Differences in the relationship between traumatic experiences, self-esteem, negative cognition, and Internet addiction symptoms among North Korean adolescent defectors and South Korean adolescents: A preliminary study

Park, Subin,Lee, Yeeun,Jun, Jin Yong Elsevier/North Holland Biomedical Press 2017 Psychiatry research Vol.257 No.-

<P><B>Abstract</B></P> <P>North Korean adolescent defectors experience adaptation difficulties along with a wide range of psychosocial problems, but no study has yet examined their Internet addiction symptoms. We compared early traumatic experiences, self-esteem, negative cognition, and Internet addiction symptoms, as well as the relationships between these variables, between North Korean adolescent defectors and South Korean adolescents. Fifty-six North Korean adolescent defectors and 112 age- and sex- matched South Korean adolescents participated. The analyses examined the relationship between traumatic experiences and Internet addiction symptoms, with negative automatic thoughts or low self-esteem as mediators of these relations. North Korean adolescent defectors tended to have higher levels of negative automatic thoughts and more severe Internet addiction symptoms, as well as better self-esteem, than did South Korean adolescents. Furthermore, only among North Korean adolescent defectors, traumatic experiences were positively associated with Internet addition symptoms via increasing negative automatic thoughts. North Korean adolescent defectors are more susceptible to Internet addiction, negative cognitions, and early traumatic experiences compared to South Korean adolescents. However, the cross-sectional design of this study precludes consideration of the causality of these relationships. Interventions aiming to correct negative cognitions and increase self-esteem may be helpful for North Korean adolescent defectors with problematic Internet use.</P> <P><B>Highlights</B></P> <P> <UL> <LI> North Korean adolescent defectors had higher trauma and Internet addiction (IA). </LI> <LI> North Korean defectors also had greater self-esteem and negative automatic thoughts. </LI> <LI> Self-esteem and negative thoughts were mediators in the relation of trauma and IA. </LI> <LI> Country of origin (North vs. South Korea) moderated the mediating effects. </LI> </UL> </P>

Pulchellamin G, an amino acid-sesquiterpene lactone, from Saussurea pulchella suppresses lipopolysaccharide-induced inflammatory responses via heme oxygenase-1 expression in murine peritoneal macrophages

Lee, D.S.,Choi, H.G.,Wan Woo, K.,Kang, D.G.,Lee, H.S.,Oh, H.,Ro Lee, K.,Kim, Y.C. North-Holland ; Elsevier Science Ltd 2013 european journal of pharmacology Vol.715 No.1

Saussurea pulchella (Asteraceae) is widely distributed in Korea and has been used in Korean folk medicine for the treatment of inflammation, hypertension, hepatitis, and arthritis. Pulchellamin G is an amino acid-sesquiterpene lactone conjugate isolated from S. pulchella. In the present study, we focused on the anti-inflammatory effect of pulchellamin G, which acts by inducing the expression of heme oxygenase (HO)-1. HO-1 plays important roles in cytoprotection since it has antioxidant, anti-inflammatory, antiproliferative, and antiapoptotic properties. Pulchellamin G inhibited the mRNA and protein expression of inducible nitric oxide synthase (iNOS), iNOS-derived nitric oxide (NO), and cyclooxygenase (COX)-2 and COX-derived prostaglandin E2 (PGE<SUB>2</SUB>) production in lipopolysaccharide (LPS)-stimulated murine peritoneal macrophages. The compound also reduced tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) production and suppressed the phosphorylation and degradation of IκB-α and nuclear translocation of p65 in murine peritoneal macrophages in response to LPS stimulus. The inhibitory effects of pulchellamin G on nuclear factor kappa B (NF-κB) translocation was impaired by co-treatment of the cells with HO activity inhibitor tin protoporphyrin (SnPP). By using SnPP, we verified that the inhibitory effects of pulchellamin G on the pro-inflammatory mediators NO, PGE<SUB>2</SUB>, TNF-α, and IL-1β are associated with induction of HO-1 expression. Our data suggest that pulchellamin G might have potent therapeutic effects and it should be considered in the development of treatments for various inflammatory diseases.

(-)-Epigallocatechin-3-gallate inhibits voltage-gated proton currents in BV2 microglial cells

Jin, S.,Park, M.,Song, J.H. North-Holland ; Elsevier Science Ltd 2013 european journal of pharmacology Vol.698 No.1

(-)-Epigallocatechin-3-gallate (EGCG), the principal constituent of green tea, protects neurons from toxic insults by suppressing the microglial secretion of neurotoxic inflammatory mediators. Voltage-gated proton channels are expressed in microglia, and are required for NADPH oxidase-dependent reactive oxygen species generation. Brain damage after ischemic stroke is dependent on proton channel activity. Accordingly, we examined whether EGCG could inhibit proton channel function in the murine microglial BV2 cells. EGCG potently inhibited proton currents with an IC<SUB>50</SUB> of 3.7μM. Other tea catechins, (-)-epigallocatechin, (-)-epicatechin and (-)-epicatechin-3-gallate, were far less potent than EGCG. EGCG did not change the kinetics of proton currents such as the activation and the deactivation time constants, the reversal potential and the activation voltage, suggesting that the gating process of proton channels were not altered by EGCG. EGCG is known to disturb lipid rafts by sequestering cholesterol. However, neither extraction of cholesterol with methyl-β-cyclodextrin or cholesterol supplementation could reverse the EGCG inhibition of proton currents. In addition, the EGCG effect was preserved in the presence of the cytoskeletal stabilizers paclitaxel and phalloidin, phosphatase inhibitors, the antioxidant Trolox, superoxide dismutase or catalase. The proton channel inhibition can be a substantial mechanism for EGCG to suppress microglial activation and subsequent neurotoxic events.

The procyanidin trimer C1 induces macrophage activation via NF-κB and MAPK pathways, leading to Th1 polarization in murine splenocytes

Sung, N.Y.,Yang, M.S.,Song, D.S.,Byun, E.B.,Kim, J.K.,Park, J.H.,Song, B.S.,Lee, J.W.,Park, S.H.,Park, H.J.,Byun, M.W.,Byun, E.H.,Kim, J.H. North-Holland ; Elsevier Science Ltd 2013 european journal of pharmacology Vol.714 No.1

Numerous studies have shown various relationships between foods with a high nutritional value and a robust immune response, particularly studies that have focused on host protection and cytokine networks. This study aimed to clarify the role played by the procyanidin trimer C1 in innate and adaptive immunity. Procyanidin C1 did not exert cytotoxicity at concentrations ranging from 7.8 to 62.5μg/ml in macrophage cells; therefore, concentration of 62.5μg/ml was used as the maximum dose of procyanidin C1 throughout subsequent experiments. Procyanidin C1 enhanced inducible nitric oxide synthase-mediated nitric oxide production in a concentration-dependent manner. In addition, procyanidin C1 functionally induced macrophage activation by augmenting the expression of cell surface molecules (CD80, CD86, and MHC II) and proinflammatory cytokine production (tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6) via activation of mitogen-activated protein kinase (MAPK), e.g., p38, ERK, and JNK and nuclear factor (NF)-κB signaling pathways. Interestingly, procyanidin C1 effectively polarized T helper type 1 (Th1) by secreting Th1-mediated cytokines (interferon-γ, IL-12p70, and IL-2) and inducing splenocyte proliferation, indicating that procyanidin C1 contributes to Th1 polarization of the immune response. Accordingly, these findings confirms that the procyanidin C1 induces macrophage activation via NF-κB and MAPK pathways, leading to Th1 polarization in murine splenocytes, which suggests that procyanidin C1 regulates innate and adaptive immunity by macrophage activation and Th1 polarization.

A compound (DW1182v) protecting high glucose/palmitate-induced glucolipotoxicity to INS-1 beta cells preserves islet integrity and improves hyperglycemia in obese db/db mouse

Lee, S.J.,Choi, S.E.,Hwang, Y.C.,Jung, I.R.,Yi, S.A.,Jung, J.G.,Ku, J.M.,Jeoung, K.,Han, S.J.,Kim, H.J.,Kim, D.J.,Lee, K.W.,Kang, Y. North-Holland ; Elsevier Science Ltd 2012 european journal of pharmacology Vol.696 No.1

Loss of beta cells is a pathogenic cause for the development of type 2 diabetes. High glucose/free fatty acid (HG/FFA)-induced glucolipotoxicity was thought to play a role in the beta cell loss. Thus, application of small molecules capable of preventing HG/FFA-induced glucolipotoxicty to beta cells could be an avenue for a therapeutic intervention for the development of type 2 diabetes. We screened a representative library supplied from Korean Chemical Bank for prevention of high glucose/palmitate (HG/PA)-induced viability reduction of INS-1 beta cells and were able to identify a new small molecule (DW1182v) with a function to protect HG/PA-induced glucolipotoxicity. The protective effect was specific to HG/PA-induced beta cell death since DW1182v did not protect streptozotocin- or cytokine-induced INS-1 cell death. The protective effect by DW1182v was likely due to the reduction of death-promoting endoplasmic reticulum (ER) stress responses such as phospho-C-Jun N-terminal kinase (JNK) and C/EBP homologous protein (CHOP). Treatment of obese diabetic db/db mice with DW1182v preserved islet integrity and thus increased insulin secretion and lowered blood glucose after glucose infusion. These results suggest that a small molecule protecting HG/PA-induced glucolipotoxicity to beta cells can be a new therapeutic candidate to prevent the development of type 2 diabetes.

Chlorogenic acid ameliorates brain damage and edema by inhibiting matrix metalloproteinase-2 and 9 in a rat model of focal cerebral ischemia

Lee, K.,Lee, J.S.,Jang, H.J.,Kim, S.M.,Chang, M.S.,Park, S.H.,Kim, K.S.,Bae, J.,Park, J.W.,Lee, B.,Choi, H.Y.,Jeong, C.H.,Bu, Y. North-Holland ; Elsevier Science Ltd 2012 european journal of pharmacology Vol.689 No.1

Chlorogenic acid (CGA) has been reported to have various beneficial effects on the cardiovascular and central nervous systems. The purpose of the current study was to investigate whether CGA has protective effects against cerebral ischemia and whether these effects are due to modification of brain edema-related vascular factors. In a rat model of transient middle cerebral artery occlusion (MCAo, 2h of occlusion followed by 22h of reperfusion), we measured infarct volume and performed behavioral test to evaluate the effects of CGA on brain damage and sensory-motor functional deficits. Brain water content and Evans blue extravasation were measured to evaluate brain edema and blood brain barrier (BBB) damage. Lipid peroxidation (LPO) and the expressions and activities of matrix metalloproteinase (MMP)-2 and MMP-9 were measured to investigate the mechanisms of action. Intraperitoneal injection of CGA (3, 10, and 30mg/kg) at 0h and 2h after MCAo dose-dependently reduced infarct volume and sensory-motor functional deficits. It also reduced brain water content and Evans blue extravasation. Mechanistically, CGA reduced LPO and MMPs expressions and activities. These results suggest that CGA reduces brain damage, BBB damage and brain edema by radical scavenging activity and the inhibitory effects on MMP-2 and MMP-9.

Inhibition of adipocyte inflammation and macrophage chemotaxis by butein

Wang, Z.,Lee, Y.,Eun, J.S.,Bae, E.J. North-Holland ; Elsevier Science Ltd 2014 european journal of pharmacology Vol.738 No.-

Adipose tissue inflammation has been proposed as a therapeutic target for the treatment of obesity and metabolic disorders such as insulin resistance and type 2 diabetes. Butein, a polyphenol of vegetal origin, exhibits anti-inflammatory effects in macrophages but it was not reported whether butein prevents adipocyte inflammation. Here, we investigated the effects of butein on adipocyte inflammation in 3T3-L1 cells and performed functional macrophage migration assays. Butein opposed the stimulation of inducible nitric oxide synthase (iNOS) protein expression and of nitric oxide production by simultaneous treatment of adipocytes with tumor necrosis factor alpha (TNFα), lipopolysaccharide (LPS), and interferon gamma (TLI). In addition, butein inhibited mRNA expression of pro-inflammatory genes and chemokines in adipocytes stimulated with TLI or conditioned medium from RAW 264.7 macrophages treated with LPS. These effects were associated with suppression of inhibitor of kappa B alpha degradation induced by TNFα and with nuclear factor-kappa B (NF-κB) p65 phosphorylation and acetylation. Moreover, butein prevented phosphorylation of extracellular signal-regulated kinases, c-Jun N-terminal kinase, and the mitogen-activated protein kinase (MAPK) p38. These results suggest that butein suppresses adipocyte inflammation by inhibiting NF-κB/MAPK-dependent transcriptional activity. Furthermore, conditioned media from adipocytes stimulated macrophage chemotaxis, whereas media from adipocytes treated with butein blocked macrophage migration, an effect that was consistent with suppression of MCP-1 secretion by adipocytes treated with butein. In addition, macrophages treated with butein exhibited a reduced ability to migrate toward adipocyte CM. In conclusion, butein may represent a therapeutic agent to prevent adipose tissue inflammation and the obesity-linked insulin resistance.

Wound-healing effect of ginsenoside Rd from leaves of Panax ginseng via cyclic AMP-dependent protein kinase pathway

Kim, W.K.,Song, S.Y.,Oh, W.K.,Kaewsuwan, S.,Tran, T.L.,Kim, W.S.,Sung, J.H. North-Holland ; Elsevier Science Ltd 2013 european journal of pharmacology Vol.702 No.1

Panax ginseng is considered as one of the most valuable medicinal herbs in traditional medicine, and ginsenoside Rd is one of the main active ingredients in P. ginseng leaf. Although there is significant number of evidences implicated on the beneficial effects of the ginsenosides with diverse associated mechanisms, reports on the skin regeneration by the ginsenoside Rd are not sufficient. Therefore, we examined the mitogenic and protective effects of the ginsenoside Rd in the keratinocyte progenitor cells (KPCs) and human dermal fibroblasts (HDFs). Furthermore, the signaling pathways involved in the activation of KPCs and HDFs were investigated, and wound-healing effect is evaluated in vivo through animal wound models. We found that the ginsenoside Rd significantly increased the proliferation and migration level of KPCs and HDFs in a dose-dependent manner. Additionally, the cell survival was significantly increased in H<SUB>2</SUB>O<SUB>2</SUB> treated KPCs. Moreover, the ginsenoside Rd effectively induced collagen type 1 and down-regulated matrix metalloprotinase-1 (MMP-1) in a dose-dependent manner. All of these beneficial effects are associated with an induction of intracellular cAMP levels and phosphorylated cAMP response element-binding protein expression in nucleus, which both attenuated by adenine 9-β-d-arabinofuranoside, an adenylate cyclase inhibitor. Application of the ginsenoside Rd to an excision wound in mice showed an effective healing process. As skin regeneration is mainly associated with the activation of HDFs and KPCs, P. ginseng leaf, an alternative source of the ginsenoside Rd, can be used as a natural source for skin regeneration.

Strong matching preclusion under the conditional fault model

Park, J.H.,Ihm, I. North Holland ; Elsevier Science Ltd 2013 Discrete applied mathematics Vol.161 No.7

Strong matching preclusion that additionally permits more destructive vertex faults in a graph [J.-H. Park, I. Ihm, Strong matching preclusion, Theoretical Computer Science 412 (2011) 6409-6419] is an extended form of the original matching preclusion that assumes only edge faults [R.C. Brigham, F. Harary, E.C. Violin, J. Yellen, Perfect-matching preclusion, Congressus Numerantium 174 (2005) 185-192]. In this paper, we study the problem of strong matching preclusion under the condition that no isolated vertex is created as a result of faults. After briefly discussing some fundamental classes of graphs in the point of the conditional matching preclusion, we establish the conditional strong matching preclusion number for the class of restricted hypercube-like graphs, which include most nonbipartite hypercube-like networks found in the literature.

High-speed inter-view frame mode decision procedure for multi-view video coding

Liu, X.,Yang, L.T.,Sohn, K. North-Holland ; Elsevier Science Ltd 2012 Future generations computer systems Vol.28 No.6

With the amazing development of visual identification systems, multi-view video which is one of the main types of three-dimensional (3D) video signals, captured by a set of video cameras from various viewpoints, has attracted much interest recently. The multi-view video coding (MVC) uses the joint multi-view video model (JMVM) established on H.264/AVC as the core codec to achieve excellent coding efficiency. However, the concomitant problem is the huge encoding complexity especially due to the heavy Rate-to-Distortion Cost (RDCost) computational load of the mode decision (MD) process, which limits the applications of MVC for mobile terminals and embedded systems. In this paper, a high-speed MD (HSMD) algorithm is proposed for the inter-view frames of multi-view video signal. The redundant candidate modes of each macroblock (MB) in the inter-view frames are eliminated to reduce the original RDCost computational load by utilizing multiple efficiency parameters. The quantitative analysis verifies our proposal in theory and the simulation results show that the proposed HSMD algorithm can reduce the encoding time by over 90% for the inter-view video frames with negligible quality loss compared with the original JMVM codec. The proposed algorithm can be widely employed for real-time multi-view signal encoding especially under the mobile and embedded environments to realize the real-time encoding process.