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Search Results: 1 - 10 of 85317 matches for " Yen-Chin Liu "
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Acute morphine activates satellite glial cells and up-regulates IL-1β in dorsal root ganglia in mice via matrix metalloprotease-9
Temugin Berta, Tong Liu, Yen-Chin Liu, Zhen-Zhong Xu, Ru-Rong Ji
Molecular Pain , 2012, DOI: 10.1186/1744-8069-8-18
Abstract: Subcutaneous morphine injection (10 mg/kg) induced robust peripheral glial responses, as evidenced by increased GFAP expression in DRGs but not in spinal cords. The acute morphine-induced GFAP expression is transient, peaking at 2 h and declining after 3 h. Acute morphine treatment also increased IL-1β immunoreactivity in SGCs and IL-1β activation in DRGs. MMP-9 and GFAP are expressed in DRG neurons and SGCs, respectively. Confocal analysis revealed a close proximity of MMP-9 and GFAP immunostaining. Importantly, morphine-induced DRG up-regulation of GFAP expression and IL-1β activation was abolished after Mmp9 deletion or naloxone pre-treatment. Finally, intrathecal injections of IL-1β-selective siRNA not only reduced DRG IL-1β expression but also prolonged acute morphine-induced analgesia.Acute morphine induces opioid receptors- and MMP-9-dependent up-regulation of GFAP expression and IL-1β activation in SGCs of DRGs. MMP-9 could mask and shorten morphine analgesia via peripheral neuron-glial interactions. Targeting peripheral glial activation might prolong acute opioid analgesia.Mounting evidence indicates that activation of spinal cord glial cells such as microglia and astrocytes plays a crucial role in the pathogenesis of chronic pain [1-7]. In particular, chronic opioid exposure induces profound changes in spinal cord microglia and astrocytes [8-10]. Upon activation spinal glial cells produce multiple proinflammatory cytokines such as TNF-α, IL-1β, and IL-6 to antagonize morphine analgesia and promote morphine tolerance [11-14], via sensitization of spinal cord dorsal horn neurons [15-17]. For example, IL-1β has been shown to counteract opioid-induced analgesia following both chronic and acute administration of morphine [18]. While intrathecal injection of the inteurleukin-1 receptor (IL-1R) antagonist potentiates acute morphine analgesia [11], intrathecal administration of IL-1β induces heat hyperalgesia [15]. Of interest genetic polymorphism of IL-1R antagon
Acute morphine induces matrix metalloproteinase-9 up-regulation in primary sensory neurons to mask opioid-induced analgesia in mice
Yen-Chin Liu, Temugin Berta, Tong Liu, Ping-Heng Tan, Ru-Rong Ji
Molecular Pain , 2012, DOI: 10.1186/1744-8069-8-19
Abstract: Subcutaneous morphine induced a marked up-regulation of MMP-9 protein in DRGs but not spinal cords. Morphine also increased MMP-9 activity and mRNA expression in DRGs. MMP-9 up-regulation peaked at 2 h but returned to the baseline after 24 h. In DRG tissue sections, MMP-9 is expressed in small and medium-sized neurons that co-express mu opioid receptors (MOR). In DRG cultures, MOR agonists morphine, DAMGO, and remifentanil each increased MMP-9 expression in neurons, whereas the opioid receptor antagonist naloxone and the MOR-selective antagonist D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP) suppressed morphine-induced MMP-9 expression. Notably, subcutaneous morphine-induced analgesia was enhanced and prolonged in Mmp9 knockout mice and also potentiated in wild-type mice receiving intrathecal injection of MMP-9 inhibitors. Consistently, intrathecal injection of specific siRNA targeting MMP-9 reduced MMP-9 expression in DRGs and enhanced and prolonged morphine analgesia. Subcutaneous morphine also produced heat hyperalgesia at 24 h, but this opioid-induced hyperalgesia was not enhanced after MMP-9 deletion or inhibition.Transient MMP-9 up-regulation in DRG neurons can mask opioid analgesia, without modulating opioid-induced hyperalgesia. Distinct molecular mechanisms (MMP-9 dependent and independent) control acute opioid-induced pronociceptive actions (anti-analgesia in the first several hours and hyperalgesia after 24 h). Targeting MMP-9 may improve acute opioid analgesia.Opioids especially mu opioid receptor (MOR) agonists remain to be the most effective treatment for moderate to severe pain. MOR is expressed by primary sensory neurons including small-sized (C-fiber) and medium-sized (Aδ-fiber) neurons in the dorsal root ganglia (DRGs) [1-5]. MOR is also expressed in primary afferent terminals and lamina II interneurons in the spinal cord [1,6-8]. MOR agonist, such as [D-Ala2, N-Me-Phe4, Gly5-ol]-enkephalin (DAMGO) elicits potent presynaptic inhibition via suppress
Differential protection against oxidative stress and nitric oxide overproduction in cardiovascular and pulmonary systems by propofol during endotoxemia
Yen-Chin Liu, Alice YW Chang, Yu-Chuan Tsai, Julie YH Chan
Journal of Biomedical Science , 2009, DOI: 10.1186/1423-0127-16-8
Abstract: Experimental endotoxemia was induced by systemic injection of E. coli lipopolysaccharide (LPS, 15 mg/kg) to Sprague-Dawley rats that were maintained under propofol (15 or 30 mg/kg/h, i.v.) anesthesia. Mean systemic arterial pressure (MSAP) and heart rate (HR) were monitored for 6 h after the endotoxin. Tissue level of NO was measured by chemical reduction-linked chemiluminescence and oxidative burst activity was determined using dihydroethidium method. Expression of NO synthase (NOS) was determined by immunoblotting. The Scheffé multiple range test was used for post hoc statistical analysis.Systemic injection of LPS (15 mg/kg) induced biphasic decreases in MSAP and HR. In the heart, lung and aorta, an abrupt increase in lipid peroxidation, our experimental index of oxidative tissue injury, was detected in early stage and sustained during late stage cardiovascular depression. LPS injection, on the other hand, induced a gradual increase in tissue nitrite and nitrate levels in the same organs that peaked during late stage endotoxemia. Propofol infusion (15 or 30 mg/kg/h, i.v.) significantly attenuated lipid peroxidation in the heart, lung and aorta during early and late stage endotoxemia. High dose (30 mg/kg/h, i.v.) propofol also reversed the LPS-induced inducible NO synthase (iNOS) upregulation and NO production in the aorta, alongside a significant amelioration of late stage cardiovascular depression and increase in survival time during endotoxemia.Together these results suggest that oxidative injury and NO may play a differential role in LPS-induced cardiovascular depression. Oxidative tissue injury is associated with both early and late stage; whereas NO is engaged primarily in late stage cardiovascular depression. Moreover, propofol anesthesia may protect against fatal cardiovascular depression during endotoxemia by attenuating the late stage NO surge in the aorta, possibly via inhibition of iNOS upregulation by the endotoxin.Sepsis poses a major clinical problem
Critical Factors Governing the Difference in Antizyme-Binding Affinities between Human Ornithine Decarboxylase and Antizyme Inhibitor
Yen-Chin Liu,Yi-Liang Liu,Jia-Yang Su,Guang-Yaw Liu,Hui-Chih Hung
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0019253
Abstract: Both ornithine decarboxylase (ODC) and its regulatory protein, antizyme inhibitor (AZI), can bind with antizyme (AZ), but the latter has a higher AZ-binding affinity. The results of this study clearly identify the critical amino acid residues governing the difference in AZ-binding affinities between human ODC and AZI. Inhibition experiments using a series of ODC mutants suggested that residues 125 and 140 may be the key residues responsible for the differential AZ-binding affinities. The ODC_N125K/M140K double mutant demonstrated a significant inhibition by AZ, and the IC50 value of this mutant was 0.08 μM, three-fold smaller than that of ODC_WT. Furthermore, the activity of the AZ-inhibited ODC_N125K/M140K enzyme was hardly rescued by AZI. The dissociation constant (Kd) of the [ODC_N125K/M140K]-AZ heterodimer was approximately 0.02 μM, which is smaller than that of WT_ODC by approximately 10-fold and is very close to the Kd value of AZI_WT, suggesting that ODC_N125K/M140K has an AZ-binding affinity higher than that of ODC_WT and similar to that of AZI. The efficiency of the AZI_K125N/K140M double mutant in the rescue of AZ-inhibited ODC enzyme activity was less than that of AZI_WT. The Kd value of [AZI_K125N/K140M]-AZ was 0.18 μM, nine-fold larger than that of AZI_WT and close to the Kd value of ODC_WT, suggesting that AZI_K125N/K140M has an AZ-binding affinity lower than that of AZI_WT and similar to that of ODC. These data support the hypothesis that the differences in residues 125 and 140 in ODC and AZI are responsible for the differential AZ-binding affinities.
Determinants of the Differential Antizyme-Binding Affinity of Ornithine Decarboxylase
Yen-Chin Liu, Den-Hua Hsu, Chi-Liang Huang, Yi-Liang Liu, Guang-Yaw Liu, Hui-Chih Hung
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0026835
Abstract: Ornithine decarboxylase (ODC) is a ubiquitous enzyme that is conserved in all species from bacteria to humans. Mammalian ODC is degraded by the proteasome in a ubiquitin-independent manner by direct binding to the antizyme (AZ). In contrast, Trypanosoma brucei ODC has a low binding affinity toward AZ. In this study, we identified key amino acid residues that govern the differential AZ binding affinity of human and Trypanosoma brucei ODC. Multiple sequence alignments of the ODC putative AZ-binding site highlights several key amino acid residues that are different between the human and Trypanosoma brucei ODC protein sequences, including residue 119, 124,125, 129, 136, 137 and 140 (the numbers is for human ODC). We generated a septuple human ODC mutant protein where these seven bases were mutated to match the Trypanosoma brucei ODC protein sequence. The septuple mutant protein was much less sensitive to AZ inhibition compared to the WT protein, suggesting that these amino acid residues play a role in human ODC-AZ binding. Additional experiments with sextuple mutants suggest that residue 137 plays a direct role in AZ binding, and residues 119 and 140 play secondary roles in AZ binding. The dissociation constants were also calculated to quantify the affinity of the ODC-AZ binding interaction. The Kd value for the wild type ODC protein-AZ heterodimer ([ODC_WT]-AZ) is approximately 0.22 μM, while the Kd value for the septuple mutant-AZ heterodimer ([ODC_7M]-AZ) is approximately 12.4 μM. The greater than 50-fold increase in [ODC_7M]-AZ binding affinity shows that the ODC-7M enzyme has a much lower binding affinity toward AZ. For the mutant proteins ODC_7M(-Q119H) and ODC_7M(-V137D), the Kd was 1.4 and 1.2 μM, respectively. These affinities are 6-fold higher than the WT_ODC Kd, which suggests that residues 119 and 137 play a role in AZ binding.
Current Evidence of the Monoaminergic Regulation of Romantic Love and Relationship  [PDF]
Wei-Hsi Chen, Mei-Yen Chu, Yuan-Hsiang Chu, Yen-Chin Lin, Kuo-Yen Chen
Advances in Sexual Medicine (ASM) , 2017, DOI: 10.4236/asm.2017.73011
Introduction: Sexual response cycle is modulated by a variety of biological factors, especially antidepressants and antipsychotics. Although the circuit of romantic love has recently been delineated, the biological impact on romantic love is barely mentioned in human, however. Methods: In thus study, a comprehensive literature review was completed to elucidate the role of central monoamines, including dopamine, serotonin, norepinephrine, epinephrine, melatonin and histamine, for the romantic love and relationship in human. Results: The central circuit of romantic love includes the mesolimbic and mesocortical tract and their extensions widely distributed in cortical, subcortical and brainstem structures. The activation of brain foci progressively decreases along with the romantic relationship in many areas, including the bilateral caudate and ventral tegmentum area without change of passionate love. Hyperactivity of dopamine and serotonin is suggested at the synaptic level for romantic love in lovers, probably through an inhibition of transporters or increase of terminal release. Romantic love can be modulated by antidepressants or recreational drugs. Polymorphism of dopamine and serotonin receptor relates to the romantic relationship. The effect of other monoamines is barely mentioned. Conclusions: Romantic love is vulnerable for secondary effect, such as drugs which modulate the dopamine and serotonin, in human. Romantic relationship is also impacted by the polymorphism of monoamine receptors. Therefore, the biological effect is not limited to sexual response cycle but also the romantic love and relationship. Further investigation is warranted for understanding the secondary effect in romantic love for romantic dissolution or divorce.
Cytoplasmic Viral RNA-Dependent RNA Polymerase Disrupts the Intracellular Splicing Machinery by Entering the Nucleus and Interfering with Prp8
Yen-Chin Liu,Rei-Lin Kuo,Jing-Yi Lin,Peng-Nien Huang,Yi Huang,Hsuan Liu,Jamine J. Arnold,Shu-Jen Chen,Robert Yung-Liang Wang,Craig E. Cameron,Shin-Ru Shih
PLOS Pathogens , 2014, DOI: doi/10.1371/journal.ppat.1004199
Abstract: The primary role of cytoplasmic viral RNA-dependent RNA polymerase (RdRp) is viral genome replication in the cellular cytoplasm. However, picornaviral RdRp denoted 3D polymerase (3Dpol) also enters the host nucleus, where its function remains unclear. In this study, we describe a novel mechanism of viral attack in which 3Dpol enters the nucleus through the nuclear localization signal (NLS) and targets the pre-mRNA processing factor 8 (Prp8) to block pre-mRNA splicing and mRNA synthesis. The fingers domain of 3Dpol associates with the C-terminal region of Prp8, which contains the Jab1/MPN domain, and interferes in the second catalytic step, resulting in the accumulation of the lariat form of the splicing intermediate. Endogenous pre-mRNAs trapped by the Prp8-3Dpol complex in enterovirus-infected cells were identified and classed into groups associated with cell growth, proliferation, and differentiation. Our results suggest that picornaviral RdRp disrupts pre-mRNA splicing processes, that differs from viral protease shutting off cellular transcription and translation which contributes to the pathogenesis of viral infection.
Compact Dual-Mode Double Square-Loop Resonators for WLAN and Wimax Tri-Band Filter Design
Ji-Chyun Liu;Feng-Seng Huang;Ching-Pin Kuei;Chin-Yen Liu
PIER C , 2013, DOI: 10.2528/PIERC13012002
Abstract: The improved configurations with dual-mode double-square-loop resonators (DMDSLR) for tri-band application are proposed in this paper. Two sets of loops including double-square-loop and G-shaped loop are involved in the resonators. The resonant frequency equations related to DMDSLR geometries are introduced for simply designing tri-band bandpass filter (BPF). Resonant frequencies and transmission zeroes can be controlled by tuning the perimeter ratio of the square rings and the couples. To obtain lower insertion loss, higher out-of-band rejection level, wider bandwidth of tri-band, and compact applications, the miniaturized DMDSLR structure is designed. The effective design procedure is provided. The proposed filter is successfully simulated and measured. It can be applied to WLAN (2.45, 5.20 and 5.80 GHz) and WiMAX (3.50 GHz) systems.
Physical and Electrical Characteristics of Carbon Nanotube Network Field-Effect Transistors Synthesized by Alcohol Catalytic Chemical Vapor Deposition
Chin-Lung Cheng,Chien-Wei Liu,Bau-Tong Dai,Ming-Yen Lee
Journal of Nanomaterials , 2011, DOI: 10.1155/2011/125846
Abstract: Carbon nanotubes (CNTs) have been explored in nanoelectronics to realize desirable device performances. Thus, carbon nanotube network field-effect transistors (CNTNFETs) have been developed directly by means of alcohol catalytic chemical vapor deposition (ACCVD) method using Co-Mo catalysts in this work. Various treated temperatures, growth time, and Co/Mo catalysts were employed to explore various surface morphologies of carbon nanotube networks (CNTNs) formed on the SiO2/n-type Si(100) stacked substrate. Experimental results show that most semiconducting single-walled carbon nanotube networks with 5–7?nm in diameter and low disorder-induced mode ( -band) were grown. A bipolar property of CNTNFETs synthesized by ACCVD and using HfO2 as top-gate dielectric was demonstrated. Various electrical characteristics, including drain current versus drain voltage , drain current versus gate voltage , mobility, subthreshold slope (SS), and transconductance , were obtained. 1. Introduction Carbon nanotube field-effect transistors (CNTFETs) have been explored in nanoelectronics to realize desirable device characteristics [1–11]. Both n-type and p-type single-walled carbon nanotube (SWCNT) field-effect transistors (FETs) with top-gate electrodes in the conventional metal-oxide-semiconductor field-effect transistor (MOSFET) structures were demonstrated [1]. Two methods, including conventional doping and annealing metal/carbon nanotubes (CNTs) contact in vacuum, were used for the CNTFETs conversion from p- to n-type devices [2]. Moreover, the fabrication of the n-type CNTFET by Al-doped CNTs as channel was also achieved [12]. The primary potential advantage of CNTs is their very high carrier mobility ( ?cm2/V-s) [13]. However, one of challenges of CNTs to be viable in high-performance FETs is the requirement for processes that provide each CNTs placed in a desired location and direction [14]. Recently, an architecture based on the assembly of two- and three-dimensional networks of SWNTs using chemical vapor deposition (CVD) was demonstrated [15]. The field-effect mobility of random networks of SWCNT as thin-film transistor can exceed 100?cm2/V-s [16]. SWCNT random network thin film transistor with a 105 of on/off ratio and a ~8?cm2/C-s of field-effect mobility was demonstrated using water-assisted plasma-enhanced CVD (PECVD) [17]. Although various methods were used to synthesize the carbon nanotube networks (CNTNs), some electrical characteristics of CNTNs fabricated by alcohol catalytic CVD (ACCVD) remain not totally understood. We, therefore, attempt to explore some
Endothelial [Ca2+]i is an integrating signal for the vascular tone in rat aortae
Tung-Yi Huang, Hsiun-ing Chen, Chin-Yen Liu, Chauying J Jen
BMC Physiology , 2001, DOI: 10.1186/1472-6793-1-5
Abstract: Receptor-dependent (acetylcholine) or independent (ionomycin) agonists caused immediate EC [Ca2+]i elevation followed by vasorelaxation in preparations pre-contracted with phenylephrine. Low doses of agonists induced small EC [Ca2+]i elevations (about 100 nmol/L) and concomitant half-maximal vasorelaxation. At high doses, agonists elevated EC [Ca2+]i to μmol/L range with little additional vasodilatation. When EC [Ca2+]i was plotted against the vasorelaxation, the curves were almost identical for both acetylcholine and ionomycin treatments, in the presence or absence of various endothelial autacoid inhibitors. Calcium-free solution reduced basal EC [Ca2+]i and induced a drastic vasoconstriction. Endothelial autacoid inhibitors reduced EC [Ca2+]i changes and abolished both agonist-induced vasodilatation and calcium-free solution-induced vessel contraction. When the EC [Ca2+]i was completely chelated by 40 μmol/L BAPTA, the acetylcholine-evoked vasorelaxation could be abolished as well. However, when the EC [Ca2+]i was partially chelated by 20 μmol/L BAPTA, the acetylcholine-evoked vasorelaxation was almost unaffected.These results indicate that vascular tone is modulated by subtle changes of EC [Ca2+]i level, which seems to serve as an integrating signal in both basal and stimulated states.Vascular endothelium plays an important role in controlling vascular tone by secreting a variety of endothelium-derived relaxing factors (endothelial autacoids), namely NO, prostacyclin (PGI2), and L-NNA/indomethacin-insensitive relaxing factor [1,2,3]. In response to various chemical and physical stimuli, an elevation of endothelial cytosolic free Ca2+ concentration (EC [Ca2+]i) followed by the activation of calcium-dependent enzymes/channels and the consequent production of endothelial autacoids [4]. Although EC [Ca2+]i appears to mediate the release of endothelial autacoids, the direct relationship between EC [Ca2+]i and vascular contractility in intact vessels remains to be esta
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