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Han, Rafael Taeho,Kim, Hye Young,Ryu, Hyun,Jang, Wooyoung,Cha, Seung Ha,Kim, Hyo Young,Lee, JaeHee,Back, Seung Keun,Kim, Hee Jin,Na, Heung Sik Elsevier 2018 Journal of dermatological science Vol.90 No.3
<P><B>Abstract</B></P> <P><B>Background</B></P> <P>Atopic dermatitis (AD) is a highly pruritic, chronic inflammatory skin disease associated with hyperreactivity to environmental triggers. Among those, outdoor air pollutants such as particulate matter (PM) have been reported to aggravate pre-existing AD. However, underlying mechanisms of air pollution-induced aggravation of AD have hardly been studied.</P> <P><B>Objective</B></P> <P>To investigate the molecular mechanisms by which glyoxal, a PM-forming organic compound, exacerbates the symptoms of AD induced by neonatal capsaicin treatment.</P> <P><B>Methods</B></P> <P>Naïve and AD rats had been exposed to either fresh air or vaporized glyoxal for 5 weeks (2 h/day and 5 days/week) since one week of age. Pruritus and dermatitis were measured every week. The skin and blood were collected and immunological traits such as Staphylococcus aureus skin colonization, production of antimicrobial peptides and immunoglobulin, and mRNA expression of inflammatory cytokines were analyzed.</P> <P><B>Results</B></P> <P>Exposure to glyoxal aggravated pruritus and dermatitis in AD rats, but did not induce any symptoms in naïve rats. Staphylococcus aureus skin colonization was increased in the skin of both naïve and AD rats. Expression of antimicrobial peptides such as LL-37 and β-defensin-2 was also increased by exposure to glyoxal in the skin of both naïve and AD rats. The mRNA expression of Th1-related cytokines was elevated on exposure to glyoxal. However, serum immunoglobulin production was not significantly changed by exposure to glyoxal.</P> <P><B>Conclusion</B></P> <P>In AD rats, exposure to glyoxal exacerbated pruritus and cutaneous inflammation, which was associated with increased colonization of <I>S. aureus</I> and subsequent immunological alterations in the skin.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Exposure to glyoxal aggravated the symptoms in AD rats, but did not induce AD in naïve rats. </LI> <LI> <I>S. aureus</I> skin colonization and subsequent expression of antimicrobial peptides were increased after exposure to glyoxal. </LI> <LI> Exposure to glyoxal elevated the production of Th1-related cytokines such as TNF-α and IFN-γ in the AD lesional skin. </LI> </UL> </P>
Are Spinal GABAergic Elements Related to the Manifestation of Neuropathic Pain in Rat?
Jaehee Lee,Seung Keun Back,Eun Jeong Lim,Gyu Chong Cho,Myung Ah Kim,Hee Jin Kim,Min Hee Lee,Heung Sik Na 대한생리학회-대한약리학회 2010 The Korean Journal of Physiology & Pharmacology Vol.14 No.2
Impairment in spinal inhibition caused by quantitative alteration of GABAergic elements following peripheral nerve injury has been postulated to mediate neuropathic pain. In the present study, we tested whether neuropathic pain could be induced or reversed by pharmacologically modulating spinal GABAergic activity, and whether quantitative alteration of spinal GABAergic elements after peripheral nerve injury was related to the impairment of GABAergic inhibition or neuropathic pain. To these aims, we first analyzed the pain behaviors following the spinal administration of GABA antagonists (1Ռg bicuculline/rat and 5Ռg phaclofen/rat), agonists (1Ռg muscimol/rat and 0.5Ռg baclofen/rat) or GABA transporter (GAT) inhibitors (20Ռg NNC-711/rat and 1Ռg SNAP-5114/rat) into naïve or neuropathic animals. Then, using Western blotting, PCR or immunohistochemistry, we compared the quantities of spinal GABA, its synthesizing enzymes (GAD65, 67) and its receptors (GABA<sub>A</sub> and GABA<sub>B</sub>) and transporters (GAT-1, and -3) between two groups of rats with different severity of neuropathic pain following partial injury of tail-innervating nerves; the allodynic and non-allodynic groups. Intrathecal administration of GABA antagonists markedly lowered tail-withdrawal threshold in naïve animals, and GABA agonists or GAT inhibitors significantly attenuated neuropathic pain in nerve-injured animals. However, any quantitative changes in spinal GABAergic elements were not observed in both the allodynic and non-allodynic groups. These results suggest that although the impairment in spinal GABAergic inhibition may play a role in mediation of neuropathic pain, it is not accomplished by the quantitative change in spinal elements for GABAergic inhibition and therefore these elements are not related to the generation of neuropathic pain following peripheral nerve injury.
Jang, In Jeong,Davies, Alexander J.,Akimoto, Nozomi,Back, Seung Keun,Lee, Pa Reum,Na, Heung Sik,Furue, Hidemasa,Jung, Sung Jun,Kim, Yong Ho,Oh, Seog Bae John Wiley and Sons Inc. 2017 Physiological reports Vol.5 No.8
<P><B>Abstract</B></P><P>Gamma‐aminobutyric acid (GABA) depolarizes dorsal root ganglia (DRG) primary afferent neurons through activation of Cl<SUP>−</SUP> permeable GABAA receptors but the physiologic role of GABAA receptors in the peripheral terminals of DRG neurons remains unclear. In this study, we investigated the role of peripheral GABAA receptors in nociception using a mouse model of acute inflammation. In vivo, peripheral administration of the selective GABAA receptor agonist muscimol evoked spontaneous licking behavior, as well as spinal wide dynamic range (WDR) neuron firing, after pre‐conditioning with formalin but had no effect in saline‐treated mice. GABAA receptor‐mediated pain behavior after acute formalin treatment was abolished by the GABAA receptor blocker picrotoxin and cyclooxygenase inhibitor indomethacin. In addition, treatment with prostaglandin E2 (PGE<SUB>2</SUB>) was sufficient to reveal muscimol‐induced licking behavior. In vitro, GABA induced sub‐threshold depolarization in DRG neurons through GABAA receptor activation. Both formalin and PGE<SUB>2</SUB> potentiated GABA‐induced Ca<SUP>2+</SUP> transients and membrane depolarization in capsaicin‐sensitive nociceptive DRG neurons; these effects were blocked by the prostaglandin E2 receptor 4 (EP4) antagonist AH23848 (10 <I>μ</I>mol/L). Furthermore, potentiation of GABA responses by PGE<SUB>2</SUB> was prevented by the selective Na<SUB>v</SUB>1.8 antagonist A887826 (100 nmol/L). Although the function of the Na<SUP>+</SUP>‐K<SUP>+</SUP>‐2Cl<SUP>‐</SUP> co‐transporter NKCC1 was required to maintain the Cl<SUP>‐</SUP> ion gradient in isolated DRG neurons, NKCC1 was not required for GABAA receptor‐mediated nociceptive behavior after acute inflammation. Taken together, these results demonstrate that GABAA receptors may contribute to the excitation of peripheral sensory neurons in inflammation through a combined effect involving PGE<SUB>2</SUB>‐EP4 signaling and Na<SUP>+</SUP> channel sensitization.</P>
허근태,나중균 경성대학교 생산기술연구소 1996 생산기술연구지 Vol.3 No.-
The flame retardant ABS polymer was prepared with various inorganic and organic flame retardant agents. Especially, PVC was known a good flame retardant polymer and economical substrate. The effect of retardant agents concentration and mechanical and optical properties of the blends (ABS-PVC) were studied. Blends structures were investigated by scanning electron microscopy. A viriuos mechanical and optical properties were affected by additives, monomers, and pre-polymers.
임근우,박일영,유승진,나병호,오동렬,전해명,황주일,김세경 대한응급의학회 1995 대한응급의학회지 Vol.6 No.1
We reviewed retrospectively 230 patients who came to emergency room of Kang Nam St. Mary's Hospital and Uijongbu St. Mary's Hospital between 1. January and 31. December 1994. We classified them according to their age, sex, a sort of drug, the cause of poisoning, prehospital care, time-lapse to arrive at hospital after poisoning, psychiatric problem the status of patients. *We conclude as follows; 1. The male to female ratio was totally 1 : 1.98, 1 : 1.24 in a urban area, 1 : 2.43 in a rural area. 2. On age of the patients in this study, the peake incidence was between 20 and 39(55.2%). 3. On seasonal prevalence, the poisoning was most common in summer and spring, in urban area(35.7%) and rural area(37.0%) respectively. 4. The common drug were as follow; Doxylamine, Organophosphate, Acetaminophen in urban area, Paraquat, Organophospate, Doxylamine in rural area 5. The percentage of suicidal attempt were 81.8% and 87.7% in urban area and rural area respectively. 6. The poisoning patients had psychatric problem in 19.4% and 24.6%, in urban area and rural area respectively. 7. Before arrival to emergency room, 27.7% of patient was done prehospital care in rural area. 8. On arrival to emergency room, 95.1% and 73.8% of patients show stable vital sign in urban area and rural area respectively.