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Surface-enhanced Raman Spectroscopy (SERS) is a powerful optical sensing technique that amplifies the signal generated by Raman scattering by many orders of magnitude. Although the extreme sensitivity of SERS enables an extremely low limit of detection, even down to single molecule levels, it is also a primary limitation of the technique due to its tendency to equally amplify 'noise' generated by non-specifically adsorbed molecules at (or near) SERS-active interfaces. Eliminating interference noise is thus critically important to SERS biosensing and typically involves onerous extraction/purification/washing procedures and/or heavy dilution of biofluid samples. Consequently, direct analysis within biofluid samples or in vivo environments is practically impossible. In this study, an anti-fouling coating of recombinant human Lubricin (LUB) was self-assembled onto AuNP-modified glass slides via a simple drop-casting method. A series of Raman spectra were collected using rhodamine 6G (R6G) as a model analyte, which was spiked into NaCl solution or unprocessed whole blood. Likewise, we demonstrate the same sensing system for the quantitative detection of L-cysteine spiked in undiluted milk. It was demonstrated for the first time that LUB coating can mitigate the deleterious effect of fouling in a SERS sensor without compromising the detection of a target analyte, even in a highly fouling, complex medium like whole blood or milk. This feat is achieved through a molecular sieving property of LUB that separates small analytes from large fouling species directly at the sensing interface resulting in SERS spectra with low background ( i.e. , noise) levels and excellent analyte spectral fidelity. These findings indicate the great potential for using LUB coatings together with an analyte-selective layer to form a hierarchical separation system for SERS sensing of relevant analytes directly in complex biological media, aquaculture, food matrix or environmental samples.

Non-viral gene transfer into skeletal muscle in vivo is enhanced by electroporation (EP) to efficiencies far beyond any other (non-EP) method reported to date. Electroporation consistently delivers high levels of transgene to muscle and has been used extensively for the delivery of therapeutic transgenes to dystrophic mouse muscle such as the mdx mouse model of human Duchenne muscular dystrophy (DMD). Since the earliest applications, electroporation has consistently and reproducibly achieved highly efficient DNA delivery to a high proportion (greater than 70%) of fibres in treated muscles. This manuscript describes a methodology for introduction of corrective nucleic acids (CNAs) for the purpose of correcting the dystrophin gene (DMD ( mdx )) mutation responsible for muscular dystrophy in the mdx mouse model of human DMD by targeted corrective gene conversion (TCGC).