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- 저자 : ( David. A. Norris ) (검색결과 5 건)
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류순효,Lindsey Broussard,윤차경,Brendon Song,David Norris,Cheryl A. Armstrong,Beom Joon Kim,Peter I Song 전남대학교 의과학연구소 2019 전남의대학술지 Vol.55 No.2
Psoriasis is a chronic, recurrent, heterogeneous, cutaneous inflammatory skin disease for which there is no cure. It affects approximately 7.5 million people in the United States. Currently, several biologic agents that target different molecules implicated in the pathogenic processes of psoriasis are being assessed in diverse clinical studies. However, relapse usually occurs within weeks or months, meaning there is currently no cure for psoriasis. Therefore, recent studies have discovered diverse new potential treatments for psoriasis: inhibitors of bacteria such as Staphylococcus aureus, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and neuropilin 1 (NRP1). A promising approach that has recently been described involves modifying antimicrobial peptides to develop new cutaneous anti-bacterial agents that target inflammatory skin disease induced by Staphylococcus. Increased expression of TRAIL and its death receptors DR4 and DR5 has been implicated in the pathogenesis of plaque psoriasis. In addition, TRAIL has the ability to inhibit angiogenesis by inducing endothelial cell death and by negative regulation of VEGF-induced angiogenesis via caspase-8-mediated enzymatic and non-enzymatic functions. Since NRP1 regulates angiogenesis induced by multiple signals, including VEGF, ECM and semaphorins, and also initiates proliferation of keratinocytes through NF-kB signaling pathway in involved psoriatic skin, targeting NRP1 pathways may offer numerous windows for intervention in psoriasis. In this review, we will focus on the current knowledge about the emerging role of synthetic antimicrobial peptides, TRAIL and NRP1 blocking peptides in the pathogenesis and treatment of psoriasis.
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Melanoma Cell Death Mechanisms
Lindsey Broussard,Amanda Howland,류순효,Kyungsup Song,David Norris,Cheryl A. Armstrong,Peter I Song 전남대학교 의과학연구소 2018 전남의대학술지 Vol.54 No.3
Over recent years, several new molecular and immunogenic therapeutic approaches to melanoma treatment have been approved and implemented in clinical practice. Mechanisms of resistance to these new therapies have become a major problem. Mutation-specific pharmacotherapy can result in simultaneous emergence of resistant clones at many separate body sites despite an initially positive therapeutic response. Additionally, treatments aimed at inducing apoptosis are subject to resistance due to escape through other known mechanisms of regulated cell death (RCD). In this review, we discuss the complexity in pharmacological manipulation of melanoma with c-Kit, BRAF, MEK, and/or mTOR mutant cell lines. This study also addresses melanoma evasion of cell death through modalities of RCD such as apoptosis, autophagy, and necroptosis. This study also examines new combination therapies which have been approved to target both cell cycle dysregulation and cell death pathways. Lastly, we recognize the importance of immunomodulation though manipulation of the body’s natural killing mechanisms with CTLA4, PD1, and CSF1 inhibition. As we begin to recognize tumor cell activation of alternate pathways, evasion of programmed cell death, and manipulation of the tumor microenvironment, it is increasingly important to grasp the complexity of personalized therapy in melanoma treatment.
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인체 각질형성세포와 KB 세포에서의 Fas 항체 , IFN - γ , IL - 1α에 의한 apoptosis 유발에 관한 연구
이홍규,황규왕,박영립,김영근,( Hong Kyu Lee,Kyu Uang Whang,Young Lip Park,Young Keun Kim,David A Norris ) 대한피부과학회 1997 大韓皮膚科學會誌 Vol.35 No.2
Background: The Fas antigen is a cell surface molecule that mediates apoptosis in many cell types. Matsues group indicated that keratinocytes constitutively express the Fas antigen and apoptosis was induced only on pretreatment with interferon-r(IFN-y) in cultured normal human keratinocytes(NHK). Objective : We undertook this study to determine the induction of apoptosis by Fas antibody alone and/or in combination with IFN y, IL-1a in normal human keratinocytes(NHK) and transitional epithelioma cell lines(KB cell) which had lower levels of intracellular IL-1 receptor antago- nists(IL-1ra ). Methods : We used cultured NHK and KB cells. Each cell was treated with IFN-r, IL-la and Fas antibody for induction of apoptosis. For quantifying the apoptosis, index fluorescent DNA- binding dyes were used. Result: Fas antibody alone could induce apoptosis not only in KB cells but also in NHK cells. The combination of Fas antibody and IFN-r enhanced the induction of apoptosis in NHK and KB cells. The IL-la alone could induce apoptosis only in KB cells which had relatively small amounts of IL-1ra compared to NHK. Conclusion : Our result may indicate that Fas antigen in human keratinocytes can regulate normal epidermal cellular differentiation and proliferation. (Kor J Dermatol 1997;35(2): 273-278)
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Complex Chiral Colloids and Surfaces via High-Index Off-Cut Silicon
McPeak, Kevin M.,van Engers, Christian D.,Blome, Mark,Park, Jong Hyuk,Burger, Sven,Gosá,lvez, Miguel A.,Faridi, Ava,Ries, Yasmina R.,Sahu, Ayaskanta,Norris, David J. American Chemical Society 2014 NANO LETTERS Vol.14 No.5
<P>Silicon wafers are commonly etched in potassium hydroxide solutions to form highly symmetric surface structures. These arise when slow-etching {111} atomic planes are exposed on standard low-index surfaces. However, the ability of nonstandard high-index wafers to provide more complex structures by tilting the {111} planes has not been fully appreciated. We demonstrate the power of this approach by creating chiral surface structures and nanoparticles of a specific handedness from gold. When the nanoparticles are dispersed in liquids, gold colloids exhibiting record molar circular dichroism (>5 × 10<SUP>9</SUP> M<SUP>–1</SUP> cm<SUP>–1</SUP>) at red wavelengths are obtained. The nanoparticles also present chiral pockets for binding.</P><P><B>Graphic Abstract</B> <IMG SRC='http://pubs.acs.org/appl/literatum/publisher/achs/journals/content/nalefd/2014/nalefd.2014.14.issue-5/nl501032j/production/images/medium/nl-2014-01032j_0005.gif'></P><P><A href='http://pubs.acs.org/doi/suppl/10.1021/nl501032j'>ACS Electronic Supporting Info</A></P>
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