Polystyrene microplastics facilitate the biotoxicity and biomagnification of ZnO nanoparticles in the food chain from algae to daphnia.

Ubiquitous microplastics (MPs) may affect the trophic transfer of nanoparticles (NPs), in turn threatening aquatic organisms and even human health. Thus, this study explored the influence of polystyrene microplastics (PS MPs) on the biotoxicity and biomagnification of ZnO nanoparticles (ZnO NPs) in the aquatic food chain from Chlorella vulgaris (C. vulgaris) to Daphnia magna (D. magna). The results showed that PS MPs facilitated the biotoxicity of ZnO NPs towards D. magna after dietary exposure. Compared to the control (single ZnO NPs), the heart rate and the level of reactive oxygen species were remarkably increased by 21.25% and 16.32% in the combined system (PS MPs + ZnO NPs), respectively. Notably, PS MPs suppressed the ZnO NPs accumulation in C. vulgaris, while remarkably facilitating the trophic transfer of ZnO NPs to D. magna. The biomagnification of ZnO NPs was evident with a maximal biomagnification factor (BMF) of 1.49 under acute dietary exposure of PS MPs (72 h), but was absent in the single ZnO NPs system (BMF <0.90). Moreover, PS MPs resulted in a larger biomagnification of ZnO NPs with a maximal BMF of 2.11 under chronic dietary exposure (21 days). Furthermore, the Zn element (including ZnO NPs and released Zn2+) was observed to accumulate in the intestine, thus causing ultrastructural damage and lipid droplet (LD) aggregate. Overall, these findings highlight the importance of considering the impact of MPs on co-existed pollutants and contribute to a better understanding of the ecological risks of MPs in aquatic ecosystems.

Retrospective analysis of Porphyromonas gingivalis in patients with nasopharyngeal carcinoma in central China.

Little is known about the presence and possible role of Porphyromonas gingivalis (P. gingivalis) in nasopharyngeal carcinoma (NPC), its co-infection with Epstein-Barr virus (EBV), or their association with clinical characteristics of patients with NPC in Central China, where NPC is non-endemic. A total of 45 NPC formalin-fixed paraffin-embedded (FFPE) tissues were retrospectively analyzed using immunohistochemistry (IHC) and a nested PCR combined with DNA sequencing to detect the presence of P. gingivalis, and using reverse transcription-quantitative PCR to detect the presence of EBV. Clinical data including EBV and P. gingivalis status were associated with overall survival (OS). All tumors were undifferentiated, non-keratinizing carcinomas, of which 40/45 (88.9%) were positive for EBV (EBV+), 26/45 (57.8%) were positive for P. gingivalis (by IHC), and 7/45 (15.6%) were positive for P. gingivalis DNA (P. gingivalis +). All seven P. gingivalis DNA-positive NPCs were co-infected with EBV. The 5-year survival rates of the patients with EBV-/P. gingivalis -, EBV+/P. gingivalis -, and EBV+/P. gingivalis + tumors were 60.0% (3/5), 39.4% (13/33) and 42.9% (3/7), respectively. No significant difference was found between the OS of NPC patients among the different infection groups (P=0.793). In conclusion, to the best of our knowledge, this is the first study to describe and confirm the presence of P. gingivalis in FFPE tissues from patients with NPC. P. gingivalis was found to co-exist with EBV in NPC tumor tissues, but is not etiologically relevant to NPC in non-endemic areas, such as Central China.

RGD-modified injectable hydrogel maintains islet beta-cell survival and function.

OBJECTIVE: A potential solution for islet transplantation and drug discovery vis-à-vis treating diabetes is the production of functional islets in a three-dimensional extracellular matrix. Although several scaffold materials have been reported as viable candidates, a clinically applicable one that is injectable and can maintain long-term functionality and survival of islet pancreatic beta-cells (ß-cells) is far from being established. RESULTS: In the current study, we evaluated a ready-to-use and injectable hydrogel's impact on ß-cells' function and viability, both in vitro and in vivo. We found that ß-cells in high concentration with hydrogels functionalized via Arg-Gly-Asp (RGD) demonstrated better viability and insulin secretory capacity in vitro. Moreover, it is a biocompatible hydrogel that can maintain ß-cell proliferation and vascularization without stimulating inflammation after subcutaneous injection. Meanwhile, modifying the hydrogel with RGD can maintain ß-cells' secretion of insulin, regulating the blood glucose levels of mice with streptozotocin-induced diabetes. CONCLUSIONS: Thus, these preliminary results indicate that this RGD-modified hydrogel is a potential extracellular matrix for islet transplantation at extrahepatic sites, and they also provide a reference for future tissue engineering study.

Polybrene induces neural degeneration by bidirectional Ca2+ influx-dependent mitochondrial and ER-mitochondrial dynamics.

Hexadimethrine bromide (Polybrene) was once used clinically as a heparin neutralizer and has recently found use as a promoter in virus-mediated gene therapy trials and gene transfer in research. However, the potential for tissue-specific toxicity of polybrene at low doses has been ignored so far. Here, we found that after intracerebroventricular (ICV) polybrene injection, mice showed disability of movement accompanied neural death and gliosis in brain, and in human neurons, polybrene induces concentration-dependent neuritic beading and fragmentation. Mechanistically, polybrene induces a rapid voltage-dependent calcium channel (VDCC)-mediated influx of extracellular Ca2+. The elevated cytoplasmic Ca2+ activates DRP1, which leads to mitochondrial fragmentation and metabolic dysfunction. At the same time, Ca2+ influx induces endoplasmic reticulum (ER) fragmentation and tightened associations between ER and mitochondria, which makes mitochondria prone to Ca2+ overloading and ensuing permeability transition. These results reveal an unexpected neuronal toxicity of polybrene, wherein Ca2+ influx serves as a regulator for both mitochondrial dynamics and ER-mitochondrial remodeling.