Matrix Assisted Pulsed Laser Evaporation of Dexamethasone Thin Films
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Matrix Assisted Pulsed Laser Evaporation of Dexamethasone Thin Films Timothy M. Patz1, Anand Doraiswamy1, Roger J. Narayan1 Nicola Menegazzo2, Christine Kranz2, Boris Mizakoff2 Yinghui Zhong3, Ravi Bellamkonda3 Rohit Modi4, Douglas B. Chrisey4 1
Bioengineering Program and School of Material Science and Engineering, Georgia Institute of Technology, Atlanta, GA, USA 2 Georgia Institute of Technology, School of Chemistry and Biochemistry, Atlanta - GA 30332-0400, USA 3 Coulter Department of Biomedical Engineering, Georgia Institute of Technology, NW, Atlanta, GA, USA 4 US Naval Research Laboratory, Washington, DC, USA ABSTRACT We have demonstrated deposition of dexamethasone thin films via matrix assisted pulsed laser evaporation (MAPLE). Infrared analysis revealed that dexamethasone thin films deposited by MAPLE and by drop casting had a similar absorbance spectra. AFM imaging of the MAPLE-deposited dexamethasone thin film revealed 2-10 µm punctuate ring-like structures. Deposited dexamethasone was tested for positive bioactivity by treating primary microglia cells with lipopolysacchride and measuring nitric oxide (NO) production. The successful deposition of dexamethasone thin films can be used on neural implants to prevent tissue injury and inflammatory response. INTRODUCTION The implantation of neural sensors is characterized by several vascular and cellular processes, including fibroblast proliferation, collagen synthesis, and blood vessel proliferation [1-2]. These events lead to the formation of an avascular connective tissue capsule that surrounds the implant. The connective tissue capsule consists of several different cellular layers, including an inner layer of macrophages, a concentric layer of fibrous tissue and fibroblasts (30–100 µm), and an outer vascularized tissue layer. This dense fibrous tissue retards the transport of low-molecular weight molecules (e.g., glucose) due to steric hindrance and increased diffusion path tortuosity. Steroidal antiinflammatory agents may serve to counter inflammation through release of vasoactive and chemoattractive factors, changes in the circulatory kinetics of leukocytes, alterations in the function of inflammatory cells, and modification of soluble mediators. These antiinflammatory actions must be provided during acute (24-48 hours) and chronic (1-2 weeks) phases of the inflammatory response in order to prevent encapsulation and ensure normal tissue growth. Long-term systemic use of steroids is not desirable. Individuals on systemic steroid therapy are more susceptible to viral, bacterial, and fungal infections. In addition, many side effects, including posterior subcapsular cataracts, glaucoma, and peptic ulcers, may result from systemic use of corticosteroids. Local, continuous,
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controlled release of steroids reduces systemic side effects and improves the therapeutic response at the implant site [3]. One of the most widely used methods for coating organic materials onto implants is dip coating, in which an implant is placed in an appropriate sol
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