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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. National Research Foundation (NRF) Published version This work was supported by the National Research Foundation of Singapore through a Proof-of-Concept grant (NRF2015NRF-POC0001-19) and by National Research Foundation of Korea (NRF) grants funded by the Korean government (MSIT) (2020R1C1C1004385 and2020R1C1C1005523). In addition, this work was supported by Brain Pool Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science and ICT (2019H1D3A1A01070318). This research was also supported by the International Research & Development Program of the National Research Foundation of Korea (NRF) funded by the Ministry of Science and ICT(2020K1A3A1A39112724).

Glehnia littoralis has been reported to have several pharmacological properties but no reports describing the antiadipogenic effect of this plant have been published. This study was conducted to investigate the effects of Glehnia littoralis root hot water extract (GLE) and its underlying mechanism on 3T3-L1 cell adipogenesis and in high-fat diet- (HFD-) induced obese mice. We measured intracellular lipid accumulation using oil red O staining in vitro. For in vivo study, twenty-eight C57BL/6J male mice were randomly divided into four groups, Control, HFD, HFD + 1% GLE, and HFD + 5% GLE, which was performed for eight weeks. We determined the expression levels of the adipogenesis-related proteins by RT-PCR and western blotting in HFD-induced obese mice. The GLE dose-dependently inhibited 3T3-L1 adipocyte differentiation and intracellular lipid accumulation in differentiated adipocytes. Further, body weight gain and fat accumulation were significantly lower in the GLE-treated HFD mice than in the untreated HFD mice. GLE treatment suppressed the expression of adipogenic genes such as peroxisome proliferator-activated receptor (PPAR) γ, CCAAT/enhancer-binding protein (C/EBP) α, fatty acid synthase (aP2), and fatty acid synthase (FAS). These results suggest that the GLE inhibits adipocyte differentiation and intracellular lipid accumulation by downregulating the adipogenic gene expression both in vitro and in vivo.

Microglia are a type of resident macrophage that functions as an inflammation modulator in the central nervous system. Over-activation of microglia by a range of stimuli disrupts the physiological homeostasis of the brain, and induces inflammatory response and degenerative processes, such as those implicated in neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease. Therefore, we investigated the possible anti-inflammatory mechanisms of inflexanin B in murine microglial BV2 cells. Lipopolysaccharide (LPS) activated BV2 cells and induced the production of pro-inflammatory mediators such as nitric oxide (NO), prostaglandin E2 (PGE2), and cytokines (interleukins-1β and -6, and tumour necrosis factor α). The LPS-induced production of pro-inflammatory mediators was associated with the enhancement of nuclear factor-kappaB (NF-κB) nuclear translocation and the activation of mitogen-activated protein kinase (MAPK) including ERK1/2 and JNK. Conversely, pretreatment of cells with inflexanin B (10 and 20 μg/mL) significantly reduced the production of pro-inflammatory mediators. This was accompanied with the reduced nuclear translocation of NF-κB and reduced activation of MAPKs. These results suggest that inflexanin B attenuated the LPS-induced inflammatory process by inhibiting the activation of NF-κB and MAPKs.

Toluene, a clear, colorless liquid with a distinctive smell, is the most commonly used industrial organic solvent. The adverse effects of chronic toluene exposure have been reported. The abuse of volatile substances is practiced mainly by adolescents and young adults. Chronic toluene abuse causes permanent changes in brain structure correlated with brain dysfunction; therefore, it is important to monitor the level of toluene exposure to prevent neurological damages. In this study, immunochromatographic analysis was performed to measure a level of the exposed toluene easily and accurately in urine. Inhaled toluene is metabolized to hippuric acid (HA) in the liver and secreted in urine. Therefore, the monoclonal antibodies against HA were generated and characterized by indirect competitive ELISA. The sensitivity was then monitored in order to adjust the cutoff concentration to 2 mg of HA/mL of urine. Using these monoclonal antibodies as raw materials, the immunochromatographic device was manufactured with the lateral flow system. The clinical studies were performed with suspected users' urine samples, and the results were confirmed by high-performance liquid chromatography.

We have cloned and characterized two genes for Photosystem II from chloroplasts ofPanax ginseng. These genes,psbl andpsbJ, 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 thatpsbL andpsb) 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 ofin vivo accumulation ofpsbLJ transcript

The phosphate-specific transport substrate binding protein-1 (PstS1) is a potential antigen used for the serological diagnosis of tuberculosis. For a highly specific diagnostic result, it is important that the recombinant PstS1 be highly pure and correctly folded. In this study, the PstS1 was expressed as fusion protein with glutathione-S-transferase (PstS1-GST) and Escherichia coli trigger factor (PstS1-TF) and their immunodiagnostic potentials were evaluated. The insoluble PstS1-GST was denatured and refolded to the native conformation by a step-gradient dilution, followed by purification with affinity chromatography on immobilized glutathione whereas the soluble PstS1-TF was directly purified by Ni-NTA affinity and size-exclusion chromatographies. The levels of antibody responses to PstS1-TF and PstS1-GST were measured by enzyme-linked immunosorbent assay (ELISA) in the sera of 22 tuberculosis patients with smear-positive and culture-positive tuberculosis as well as 20 healthy individuals; the antigenicities of the samples were evaluated in terms of sensitivity and specificity. To determine the diagnostic accuracy, receiver operation characteristic (ROC) curves were constructed and then the areas under the ROC curves (AUC) were calculated; the AUC values for PstS1-TF and PstS1-GST were 0.971 and 0.877 with 95% confidence intervals (CI) of 0.927-1.000 and 0.768-0.986, respectively. The specificity of PstS1-TF was reduced from 89.5% to 84.2%, but in case of PstS1-GST it dropped drastically from 78.9% to 26.3% when the sensitivity was raised from 86.4% up to 95.5%. These results indicate that PstS1-TF is capable of producing more accurate and consistent serodiagnostic results than PstS1-GST, possibly due to its conformation being closer to the native state.

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.

Alzheimer’s disease (AD) is one of the most well-known neurodegenerative diseases and explains 50–60% of dementia in patients. The prevalence rate of AD is positively correlated with age and AD affects ≥ 40% of those over 85 years old. The major AD therapeutics available on the market are acetylcholinesterase inhibitors, such as tacrine and donepezil. New therapeutic agents that can block the disease-inducing mechanisms are essential. Diverse efforts have been made to discover anti-AD agents from natural sources. In this review article, we describe some representative terpenoids such as ginsenosides, gingkolides, and canabinoids as potential anti-AD agents. These compounds exhibit promising in vitro and in vivo biological activities, but are still waiting clinical trials. Additionally, we also discuss some terpenoids including cornel iridoid glycoside, oleanolic acid, tenuifolin, cryptotanshinone, and ursolic acid, which are under investigation for their in vitro and in vivo animal studies.