• IMMUNE NETWORK
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• v.13 no.6
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• pp.289-294
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• 2013

Lipocalin-2 (LCN2) is an acute-phase protein induced by injury, infection, or other inflammatory stimuli. LCN2 binds small hydrophobic ligands and interacts with cell surface receptor to regulate diverse cellular processes. The role of LCN2 as a chemokine inducer in the central nervous system (CNS) has been previously reported. Based on the previous participation of LCN2 in neuroinflammation, we investigated the role of LCN2 in formalin-induced nociception and pathological pain. Formalin-induced nociceptive behaviors (licking/biting) and spinal microglial activation were significantly reduced in the second or late phase of the formalin test in Lcn2 knockout mice. Likewise, antibody-mediated neutralization of spinal LCN2 attenuated the mechanical hypersensitivity induced by peripheral nerve injury in mice. Taken together, our results suggest that LCN2 can be therapeutically targeted, presumably for both prevention and reversal of acute inflammatory pain as well as pathological pain.

• IMMUNE NETWORK
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• v.11 no.6
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• pp.342-347
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• 2011

Background: Glial cells are involved in immune and inflammatory responses in the central nervous system (CNS). Glial cells such as microglia and astrocytes also provide structural and functional support for neurons. Migration and morphological changes of CNS cells are associated with their physiological as well as pathological functions. The secreted protein lipocalin-2 (LCN2) has been previously implicated in regulation of diverse cellular processes of glia and neurons, including cell migration and morphology. Methods: Here, we employed a zebrafish model to analyze the role of LCN2 in CNS cell migration and morphology in vivo. In the first part of this study, we examined the indirect effect of LCN2 on cell migration and morphology of microglia, astrocytes, and neurons cultured in vitro. Results: Conditioned media collected from LCN2-treated astrocytes augmented migration of glia and neurons in the Boyden chamber assay. The conditioned media also increased the number of neuronal processes. Next, in order to further understand the role of LCN2 in the CNS in vivo, LCN2 was ectopically expressed in the zebrafish spinal cord. Expression of exogenous LCN2 modulated neuronal cell migration in the spinal cord of zebrafish embryos, supporting the role of LCN2 as a cell migration regulator in the CNS. Conclusion: Thus, LCN2 proteins secreted under diverse conditions may play an important role in CNS immune and inflammatory responses by controlling cell migration and morphology.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.12
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• pp.4965-4969
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• 2015

LCN2 (Lipocalin 2) is a 25 KD secreted acute phase protein, reported to be a novel regulator of angiogenesis in breast cancer. Up regulation of LCN2 had been observed in multiple cancers including breast cancer, pancreatic cancer and ovarian cancer. However, the role of LCN2 promoter methylation in the formation of microvessels is poorly understood. The aim of this study was to analyze the association of LCN 2 promoter methylation with microvessel formation and tumor cell proliferation in breast cancer patients. The LCN2 promoter methylation status was studied in 64 breast cancer tumors by methylation specific PCR (MSP). Evaluation of microvessel density (MVD) and Ki67 cell proliferation index was achieved by immunohistochemical staining using CD34 and MIB-1 antibodies, respectively. LCN2 promoter unmethylation status was observed in 43 (67.2%) of breast cancer patients whereas LCN2 methylation status was seen in 21 (32.8%). Further, LCN2 promoter unmethylation status was associated with aggressive tumor phenotype and elevated mean MVD in breast cancer patients.

• Journal of Electrochemical Science and Technology
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• v.11 no.4
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• pp.336-345
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• 2020

Nickel-doped lanthanum cobalt oxide (LaCo_1-xNi_xO_3-δ, LCN) was investigated as an alternative anode material for solid oxide fuel cells. To improve its catalytic activity for steam methane reforming (SMR) reaction, Ni²⁺ was substituted into Co³⁺ lattice in LaCoO₃. LCN anode, synthesized using the Pechini method, reacts with yttria-stabilized zirconia (YSZ) electrolyte at high temperatures to form an electrochemically inactive phase such as La₂Zr₂O₇. To minimize the interlayer by-products, the LCN was coated via a double-tape casting method on the Ni/YSZ anode as a catalytic functional layer. By increasing the Ni doping amount, oxygen vacancies in the LCN increased and the cell performance improved. CH₄ fuel decomposed to H₂ and CO via SMR reaction in the LCN functional layer. Hence, the LCN-coated Ni/YSZ anode exhibited better cell performance than the Ni/YSZ anode under H₂ and CH₄ fuels. LCN with 12 mol% of Ni (LCN12)-modified Ni/YSZ anode showed excellent long-term stability under H₂ and CH₄ conditions.

• Analytical Science and Technology
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• v.24 no.1
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• pp.51-59
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• 2011

Genetic Identification has become an important forensic investigation method which discerns identity through analysis of physical samples discovered in various crime scenes. Recently more samples are being requested to undergo A-STR analysis of low copy number (LCN) DNA, which is known as touch evidence-type sample and left on various objects such as a pen briefly used by the criminal, the gear of the car used for driving, the handle, and various buttons inside a car. This research attempted to extract the LCN DNA of the touch evidencetype left on crushed fingerprints on firearms, etc. and examine the genotyping success rate. Four types of firearms (M16, K1A, COLT 45 Pistol, M29 Revolver) were fired individually and physical samples were gathered from four parts of each firearm. Subsequently, in order to extract the LCN DNA, Microkit and $Prepfiler^{TM}$ were used to compare and analyze the quantity of DNA extracted and the genotyping success rate. Analysis results showed that the quantity of DNA extracted by $Prepfiler^{TM}$ was on average 1.7 times higher than that of Microkit, and in genotype analysis success rate $Prepfiler^{TM}$ also demonstrated 24.9% on average in contrast to 0% for Microkit. In regards to the grip part of the K1A, $Prepfiler^{TM}$'s success rate was as high as 50.6%.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.2
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• pp.837-845
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• 2014

Background: Overweight and obesity are recognized as major drivers of cancers including breast cancer. Several cytokines, including interleukin-6 (IL-6), IL-10 and lipocalin 2 (LCN2), as well as dysregulated cell cycle proteins are implicated in breast carcinogenesis. The nuclear, casein kinase and cyclin-dependent kinase substrate-1 (NUCKS-1), is a nuclear DNA-binding protein that has been implicated in several human cancers, including breast cancer. Objectives: The present study was conducted to evaluate NUCKS-1 mRNA expression in breast tissue from obese patients with and without breast cancer and lean controls. NUCKS-1 expression was correlated to cytokine profiles as prognostic and monitoring tools for breast cancer, providing a molecular basis for a causal link between obesity and risk. Materials and Methods: This study included 39 females with breast cancer (G III) that was furtherly subdivided into two subgroups according to cancer grading (G IIIa and G IIIb) and 10 control obese females (G II) in addition to 10 age-matched healthy lean controls (G I). NUCKS-1 expression was studied in breast tissue biopsies by means of real-time PCR (RT-PCR). Serum cytokine profiles were determined by immunoassay. Lipid profiles and glycemic status as well as anthropometric measures were also recorded for all participants. Results: IL-6, IL-12 and LCN2 were significantly higher in control obese and breast cancer group than their relevant lean controls (p<0.05), while NUCKS-1 mRNA expression was significantly higher in the breast cancer group compared to the other groups (p<0.05). Significant higher levels of IL-6, IL-12, and LCN2 as well as NUCKS-1 mRNA levels were reported in G IIIb than G IIIa, and positively correlated with obesity markers in all obese patients. Conclusions: Evaluation of cytokine levels as well as related gene expression may provide a new tool for understanding interactions for three axes of carcinogenesis, innate immunity, inflammation and cell cycling, and hope for new strategies of management.

• Journal of Hydrogen and New Energy
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• v.29 no.3
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• pp.251-259
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• 2018

Metal hydride based hydrogen storage under moderate temperature and pressure gives the safety advantage over the gas and liquid storage methods. Still solid-state hydrogen storage including metal hydride is below the DOE target level for automotive applications, but it can be adapted to stationary or miliary application reasonably. In order to develop a modular solid state hydrogen storage system that can be applied to a distributed power supply system composed of renewable energy - water electrolysis - fuel cell, the heat transfer and hydrogen storage characteristics of the metal hydride necessary for the module system design were investigated using AB5 type metal hydride, LCN2 ($La_{0.9}Ce_{0.1}Ni_5$). The planetary high energy mill (PHEM) treatment of LCN2 confirmed the initial hydrogen storage activation and hydrogen storage capacity through surface modification of LCN2 material. Expanded natural graphite (ENG) addition to LCN2, and compression molding at 500 atm improved the thermal conductivity of the solid hydrogen storage material.

• The Korean Journal of Physiology and Pharmacology
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• v.23 no.5
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• pp.335-344
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• 2019

Obesity causes inflammation and impairs thermogenic functions in brown adipose tissue (BAT). The adipokine lipocalin 2 (LCN2) has been implicated in inflammation and obesity. Herein, we investigated the protective effects of caloric restriction (CR) on LCN2-mediated inflammation and oxidative stress in the BAT of high-fat diet (HFD)-fed mice. Mice were fed a HFD for 20 weeks and then either continued on the HFD or subjected to CR for the next 12 weeks. CR led to the browning of the white fat-like phenotype in HFD-fed mice. Increased expressions of LCN2 and its receptor in the BAT of HFD-fed mice were significantly attenuated by CR. Additionally, HFD+CR-fed mice had fewer neutrophils and macrophages expressing LCN2 and iron-positive cells than HFD-fed mice. Further, oxidative stress and mitochondrial fission induced by a HFD were also significantly attenuated by CR. Our findings indicate that the protective effects of CR on inflammation and oxidative stress in the BAT of obese mice may be associated with regulation of LCN2.

• 한국체육학회지인문사회과학편
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• v.51 no.2
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• pp.305-314
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• 2012

This study estimated the causal relationship among leisure identity salience (LIS), leisure constraints negotiation (LCN), and intentions to participate in leisure activity (IPLA). For this, we estimated structural equation models controlled by leisure constraints, and we used data collected from 296 college students residing in Seoul and Kyoung-gi providence. The following was obtained. First, for both groups with high and low levels of leisure constraints, LIS positively caused LCN, and this became more evident for the group with high level of leisure constraint. Second, for the group with low level of leisure constraints, LIS positively and directly caused IPLA, whereas this causal relationship could not observed from the group with high level of leisure constraints. Nevertheless, it indirectly and positively caused IPLA though LCN for the same group. This implies that the mediative role of LCN became more important as the level of leisure constraints became more restrictive. Further, we separately showed that the role of LIS was important in the process of LCN.

• Biomolecules & Therapeutics
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• v.29 no.2
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• pp.135-143
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• 2021

Drug addiction influences most communities directly or indirectly. Increasing studies have reported the relationship between circadian-related genes and drug addiction. Per2 disrupted mice exhibited more vulnerable behavioral responses against some drugs including methamphetamine (METH). However, its roles and mechanisms are still not clear. Transcriptional profiling analysis in Per2 knockout (KO) mice may provide a valuable tool to identify potential genetic involvement and pathways in enhanced behavioral responses against drugs. To explore the potential genetic involvement, we examined common differentially expressed genes (DEGs) in the striatum of drug naïve Per2 KO/wild-type (WT) mice, and before/after METH treatment in Per2 KO mice, but not in WT mice. We selected 9 common DEGs (Ncald, Cpa6, Pklr, Ttc29, Cbr2, Egr2, Prg4, Lcn2, and Camsap2) based on literature research. Among the common DEGs, Ncald, Cpa6, Pklr, and Ttc29 showed higher expression levels in drug naïve Per2 KO mice than in WT mice, while they were downregulated in Per2 KO mice after METH treatment. In contrast, Cbr2, Egr2, Prg4, Lcn2, and Camsap2 exhibited lower expression levels in drug naïve Per2 KO mice than in WT mice, while they were upregulated after METH treatment in Per2 KO mice. qRT-PCR analyses validated the expression patterns of 9 target genes before/after METH treatment in Per2 KO and WT mice. Although further research is required to deeply understand the relationship and roles of the 9 target genes in drug addiction, the findings from the present study indicate that the target genes might play important roles in drug addiction.