Chemical characterization and source apportionment of PM2.5 in a Northeastern China city during the epidemic period.

To investigate the influence of COVID-19 lockdown measures on PM2.5 and its chemical components in Shenyang, PM2.5 samples were continuously collected from January 1 to May 31, 2020. The samples were then analyzed for water-soluble inorganic ions, metal elements, organic carbon, and elemental carbon. The findings indicated a significant decrease in PM2.5 and its various chemical components during the lockdown period, compared to pre-lockdown levels (p < 0.05), suggesting a substantial improvement in air quality. Water-soluble inorganic ions (WSIIs) were identified as the primary contributors to PM2.5, accounting for 47% before the lockdown, 46% during the lockdown, and 37% after the lockdown. Ionic balance analysis revealed that PM2.5 exhibited neutral, weakly alkaline, and alkaline characteristics before, during, and after the lockdown, respectively. NH4+ was identified as the main balancing cation and was predominantly present in the form of NH4NO3 in the absence of complete neutralization of SO42- and NO3-. Moreover, the higher sulfur oxidation ratio (SOR) and nitrogen oxidation ratio (NOR), along with the significant increase in PM2.5/EC, suggested intense secondary transformation during the lockdown period. The elevated OC/EC ratio during the lockdown period implied higher secondary organic carbon (SOC), and the notable increase in SOC/EC ratio indicated a significant secondary transformation of total carbon. The enrichment factor (EF) results revealed that during the lockdown, 9 metal elements (As, Sn, Pb, Zn, Cu, Sb, Ag, Cd, and Se) were substantially impacted by anthropogenic emissions. Source analysis of PMF was employed to identify the sources of PM2.5 in Shenyang during the study period, and the analysis identified six factors: secondary sulfate and vehicle emissions, catering fume sources, secondary nitrate and coal combustion emissions, dust sources, biomass combustion, and industrial emissions, with secondary sulfate and vehicle emissions and catering fume sources contributing the most to PM2.5.

Biochar alters the soil fauna functional traits and community diversity: A quantitative and cascading perspective.

With the widespread use of biochar, the cascading effects of biochar exposure on soil fauna urgently require deeper understanding. A meta-analysis quantified hierarchical changes in functional traits and community diversity of soil fauna under biochar exposure. Antioxidant enzymes (24.1 %) did not fully mitigate the impact of MDA (13.5 %), leading to excessive DNA damage in soil fauna (21.2 %). Concurrently, reproduction, growth, and survival rates decreased by 20.2 %, 8.5 %, and 21.2 %, respectively. Due to a 39.7 % increase in avoidance behavior of soil fauna towards biochar, species richness ultimately increased by 80.2 %. Compared to other feeding habits, biochar posed a greater threat to the survival of herbivores. Additionally, macrofauna were the most sensitive to biochar. The response of soil fauna also depended on the type, size, concentration, and duration of biochar exposure. It should be emphasized that as exposure concentration increased, the damage to soil fauna became more severe. Furthermore, the smaller the biochar sizes, the greater the damage to soil fauna. To mitigate the adverse effects on soil fauna, this study recommens applying biochar at appropriate times and selecting large sizes in low to medium concentrations. These findings confirm the threat of biochar to soil health from the perspective of soil fauna.

Tazarotene-induced Gene 1 Induces Melanoma Cell Death by Triggering Endoplasmic Reticulum Stress Response.

BACKGROUND: This study investigated the mechanism by which tazarotene-induced gene 1 (TIG1) inhibits melanoma cell growth. The main focus was to analyze downstream genes regulated by TIG1 in melanoma cells and its impact on cell growth. METHODS: The effects of TIG1 expression on cell viability and death were assessed using water-soluble tetrazolium 1 (WST-1) mitochondrial staining and lactate dehydrogenase release assays. RNA sequencing and Western blot analysis were employed to investigate the genes regulated by TIG1 in melanoma cells. Additionally, the correlation between TIG1 expression and its downstream genes was analyzed in a melanoma tissue array. RESULTS: TIG1 expression in melanoma cells was associated with decreased cell viability and increased cell death. RNA-sequencing (RNA-seq), quantitative reverse transcription PCR (reverse RT-QPCR), and immunoblots revealed that TIG1 expression induced the expression of Endoplasmic Reticulum (ER) stress response-related genes such as Homocysteine-responsive endoplasmic reticulum-resident ubiquitin-like domain member 1 (HERPUD1), Binding immunoglobulin protein (BIP), and DNA damage-inducible transcript 3 (DDIT3). Furthermore, analysis of the melanoma tissue array revealed a positive correlation between TIG1 expression and the expression of HERPUD1, BIP, and DDIT3. Additionally, attenuation of the ER stress response in melanoma cells weakened the impact of TIG1 on cell growth. CONCLUSIONS: TIG1 expression effectively hinders the growth of melanoma cells. TIG1 induces the upregulation of ER stress response-related genes, leading to an increase in caspase-3 activity and subsequent cell death. These findings suggest that the ability of retinoic acid to prevent melanoma formation may be associated with the anticancer effect of TIG1.

LINC00606 promotes glioblastoma progression through sponge miR-486-3p and interaction with ATP11B.

BACKGROUND: LncRNAs regulate tumorigenesis and development in a variety of cancers. We substantiate for the first time that LINC00606 is considerably expressed in glioblastoma (GBM) patient specimens and is linked with adverse prognosis. This suggests that LINC00606 may have the potential to regulate glioma genesis and progression, and that the biological functions and molecular mechanisms of LINC00606 in GBM remain largely unknown. METHODS: The expression of LINC00606 and ATP11B in glioma and normal brain tissues was evaluated by qPCR, and the biological functions of the LINC00606/miR-486-3p/TCF12/ATP11B axis in GBM were verified through a series of in vitro and in vivo experiments. The molecular mechanism of LINC00606 was elucidated by immunoblotting, FISH, RNA pulldown, CHIP-qPCR, and a dual-luciferase reporter assay. RESULTS: We demonstrated that LINC00606 promotes glioma cell proliferation, clonal expansion and migration, while reducing apoptosis levels. Mechanistically, on the one hand, LINC00606 can sponge miR-486-3p; the target gene TCF12 of miR-486-3p affects the transcriptional initiation of LINC00606, PTEN and KLLN. On the other hand, it can also regulate the PI3K/AKT signaling pathway to mediate glioma cell proliferation, migration and apoptosis by binding to ATP11B protein. CONCLUSIONS: Overall, the LINC00606/miR-486-3p/TCF12/ATP11B axis is involved in the regulation of GBM progression and plays a role in tumor regulation at transcriptional and post-transcriptional levels primarily through LINC00606 sponging miR-486-3p and targeted binding to ATP11B. Therefore, our research on the regulatory network LINC00606 could be a novel therapeutic strategy for the treatment of GBM.