) play an important role in the induction of peripheral neuropathic pain, there is limited understanding of the role that the neurosteroidogenic enzymes, which produce Sig-1R endogenous ligands, play during the development of neuropathic pain. We examined whether sciatic nerve injury upregulates the neurosteroidogenic enzymes, cytochrome P450c17 and 3β-hydroxysteroid dehydrogenase (3β-HSD), which modulate the expression and/or activation of Sig-1Rs leading to the development of peripheral neuropathic pain. Chronic constriction injury (CCI) of the sciatic nerve induced a significant increase in the expression of P450c17, but not 3β-HSD, in the ipsilateral lumbar spinal cord dorsal horn at postoperative day 3. Intrathecal administration of the P450c17 inhibitor, ketoconazole during the induction phase of neuropathic pain (day 0 to day 3 post-surgery) significantly reduced the development of mechanical allodynia and thermal hyperalgesia in the ipsilateral hind paw. However, administration of the 3β-HSD inhibitor, trilostane had no effect on the development of neuropathic pain. Sciatic nerve injury increased astrocyte Sig-1R expression as well as dissociation of Sig-1Rs from BiP in the spinal cord. These increases were suppressed by administration of ketoconazole, but not by administration of trilostane. Co-administration of the Sig-1R agonist, PRE084 restored the development of mechanical allodynia originally suppressed by the ketoconazole administration. However, ketoconazole-induced inhibition of thermal hyperalgesia was not affected by co-administration of PRE084. Collectively these results demonstrate that early activation of P450c17 modulates the expression and activation of astrocyte Sig-1Rs, ultimately contributing to the development of mechanical allodynia induced by peripheral nerve injury.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Sciatic nerve injury increases P450c17 expression in astrocytes of the ipsilateral lumbar spinal cord dorsal horn. </LI> <LI> Spinal P450c17 contributes to the CCI-induced development of neuropathic pain. </LI> <LI> Spinal P450c17 modulates the CCI-induced increase in astrocyte Sig-1R expression. </LI> <LI> P450c17 increases the dissociation of Sig-1Rs from BiP in the spinal cord dorsal horn of CCI mice. </LI> <LI> Sig-1R plays an important role in the P450c17-induced development of mechanical allodynia in neuropathic mice. </LI> </UL> </P>

Inhibition of cytochrome P450c17 reduces spinal astrocyte activation in a mouse model of neuropathic pain via regulation of p38 MAPK phosphorylation

Choi, Sheu-Ran,Beitz, Alvin J.,Lee, Jang-Hern Elsevier 2019 BIOMEDICINE AND PHARMACOTHERAPY Vol.118 No.-

<P><B>Abstract</B></P> <P>We have recently demonstrated that the neurosteroid-metabolizing enzyme, cytochrome P450c17 is increased in spinal astrocytes contributing to the development of mechanical allodynia in chronic constriction injury (CCI)-induced neuropathic mice. However, the mechanisms by which spinal P450c17 modulates pathological changes in astrocytes remain unclear. In this study we investigated whether P450c17 modulates astrocyte activation and whether this process is mediated by spinal p38 mitogen-activated protein kinase phosphorylation ultimately leading to the development of mechanical allodynia in CCI mice. Sciatic nerve injury induced a significant increase in glial fibrillary acidic protein (GFAP) expression in the superficial dorsal horn (SDH, laminae I-II) and nucleus proprius (NP, laminae III-IV) regions of the spinal cord dorsal horn. Repeated daily (from days 0–3 post-surgery) intrathecal administration of the P450c17 inhibitor, ketoconazole (10 nmol) significantly inhibited the CCI-induced increase in GFAP-immunoreactivity, but had no effect on the CCI-induced increase in Iba-1-immunoreactivity. In addition, intrathecal administration of ketoconazole significantly inhibited the CCI-induced increase in p38 phosphorylation, while the levels of ERK and JNK phosphorylation remained unchanged. The CCI-induced development of mechanical allodynia was attenuated by administration of either ketoconazole (10 nmol) or the p38 MAPK inhibitor, SB203580 (5 nmol). Administration of a sub-effective dose of SB203580 (0.5 nmol) potentiated the pharmacological effect of ketoconazole (1 nmol) on spinal GFAP-immunostaining, as well as, the development of mechanical allodynia following CCI. Collectively these data suggest that spinal P450c17 activates astrocytes via p38 phosphorylation, ultimately leading to the development of mechanical allodynia in a model of peripheral neuropathy.</P> <P><B>Highlights</B></P> <P> <UL> <LI> P450c17 inhibition suppresses the activation of spinal astrocytes in CCI mice. </LI> <LI> P450c17 inhibition has no effect on the activation of spinal microglial cells in CCI mice. </LI> <LI> Spinal P450c17 increases p38 MAPK phosphorylation in the spinal cord of CCI mice. </LI> <LI> SB203580 potentiates the pharmacological effects of ketoconazole on neuropathic pain and astrocyte activation. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>

특강연자 약력

( Hamm Ming Sheu ) 한국피부장벽학회 2004 한국피부장벽학회지 Vol.6 No.1

Hybrid Digital and Analogue Beamforming Design for Millimeter Wave Relaying Systems

Jeng Shin Sheu 한국통신학회 2017 Journal of communications and networks Vol.19 No.5

Millimeter-wave (mm-wave) communication has beenconsidered as a potential technology for next-generation mobile cellularnetworks because of the vast amount of underutilised spectrumin these frequency bands. The very short wavelength enablesthe use of a massive number of antenna arrays to obtain sufficientbeamforming gains and received power. In practice, mm-wavecommunications adopt a hybrid radio frequency (RF) and baseband(BB) beamforming design to avoid allocating a dedicated RFchain for each antenna. In this paper, we propose hybrid beamformingschemes for multiuser mm-wave relaying systems. In particular,the RF and BB beamforming designs are separated to avoidthe intractable searching problem in a joint optimization. Simulationresults show that the proposed hybrid beamforming can usea small number of RF chains to approach the performance of conventionaldigital beamforming, in which each antenna is assigned toan individual RF chain. Results also demonstrate that the proposeddesign outperforms the conventional joint RF/BB design. Finally,the proposed hybrid beamforming method is further validated byintroducing channel estimation error, to which it is shown to berobust.

The Root Extract of Gentiana macrophylla Pall. Alleviates B19-NS1-Exacerbated Liver Injuries in NZB/W F1 Mice

Ming-Jen Sheu,Chun-Ching Chiu,Deng-Jye Yang,Tsai-Ching Hsu,Bor-Show Tzang 한국식품영양과학회 2017 Journal of medicinal food Vol.20 No.1

The nonstructural protein NS1 of human parvovirus B19 (B19) is known to exacerbate disease activity in systemic lupus erythematosus (SLE). However, no specific medicine for B19 infection is available. The roots of Gentiana macrophylla Pall. (GM), the traditional Chinese medicine “Qinjiao,” have been used for centuries to treat rheumatic disease, including SLE. Herein, we aimed to investigate the effects of GM root extract (100 and 300 mg/kg body weight) on B19-NS1-exacerbated liver injury in NZB/W F1 mice; liver tissues were assessed by hematoxylin–eosin staining and immunoblotting. The GM root extract significantly decreased B19-NS1-exacerbated liver inflammation by suppressing the expressions of hepatic inducible nitric oxide synthase, cyclooxygenase type 2 (COX-2), interleukin (IL)-1β proteins, values of serum asparate transaminase (AST) and alanine transaminase (ALT), and lymphocyte infiltration (P < .05). It also significantly reduced the B19-NS1-exacerbated hepatic matrix metalloproteinase-9 (MMP-9) and urokinase plasminogen activator (uPA) expressions by downregulating tumor necrosis factor (TNF)-α/NF-κB (p65) signaling. These findings suggest a therapeutic potential of GM root extract against B19-NS1-exacerbated liver inflammation in SLE.

Mucilaginibacter limnophilus sp. nov., isolated from a lake

Shih-Yi Sheu,Yi-Ru Xie,Wen-Ming Chen 한국미생물학회 2019 The journal of microbiology Vol.57 No.11

A polyphasic taxonomy approach was used to characterize strain YBJ-36T, isolated from a freshwater lake in Taiwan. Phylogenetic analyses, based on 16S rRNA gene sequences and coding sequences of an up-to-date bacterial core gene set (92 protein clusters), indicated that strain YBJ-36T formed a phylogenetic lineage in the genus Mucilaginibacter. 16S rRNA gene sequence similarity indicated that strain YBJ-36T is closely related to species within the genus Mucilaginibacter (93.8–97.8% sequence similarity) and is most similar to Mucilaginibacter fluminis TTM-2T (97.8%), followed by Mucilaginibacter roseus TTM-1T (97.2%). Microbiological analyses demonstrated that strain YBJ-36T is Gram-negative, aerobic, non-motile, rod-shaped, surrounded by a thick capsule, and forms pink-colored colonies. Strain YBJ-36T grew between 20–40°C (optimal range, 35–37°C), pH 5.5–7.0 (optimal pH of 6) and 0–2% NaCl (optimal concentration, 0.5%). The predominant fatty acids of strain YBJ-36T are iso-C15:0 and summed feature 3 (C16:1 ω7c and/or C16:1 ω6c), the major polar lipid is phosphatidylethanolamine, the major polyamine is homospermidine, and the major isoprenoid quinone is MK-7. The draft genome is approximately 4.63 Mb in size with a G+C content of 42.8 mol%. Strain YBJ-36T exhibited less than 35% DNA-DNA relatedness with Mucilaginibacter fluminis TTM-2T and Mucilaginibacter roseus TTM-1T. Based on phenotypic and genotypic properties and phylogenetic inference, strain YBJ-36T should be classified in a novel species of the genus Mucilaginibacter, for which the name Mucilaginibacter limnophilus sp. nov. is proposed. The type strain is YBJ-36T (= BCRC 81056T = KCTC 52811T = LMG 30058T).

Bioactive Cadinane-type Compounds from the Soft Coral Sinularia scabra

Jyh-Horng Sheu,Jui-Hsin Su,Chiung-Yao Huang,Po-Ju Li,Yi Lu,Zhi-Hong Wen,Yao-Haur Kao 대한약학회 2012 Archives of Pharmacal Research Vol.35 No.5

Two new cadinane-type sesquiterpenoids, scabralins A (1) and B (2) were obtained from the soft coral Sinularia scabra. Metabolite 1 was shown to exhibit moderate to weak cytotoxicity against MCF-7, WiDr, Daoy, and HEp 2 cancer cell lines. Also, incubation with 10 μM compound 1 significantly inhibited the accumulation of the pro-inflammatory inducible nitric oxide synthase protein in lipopolysaccharide-stimulated RAW264.7 macrophage cells.

On Antenna Orientation for Inter-Cell Interference Coordination in Cellular Network MIMO Systems

Jeng-Shin Sheu,Shin-Hong Lyu,Chuan-Yuan Huang 한국통신학회 2016 Journal of communications and networks Vol.18 No.4

Next-generation (4G) systems are designed to supportuniversal frequency reuse (UFR) to achieve best use of valuablespectra. However, it leads to undesirable interference level nearcell borders. To control this, 4G systems adopt techniques, suchas network multiple-input multiple-output (MIMO) and inter-cellinterference coordination (ICIC), to improve cell-edge throughput. Network MIMO aims at mitigating inter-cell interference towardscell-edge users (CEUs) through multi-cell cooperation, where eachcollaborative base station serves both cell-center users (CCUs) andCEUs, including other cells’ CEUs, under a power constraint. The present ICIC strategies cannot be directly applied to networkMIMO because they were designed in absence of multi-cell coordination. In the presence of network MIMO, this paper investigatesantenna orientations in ICIC and the method of power management. Results show that a proper antenna orientation can improvethe cell-edge capacity and meantime lower the interferenceto CCUs. Capacity inconsistency between CCUs and CEUs is detrimentaltomobile communications. Simulation results show that theproposed power management for ICIC in network MIMO systemscan achieve a uniform data rate regardless users’ position.

On the fail-safe design of tendon-driven manipulators with redundant tendons

Jinn-Biau Sheu,Tyng Liu,Jyh-Jone Lee 대한기계학회 2012 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.26 No.6

A tendon-driven manipulator having redundant tendons may possess more flexibility in operation, such as optimizing the performance of tendons, reducing the burden of each tendon, and providing fail-safe features. The purpose of this paper is to investigate the design of tendon-driven manipulators with a fail-safe feature, that is, to synthesize a system that may still remain controllable as any of the tendons have broken down or malfunctioned. Characteristics of tendon-driven manipulators are briefly discussed. Criteria for tendon-driven manipulators with redundant tendons and fail-safe feature are then established. Subsequently, constraints for such system are derived from the structure of tendon-driven manipulator. Associated with the criteria, manipulators can remain controllable when any of the tendons fails to function. Finally, a geometric method for determining the structure is developed. Examples of two-DOF and three-DOF tendondriven manipulators are demonstrated.