Titanium dioxide nanoparticles (nano‐TiO2) are widely used in consumer products, raising environmental and health concerns. An overview of the toxic effects of nano‐TiO2 on human and environmental health is provided. A meta‐analysis is conducted to analyze the toxicity of nano‐TiO2 to the liver, circulatory system, and DNA in humans. To assess the environmental impacts of nano‐TiO2, aquatic environments that receive high nano‐TiO2 inputs are focused on, and the toxicity of nano‐TiO2 to aquatic organisms is discussed with regard to the present and predicted environmental concentrations. Genotoxicity, damage to membranes, inflammation and oxidative stress emerge as the main mechanisms of nano‐TiO2 toxicity. Furthermore, nano‐TiO2 can bind with free radicals and signal molecules, and interfere with the biochemical reactions on plasmalemma. At the higher organizational level, nano‐TiO2 toxicity is manifested as the negative effects on fitness‐related organismal traits including feeding, reproduction and immunity in aquatic organisms. Bibliometric analysis reveals two major research hot spots including the molecular mechanisms of toxicity of nano‐TiO2 and the combined effects of nano‐TiO2 and other environmental factors such as light and pH. The possible measures to reduce the harmful effects of nano‐TiO2 on humans and non‐target organisms has emerged as an underexplored topic requiring further investigation.

Peptide antigens have been widely used in the development of vaccines, especially for those against autoimmunity-inducing pathogens and cancers. However, peptide-based vaccines require adjuvant and/or a delivery system to stimulate desired immune responses. Here, we explored the potential of self-adjuvanting poly­(hydrophobic amino acids) (pHAAs) to deliver peptide-based vaccine against Group A Streptococcus (GAS). We designed and synthesized self-assembled nanoparticles with a variety of conjugates bearing a peptide antigen (J8-PADRE) and polymerized hydrophobic amino acids to evaluate the effects of structural arrangement and pHAAs properties on a system’s ability to induce humoral immune responses. Immunogenicity of the developed conjugates was also compared to commercially available human adjuvants. We found that a linear conjugate bearing J8-PADRE and 15 copies of leucine induced equally effective, or greater, immune responses than commercial adjuvants. Our fully defined, adjuvant-free, single molecule-based vaccine induced the production of antibodies capable of killing GAS bacteria.

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Dictamni Cortex (DC) has been reported to be associated with acute hepatitis in clinic and may lead to a selective sub-chronic hepatotoxicity in rats. Nevertheless, the potent toxic ingredient and the underlying mechanism remain unknown. Dictamnine (DTN), the main alkaloid from DC, possesses a furan ring which was suspected of being responsible for hepatotoxicity via metabolic activation primarily by CYP3A4. Herein, the present study aimed to evaluate the role of CYP3A4 in DTN-induced liver injury. The in vitro results showed that the EC50 values in primary human hepatocytes (PHH), L02, HepG2 and NIH3T3 cells were correlated with the CYP3A4 expression levels in corresponding cells. Furthermore, the toxicity was increased in CYP3A4-induced PHH by rifampicin, and CYP3A4 over-expressed (OE) HepG2 and L02 cells. Contrarily, the cytotoxicity was decreased in CYP3A4-inhibited PHH and CYP3A4 OE HepG2 and L02 cells inhibited by ketoconazole (KTZ). In addition, the hepatotoxicity of DTN in enzyme induction/inhibition mice was further investigated in the aspects of biochemistry, histopathology, and pharmacokinetics. Administration of DTN in combination with KTZ resulted in attenuated liver injury, including lower alanine transaminase and aspartate transaminase activities and greater AUC and Cmax of serum DTN, whereas, pretreatment with dexamethasone aggravated the injury. Collectively, our findings illustrated that DTN-induced hepatotoxicity correlated well with the expression of CYP3A4, namely inhibition of CYP3A4 alleviated the toxicity both in vitro and in vivo, and induction aggravated the toxicity effects.

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Tibetan nomads in the Tibetan Autonomous Region of China have experienced profound transitions in recent decades with important implications for land use, livelihoods, and health development. The change from being traditional nomads to agropastoralists engaged in permanent agriculture, a sedentary village life (known as "sedentarization"), has been associated with a remarkable change in diet and lifestyle, decline in spatial mobility, increase in food production, and emerging infectious and noncommunicable diseases. The overarching response of the government has been to emphasize infrastructure and technological solutions. The local adaptation strategies of Tibetan nomads through maintaining balanced mobile herding, reindeer husbandry, as well as off-farm labor and trade could address both the cause of environmental degradation and improve the well-being of local people. Drawing on transdisciplinary, preliminary field work in Gangga Township of Dingri County in the foothills of Mt. Everest, we identify pertinent linkages between land use and health, and spatial and temporal mismatch of livelihoods and health care services, in the transition to sedentary village life. We suggest emerging imperatives in Ecohealth to help restore Tibetan livelihoods in transition to a sedentary lifestyle.

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The use of herbal medicines continues to expand globally, meanwhile, herb-associated hepatotoxicity is becoming a safety issue. As a conventional Chinese medicinal herb, Dioscorea bulbifera rhizome (DBR) has been documented to cause hepatic toxicity. However, the exact underlying mechanism remains largely unexplored. In the present study, we aimed to profile entire endogenous metabolites in a biological system using a multisample integrated metabolomics strategy. Our findings offered additional insights into the molecular mechanism of the DBR-induced hepatotoxicity. We identified different metabolites from rat plasma, urine, and feces by employing gas chromatography-mass spectrometry in combination with multivariate analysis. In total, 55 metabolites distributed in 33 metabolic pathways were identified as being significantly altered in DBR-treated rats. Correlation network analysis revealed that the hub metabolites of hepatotoxicity were mainly associated with amino acid, bile acid, purine, pyrimidine, lipid, and energy metabolism. As such, DBR affected the physiological and biological functions of liver via the regulation of multiple metabolic pathways to an abnormal state. Notably, our findings also demonstrated that the multisample integrated metabolomics strategy has a great potential to identify more biomarkers and pathways in order to elucidate the mechanistic complexity of toxicity of traditional Chinese medicine.