Insight study of rare earth elements in PM2.5 during five years in a Chinese inland city: Composition variations, sources, and exposure assessment.

The booming development of rare earth industry and the extensive utilization of its products accompanied by urban development have led to the accelerated accumulation of rare earth elements (REEs) as emerging pollutants in atmospheric environment. In this study, the variation of REEs in PM2.5 with urban (a non-mining city) transformation was investigated through five consecutive years of sample collection. The compositional variability and provenance contribution of REEs in PM2.5 were characterized, and the REEs exposure risks of children and adults via inhalation, ingestion and dermal absorption were also evaluated. The results showed an increase in the total REEs concentration from 46.46 ± 35.16 mg/kg (2017) to 81.22 ± 38.98 mg/kg (2021) over the five-year period, with Ce and La making the largest contribution. The actual increment of industrial and traffic emission source among the three pollution sources was 1.34 ng/m3. Coal combustion source displayed a downward trend. Ingestion was the main exposure pathway for REEs in PM2.5 for both children and adults. Ce contributed the most to the total intake of REEs in PM2.5 among the population, followed by La and Nd. The exposure risks of REEs in PM2.5 in the region were relatively low, but the trend of change was of great concern. It was strongly recommended to strengthen the concern about traffic-related non-exhaust emissions of particulate matter.

Ambra1 in cancer: implications for clinical oncology.

Activating molecule in Beclin-1-regulated autophagy protein 1 (Ambra1) is well known to mediate the autophagy process and promote the formation of autophagosomes. In addition, Ambra1 is involved in the execution of apoptosis. A growing number of studies have revealed that this protein modifies the sensitivity of cancer cells to anticancer drugs by controlling the balance between autophagy and apoptosis. In addition, Ambra1 is a key factor in regulating the cell cycle, proliferation, invasion and migration. Therefore, it plays a key role in tumorigenesis and progression. Moreover, Ambra1 is highly expressed in a variety of cancers and is closely related to the prognosis of patients. Thus, it appears that Ambra1 has multiple roles in tumorigenesis and progression, which may have implications for clinical oncology. The present review focuses on recent advances in the study of Ambra1, especially the role of the protein in tumorigenesis, progression and effects on anticancer drug sensitivity.

Ambra1 regulates apoptosis and chemosensitivity in breast cancer cells through the Akt-FoxO1-Bim pathway.

The sensitivity of cells to chemotherapeutic agents has a major effect on disease outcome in breast cancer patients. Unfortunately, there are numerous factors involved in the regulation of chemosensitivity, and the mechanisms need to be further investigated. Autophagy/Beclin 1 regulator 1 (Ambra1) is a key protein in the crosstalk between autophagy and apoptosis. It controls the switch between these two processes, which determines whether cells survive or die. Induction of apoptosis is the primary mechanism by which most chemotherapeutic drugs eliminate cancer cells. Recently, Ambra1 has been shown to modulate paclitaxel-induced apoptosis in breast cancer cells via the Bim/mitochondrial pathway, thereby modifying the sensitivity of cells to paclitaxel. However, how Ambra1 regulates Bim expression remains unclear. Here, we further confirmed that Bim plays an indispensable role in Ambra1's regulation of apoptosis and chemosensitivity in breast cancer cells. Furthermore, Ambra1 was found to regulate Bim expression at the transcriptional level through the Akt-FoxO1 pathway. Therefore, we propose a novel pathway, Ambra1-Akt-FoxO1-Bim, which regulates apoptosis and chemosensitivity in breast cancer cells. Thus, Ambra1 may represent a potential target for breast cancer treatment.

Application of New Energy Thermochromic Composite Thermosensitive Materials of Smart Windows in Recent Years.

Thermochromic smart windows technology can intelligently regulate indoor solar radiation by changing indoor light transmittance in response to thermal stimulation, thus reducing energy consumption of the building. In recent years, with the development of new energy-saving materials and the combination with practical technology, energy-saving smart windows technology has received more and more attention from scientific research. Based on the summary of thermochromic smart windows by Yi Long research groups, this review described the applications of thermal responsive organic materials in smart windows, including poly(N-isopropylacrylamide) (PNIPAm) hydrogels, hydroxypropyl cellulose (HPC) hydrogels, ionic liquids and liquid crystals. Besides, the mechanism of various organic materials and the properties of functional materials were also introduced. Finally, opportunities and challenges relating to thermochromic smart windows and prospects for future development are discussed.

Wettability-regulated extracellular electron transfer from the living organism of Shewanella loihica PV-4.

C-type cytochromes located on the outer membrane (OMCs) of genus Shewanella act as the main redox-active species to mediate extracellular electron transfer (EET) from the inside of the outer membrane to the external environment: the central challenge that must be met for successful EET. The redox states of OMCs play a crucial role in dictating the rate and extent of EET. Here, we report that the surface wettability of the electrodes strongly influences the EET activity of living organisms of Shewanella loihica PV-4 at a fixed external potential: the EET activity on a hydrophilic electrode is more than five times higher than that on a hydrophobic one. We propose that the redox state of OMCs varies significantly at electrodes with different wettability, resulting in different EET activities.

Decryption analysis of antimony pollution sources in PM2.5 through a multi-source isotope mixing model based on lead isotopes.

Antimony (Sb) in PM2.5 has attracted close attention as a new air pollutant due to its extensive use in daily life. The identification of antimony sources in PM2.5 by scientific methods is important to control its pollution. In this study, the Sb and other elements concentrations and Pb isotopic compositions in PM2.5 and possible pollution sources (soil, road dust, traffic emission, coal-fired fly ash, local factory emission dust and cement dust) were analyzed. The results showed that the Sb in the PM2.5 samples had seasonal change. The enrichment factors of Sb in PM2.5 samples were all above 100 in four seasons, which indicated anthropogenic pollution. The average value of potential ecological risk index was at extremely high-risk level greater than 320. Based on Pearson correlation coefficient and hierarchical cluster analysis results, the pollution sources of antimony and lead in PM2.5 samples were highly consistent which means that Pb isotopes might be a new and feasible tracer for Sb pollution in air. The sources analysis results based on Pb isotopes indicated that the proportion of Pb and Sb from coal-fired fly ash was the highest in winter (47.7%) and inclined to road dust in spring (34.5%), but it was mainly from traffic emissions in summer and autumn (34.2% and 32.8%). This study showed that Pb isotope tracing can be applied to predict the potential pollution sources, and it was also a feasible substitute for tracing Sb pollution in PM2.5.

[Expression of oxidative stress proteins in the clear-cell renal cell carcinoma].

AIM: To investigate the expression of the oxidative stress proteins in human clear-cell renal cell carcinoma (CRCC) cell line (RLC-310) and normal renal proximal tubule epithelial cell line (HK-2), the CRCC and the corresponding normal renal tissues. METHODS: RLC-310 and HK-2 cells were cultured in vitro. Total proteins of the two cell lines were separated by PF-2D protein fractionation system. The differentially expressed proteins of the two cell lines were analyzed using capillary LC-ESI-MS/MS and identified using the protein database. The representative differential oxidative stress proteins were verified by immunohistochemistry in the CRCC and corresponding normal renal tissues. RESULTS: Twelve differentially expressed oxidative stress proteins were identified, including peroxiredoxin-1, peroxiredoxin-6 (PRX-6), superoxide dismutase[Cu-Zn] SOD1, catalase, glutathione peroxidase 1, glutathione synthetase, glutathione S-transferase Pi (GSTPi), thioredoxin, heat shock protein 10 (HSP10), HSP60, HSP70 and HSP90. Three representative differential proteins PRX-6, HSP60 and GSTPi were both expressed in RLC-310 and HK-2, and the levels of these proteins were significantly higher in RLC-310 than those in HK-2 (P<0.05). The levels of these proteins were significantly higher in CRCC than those in corresponding normal renal tissues (P<0.05). CONCLUSION: A series of oxidative stress proteins are overexpressed in the CRCC. They play an important role in preventing oxidative damage of CRCC cells.