• BMB Reports
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• 제46권2호
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• pp.124-129
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• 2013

FK506 binding protein 12 (FK506BP) belongs to a family of immunophilins, and is involved in multiple biological processes. However, the function of FK506BP in corneal disease remains unclear. In this study, we examined the protective effects on dry eye disease in a Botulinum toxin A (BTX-A) induced mouse model, using a cell-permeable PEP-1-FK506BP protein. PEP-1-FK506BP efficiently transduced into human corneal epithelial cells in a time- and dose-dependent manner, and remained stable in the cells for 48 h. In addition, we demonstrated that topical application of PEP-1-FK506BP was transduced into mouse cornea and conjunctiva by immunohistochemistry. Furthermore, topical application of PEP-1-FK506BP to BTX-A-induced mouse model markedly inhibited expression levels of pro-inflammatory cytokines such as interleukin-$1{\beta}$ (IL-$1{\beta}$), tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) and macrophage inhibitory factor (MIF) in corneal and conjunctival epithelium. These results suggest PEP-1-FK506BP as a potential therapeutic agent for dry eye diseases.

• 한국통신학회논문지
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• 제38B권9호
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• pp.700-706
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• 2013

본 논문에서는 위성 통신에서 신뢰성 향상을 위한 랜덤 선형 네트워크 코딩 적용 기술을 제안한다. 제안하는 프로토콜에서는 PEP (Performance Enhancement Proxy)에서 네트워크 코딩된 여분의 패킷을 전송하여 만약 데이터 패킷이 무선 채널 에러에 의해 손실되었다 할지라도 복구 할 수 있다. 또한 본 논문에서는 제안한 프로토콜을 위성 통신에 적용했을 때의 TCP 처리율 수학적 모델을 제시하고 제안한 프로토콜의 성능을 평가했다. 성능 평가 결과, 제안하는 프로토콜은 발신 측 PEP에서 여분의 네트워크 코딩된 패킷을 전송하고 수신 측 PEP에서 여분의 네트워크 코딩된 패킷을 이용하여 손실된 패킷을 복구하기 때문에 패킷 손실률을 감소시켜 기존 TCP보다 처리율 측면에서 우수한 성능을 나타냈다.

• BMB Reports
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• 제53권2호
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• pp.106-111
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• 2020

Glutaredoxin 1 (GLRX1) has been recognized as an important regulator of redox signaling. Although GLRX1 plays an essential role in cell survival as an antioxidant protein, the function of GLRX1 protein in inflammatory response is still under investigation. Therefore, we wanted to know whether transduced PEP-1-GLRX1 protein inhibits lipopolysaccharide (LPS)- and 12-O-tetradecanoyl phorbol-13-acetate (TPA)-induced inflammation. In LPS-exposed Raw 264.7 cells, PEP-1-GLRX1 inhibited cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), activation of mitogen activated protein kinases (MAPKs) and nuclear factor-kappaB (NF-κB) expression levels. In a TPA-induced mouse-ear edema model, topically applied PEP-1-GLRX1 transduced into ear tissues and significantly ameliorated ear edema. Our data reveal that PEP-1-GLRX1 attenuates inflammation in vitro and in vivo, suggesting that PEP-1-GLRX1 may be a potential therapeutic protein for inflammatory diseases.

• 기술혁신연구
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• 제16권2호
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• pp.95-123
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• 2008

As a medium for communication on science and technology, science museum could be important to adults who finished formal school education. By analysing all the exhibits at the National Science Museum and conducting a face-to-face interview survey toward 100 adult visitors, based on the PEP / IS model's perspective(Kim, 2007), this study aimed to find a way to induce many adults to visit science museum from the information consumer's viewpoint, not the information provider's one. The result was that most of the exhibits were not related to problems which people focused attention on. About half of visitors, therefore, did not relate their problems with exhibits and responded that there was no relationship between exhibits and their everyday life. However, they had an idea that science and technology could contribute to solving their problems. These findings could suggest that first, science exhibits in relation to people's focused problems or issues are to be developed, second, programs for parents who are accompanied by their children are to be developed, and last, adults' engagement in planning the science museum exhibits is to be considered.

• BMB Reports
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• 제49권7호
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• pp.382-387
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• 2016

Reactive oxygen species generated under oxidative stress are involved in neuronal diseases, including ischemia. Glutathione S-transferase pi (GSTpi) is a member of the GST family and is known to play important roles in cell survival. We investigated the effect of GSTpi against oxidative stress-induced hippocampal HT-22 cell death, and its effects in an animal model of ischemic injury, using a cell-permeable PEP-1-GSTpi protein. PEP-1-GSTpi was transduced into HT-22 cells and significantly protected against H2O2-treated cell death by reducing the intracellular toxicity and regulating the signal pathways, including MAPK, Akt, Bax, and Bcl-2. PEP-1-GSTpi transduced into the hippocampus in animal brains, and markedly protected against neuronal cell death in an ischemic injury animal model. These results indicate that PEP-1-GSTpi acts as a regulator or an antioxidant to protect against oxidative stress-induced cell death. Our study suggests that PEP-1-GSTpi may have potential as a therapeutic agent for the treatment of ischemia and a variety of oxidative stress-related neuronal diseases.

• BMB Reports
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• 제45권9호
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• pp.532-537
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• 2012

P18, a member of the INK4 family of cyclin-dependent kinase inhibitors, is a tumor suppressor protein and plays a key cell survival role in a variety of human cancers. Under pathophysiological conditions, the INK4 group proteins participate in novel biological functions associated with neuronal diseases and oxidative stress. Parkinson's disease (PD) is characterized by loss of dopaminergic neurons, and oxidative stress is important in its pathogenesis. Therefore, we examined the effects of PEP-1-p18 on oxidative stress-induced SH-SY5Y cells and in a PD mouse model. The transduced PEP-1-p18 markedly inhibited 1-methyl-4-phenyl pyridinium-induced SH-SY5Y cell death by inhibiting Bax expression levels and DNA fragmentation. Additionally, PEP-1-p18 prevented dopaminergic neuronal cell death in the substantia nigra of a 1-methyl-4-phenyl-1,2,3,6,-tetrahydropyridine-induced PD mouse model. These results indicate that PEP-1-p18 may be a useful therapeutic agent against various diseases and is a potential tool for treating PD.

• BMB Reports
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• 제48권7호
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• pp.395-400
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• 2015

Parkinson's disease (PD) is a neurodegenerative disability caused by a decrease of dopaminergic neurons in the substantia nigra (SN). Although the etiology of PD is not clear, oxidative stress is believed to lead to PD. Catalase is antioxidant enzyme which plays an active role in cells as a reactive oxygen species (ROS) scavenger. Thus, we investigated whether PEP-1-Catalase protects against 1-methyl-4-phenylpyridinium (MPP⁺) induced SH-SY5Y neuronal cell death and in a 1-methyl-4-phenyl-1,2,3,6-trtrahydropyridine (MPTP) induced PD animal model. PEP-1-Catalase transduced into SH-SY5Y cells significantly protecting them against MPP⁺-induced death by decreasing ROS and regulating cellular survival signals including Akt, Bax, Bcl-2, and p38. Immunohistochemical analysis showed that transduced PEP-1-Catalase markedly protected against neuronal cell death in the SN in the PD animal model. Our results indicate that PEP-1-Catalase may have potential as a therapeutic agent for PD and other oxidative stress related diseases. [BMB Reports 2015; 48(7): 395-400]

• 대한방사성의약품학회지
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• 제2권2호
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• pp.96-102
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• 2016

Apoptosis, a genetically determined process of programmed cell death, is considered a vital component of various processes including normal cell turnover, animal development, and tissue homeostasis. It has a crucial role in many medical disorders and hence the development of non-invasive imaging tool is highly demanded. Recently, we have developed a peptide-based radioactive probe (ApoPep-1) for apoptosis detection. In that work the potential of probe for apoptosis detection was verified, however in vivo stability of radiolabeled peptide was not enough to monitor apoptosis for extended period. In current study, we prepared cyclic ApoPep-1 peptides to improve the stability of origianl linear ApoPep-1 and carried out direct comparison studies in vitro and in vivo. A targeting efficacy of newly synthesized cyclic ApoPep-1 peptide for apoptosis was confirmed in acute myocardial infarct model.

• 정보처리학회논문지D
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• 제16D권4호
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• pp.561-570
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• 2009

모바일 환경에서 유지보수의 효율적인 관리를 위해서는 서비스를 정책으로 관리하기 위한 시스템 구조와 정책정의언어가 필요하다. 본 연구는 IETF의 정책 프레임웍 중에 정책 실행자인 PEP 구조를 정의하고, PEP 구조하에서 수행될 수 있는 정책정의언어를 제안한다. 제안한 정책정의언어는 문헌자료와 모바일 특성을 기반으로 하여 요구사항을 도출하고, 3단계 접근 방법으로 정책정보모델을 설계하여 정책정의언어로 정의하였다. 3단계 접근 방법은 정책이 적용될 범위를 결정하는 정책도메인, 정책 적용 및 제어하는 종류를 구분하는 정책규칙, 정책 구조를 문맥화하는 정책문법으로 구성된다. 제안한 정책정의언어의 효율성을 검증하기 위하여 시나리오를 정책정의언어로 정의하여 정책 도구를 이용하여 검증하였고, 타 정책정의언어들과 비교 분석하여 확장성을 입증하였다.

• BMB Reports
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• 제48권11호
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• pp.618-623
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• 2015

FK506 binding protein 12 (FK506BP) is a small peptide with a single FK506BP domain that is involved in suppression of immune response and reactive oxygen species. FK506BP has emerged as a potential drug target for several inflammatory diseases. Here, we examined the protective effects of directly applied cell permeable FK506BP (PEP-1-FK506BP) on corneal alkali burn injury (CAI). In the cornea, there was a significant decrease in the number of cells expressing pro-inflammation, apoptotic, and angiogenic factors such as TNF-α, COX-2, and VEGF. Both corneal opacity and corneal neovascularization (CNV) were significantly decreased in the PEP-1-FK506BP treated group. Our results showed that PEP-1-FK506BP can significantly inhibit alkali burn-induced corneal inflammation in rats, possibly by accelerating corneal wound healing and by reducing the production of angiogenic factors and inflammatory cytokines. These results suggest that PEP-1-FK506BP may be a potential therapeutic agent for CAI.