Co-Culturing Rat Dorsal Root Ganglion Neurons With Rat Schwann Cells Protects Them Against the Cytotoxic Effects of Silver and Gold Nanoparticles.

Previous studies using monotypic nerve cell cultures have shown that nanoparticles induced neurotoxic effects on nerve cells. Interactions between neurons and Schwann cells may protect against the neurotoxicity of nanoparticles. In this study, we developed a co-culture model consisting of immortalized rat dorsal root ganglion (DRG) neurons and rat Schwann cells and employed it to investigate our hypothesis that co-culturing DRG neurons with Schwann cells imparts protection on them against neurotoxicity induced by silver or gold nanoparticles. Our results indicated that neurons survived better in co-cultures when they were exposed to these nanoparticles at the higher concentrations compared to when they were exposed to these nanoparticles at the same concentrations in monotypic cultures. Synapsin I expression was increased in DRG neurons when they were co-cultured with Schwann cells and treated with or without nanoparticles. Glial fibrillary acidic protein (GFAP) expression was increased in Schwann cells when they were co-cultured with DRG neurons and treated with nanoparticles. Furthermore, we found co-culturing with Schwann cells stimulated neurofilament polymerization in DRG neurons and produced the morphological differentiation. Silver nanoparticles induced morphological disorganization in monotypic cultures. However, there were more cells displaying normal morphology in co-cultures than in monotypic cultures. All of these results suggested that co-culturing DRG neurons with Schwann cells imparted some protection on them against neurotoxicity induced by silver or gold nanoparticles, and altering the expression of neurofilament-L, synapsin I, and GFAP could account for the phenomenon of protection in co-cultures.

Evaluating Litigation as a Structural Strategy for Addressing Bias-Based Bullying Among Youth.

Importance: Homophobic bullying-which is motivated by actual or perceived sexual orientation-is a common experience among youth and is more strongly associated with adverse outcomes than bullying unrelated to bias. Yet current approaches to reducing homophobic bullying either lack empirical evidence or encounter significant obstacles. Thus, the field requires the identification of strategies that hold promise for reducing homophobic bullying. Objective: To examine whether litigation is associated with reductions in homophobic bullying. Design, Setting, and Participants: In this quasi-experimental study, difference-in-difference analysis was used to estimate the association between litigation and homophobic bullying, comparing students in schools that experienced litigation with students in schools that did not experience litigation, controlling for individual and school characteristics, study year, and county. Survey responses came from high school students from 499 schools participating in the California Healthy Kids Survey, the largest statewide survey of youth risk behaviors and protective factors, between 2001 and 2016. Legal data were collected from September 2018 to September 2019, and data were analyzed from February 2020 to April 2021. Exposures: Outcomes of litigation related to sexual orientation-based harassment and discrimination in California schools occurring after 2000. Main Outcomes and Measures: Student reports of homophobic bullying. Results: Of 1 448 778 included participants, 706 258 (48.7%) were male, 563 973 (38.9%) were White, and the mean (SD) age was 14.6 (1.7) years. For cases where the plaintiff (student) secured monetary and/or injunctive relief through settlement or court decision, there was a 23% reduction in the ratio of odds ratios (ROR) of homophobic bullying in schools directly involved in the litigation relative to schools that did not experience litigation (ROR, 0.77; 95% CI, 0.68-0.86). These benefits of litigation spilled over into schools in the same district as the schools experiencing litigation (ROR, 0.76; 95% CI, 0.70-0.81). However, homophobic bullying slightly increased in the school and district where the defendant (school) avoided adverse legal consequences, suggesting potential backlash. Conclusions and Relevance: Litigation seeking to address alleged violations of the rights of students who are (or are perceived to be) lesbian, gay, bisexual, or transgender under laws prohibiting harassment or discrimination may lead to reductions in rates of homophobic bullying, with effect sizes comparable with that of resource-intensive school-based bullying interventions. These findings set the stage for future studies to evaluate the consequences of different litigation efforts aimed at redressing stigma-based harms among youth.

Functional enhancement of chitosan and nanoparticles in cell culture, tissue engineering, and pharmaceutical applications.

As a biomaterial, chitosan has been widely used in tissue engineering, wound healing, drug delivery, and other biomedical applications. It can be formulated in a variety of forms, such as powder, film, sphere, gel, and fiber. These features make chitosan an almost ideal biomaterial in cell culture applications, and cell cultures arguably constitute the most practical way to evaluate biocompatibility and biotoxicity. The advantages of cell cultures are that they can be performed under totally controlled environments, allow high throughput functional screening, and are less costly, as compared to other assessment methods. Chitosan can also be modified into multilayer composite by combining with other polymers and moieties to alter the properties of chitosan for particular biomedical applications. This review briefly depicts and discusses applications of chitosan and nanoparticles in cell culture, in particular, the effects of chitosan and nanoparticles on cell adhesion, cell survival, and the underlying molecular mechanisms: both stimulatory and inhibitory influences are discussed. Our aim is to update the current status of how nanoparticles can be utilized to modify the properties of chitosan to advance the art of tissue engineering by using cell cultures.

Treatment of human astrocytoma U87 cells with silicon dioxide nanoparticles lowers their survival and alters their expression of mitochondrial and cell signaling proteins.

Recent evidence suggests silicon dioxide micro- and nanoparticles induce cytotoxic effects on lung cells. Thus, there is an increasing concern regarding their potential health hazard. Nevertheless, the putative toxicity of nanoparticles in mammalian cells has not yet been systematically investigated. We previously noted that several metallic oxide nanoparticles exert differential cytotoxic effects on human neural and nonneural cells. Therefore, we hypothesized that silicon dioxide nanoparticles induce cytotoxicity in U87 cells by lowering their survival by decreasing cell survival signaling and disturbing mitochondrial function. To investigate this hypothesis, we determined the activities of the key mitochondrial enzymes, citrate synthase and malate dehydrogenase, in astrocytoma U87 cells treated with silicon dioxide nanoparticles. In addition, we studied the expression of the mitochondrial DNA-encoded proteins, cytochrome C oxidase II and nicotinamide adenine dinucleotide (NADPH) dehydrogenase subunit 6, and cell signaling pathway protein extracellular signal-regulated kinase (ERK) and phosphorylated ERK in treated U87 cells. The activated form of ERK controls cell growth, differentiation, and proliferation. In parallel, we determined survival of U87 cells after treating them with various concentrations of silicon dioxide nanoparticles. Our results indicated that treatment with silicon dioxide nanoparticles induced decreases in U87 cell survival in a dose-related manner. The activities of citrate synthase and malate dehydrogenase in treated U87 cells were increased, possibly due to an energetic compensation in surviving cells. However, the expression of mitochondrial DNA-encoded cytochrome C oxidase subunit II and NADH dehydrogenase subunit 6 and the cell signaling protein ERK and phosphorylated ERK were altered in the treated U87 cells, suggesting that silicon dioxide nanoparticles induced disruption of mitochondrial DNA-encoded protein expression, leading to decreased mitochondrial energy production and decreased cell survival/proliferation signaling. Thus, our results strongly suggest that the cytotoxicity of silicon dioxide nanoparticles in human neural cells implicates altered mitochondrial function and cell survival/proliferation signaling.

A new approach to characterize biodegradation of organics by molecular mass distribution in landfill leachate.

This study provides biodegradability of organics in leachate according to their molecular mass distributions (<0.5, 0.5 to 1, 1 to 3, 10, and >10 KDa). Organics with molecular mass values lower than 0.5 KDa were the predominant species in the raw leachate filtrate, and the aerated lagoon process was very effective in treating these highly biodegradable organics; the Fenton's oxidation process was very effective in treating not-so-biodegradable organics with molecular mass values higher than 0.5 KDa, but a portion of these organics were converted into organics <0.5 KDa after Fenton's oxidation. An oxygen uptake measurement using a respirometer was more sensitive than a conventional biochemical oxygen demand measurement to evaluate bioactivities, especially when bioactivities were low.

Exposure to titanium dioxide and other metallic oxide nanoparticles induces cytotoxicity on human neural cells and fibroblasts.

The use of titanium dioxide (TiO(2)) in various industrial applications (eg, production of paper, plastics, cosmetics, and paints) has been expanding thereby increasing the occupational and other environmental exposure of these nanoparticles to humans and other species. However, the health effects of exposure to TiO(2) nanoparticles have not been systematically assessed even though recent studies suggest that such exposure induces inflammatory responses in lung tissue and cells. Because the effects of such nanoparticles on human neural cells are unknown, we have determined the putative cytotoxic effects of these nanoparticles on human astrocytes-like astrocytoma U87 cells and compared their effects on normal human fibroblasts. We found that TiO(2) micro- and nanoparticles induced cell death on both human cell types in a concentration-related manner. We further noted that zinc oxide (ZnO) nanoparticles were the most effective, TiO(2) nanoparticles the second most effective, and magnesium oxide (MgO) nanoparticles the least effective in inducing cell death in U87 cells. The cell death mechanisms underlying the effects of TiO(2) micro- and nanoparticles on U87 cells include apoptosis, necrosis, and possibly apoptosis-like and necrosis-like cell death types. Thus, our findings may have toxicological and other pathophysiological implications on exposure of humans and other mammalian species to metallic oxide nanoparticles.