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Byungwook Kim

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Articles

Tobramycin pharmacokinetic and pharmacodynamic targets in people with cystic fibrosis

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By Byungwook Kim, Kiera H. Harwood, Sarah Bannister
| British Pharmacological Society
1 INTRODUCTION Cystic fibrosis (CF) is a life-limiting, monogenetic disorder caused by a mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, characterized by chronic lung disease and affecting approximately 1 in 3000 births.1 People with CF are vulnerable to recurrent pulmonary infections with bacteria such as Staphylococcus aureus, Haemophilus influenzae and Pseudomonas aeruginosa.2 The prevalence of P.
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Deletion of SPI1 in microglia exacerbates amyloid pathology by impairing microglial response in Alzheimer’s disease models

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By Byungwook Kim, Hande Karahan, H.R. Sagara Wijeratne, Ahmad Daniel Sharify, Selena Wang, Justin Kim, Mamun Al-Amin, Kelly Hartigan, Luke Child Dabin, Dominic J Acri, Emma H. Doud, Sutha K. John, Amber L. Mosley, Jungsu Kim, Mason Douglas Tate, Sunwoo Chung
| Cell Press Verified
Keywords Alzheimer’s disease amyloid amyloidosis microglia SPI1 PU.1 Syk Lyn Fcgr1 phagocytosis Introduction Alzheimer’s disease (AD) is a progressive neurodegenerative disorder histologically characterized by the accumulation of amyloid-beta (Aβ) plaques, neurofibrillary tangles, and dystrophic neurites.
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The acetyltransferase GCN5 contributes to neuroinflammation in mice by acetylating and activating the NF-κB subunit p65 in microglia

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By Byungwook Kim, Duk-Yeon Cho, Amy Baek, Jun-Hyuk Han
| Science Magazine Verified
Editor’s summary The acetyltransferase GCN5 is implicated in various diseases involving inflammation in peripheral tissues. Cho et al. found that GCN5 mediates inflammation in the brain as well, suggesting that it may be a target for treating neuroinflammatory diseases. In mice, inducing an innate immune response in the periphery (to mimic an infection) selectively increased the abundance of GCN5 in microglia in the brain.
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