Pharmaceutical drugs and vaccines require the use of material containers for protection, storage, and transportation. Glass and plastic materials are widely used for packaging, and a longstanding challenge in the field is the nonspecific adsorption of pharmaceutical drugs to container walls -the so-called "sticky containers, vanishing drugs" problem -that effectively reduces the active drug concentration and can cause drug denaturation. This challenge has been frequently discussed in the case of the anticancer drug, paclitaxel, and the ongoing coronavirus disease 2019 (COVID-19) pandemic has brought renewed attention to this material science challenge in light of the need to scale up COVID-19 vaccine production and to secure sufficient quantities of packaging containers. To reduce nonspecific adsorption on inner container walls, various strategies based on siliconization and thin polymer films have been explored, while it would be advantageous to develop mass-manufacturable, natural material solutions, especially ones involving pharmaceutical grade excipients. Inspired by how lipid nanoparticles have revolutionized the vaccine field, in this perspective, we discuss the prospects for developing lipid bilayer coatings to prevent nonspecific adsorption of pharmaceutical drugs and vaccines and how recent advances in lipid bilayer coating fabrication technologies are poised to accelerate progress in the field. We critically discuss recent examples of how lipid bilayer coatings can prevent nonspecific sticking of proteins and vaccines to relevant material surfaces and examine future translational prospects.

The innate immune response is a central process that is activated during pathogenic infection in order to maintain physiological homeostasis. It is well known that dexamethasone (Dex), a synthetic glucocorticoid, is a potent immunosuppressant that inhibits the cytokine production induced by bacterial lipopolysaccharides (LPS). Nevertheless, the extent to which the functional groups of Dex control the excessive activation of inflammatory reactions remains unknown. Furthermore, importantly, the role of Dex in the innate immune response remains unclear. Here we explore the mechanism of LPS-induced TNF-α secretion and reveal p38 MAPK signaling as a target of Dex that is involved in control of tumor necrosis factor-α (TNF-α)-converting enzyme (TACE) activity; that later mediates the shedding of TNF-α that allows its secretion. We further demonstrate that the 11-hydroxyl and 21-hydroxyl groups of Dex are the main groups that are involved in reducing LPS-induced TNF-α secretion by activated macrophages. Blockage of the hydroxyl groups of Dex inhibits immunosuppressant effect of Dex during LPS-induced TNF-α secretion and mouse mortality. Our findings demonstrate Dex signaling is involved in the control of innate immunity.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) is an environmental toxicant with a polyhalogenated aromatic hydrocarbon structure and is one of the most toxic man-made chemicals. Exposure to 2,3,7,8-TCDD induces reproductive toxicity, immunotoxicity, and hepatotoxicity. In this study, we evaluated how 2,3,7,8-TCDD-induced hepatotoxicity affect the expression of heat shock proteins and antioxidant enzymes using the real-time polymerase chain reaction (PCR) in rat. 2,3,7,8-TCDD increased heat shock protein (Hsp27, α-B-crystallin, Mortalin, Hsp105, and Hsp90s) and antioxidant enzymes (SOD-3, GST and catalase) expression after a 1 day exposure in livers of rats, whereas heat shock protein (α-B-crystallin, Hsp90, and GRP78) and antioxidant enzymes (SOD-1, SOD-3, catalase, GST, and GPXs) expression decreased on day 2 and then slowly recovered back to control levels on day 8. These results suggest that heat shock proteins and antioxidant enzymes were induced as protective mechanisms against 2,3,7,8-TCDD induced hepatotoxicity, and that prolonged exposure depressed their levels, which recovered to control levels due to reduced 2,3,7,8-TCDD induced hepatotoxicity.

The enzyme-linked immunosorbent assay (ELISA) is a widely used method for protein detection and relies on the specific capture of target proteins while minimizing the nonspecific binding of other interfering proteins and biomolecules. To prevent nonspecific binding events, blocking agents such as bovine serum albumin (BSA) protein, mixtures of proteins in media such as milk or serum, and/or surfactants are typically added to ELISA plates after probe attachment and before analyte capture. Herein, we developed a streamlined ELISA strategy in which readily prepared lipid nanoparticles are utilized as the blocking agent and are added together with the probe molecule to the ELISA plate, resulting in fewer processing steps, quicker protocol time, and superior detection performance compared to conventional BSA blocking. These measurement capabilities were established for coronavirus disease-2019 (COVID-19) antibody detection in saline and human serum conditions and are broadly applicable for developing rapid ELISA diagnostics.

We have cloned and characterized two genes for Photosystem II from chloroplasts of Panax ginseng. These genes, psbL and psbJ, comprise 117 and 123 nucleotides, respectively. When compared with monocots, dicots, or liverwort, the overall amino acid sequence identity of the former is >97%, whereas that of the latter is approximately 95 to 100%. Southern blot analysis revealed that a single copy of each gene exists in the chloroplast genome. Our Northern blot analysis indicated that psbL and psbJ are co-transcribed as a polycistron and are not subjected to further processing into smaller transcripts. We also determined that varying daylight intensities (5, 10, 20, or 100%) did not significantly change the level of in vivo accumulation of psbLJ transcript.