Effect of Aeration and External Carbon Source on Nitrogen Removal and Distribution Patterns of Related-Microorganisms in Horizontal Subsurface Flow Constructed Wetlands

Nitrogen pollution of surface water is still a critical issue worldwide. In this study, a total of four treatments were conducted in horizontal subsurface flow constructed wetlands (HSSFCWs) to explore the removal rate of nitrogen in the carbon-deficient wastewater, including combination of aeration and external carbon source (CW_CA), external carbon source (CW_C), aeration (CW_A), and control group without aeration and carbon source (CW_CK). Results showed that the removal rates of total nitrogen (TN) in the enhanced treatments were increased compared with CW_CK. The highest removal rates of COD (66.56%), NH4+-N (73.51%), NO3−-N (79.31%), and TN (76.19%) were observed in the CW_CA treatment. The bacterial community structure at the fore and rear ends of HSSFCWs was simultaneously changed in the CW_CA and CW_C treatments, respectively. The highest richness index at both the fore and rear ends of HSSFCWs was found in the CW_CA treatment. The richness and diversity indices of CW_C declined at the fore ends of HSSFCWs, but increased at the rear ends of HSSFCWs. Furthermore, the functional bacteria and genes significantly changed among different treatments. At the fore ends of HSSFCWs, the highest relative abundance of nitrifiers and absolute abundance of amoA and nxrA were obtained in CW_A, and the highest relative abundance of denitrifying bacteria and absolute abundance of nirS, nirK, nosZ were found in CW_C. However, at the rear ends of HSSFCWs, the highest relative abundance of nitrifiers and denitrifying bacteria as well as the absolute abundance of related genes were also observed in the CW_CA treatment. Overall, CW_CA improved the nitrogen removal rate by increasing the abundance of nitrogen-converting functional microbes and the genes associated with nitrification and denitrification

Long non-coding RNA CASC2 suppresses pulmonary artery smooth muscle cell proliferation and phenotypic switch in hypoxia-induced pulmonary hypertension

Abstract Background In this study, we aimed to investigate whether and how lncRNA CASC2 was involved in hypoxia-induced pulmonary hypertension (PH)-related vascular remodeling. Methods The expression of lncRNAs or mRNAs was detected by qRT-PCR, and western blot analysis or immunochemistry was employed for detecting the protein expression. Cell number assay and EdU (5-ethynyl-2′-deoxyuridine) staining were performed to assess cell proliferation. Besides, flow cytometry and wound healing assay were employed for assessments of cell apoptosis and cell migration, respectively. Rat model of hypoxic PH was established and the hemodynamic measurements were performed. Hematoxylin and eosin (HE) and Masson′s trichrome staining were carried out for pulmonary artery morphometric analysis. Results The expression of lncRNA CASC2 was decreased in hypoxia-induced rat pulmonary arterial tissues and pulmonary artery smooth muscle cells (PASMCs). Up-regulation of lncRNA CASC2 inhibited cell proliferation, migration yet enhanced apoptosis in vitro and in vivo in hypoxia-induced PH. Western blot analysis and immunochemistry showed that up-regulation of lncRNA CASC2 greatly decreased the expression of phenotype switch-related marker α-SMA in hypoxia-induced PH. Furthermore, it was indicated by the pulmonary artery morphometric analysis that lncRNA CASC2 suppressed vascular remodeling of hypoxia-induced rat pulmonary arterial tissues. Conclusion LncRNA CASC2 inhibited cell proliferation, migration and phenotypic switch of PASMCs to inhibit the vascular remodeling in hypoxia-induced PH

Comprehensive multi-omics analysis reveals WEE1 as a synergistic lethal target with hyperthermia through CDK1 super-activation

Abstract Hyperthermic intraperitoneal chemotherapy’s role in ovarian cancer remains controversial, hindered by limited understanding of hyperthermia-induced tumor cellular changes. This limits developing potent combinatory strategies anchored in hyperthermic intraperitoneal therapy (HIPET). Here, we perform a comprehensive multi-omics study on ovarian cancer cells under hyperthermia, unveiling a distinct molecular panorama, primarily characterized by rapid protein phosphorylation changes. Based on the phospho-signature, we pinpoint CDK1 kinase is hyperactivated during hyperthermia, influencing the global signaling landscape. We observe dynamic, reversible CDK1 activity, causing replication arrest and early mitotic entry post-hyperthermia. Subsequent drug screening shows WEE1 inhibition synergistically destroys cancer cells with hyperthermia. An in-house developed miniaturized device confirms hyperthermia and WEE1 inhibitor combination significantly reduces tumors in vivo. These findings offer additional insights into HIPET, detailing molecular mechanisms of hyperthermia and identifying precise drug combinations for targeted treatment. This research propels the concept of precise hyperthermic intraperitoneal therapy, highlighting its potential against ovarian cancer