Introduction: Humans are intentionally exposed to gold nanoparticles (AuNPs) where they are used in variety of biomedical applications as imaging and drug delivery agents as well as diagnostic and therapeutic agents currently in clinic and in a variety of upcoming clinical trials. Consequently, it is critical that we gain a better understanding of how physiochemical properties such as size, shape, and surface chemistry drive cellular uptake and AuNP toxicity in vivo. Understanding and being able to manipulate these physiochemical properties will allow for the production of safer and more efficacious use of AuNPs in biomedical applications. Methods and Materials: Here, AuNPs of three sizes, 5 nm, 10 nm, and 20 nm, were coated with a lipid bilayer composed of sodium oleate, hydrogenated phosphatidylcholine, and hexanethiol. To understand how the physical features of AuNPs influence uptake through cellular membranes, sum frequency generation (SFG) was utilized to assess the interactions of the AuNPs with a biomimetic lipid monolayer composed of a deuterated phospholipid 1.2-dipalmitoyl-d62-sn-glycero-3-phosphocholine (dDPPC). Results and Discussion: SFG measurements showed that 5 nm and 10 nm AuNPs are able to phase into the lipid monolayer with very little energetic cost, whereas, the 20 nm AuNPs warped the membrane conforming it to the curvature of hybrid lipid-coated AuNPs. Toxicity of the AuNPs were assessed in vivo to determine how AuNP curvature and uptake influence cell health. In contrast, in vivo toxicity tested in embryonic zebrafish showed rapid toxicity of the 5 nm AuNPs, with significant 24 hpf mortality occurring at concentrations ≥20 mg/L, whereas the 10 nm and 20 nm AuNPs showed no significant mortality throughout the five-day experiment. Conclusion: By combining information from membrane models using SFG spectroscopy with in vivo toxicity studies, a better mechanistic understanding of how nanoparticles (NPs) interact with membranes is developed to understand how the physiochemical features of AuNPs drive nanoparticle-membrane interactions, cellular uptake, and toxicity.

Petroleum asphaltenes are surface-active compounds found in crude oils, and their interactions with surfaces and interfaces have huge implications for many facets of reservoir exploitation, including production, transportation, and oil−water separation. The asphaltene fraction in oil, found in the highest boiling-point range, is composed of many different molecules that vary in size, functionality, and polarity. Studies done on asphaltene fractions have suggested that they interact via polyaromatic and heteroaromatic ring structures and functional groups containing nitrogen, sulfur, and oxygen. However, isolating a single pure chemical structure of asphaltene in abundance is challenging and often not possible, which impairs the molecular-level study of asphaltenes of various architectures on surfaces. Thus, to further the molecular fundamental understanding, we chose to use functionalized model asphaltenes (AcChol-Th, AcChol-Ph, and 1,6-DiEtPy[Bu-Carb]) and model self-assembled monolayer (SAM) surfaces with precisely known chemical structures, whereby the hydrophobicity of the model surface is controlled. We applied solutions of asphaltenes to these SAM surfaces and then analyzed them with surface-sensitive techniques of near-edge X-ray absorption fine structure (NEXAFS) and X-ray photoelectron spectroscopy (XPS). We observe no adsorption of asphaltenes to the hydrophobic surface. On the hydrophilic surface, AcChol-Ph penetrates into the SAM with a preferential orientation parallel to the surface; AcChol-Th adsorbs in a similar manner, and 1,6-DiEtPy[Bu-Carb] binds the surface with a bent binding geometry. Overall, this study demonstrates the need for studying pure and fractionated asphaltenes at the molecular level, as even within a family of asphaltene congeners, very different surface interactions can occur.

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While in most cases, jaundice can be effectively treated using phototherapy, severe cases require exchange transfusion, a relatively risky procedure in which the neonate's bilirubin-rich blood is replaced with donor blood. Here, we examine extracorporeal blood treatment in a microfluidic photoreactor as an alternative to exchange transfusion. This new treatment approach relies on the same principle as phototherapy but leverages microfluidics to speed up bilirubin removal. Our results demonstrate that high-intensity light at 470 nm can be used to rapidly reduce bilirubin levels without causing appreciable damage to DNA in blood cells. Light at 470 nm was more effective than light at 505 nm. Studies in Gunn rats show that photoreactor treatment for 4 h significantly reduces bilirubin levels, similar to the bilirubin reduction observed for exchange transfusion and on a similar time scale. Predictions for human neonates demonstrate that this new treatment approach is expected to exceed the performance of exchange transfusion using a low blood flow rate and priming volume, which will facilitate vascular access and improve safety.