RESUMEN
Marine phytoplankton are primary producers in ocean ecosystems and emit dimethyl sulfide (DMS) into the atmosphere. DMS emissions are the largest biological source of atmospheric sulfur and are one of the largest uncertainties in global climate modeling. DMS is oxidized to methanesulfonic acid (MSA), sulfur dioxide, and hydroperoxymethyl thioformate, all of which can be oxidized to sulfate. Ice core records of MSA are used to investigate past DMS emissions but rely on the implicit assumption that the relative yield of oxidation products from DMS remains constant. However, this assumption is uncertain because there are no long-term records that compare MSA to other DMS oxidation products. Here, we share the first long-term record of both MSA and DMS-derived biogenic sulfate concentration in Greenland ice core samples from 1200 to 2006 CE. While MSA declines on average by 0.2 µg S kg-1 over the industrial era, biogenic sulfate from DMS increases by 0.8 µg S kg-1. This increasing biogenic sulfate contradicts previous assertions of declining North Atlantic primary productivity inferred from decreasing MSA concentrations in Greenland ice cores over the industrial era. The changing ratio of MSA to biogenic sulfate suggests that trends in MSA could be caused by time-varying atmospheric chemistry and that MSA concentrations alone should not be used to infer past primary productivity.
RESUMEN
Gold nanoparticle (AuNP)-Au film constructs were prepared using antibody-antigen interactions or a small organic cross-linker to systematically control the gap between the AuNP and Au film. Surface-enhanced Raman spectroscopy (SERS), scanning electron micrsocopy (SEM), and atomic force microscopy (AFM) were used to characterize each construct and elucidate structure-activity relationships. Interestingly, plasmonic coupling and SERS intensity were reversibly modulated with wetting/drying cycles for the protein immobilized AuNP, and this effect was attributed to changes in protein size with hydration state. This work provides insight into fundamental limitations of AuNP-enabled SERS bioassays and will facilitate rational design of novel biospecific ligands that maximize SERS sensitivity.