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안구적출에 따른 위둔덕의 칼슘결합단백질의 재구축 및 상호 연관성
안병수,고길석,안명수,김경주,권안성,정명섭,박춘매,조병옥,김진우,Samudra Acharya,Parmeshwar Narayan Amatya,장인엽 朝鮮大學校 附設 醫學硏究所 2007 The Medical Journal of Chosun University Vol.32 No.1
Background: Superior colliculus is a part of midbrain, and participates in the visual reflexes, It receives afferent fibers from optic nerve, visual cortex, and spinotectal tract. After optic deprivation, the microscopic structure of the superior colliculus changed. Calcium-binding proteins (CBPs) Play an important role in the neuronal protection, differentiation and reorganization of the central nervous system, Objectives and Methods: The effects of neonatal retinal deafferentation on a CBPs, calbindm D-28k (CB), Parvalbumin (PB) and calretimn (CR), and the existence of colocalization between the CBPs were examined immunohistochemically in the rat superior colliculus. Results: On the experimental (contralateral to enucleation) side of superior colliculus, the number of CB-immunoreactive (IR) cells was reduced (77.4% compared to control), but not fibers. The number of PB-IR neurons and fibers was also reduced on the experimental side (88.5% compared to control), In the other hand, the CR-IR cells were dramatically increased (642% compared to control), but CR-IR fibers were markedly decreased on the experimental side. The colocalization between CB-CR and PV-CR was rarely observed in the superior colliculus Conclusion: These results suggest that the changes of retinotectal projection may alter the expressional pattern of CBPs in different manners; relatively stable in CB- and PV-IR neurons and plastic in CR-IR neurons.
아마티아 파머셔 나라얀,아카랴 사무드라,유호진 朝鮮大學校 附設 醫學硏究所 2007 The Medical Journal of Chosun University Vol.32 No.1
The response of eukaryotic cells to double-strand breaks in genomic DNA includes the sequestration of many factors into nuclear foci. Recently it has been reported that a member of the histone H2A family, H2AX, becomes extensively phosphorylated within 10-30 minutes of DNA damage and forms foci at break sites. Histone H2AX has a role in suppressing genomic instability and cancer. Phosphorylated H2AX (gamma-HZAX) is essential to the efficient recognition and (or) repair of DNA double strand breaks (DSBs), and many molecules, often thousands, of H2AX become rapidly phosphorylated at the site of each nascent DSB. gamma-H2AX foci formation is a sensitive biological dosimeter and presents new and exciting opportunities to understand important biological processes, human diseases, and individual variations in radiation sensitivity. These potentialities demonstrate the importance of understanding the parameters and functions of gamma-H2AX formation.
Kim, Mi-Hwa,Kim, Hong-Beum,Acharya, Samudra,Sohn, Hong-Moon,Jun, Jae Yeoul,Chang, In-Youb,You, Ho Jin American Society for Microbiology 2009 Molecular and cellular biology Vol.29 No.8
<B>ABSTRACT</B><P>Apurinic/apyrimidinic endonuclease 1 (Ape1/Ref-1) dysregulation has been identified in several human tumors and in patients with a variety of neurodegenerative diseases. However, the function of Ape1/Ref-1 is unclear. We show here that Ape1/Ref-1 increases the expression of glial cell-derived neurotropic factor (GDNF) receptor α1 (GFRα1), a key receptor for GDNF. Expression of Ape1/Ref-1 led to an increase in the GDNF responsiveness in human fibroblast. Ape1/Ref-1 induced <I>GFRα1</I> transcription through enhanced binding of NF-κB complexes to the <I>GFRα1</I> promoter. GFRα1 levels correlate proportionally with Ape1/Ref-1 in cancer cells. The knockdown of endogenous Ape1/Ref-1 in pancreatic cancer cells markedly suppressed GFRα1 expression and invasion in response to GNDF, while overexpression of GFRα1 restored invasion. In neuronal cells, the Ape1/Ref-1-mediated increase in GDNF responsiveness not only stimulated neurite outgrowth but also protected the cells from β-amyloid peptide and oxidative stress. Our results show that Ape1/Ref-1 is a novel physiological regulator of GDNF responsiveness, and they also suggest that Ape1/Ref-1-induced GFRα1 expression may play important roles in pancreatic cancer progression and neuronal cell survival.</P>
Ryu, Sunhyo,Choi, Soon-Yong,Acharya, Samudra,Chun, Young-Jin,Gurley, Catherine,Park, Yoonkyung,Armstrong, Cheryl A,Song, Peter I,Kim, Beom-Joon The Society for Investigative Dermatology, Inc 2011 The Journal of investigative dermatology Vol.131 No.8
The lipophilic fungus Malassezia furfur (M. furfur) is a commensal microbe associated with several chronic diseases such as pityriasis versicolor, folliculitis, and seborrheic dermatitis. Because M. furfur-related diseases are difficult to treat and require prolonged use of medications, the treatment for M. furfur-related skin diseases is supposed to gain control over M. furfur growth and the inflammation associated with it, as well as to prevent secondary infections. In this study, we investigated the antifungal and anti-inflammatory effects of cecropin A(1-8)–magainin 2(1-12) hybrid peptide analog P5 on M. furfur. The minimal inhibitory concentration of P5 against M. furfur was 0.39 μM, making it 3–4 times more potent than commonly used antifungal agents such as ketoconazole (1.5 μM) or itraconazole (1.14 μM). P5 efficiently inhibited the expression of IL-8 and Toll-like receptor 2 in M. furfur-infected human keratinocytes without eukaryotic cytotoxicity at its fungicidal concentration. Moreover, P5 significantly downregulated NF-κB activation and intracellular calcium fluctuation, which are closely related with enhanced responses of keratinocyte inflammation induced by M. furfur infection. Taken together, these observations suggest P5 may be a potential therapeutic agent for M. furfur-associated human skin diseases because of its distinct antifungal and anti-inflammatory action.