• Title/Summary/Keyword: Functional modulation

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Characterization and expression profiles of aquaporins (AQPs) 1a and 3a in mud loach Misgurnus mizolepis after experimental challenges

  • Lee, Sang Yoon;Nam, Yoon Kwon;Kim, Yi Kyung
    • Fisheries and Aquatic Sciences
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    • v.20 no.9
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    • pp.23.1-23.9
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    • 2017
  • Two distinct cDNAs encoding aquaporins (mmAQPs 1a and 3a) were isolated and characterized from mud loach Misgurnus mizolepis. The identified mud loach AQP cDNAs encode for polypeptides of 260 and 302 amino acids. Topology predictions confirmed six putative membrane-spanning domains connected by five loops and the N- and C-terminal domains being cytoplasmic. The mud loach AQPs 1a and 3a showed broad distribution in multiple tissues including immune-responsive tissues as well as osmoregulatory tissues. Hence, the diversity of AQP distribution and expression possibly indicated its differential functions in the regulation of fluid movement in response to environmental stimuli. The transcription of mmAQP genes was differentially modulated by immune challenges. In particular, the mmAQP3a expression level in the liver was more responsive to immune challenges than that of mmAQP1a. Taken together, fish stimulation or infection resulted in significant modulation of mud loach AQP genes, suggesting potential functional roles of these proteins in piscine pathophysiological process.

Regulation of Inflammatory Response in Periodontal Ligament Cells by Transglutaminase 2

  • Lee, Sun Young;Jang, Cheol Hun;Ryu, Je-Hwang
    • International Journal of Oral Biology
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    • v.42 no.4
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    • pp.191-196
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    • 2017
  • Transglutaminase2 (TGM2) is a multi-functional calcium dependent enzyme that affects angiogenesis, apoptosis, differentiation, attachment, and changes in the extracellular matrix. However, its function in periodontal tissue has not yet been studied. The aim of this study was to investigate the association of the TGM2 expression and the modulation of inflammatory mediators in inflamed periodontal ligament (PDL) cells induced by pro-inflammatory cytokines such as Interleukin-$1{\beta}$ and the Tumor necrosis $factor-{\alpha}$. The expression of TGM2 was increased in the inflamed periodontal tissue and PDL cells. Over-expressed TGM2 in the PDL cells increased expression of MMP1, MMP3, IL-6, CXCL8, and PTGS2. Conversely, inhibition of TGM2 activity using LDN27219, a TGM2 inhibitor, resulted in decreased expression of MMP1, MMP3, IL-6, and CXCL8. The mRNA expression was confirmed by RT-PCR and quantified by qRT-PCR. Protein levels were also confirmed by immunofluoroscence staining. These results suggest that TGM2 plays an important role in the regulation of inflammatory mediators which exacerbate tissue damage in inflamed periodontal tissue.

The Unified UE Baseband Modem Hardware Platform Architecture for 3GPP Specifications

  • Kwon, Hyun-Il;Kim, Kyung-Ho;Lee, Chung-Yong
    • Journal of Communications and Networks
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    • v.13 no.1
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    • pp.70-76
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    • 2011
  • This paper presents the unified user equipment (UE) baseband modulation and demodulation (modem) hardware platform architecture to support multiple radio access technologies. In particular, this platform selectively supports two systems; one is HEDGE system, which is the combination of third generation partnership project (3GPP) Release 7 high speed packet access evolution (HSPA+) and global system for mobile communication (GSM)/general packet radio service (GPRS)/enhanced data rates for GSM evolution (EDGE), while the other is LEDGE system, which is the combination of 3GPP Release 8 long term evolution (LTE) and GSM/GPRS/EDGE. This is done by applying the flexible pin multiplexing scheme to a hardwired pin mapping process. On the other hand, to provide stable connection, high portability, and high debugging ability, the stacking structure is employed. Here, a layered board architecture grouped by functional classifications is applied instead of the conventional one flatten board. Based on this proposed configuration, we provide a framework for the verification step in wireless cellular communications. Also, modem function/scenario test and inter-operability test with various base station equipments are verified by system requirements and scenarios.

Anti-platelet role of Korean ginseng and ginsenosides in cardiovascular diseases

  • Irfan, Muhammad;Kim, Minki;Rhee, Man Hee
    • Journal of Ginseng Research
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    • v.44 no.1
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    • pp.24-32
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    • 2020
  • Cardiovascular diseases prevail among modern societies and underdeveloped countries, and a high mortality rate has also been reported by the World Health Organization affecting millions of people worldwide. Hyperactive platelets are the major culprits in thrombotic disorders. A group of drugs is available to deal with such platelet-related disorders; however, sometimes, side effects and complications caused by these drugs outweigh their benefits. Ginseng and its nutraceuticals have been reported to reduce the impact of thrombotic conditions and improve cardiovascular health by antiplatelet mechanisms. This review provides (1) a comprehensive insight into the available pharmacological options from ginseng and ginsenosides (saponin and nonsaponin fractions) for platelet-originated cardiovascular disorders; (2) a discussion on the impact of specific functional groups on the modulation of platelet functions and how structural modifications among ginsenosides affect platelet activation, which may further provide a basis for drug design, optimization, and the development of ginsenoside scaffolds as pharmacological antiplatelet agents; (3) an insight into the synergistic effects of ginsenosides on platelet functions; and (4) a perspective on future research and the development of ginseng and ginsenosides as super nutraceuticals.

Effects of Zinc on Spontaneous Miniature GABA Release in Rat Hippocampal CA3 Pyramidal Neurons

  • Choi, Byung-Ju;Jang, Il-Sung
    • The Korean Journal of Physiology and Pharmacology
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    • v.10 no.2
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    • pp.59-64
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    • 2006
  • The effects of $Zn^{2+}$ on spontaneous glutamate and GABA release were tested in mechanically dissociated rat CA3 pyramidal neurons which retained functional presynaptic nerve terminals. The spontaneous miniature excitatory and inhibitory postsynaptic currents (mEPSCs and mIPSCs, respectively) were pharmacologically isolated and recorded using whole-cell patch clamp technique under voltage-clamp conditions. $Zn^{2+}$ at a lower concentration $(30{\mu}M)$ increased GABAergic mIPSC frequency without affecting mIPSC amplitude, but it decreased both mIPSC frequency and amplitude at higher concentrations $({\ge}300{\mu}M)$. In contrast, $Zn^{2+}$ (3 to $100{\mu}M$) did not affect glutamatergic mEPSCs, although it slightly decreased both mIPSC frequency and amplitude at $300{\mu}M$ concentration. Facilitatory effect of $Zn^{2+}$ on GABAergic mIPSC frequency was occluded either in $Ca^{2+}$-free external solution or in the presence of $100{\mu}M$ 4-aminopyridine, a non-selective $K^{+}$ channel blocker. The results suggest that $Zn^{2+}$ at lower concentrations depolarizes GABAergic nerve terminals by blocking $K^{+}$ channels and increases the probability of spontaneous GABA release. This $Zn^{2+}$-mediated modulation of spontaneous GABAergic transmission is likely to play an important role in the regulation of neuronal excitability within the hippocampal CA3 area.

Ethanol-induced Activiationof Transcription Factor NF-$\kappa$B and AP-1 in C6 Glial Cells

  • Park, Jae -Won;Shim, Young-Sup
    • Preventive Nutrition and Food Science
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    • v.4 no.3
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    • pp.209-214
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    • 1999
  • In this study, the effectof ethanol and acetaldehyde on DNA binding activities of NF-$textsc{k}$B and AP-1 were evaluated in C6 rat glial cells. Both NF-$textsc{k}$B and AP-1 are important transcription factors for the expression of various cytokines in glial cells. Our data showed that neither ethanol nor acetaldehyde induced conspicuous cell death of C6 cells at clinically realistic concentrations. When the DNA binding activities of nuclear NF-$textsc{k}$B and AP-1 were estimated using electrophoretic mobility shift assay (EMSA), ethanol(0.3%) or acetaldehyde(1mM) induced transient activation of these transcription factors, which attained peak levels at 4~8 hours and declined to basal levels at 12 hours after treatement . The supershift analysis showed that the increased activities of NF-$textsc{k}$B in ethanol/acetaldehyde-treated C6 cells were due to the preferential induction of p65/p50 heterodimer complex. The DNA binding activities of these transcriptional factors decreased below basal levels when cells were cultured with either ethanol or acetaldehyde for 24 hours, and showed the inhibitory effect of chronic ehtanol /acetaldehyde treatment on the activities of these transsriptional factors. Our data indicate that either ethanol or acetaldehyde can induce functional changes of glial cells throught bi-directional modulation of NF-$textsc{k}$B and AP-1 DNA binding activities.

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Fe-based Amorphous Alloy with High Strength and Toughness Synthesized based on nm-scale Phase Separation (nm-수준의 상분리를 이용하여 제조한 고강도 고인성 철계 비정질 합금)

  • Lee, Kwang-Bok;Park, Kyoung-Won;Yi, Sang-Ho;Lee, Jae-Chul
    • Korean Journal of Metals and Materials
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    • v.48 no.1
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    • pp.1-7
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    • 2010
  • Experiments have demonstrated that the addition of a moderate amount of V to $Fe_{52}Co_{(20-x)}B_{20}Si_4Nb_4V_x$ amorphous alloy enhances the plasticity of the alloy. In particular, $Fe_{52}Co_{17.5}B_{20}Si_4Nb_4V_{2.5}$ alloy withstood a maximum of 8.3% strain prior to fracture along with a strength exceeding 4.7 GPa. Energy dispersive x-ray spectroscopy conducted on the $Fe_{52}Co_{17.5}B_{20}Si_4Nb_4V_{2.5}$ alloy exhibited evidence of compositional modulation, indicating that nm-scale phase separation had occurred at local regions. In this study, the role played by nm-scale phase separation on the plasticity was investigated in terms of structural disordering and shear localization in order to better understand the structural origin of the enhanced plasticity shown by the developed alloy.

Complete genome sequence of Limosilactobacillus fermentum JNU532 as a probiotic candidate for the functional food and feed supplements

  • Bogun Kim;Ziayo Meng;Xiaoyue Xu;Seungwoo Baek;Duleepa Pathiraja;In-Geol Choi;Sejong Oh
    • Journal of Animal Science and Technology
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    • v.65 no.1
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    • pp.271-274
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    • 2023
  • Lactic acid bacteria (LAB) have been reported to possess various beneficial properties and are commonly used as probiotics. LAB play a crucial role in milk fermentation, industrial lactic acid fermentation, and health and medicine. Limosilactobacillus fermentum isolated from fermented dairy and food products is considered as 'Generally Recognized as Safe' by FDA. Limosilactobacillus fermentum plays an important role in modulation of the intestinal microbiota, enhancing the host immune system and improving feed digestibility. We isolated a probiotic candidate that was identified and named Limosilactobacillus fermentum JNU532. In a previous report, cell-free culture of L. fermentum JNU532 exhibited anti-melanogenic and antioxidant activities. In this study, we present the complete genome assembly of the bacterial strain JNU532. The final genome consists of one circular chromosome (2,077,416 base pairs) with a guanine + cytosine (GC) ratio of 51.5%.

KLF9 deficiency protects the heart from inflammatory injury triggered by myocardial infarction

  • Zhihong Chang;Hongkun Li
    • The Korean Journal of Physiology and Pharmacology
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    • v.27 no.2
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    • pp.177-185
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    • 2023
  • The excessive inflammatory response induced by myocardial infarction exacerbates heart injury and leads to the development of heart failure. Recent studies have confirmed the involvement of multiple transcription factors in the modulation of cardiovascular disease processes. However, the role of KLF9 in the inflammatory response induced by cardiovascular diseases including myocardial infarction remains unclear. Here, we found that the expression of KLF9 significantly increased during myocardial infarction. Besides, we also detected high expression of KLF9 in infiltrated macrophages after myocardial infarction. Our functional studies revealed that KLF9 deficiency prevented cardiac function and adverse cardiac remodeling. Furthermore, the downregulation of KLF9 inhibited the activation of NF-κB and MAPK signaling, leading to the suppression of inflammatory responses of macrophages triggered by myocardial infarction. Mechanistically, KLF9 was directly bound to the TLR2 promoter to enhance its expression, subsequently promoting the activation of inflammation-related signaling pathways. Our results suggested that KLF9 is a pro-inflammatory transcription factor in macrophages and targeting KLF9 may be a novel therapeutic strategy for ischemic heart disease.

Current understanding of nociplastic pain

  • Yeong-Min Yoo;Kyung-Hoon Kim
    • The Korean Journal of Pain
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    • v.37 no.2
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    • pp.107-118
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    • 2024
  • Nociplastic pain by the "International Association for the Study of Pain" is defined as pain that arises from altered nociception despite no clear evidence of nociceptive or neuropathic pain. Augmented central nervous system pain and sensory processing with altered pain modulation are suggested to be the mechanism of nociplastic pain. Clinical criteria for possible nociplastic pain affecting somatic structures include chronic regional pain and evoked pain hypersensitivity including allodynia with after-sensation. In addition to possible nociplastic pain, clinical criteria for probable nociplastic pain are pain hypersensitivity in the region of pain to non-noxious stimuli and presence of comorbidity such as generalized symptoms with sleep disturbance, fatigue, or cognitive problems with hypersensitivity of special senses. Criteria for definitive nociplastic pain is not determined yet. Eight specific disorders related to central sensitization are suggested to be restless leg syndrome, chronic fatigue syndrome, fibromyalgia, temporomandibular disorder, migraine or tension headache, irritable bowel syndrome, multiple chemical sensitivities, and whiplash injury; non-specific emotional disorders related to central sensitization include anxiety or panic attack and depression. These central sensitization pain syndromes are overlapped to previous functional pain syndromes which are unlike organic pain syndromes and have emotional components. Therefore, nociplastic pain can be understood as chronic altered nociception related to central sensitization including both sensory components with nociceptive and/or neuropathic pain and emotional components. Nociplastic pain may be developed to explain unexplained chronic pain beyond tissue damage or pathology regardless of its origin from nociceptive, neuropathic, emotional, or mixed pain components.