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1.
ACS Sens ; 3(7): 1392-1400, 2018 07 27.
Article in English | MEDLINE | ID: mdl-29888907

ABSTRACT

Implementing large arrays of gold nanowires as functional elements of a plasmonic biosensor is an important task for future medical diagnostic applications. Here we present a microfluidic-channel-integrated sensor for the label-free detection of biomolecules, relying on localized surface plasmon resonances. Large arrays (∼1 cm2) of vertically aligned and densely packed gold nanorods to receive, locally confine, and amplify the external optical signal are used to allow for reliable biosensing. We accomplish this by monitoring the change of the optical nanostructure resonance in the presence of biomolecules within the tight focus area above the nanoantennas, combined with a surface treatment of the nanowires for a specific binding of the target molecules. As a first application, we detect the binding kinetics of two distinct DNA strands as well as the following hybridization of two complementary strands (cDNA) with different lengths (25 and 100 bp). Upon immobilization, a redshift of 1 nm was detected; further backfilling and hybridization led to a peak shift of additional 2 and 5 nm for 25 and 100 bp, respectively. We believe that this work gives deeper insight into the functional understanding and technical implementation of a large array of gold nanowires for future medical applications.


Subject(s)
DNA/analysis , Gold/chemistry , Nanowires/chemistry , Surface Plasmon Resonance/instrumentation , Equipment Design , Immobilized Nucleic Acids/chemistry , Lab-On-A-Chip Devices , Nucleic Acid Hybridization , Refractometry
2.
PLoS One ; 13(5): e0196649, 2018.
Article in English | MEDLINE | ID: mdl-29763442

ABSTRACT

Despite the technological progress made with cochlear implants (CI), impedances and their diagnosis remain a focus of interest. Increases in impedance have been related to technical defects of the electrode as well as inflammatory and/or fibrosis along the electrode. Recent studies have demonstrated highly increased impedances as the result of corroded platinum (Pt) electrode contacts. This in vitro study examined the effects of Pt ions and compounds generated by corrosion of the electrode contacts of a human CI on cell metabolism. Since traces of solid Pt in surrounding cochlear tissues have been reported, the impact of commercially available Pt nanoparticles (Pt-NP, size 3 nm) on the cell culture model was also determined. For this purpose, the electrode contacts were electrically stimulated in a 0.5% aqueous NaCl solution for four weeks and the mass fraction of the platinum dissolute (Pt-Diss) was determined by mass spectrometry (ICP-MS). Metabolic activity of the murine fibroblasts (NIH 3T3) and the human neuroblastoma (SH-SY5Y) cells was determined using the WST-1 assay following exposure to Pt-Diss and Pt-NP. It was found that 5-50 µg/ml of the Pt-NP did not affect the viability of both cell types. In contrast, 100 µg/ml of the nanoparticles caused significant loss in metabolic activity. Furthermore, transmission electron microscopy (TEM) revealed mitochondrial swelling in both cell types indicating cytotoxicity. Additionally, TEM demonstrated internalized Pt-NP in NIH 3T3 cells in a concentration dependent manner, whereas endocytosis in SH-SY5Y cells was virtually absent. In comparison with the Pt-NP, the corrosion products (Pt-Diss) with concentrations between 1.64 µg/ml and 8.2 µg/ml induced cell death in both cell lines in a concentration dependent manner. TEM imaging revealed both mitochondrial disintegration and swelling of the endoplasmic reticulum, suggesting that Pt ions trigger cytotoxicity in both NIH 3T3 and SH-SY5Y cell lines by interacting with the respiratory chain.


Subject(s)
Cell Death/drug effects , Metal Nanoparticles/administration & dosage , Metal Nanoparticles/chemistry , Platinum/administration & dosage , Platinum/chemistry , Animals , Cell Culture Techniques , Cell Line, Tumor , Cell Survival/drug effects , Cochlear Implantation/methods , Cochlear Implants , Corrosion , Electrodes , Endocytosis/drug effects , Endoplasmic Reticulum/drug effects , Humans , Mice , Mitochondria/drug effects , NIH 3T3 Cells
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