Study on sewage characteristics in rural China and pollutants removal performance of biologically enhanced internal circulation treatment system.

With rapid economic development and urbanization in China, rural wastewater treatment has become an important issue. This study investigated 63 rural sewage treatment stations in northern, central and southern Shaanxi, China for a 1-year period, 2021 to 2022. The main purpose of the research was to investigate the quality and discharge characteristics of rural sewage, along with current problems in rural wastewater treatment, in order to provide evidence for the optimal construction and operation of rural sewage treatment stations. We found that the biodegradability of rural wastewater is adequate, and BOD5/COD ratio in sewage was 0.4, which is suitable for biological treatment. It has obvious intermittent flow cut-off characteristics, and the range of cut-off duration of sewage was 6-16 h/d, which leads to poor pollutant removal efficiency (COD: 50.0 ± 29.2%, NH4+-N: 46.0 ± 26.1%, TN: 38.5 ± 24.9% and TP: 38.3 ± 23.8%) in sewage treatment stations. In response to the above characteristics, the rural sewage biologically enhanced internal circulation treatment (BEICT) system was constructed. After 97 days of operation, the system has a stable removal effect on TN and TP with an average removal rate of 77.42% and 89.69%, respectively, under the condition of influent interruption for 12 h per day. The activated sludge of system maintained good activity and stable sedimentation performance during the whole experiment, with MLVSS/MLSS and SVI of 0.72 and 128 mL/g, respectively. This study can provide the basis and technical support for the accurate design of rural sewage treatment facilities, and has important significance for guiding the treatment of rural domestic sewage in China.

Comprehensive Analysis of the Expression, Prognosis, and Biological Significance of OVOLs in Breast Cancer.

BACKGROUND: The study aimed to investigate the expression of OVOLs in breast cancer (BRCA) tissues and their value in prognosis. METHODS: ONCOMINE was used to analyze the expressions of OVOL1, OVOL2, and OVOL3 mRNA between BRCA tissues and normal breast tissues. The Wilcoxon rank sum test and t-test were used to assess the expression of OVOLs between BRCA tissues and unpaired/paired normal breast tissues. GEPIA and ROC curves were used to analyze the relationship between OVOLs expression and clinical pathological stage. Kaplan-Meier plotter was used to analyze prognosis. cBioPortal was used to analyze the mutation of OVOLs. GEPIA was used to analyze the co-expression of OVOLs. GO and KEGG analyses were performed by the DAVID software to predict the function of OVOLs co-expression genes. RESULTS: The expression of OVOL1/2 was significantly higher in BRCA tissues than in normal breast tissues. The OVOL3 expression correlated with tumor stage. The AUC of OVOLs was 0.757, 0.754, and 0.537, respectively. OVOL1 high expression was associated with shorter overall survival (HR: 1.48; 95% CI: 1.07-2.04; P=0.018). The OVOLs were associated with pathways including axon guidance, thyroid hormone signaling pathway, and ubiquinone and other terpenoid-quinone biosynthesis. CONCLUSION: OVOL1 is a new potential marker of prognosis in BRCA, and OVOL1/2 are potential therapeutic targets in BRCA.

Knockdown of LncRNA DLX6-AS1 inhibits HK-2 cell pyroptosis via regulating miR-223-3p/NLRP3 pathway in lipopolysaccharide-induced acute kidney injury.

Sepsis-induced acute kidney injury (AKI) represents a severe medical complication. Recently, there is growing evidence indicating the regulatory role of long non-coding RNAs (lncRNAs) in AKI pathophysiology. The present study investigated lncRNA DLX6 antisense RNA 1 (DLX6-AS1) expression in septic AKI patients and to decipher the relevant mechanisms underlying DLX6-AS1-mediated HK-2 cell pyroptosis in lipopolysaccharide (LPS)-induced AKI. The results revealed that DLX6-AS1 was up-regulated in the serum from septic AKI patients. DLX6-AS1 expression were positively associated with the creatinine levels in the serum from the septic AKI patients. In vitro studies showed that LPS induced cytotoxicity and enhanced DLX6-AS1 expression of HK-2 cells; increased NLR family pyrin domain containing 3 (NLRP3), interleukin (IL)-1ß and IL-18 expression. DLX6-AS1 overexpression promoted cytotoxicity and pyroptosis of HK-2 cells; while DLX6-AS1 knockdown counteracted the LPS-induced cytotoxicity and pyroptosis of HK-2 cells. More importantly, DLX6-AS1 sponged miR-223-3p resulting in repression of miR-223-3p expression in HK-2 cells. MiR-223-3p could bind to the 3' untranslated region of NLRP3, which results in the suppressed NLRP3 expression of HK-2 cells. Further rescue experiments showed that enhanced miR-223-3p expression partially reversed the cytotoxicity and pyroptosis of HK-2 cells upon LPS stimulation or with DLX6-AS1 overexpression. Conclusively, this study identified enhanced DLX6-AS1 expression in the serum from AKI patients. Further mechanistic findings deciphered that DLX6-AS1 mediated LPS-mediated cytotoxicity and pyroptosis in HK-2 via miR-223-3p/NLRP3 axis.

Circulating microRNA-339-5p and -21 in plasma as an early detection predictors of lung adenocarcinoma.

BACKGROUND: Many studies have shown that differentially expressed miRs in body fluids can serve as biomarkers in non-invasive detection of the cancers. However, the clinical significance of plasma miRs in the diagnosis of lung adenocarcinoma (LA) is still not clear. Therefore, we examined the LA-specific miRs in plasma, which could be utilized to diagnosis and monitor LA in routine clinical practice. METHODS: Twenty-eight LA cases and twenty-eight healthy controls were recruited to our study. MiRs differential expression in plasma was measured by miRNA Microarray assay and revalidated by using qRT-PCR based absolute quantification methods The diagnostic power of circulating miRs in LA was evaluated using the receiver operating characteristics (ROC) curves and the area under the ROC curves (AUC). RESULTS: Tumor tissues and plasma levels of miR-339-5p were significantly down-regulated in LA patients compared with those in the control group, whereas the levels of miR-21 in LA patients were significantly higher than control group. ROC analysis showed that miR-339-5p and miR-21 could distinguish LA patients from healthy controls with high AUC (0.900 and 0.880, respectively), sensitivity (0.821 and 0.821, respectively) and specificity (0.929 and 0.964, respectively). Importantly, the combination of miR-339-5p and miR-21 markedly improved AUC (0.963), sensitivity (0.929) and specificity (0.929). CONCLUSION: Plasma miR-339-5p or miR-21 could serve as a potential biomarker for diagnosis of LA, however, the combination of miR-339-5p and miR-21 was more efficient for LA detection.

Inhibition of endometrial cancer by n-3 polyunsaturated fatty acids in preclinical models.

Although preclinical and epidemiologic studies have shown the importance of n-3 polyunsaturated fatty acids (PUFA) in the prevention of hormone-responsive cancers such as breast cancer, evidence of the association between n-3 PUFAs and endometrial cancer risk is limited and no previous study has examined the effect of n-3 PUFAs on endometrial cancer in cellular and animal models. In this study, we demonstrated that docosahexenoic acid (DHA) dose- and time-dependently inhibited endometrial cancer cell proliferation, colony formation, and migration and promoted apoptosis. Dietary n-3 PUFAs efficiently prevented endometrial cancer cell growth in xenograft models. Moreover, ectopic expression of fat-1, a desaturase, catalyzed the conversion of n-6 to n-3 PUFAs and produced n-3 PUFAs endogenously, also suppressed endometrial tumor cell growth and migration, and potentiated apoptosis in endometrial cancer cell lines. Interestingly, implanted endometrial cancer cells were unable to grow in fat-1 transgenic SCID mice. Further study revealed that mTOR signaling, which plays an essential role in cell proliferation and endometrial tumorigenesis, is a target of n-3 PUFAs. Exogenous or endogenous n-3 PUFAs efficiently suppressed both mTOR complex 1 (mTORC1) and mTORC2 in vitro and in vivo. Moreover, both dietary n-3 PUFAs and transgenic expression of fat-1 in mice effectively repressed mTORC1/2 signaling and endometrial growth elicited by unopposed estrogen. Taken together, our findings provide comprehensive preclinical evidences that n-3 PUFAs efficiently prevent endometrial cancer and establish mTORC1/2 as a target of n-3 PUFAs.