Distinct profile of bacterial community and antibiotic resistance genes on microplastics in Ganjiang River at the watershed level.

Microplastics are of great public concern due to their wide distribution and the potential risk to humans and animals. In this study, the microplastic pollution associated with bacterial communities, human pathogenic bacteria, and antibiotic resistance genes (ARGs) were investigated compared to water, sediment, and natural wood particles. Microplastics were widely distributed in surface water of the Ganjiang River at a watershed level with an average value of 407 particles m-3. The fragment was the main microplastic shape found in the basin. Microplastics had significantly higher observed species and Chao1 index of bacterial communities than those in water, but comparable to wood particles. However, there was no difference in the microplastics pollution and alpha diversity indices of bacterial between different reaches along the Ganjiang River. Flavobacterium, Rhodoferax, Pseudomonas, and Janthinobacterium on the microplastics were all found to be enriched compared with water and sediment. Principal component analysis of the composition and function profile of bacterial communities showed that microplastics provide a new microbial niche in the Ganjiang River, which was distinct from water, sediment, and natural wood. Pseudomonas genus dominated the composition of human pathogenic bacteria on the microplastics, which was significantly different from water and sediment. No difference was observed in the relative abundance of total ARGs among the four media. However, microplastic and wood particles showed similar composition patterns of ARGs compared with water and sediment.

Polyethyleneimine-impregnated alkali treated waste bamboo powder for effective dye removal.

In this study, the polyethyleneimine (PEI) modified waste bamboo powder (WBP-Na-PEI) was successfully prepared and applied to adsorbing Congo red (CR) dye from aqueous solution. The obtained materials were characterized by field emission scanning electron microscope, X-ray diffraction, Fourier transform-infrared, and thermogravimetric analysis. The results showed that WBP-Na-PEI(1.8 K-5) was synthesized successfully and PEI uniformly covered the WBP-Na-PEI(1.8 K-5) surface. In the process of adsorption, four kinds of influencing factors were discussed, and the adsorption mechanisms such as kinetics, isotherm, thermodynamics were explored. The maximum adsorption capacity of WBP-Na-PEI(1.8 K-5) was 992.94 mg·g-1 at 298 ± 1 K, and the removal efficiency was over 98%. Pseudo-first-order, pseudo-second-order and intra-particle diffusion models were studied, the results showed that the adsorption process conformed to the pseudo-second-order model, and the rate of this process was controlled by many steps. Furthermore, the removal efficiency of the adsorption kinetics reached 85% within 10 minutes. The results of the isotherm model and thermodynamics showed that the adsorption process was consistent with the Langmuir model and was mainly a spontaneous chemical endothermic process of monolayer. And the removal efficiency of the adsorbent reached 93% at the concentration of 400 mg/L, which can be expected to have a broad prospect in the treatment of CR industrial wastewater.

miR-205-5p downregulation decreases gemcitabine sensitivity of breast cancer cells via ERp29 upregulation.

Breast cancer is the most common cancer in women worldwide, and the incidence and mortality rates are increasing every year. Dysregulation of microRNAs (miRNAs or miRs) is an important step in the initiation and development of breast cancer. Previous studies demonstrated that miR-205-5p is closely associated with occurrence and development of breast cancer; however, underlying mechanisms remain unclear. In the present study, reverse transcription-quantitative polymerase chain reaction assays were used to analyze miR-195-5p and endoplasmic reticulum protein 29 (ERp29) levels in breast cancer and matched normal tissues. Western blot analysis was performed to analyze ERp29 and heat shock protein 27 (HSP27) protein expression levels. Cell viability, flow cytometry and luciferase reporter assay were used to examine cell proliferation, apoptosis and direct miRNA-mRNA binding, respectively. The results revealed that miR-205-5p expression in breast cancer tissues and cell lines was decreased compared with normal tissues and a normal cell line. Overexpression of miR-205-5p significantly augmented cytotoxicity effects of gemcitabine treatment in MDA-MB-231 and BT549 cells. It was observed that miR-205-5p negatively regulated ERp29 expression in breast cancer cells. Dual luciferase assays confirmed that ERp29 was a target of miR-205-5p in breast cancer cells. Additionally, following the established gemcitabine-resistant MDA-MB-231 cells (MDA-MB-231/GEM), ERp29 and HSP27 expression was upregulated and miR-205-5p was downregulated compared with parental cells. Overexpression of miR-205-5p reversed gemcitabine resistance in MDA-MB-231/GEM cells. In conclusion, the present study indicated that miR-205-5p may inhibit gemcitabine resistance in breast cancer cells via inhibition of ERp29 expression.

miR-107 Enhances the Sensitivity of Breast Cancer Cells to Paclitaxel.

Breast cancer remains the most commonly diagnosed cancer in Chinese women. Paclitaxel (PTX) is a chemotherapy medication used to treat breast cancer patients. However, a side effect of paclitaxel is the severe drug resistance. Previous studies demonstrated that dysregulation of microRNAs could regulate sensitivity to paclitaxel in breast cancer. Here, the present study aimed to lucubrate the underlying mechanisms of miR-107 in regulating the sensitivity of breast cancer cells to PTX. The results demonstrated that miR-107 was down-regulated in breast cancer tumor tissues, while TPD52 was significantly up-regulated compared with the non-tumor adjacent tissues. After confirming that TPD52 may be a major target of miR-107 via a dual-luciferase reporter assay, the western blot and RT-qPCR assays further demonstrated that miR-107 may reduce the expression level of TPD52 as well. In addition, miR-107 may prominently enhance PTX induced reduction of cell viability and the promotion of cell apoptosis in breast cancer, and the variation could be reversed by co-transfected with pcDNA3.1-TPD52. Finally, miR-107 could further reduce the decreased expression of TPD52, Wnt1, ß-catenin and cyclin D1 that was induced by PTX in both mRNA and protein levels, which were rescued by pcDNA3.1-TPD52 indicating that miR-107 regulated breast cancer cell sensitivity to PTX may be targeting TPD52 through Wnt/ß-catenin signaling pathway.