10 research outputs found

    Computational study for optimization of a plasmon FET as a molecular biosensor

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    Surface Plasmon Resonance (SPR) is currently being widely studied as it exhibits sensitive optical properties to changes in in the refractive index of the surrounding medium. As novel devices using SPR have been developing rapidly there is a necessity to develop models and simulation environments that will allow for continued development and optimization of these devices. A biological sensing device of interest is the Plasmon FET which has been proven experimentally to have a limit of detection (LOD) of 20pg/ml while being immune to the absorption of the medium. The Plasmon FET is a metal-semiconductor-metal detector which employ functionalized gold nanostructures on a semi-conducting layer. This direct approach has the advantages of not requiring readout optics reducing size and allowing for point-of -care measurements. Using Lumerical FDTD and Device numerical solvers, we can report an advanced simulation environment illustrating several key sensor specifications including LOD, resolution, sensitivity, and dynamic range, for a variety of biological markers providing a comprehensive analysis of a Direct Plasmon-to-Electric conversion device designed to function with colored mediums (eg.whole blood). This model allows for the simulation and optimization of a plasmonic sensor that already o ers advantages in size, operability, and multiplexing-capability, with real time monitoring

    Efficient broadband energy detection from the visible to near-infrared using a plasmon FET

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    Plasmon based field effect transistors (FETs) can be used to convert energy induced by incident optical radiation to electrical energy. Plasmonic FETs can efficiently detect incident light and amplify it by coupling to resonant plasmonic modes thus improving selectivity and signal to noise ratio. The spectral responses can be tailored both through optimization of nanostructure geometry as well as constitutive materials. In this paper, we studied various plasmonic nanostructures using gold for a wideband spectral response from visible to near-infrared. We show, using empirical data and simulation results, that detection loss exponentially increases as the volume of metal nanostructure increases and also a limited spectral response is possible using gold nanostructures in a plasmon to electric conversion device. Finally, we demonstrate a plasmon FET that offers a broadband spectral response from visible to telecommunication wavelengths

    Mutational spectrum of type I collagen genes in Korean patients with osteogenesis imperfecta

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    Mutations in the type I collagen genes COL1A1 and COL1A2 are responsible for the dominantly inherited connective tissue disorder osteogenesis imperfecta (OI). The severity of OI is diverse, ranging from perinatal lethality to a very mild phenotype that is characterized by normal stature and the absence of deformities. Although there have been several studies on the mutational spectra of COL1A1 and/or COL1A2 in Western populations, very few cases have been reported from Asia. In this study, we investigated 67 unrelated Korean probands with OI and used nucleotide sequence analysis to detect COL1A1 and COL1A2 mutations. Thirty-five different mutations were identified in the two genes, including 24 novel mutations. Among the 35 kinds of detected mutations, 15 were glycine substitutions (seven in COL1A1 and eight in COL1A2), one was a nonsense mutation, four were frameshift mutations in COL1A1, three were in-frame duplications in COL1A2, and 12 were splice site mutations (seven in COL1A1 and five in COL1A2). Until now, mutations in the COL1A1 and COL1A2 genes known to cause OI were unique and rarely repeated in other families. Interestingly, the c.982G>A (p.Gly328Ser) mutation in COL1A2 was found recurrently and was the causative mutation in five independent OI probands. Haplotype analysis of the COL1A2 gene revealed that four probands from five independent OI probands with c.982G>A (p.Gly328Ser) had a common haplotype. Our clinical data showed the heterogeneity even within a specific genotype, which suggested the complex expression of this disease.Research grant from the National Institute of Health, Korea; Grant number: 347-6111-211-207

    Intracellular amyloid beta interacts with SOD1 and impairs the enzymatic activity of SOD1: implications for the pathogenesis of amyotrophic lateral sclerosis

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    Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease caused by the degeneration of motor neurons. Mutations in Cu/Zn superoxide dismutase (SOD1), including G93A, were reportedly linked to familial ALS. SOD1 is a key antioxidant enzyme, and is also one of the major targets for oxidative damage in the brains of patients suffering from Alzheimer's disease (AD). Several lines of evidence suggest that intracellular amyloid beta (Aβ) is associated with the pathogenesis of AD. In this report we demonstrate that intracellular Aβ directly interacts with SOD1, and that this interaction decreases the enzymatic activity of the enzyme. We observed Aβ-SOD1 aggregates in the perinuclear region of H4 cells, and mapped the SOD1 binding region to Aβ amino acids 26-42. Interestingly, intracellular Aβ binds to the SOD1 G93A mutant with greater affinity than to wild-type SOD1. This resulted in considerably less mutant enzymatic activity. Our study implicates a potential role for Aβ in the development of ALS by interacting with the SOD1 G93A mutant
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