• Title/Summary/Keyword: Johns Hopkins University

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The Central Concept for Chitin Catabolic Cascade in Marine Bacterium, Vibrios

  • Jung, Byung-Ok;Roseman, Saul;Park, Jae-Kweon
    • Macromolecular Research
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    • v.16 no.1
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    • pp.1-5
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    • 2008
  • The enzymatic hydrolysis of chitin has been studied for almost a century, and early work established that at least two enzymes are required, a chitinase that mainly yields the disaccharide N,N'-diacetylchitobiose, or $(GlcNAc)_2$, and a "chitobiase", or ${\beta}$-N-acetylglucosaminidase, which gives the final product G1cNAc. This pathway has not been completely identified but has remained the central concept for the chitin catabolism through the $20^{th}$ century1 including in marine bacteria. However, the chitin catabolic cascade is quite complex, as described in this review. This report describes three biologically functional genes involved in the chitin catabolic cascade of Vibrios in an attempt to better understand the metabolic pathway of chitin.

Anti-inflammatory activity of methanol extract isolated from stem bark of Albizia julibrissin

  • Na, Ho-Jeong;Cha, Dong-Seok;Jeon, Hoon
    • Advances in Traditional Medicine
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    • v.9 no.2
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    • pp.157-163
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    • 2009
  • Albizia julibrissin (AJ) has been used widely as a traditional medicine. In macrophages nitric oxide (NO) is released as an inflammatory mediator and has been proposed to be an important modulator of many pathophysiological conditions including inflammation and carcinogenesis. In this study we have examined the NO inhibition effect of 85% methanol extracts of AJ in mouse macrophage. Lipopolysaccharide (LPS) has been reported to induce production of NO. Extracts of AJ (1, 10, $100{\mu}g/ml$) suppressed nitric oxide production in LPS-stimulated ($100{\mu}g/ml$) mouse (C57BL/6) macrophages and analyzed by ELISA. In addition, it also attenuated the expression of inflammatory products like Interleukin-6 (IL-6), cyclooxygenase-2 (COX-2), and inducible NOS (iNOS) as assessed by immunoblotting with specific antibodies. These results suggest that 85% methanol extracts of AJ would be useful in inflammatory diseases.

Cell-Based Screen Using Amyloid Mimic β23 Expression Identifies Peucedanocoumarin III as a Novel Inhibitor of α-Synuclein and Huntingtin Aggregates

  • Ham, Sangwoo;Kim, Hyojung;Hwang, Seojin;Kang, Hyunook;Yun, Seung Pil;Kim, Sangjune;Kim, Donghoon;Kwon, Hyun Sook;Lee, Yun-Song;Cho, MyoungLae;Shin, Heung-Mook;Choi, Heejung;Chung, Ka Young;Ko, Han Seok;Lee, Gum Hwa;Lee, Yunjong
    • Molecules and Cells
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    • v.42 no.6
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    • pp.480-494
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    • 2019
  • Aggregates of disease-causing proteins dysregulate cellular functions, thereby causing neuronal cell loss in diverse neurodegenerative diseases. Although many in vitro or in vivo studies of protein aggregate inhibitors have been performed, a therapeutic strategy to control aggregate toxicity has not been earnestly pursued, partly due to the limitations of available aggregate models. In this study, we established a tetracycline (Tet)-inducible nuclear aggregate (${\beta}23$) expression model to screen potential lead compounds inhibiting ${\beta}23$-induced toxicity. High-throughput screening identified several natural compounds as nuclear ${\beta}23$ inhibitors, including peucedanocoumarin III (PCIII). Interestingly, PCIII accelerates disaggregation and proteasomal clearance of both nuclear and cytosolic ${\beta}23$ aggregates and protects SH-SY5Y cells from toxicity induced by ${\beta}23$ expression. Of translational relevance, PCIII disassembled fibrils and enhanced clearance of cytosolic and nuclear protein aggregates in cellular models of huntingtin and ${\alpha}$-synuclein aggregation. Moreover, cellular toxicity was diminished with PCIII treatment for polyglutamine (PolyQ)-huntingtin expression and ${\alpha}$-synuclein expression in conjunction with 6-hydroxydopamine (6-OHDA) treatment. Importantly, PCIII not only inhibited ${\alpha}$-synuclein aggregation but also disaggregated preformed ${\alpha}$-synuclein fibrils in vitro. Taken together, our results suggest that a Tet-Off ${\beta}23$ cell model could serve as a robust platform for screening effective lead compounds inhibiting nuclear or cytosolic protein aggregates. Brain-permeable PCIII or its derivatives could be beneficial for eliminating established protein aggregates.

Motor Imagery based Brain-Computer Interface for Cerebellar Ataxia (소뇌 운동실조 이상 환자를 위한 운동상상 기반의 뇌-컴퓨터 인터페이스)

  • Choi, Young-Seok;Shin, Hyun-Chool;Ying, Sarah H.;Newman, Geoffrey I.;Thakor, Nitish
    • Journal of the Korean Institute of Intelligent Systems
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    • v.24 no.6
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    • pp.609-614
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    • 2014
  • Cerebellar ataxia is a steadily progressive neurodegenerative disease associated with loss of motor control, leaving patients unable to walk, talk, or perform activities of daily living. Direct motor instruction in cerebella ataxia patients has limited effectiveness, presumably because an inappropriate closed-loop cerebellar response to the inevitable observed error confounds motor learning mechanisms. Recent studies have validated the age-old technique of employing motor imagery training (mental rehearsal of a movement) to boost motor performance in athletes, much as a champion downhill skier visualizes the course prior to embarking on a run. Could the use of EEG based BCI provide advanced biofeedback to improve motor imagery and provide a "backdoor" to improving motor performance in ataxia patients? In order to determine the feasibility of using EEG-based BCI control in this population, we compare the ability to modulate mu-band power (8-12 Hz) by performing a cued motor imagery task in an ataxia patient and healthy control.