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Targeting Pancreatic Cancer Cells and Stellate Cells Using Designer Nanotherapeutics in vitro.
Int J Nanomedicine
June 2020
Department of Pathology, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.
Article Synopsis
- Pancreatic cancer features a dense tissue environment that hinders effective delivery of the chemotherapy drug gemcitabine, making treatment challenging.
- A targeted drug delivery system was developed using gold nanoparticles and the anti-EGFR antibody cetuximab, combined with gemcitabine and polyethylene glycol to enhance drug delivery to pancreatic cancer and associated cells.
- The new drug delivery system, particularly the PEGylated nanoconjugate ACG44P1000, showed improved effectiveness in reducing the viability of pancreatic cancer cells in lab tests, setting the stage for future studies on its potential to combat tumor growth and desmoplasia in living organisms.*
Developmental pattern of the neuronal intermediate filament inaa in the zebrafish retina.
J Comp Neurol
December 2016
Department of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei, Taiwan.
α-Internexin is a member of the neuronal intermediate filament (nIF) protein family, which also includes peripherin and neurofilament (NF) triplet proteins. Previous studies found that expression of α-internexin precedes that of the NF triplet proteins in mammals and suggested that α-internexin plays a key role in the neuronal cytoskeleton network during development. In this study, we aimed to analyze the expression patterns and function of internexin neuronal intermediate filament protein-alpha a (inaa), the encoding gene of which is a homolog of the mammalian α-internexin, during retinal development in zebrafish.
View Article and Find Full Text PDFMineral content of calcified tissues in cystic fibrosis mice.
Biol Trace Elem Res
October 2001
Dalton Cardiovascular Research Center and the Department of Veterinary Biomedical Sciences, University of Missouri-Columbia, 65211, USA.
Although abnormal hard tissue mineralization is a recognized complication of cystic fibrosis (CF), the pathogenesis leading from the defective cystic fibrosis transmembrane conductance regulator (CFTR) protein is poorly understood. We hypothesized that CFTR plays a direct role in the mineralization of bone and teeth and tested the hypothesis using CF mouse models [CFTR(-) mice]. In vivo measurements by dual-emission X-ray absorpitometry (DEXA) indicated that bone mineral density (BMD) was reduced in CF mice as compared to gender-matched littermates.
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