Dataset Information

Quantitative SERS by hot spot normalization - surface enhanced Rayleigh band intensity as an alternative evaluation parameter for SERS substrate performance.

ABSTRACT: The performance of surface-enhanced Raman spectroscopy (SERS) substrates is typically evaluated by calculating an enhancement factor (EF). However, it is challenging to accurately calculate EF values since the calculation often requires the use of model analytes and requires assumptions about the number of analyte molecules within the laser excitation volume. Furthermore, the measured EF values are target analyte dependent and thus it is challenging to compare substrates with EF values obtained using different analytes. In this study, we propose an alternative evaluation parameter for SERS substrate performance that is based on the intensity of the surface plasmon enhanced Rayleigh band (IRayleigh) that originates from the amplified spontaneous emission (ASE) of the laser. Compared to the EF, IRayleigh reflects the enhancing capability of the substrate itself, is easy to measure without the use of any analytes, and is universally applicable for the comparison of SERS substrates. Six SERS substrates with different states (solid, suspended in liquid, and hydrogel), different plasmonic nanoparticle identities (silver and gold), as well as different nanoparticle sizes and shapes were used to support our hypothesis. The results show that there are excellent correlations between the measured SERS intensities and IRayleigh as well as between the SERS homogeneity and the variation of IRayleigh acquired with the six SERS substrates. These results suggest that IRayleigh can be used as an evaluation parameter for both SERS substrate efficiency and reproducibility.

SUBMITTER: Wei H

PROVIDER: S-EPMC5709184 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature

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Quantitative SERS by hot spot normalization - surface enhanced Rayleigh band intensity as an alternative evaluation parameter for SERS substrate performance.

Wei Haoran H McCarthy Alexis A Song Junyeob J Zhou Wei W Vikesland Peter J PJ

Faraday discussions 20171201

The performance of surface-enhanced Raman spectroscopy (SERS) substrates is typically evaluated by calculating an enhancement factor (EF). However, it is challenging to accurately calculate EF values since the calculation often requires the use of model analytes and requires assumptions about the number of analyte molecules within the laser excitation volume. Furthermore, the measured EF values are target analyte dependent and thus it is challenging to compare substrates with EF values obtained ...[more]

PMID: 28926064

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Project description:Heterozygous missense mutations in the N-terminal motor or coiled-coil domains of the kinesin family member 5A (KIF5A) gene cause monogenic spastic paraplegia (HSP10) and Charcot-Marie-Tooth disease type 2 (CMT2). Moreover, heterozygous de novo frame-shift mutations in the C-terminal domain of KIF5A are associated with neonatal intractable myoclonus, a neurodevelopmental syndrome. These findings, together with the observation that many of the disease genes associated with amyotrophic lateral sclerosis disrupt cytoskeletal function and intracellular transport, led us to hypothesize that mutations in KIF5A are also a cause of amyotrophic lateral sclerosis. Using whole exome sequencing followed by rare variant analysis of 426 patients with familial amyotrophic lateral sclerosis and 6137 control subjects, we detected an enrichment of KIF5A splice-site mutations in amyotrophic lateral sclerosis (2/426 compared to 0/6137 in controls; P = 4.2 × 10-3), both located in a hot-spot in the C-terminus of the protein and predicted to affect splicing exon 27. We additionally show co-segregation with amyotrophic lateral sclerosis of two canonical splice-site mutations in two families. Investigation of lymphoblast cell lines from patients with KIF5A splice-site mutations revealed the loss of mutant RNA expression and suggested haploinsufficiency as the most probable underlying molecular mechanism. Furthermore, mRNA sequencing of a rare non-synonymous missense mutation (predicting p.Arg1007Gly) located in the C-terminus of the protein shortly upstream of the splice donor of exon 27 revealed defective KIF5A pre-mRNA splicing in respective patient-derived cell lines owing to abrogation of the donor site. Finally, the non-synonymous single nucleotide variant rs113247976 (minor allele frequency = 1.00% in controls, n = 6137), also located in the C-terminal region [p.(Pro986Leu) in exon 26], was significantly enriched in familial amyotrophic lateral sclerosis patients (minor allele frequency = 3.40%; P = 1.28 × 10-7). Our study demonstrates that mutations located specifically in a C-terminal hotspot of KIF5A can cause a classical amyotrophic lateral sclerosis phenotype, and underline the involvement of intracellular transport processes in amyotrophic lateral sclerosis pathogenesis.

Dataset Information

Quantitative SERS by hot spot normalization - surface enhanced Rayleigh band intensity as an alternative evaluation parameter for SERS substrate performance.

Publications

Quantitative SERS by hot spot normalization - surface enhanced Rayleigh band intensity as an alternative evaluation parameter for SERS substrate performance.

Similar Datasets

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