The Variation in Chemical Composition and Source Apportionment of PM2.5 before, during, and after COVID-19 Restrictions in Zhengzhou, China.

Despite significant improvements in air quality during and after COVID-19 restrictions, haze continued to occur in Zhengzhou afterwards. This paper compares ionic compositions and sources of PM2.5 before (2019), during (2020), and after (2021) the restrictions to explore the reasons for the haze. The average concentration of PM2.5 decreased by 28.5% in 2020 and 27.9% in 2021, respectively, from 102.49 µg m-3 in 2019. The concentration of secondary inorganic aerosols (SIAs) was 51.87 µg m-3 in 2019, which decreased by 3.1% in 2020 and 12.8% in 2021. In contrast, the contributions of SIAs to PM2.5 increased from 50.61% (2019) to 68.6% (2020) and 61.2% (2021). SIAs contributed significantly to PM2.5 levels in 2020-2021. Despite a 22~62% decline in NOx levels in 2020-2021, the increased O3 caused a similar NO3- concentration (20.69~23.00 µg m-3) in 2020-2021 to that (22.93 µg m-3) in 2019, hindering PM2.5 reduction in Zhengzhou. Six PM2.5 sources, including secondary inorganic aerosols, industrial emissions, coal combustion, biomass burning, soil dust, and traffic emissions, were identified by the positive matrix factorization model in 2019-2021. Compared to 2019, the reduction in PM2.5 from the secondary aerosol source in 2020 and 2021 was small, and the contribution of secondary aerosol to PM2.5 increased by 13.32% in 2020 and 12.94% in 2021. In comparison, the primary emissions, including biomass burning, traffic, and dust, were reduced by 29.71% in 2020 and 27.7% in 2021. The results indicated that the secondary production did not significantly contribute to the PM2.5 decrease during and after the COVID-19 restrictions. Therefore, it is essential to understand the formation of secondary aerosols under high O3 and low precursor gases to mitigate air pollution in the future.

LncRNA MIR210HG promotes the proliferation, migration, and invasion of lung cancer cells by inhibiting the transcription of SH3GL3.

Lung cancer (LCa), the most frequent malignancy worldwide, causes millions of mortalities each year. Overexpression of the long noncoding RNA MIR210HG in LCa has been established; however, a more comprehensive investigation into its biological role within LCa is imperative. This study aimed to validate the MIR210H levels in LCa tissues and cells. The expression of indicated genes was evaluated using quantitative real-time polymerase chain reaction (qRT-PCR) and/or Western blotting. The viability, proliferation, migration, and invasion of LCa cells were measured using the 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT), colony formation, wound healing, and transwell assays, respectively. The methylation levels of LCa cells were determined via methylation-specific PCR; additionally, chromatin immunoprecipitation or RNA immunoprecipitation assays were performed to determine the targeting relationship between DNA methyltransferase 1 (DNMT1) and the SH3-domain containing CRB2 like 3 (SH3GL3) promoters and the interaction between DNMT1 and MIR210HG, respectively. Our findings revealed the upregulation of MIR210HG, coupled with a diminished expression of SH3GL3 in LCa tissues and cells. Knockdown of MIR210HG or overexpression of SH3GL3 suppressed the proliferative, migratory, and invasive capacities of the cells. DNMT1 bound to the SH3GL3 promoter region, and MIR210HG inhibited the transcription of SH3GL3 by recruiting DNMT1. These findings indicate that MIR210HG facilitates LCa cell growth and metastasis by repressing SH3GL3 transcription via the recruitment of DNMT1 to the SH3GL3 promoter region.

BML-111 alleviates inflammatory response of alveolar epithelial cells via miR-494/Slit2/Robo4 signalling axis to improve acute lung injury.

Acute lung injury (ALI) is a common, variously induced lung cell injury with high mortality. It is also an early stage of acute respiratory distress syndrome. BML-111 is a lipoxin A4 receptor agonist that plays an important role in inflammation. However, its function on ALI remains unclear. To explore whether BML-111 is involved in ALI and its regulatory molecular mechanism, we constructed an in vitro ALI model by stimulating primary mouse alveolar epithelial cells (AECs) with lipopolysaccharide (LPS). The downstream target of microRNA (miR)-494 was predicted by Targetscan. The apoptosis and expression of inflammatory cytokines were analysed by RT-qPCR, Western blot, and ELISA. BML-111 treatment alleviated LPS-induced apoptosis and the production of inflammatory cytokines, such as tumour necrosis factor α, interleukin (IL)-6, IL-1ß, in primary mouse AECs via downregulating miR-494. MiR-494 targeted and downregulated slit guidance ligand 2 (Slit2) in primary mouse AECs. BML-111 activated the Slit2/roundabout guidance receptor 4 (Robo4) axis via downregulating miR-494 to reduce LPS-induced damage in AECs. This study elucidated that miR-494 on BML-111 alleviated LPS-induced ALI in primary mouse AECs via downregulating miR-494 and subsequently activating the Slit2/Robo4 axis. These findings provided a new idea for the prevention and treatment of ALI and respiratory distress syndrome.

Constructing an ovarian cancer metastasis index by dissecting medical records.

Globally, ovarian cancer (OC) is the leading cause of gynecological cancer-associated deaths. Metastasis, especially multi-organ metastasis, determines the speed of disease progression. A multicenter retrospective study was performed to identify the factors that drive metastasis, from medical records of 534 patients with OC. The average number of target organs per patient was 3.66, indicating multi-organ metastasis. The most common sites of metastasis were large intestine and greater omentum, which were prone to co-metastasis. Results indicated that ascites and laterality, rather than age and menopausal status, were the potential drivers for multi-organ metastasis. Cancer antigen (CA) 125 (CA-125) and nine other blood indicators were found to show a significant, but weak correlation with multi-organ metastasis. A neural network cascade-multiple linear regression hybrid model was built to create an ovarian cancer metastasis index (OCMI) by integration of six multi-organ metastasis drivers including CA-125, blood platelet count, lymphocytes percentage, prealbumin, ascites, and laterality. In an independent set of 267 OC medical records, OCMI showed a moderate correlation with multi-organ metastasis (Spearman ρ = 0.67), the value being 0.72 in premenopausal patients, and good performance in identifying multi-organ metastasis (area under the receiver operating characteristic curve = 0.832), implying a potential prognostic marker for OC.

Melatonin reduces hypoxic-ischaemic (HI) induced autophagy and apoptosis: An in vivo and in vitro investigation in experimental models of neonatal HI brain injury.

Melatonin has neuroprotective effects in many diseases, including neonatal hypoxic-ischaemic (HI) brain injury. The purpose of this study was to evaluate the neuroprotective effects of melatonin both in vivo and in vitro and associated molecular mechanisms behind these effects. Postnatal day 7 male and female rat pups were subjected to unilateral HI, melatonin was injected intraperitoneally 1h before HI and an additional six doses were administered at 24h intervals. The pups were sacrificed at 24h and 7 d after HI. Pre-treatment with melatonin significantly reduced brain damage at 7 d after HI, with 15mg/kg melatonin achieving over 30% recovery in tissue loss compared to vehicle-treated animals. Autophagy and apoptotic cell death as indicated by autophagy associated proteins, cleaved caspase 3 and Tunel staining, was significantly inhibited after melatonin treatment in vivo as well as in PC12 cells. Melatonin treatment also significantly increased the GAP43 in the cortex. In conclusion, melatonin treatment reduced neonatal rat brain injury after HI, and this appeared to be related to inhibiting autophagy as well as reducing apoptotic cell death.