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In this work, experiments and comprehensive insights into the proposed covering liquid method to intensify self-preservation effect for methane (CH4) storage are presented. The CH4 hydrate decomposition percentage was 17.6% with the pressure of 0.61 MPa after 12 h at 266.0 K without a covering liquid, which can be reduced to 12.4%, 13.8%, 13.0%, and 8.3% with the pressure of 0.26 MPa, 0.33 MPa, 0.51 MPa, and 0.37 MPa by covering with tetrahydrofuran (THF), cyclopentane (CP), cyclohexane, and n-tetradecane, respectively. When the temperature for CH4 hydrate decomposition was 274.2 K, covering with THF, CP, cyclohexane, and n-tetradecane failed to inhibit CH4 hydrate decomposition. The results suggested that the covering liquid may form a new solid layer (a hydrate layer or other solidified layer) around the CH4 hydrate, which inhibit CH4 transfer below the freezing point of water. However, the new solid layer cannot resist the fast transfer of CH4 from decomposed CH4 hydrate above the freezing point of water. The same phenomenon was also observed in a sodium dodecyl sulfonate (SDS)-dry solution CH4 hydrate formation system. Therefore, the covering method can only intensify the self-preservation effect below the freezing point of water, but cannot generate a self-preservation effect.

MicroRNAs (miRNAs) have emerged as essential regulators that could have pivotal roles in cardiac homeostasis and pathological remodeling of various cardiovascular diseases. We previously demonstrated that miRNA-122-5p overexpression exacerbated the process of vascular hypertrophy, fibrosis, and dysfunction in hypertensive rats and rat aortic adventitial fibroblasts. However, the exact roles and underlying mechanisms of miRNA-122-5p in myocardial fibroblasts remain largely unknown. In this work, neonatal rat cardiofibroblasts (CFs) were isolated and primarily cultured from the hearts of 2- to 3-d-old Sprague-Dawley rats. Stimulation of angiotensin II (Ang II) resulted in marked increases in cellular proliferation and migration and levels of collagen I, collagen III, CTGF, and TGF-β1 in cultured CFs. Furthermore, Ang II led to promoted expression of P62, Bax, and phosphorylated mTOR as well as downregulation of LC3II, beclin-1, and AMPK-phosphorylated levels, thereby contributing to imbalance of autophagy and apoptosis, and cellular injury in CFs, which were significantly ameliorated by treatment with miRNA-122-5p inhibitor. These changes were associated with decreased levels of collagen I, collagen III, CTGF, and TGF-β1. Furthermore, Ang II-induced loss of autophagy and promotion of apoptosis in CFs were prevented by the treatment with Pyr

By employing N-rich porphyrin-based MOFs PCN-224 and PCN-222 as precursors and adopting a mixed-ligand strategy, uniform dispersions of Fe SA catalysts were obtained with excellent CO2 → CO activity, super-stability, and recyclability.

Background: Ovarian cancer (OC) remains a fatal gynecological malignancy. Necroptosis may be a backup pathway that induces cell death when apoptosis is inhibited. This research aims to develop and validate an OC prognosis model based on necroptosis. Methods: The Cancer Genome Atlas (TCGA) and Genome Tissue Expression Consortium Project Genome (GTEx) databases were used in obtaining data on OC patients and normal ovarian tissues. Necroptosis-related genes were downloaded from the Kyoto Encyclopedia of Genes and Genomes (KEGG) database. Differentially expressed genes (DEGs) between tumors and normal tissues were screened. COX regression analysis was used in constructing gene signature, which was further tested and validated in the TCGA and GEO cohorts. Based on risk scores and different clinical prognostic features, Nomogram was constructed to predict OS in OC patients. Then, the patients were divided into high- and low-risk groups, and differential genes were identified between the two groups. The potential biological and pathological functions of the differential genes were explored through Gene Ontology (GO) and KEGG analyses. Immunoassays were used to analyze immune status. Immunohistochemistry (IHC) further confirmed the expression levels of core prognostic genes and their correlations with overall survival (OS) rates. Drug sensitivity analysis in different risk groups was performed to screen out potential drugs for the treatment of OC. Finally, a consensus clustering analysis was used in subtyping ovarian tumors. Results: A three-gene signature was identified, including JAK1, PYGB, and STAT1. The high-risk group had lower OS than the low-risk group and the risk score was acceptable for predicting prognosis independent of any other clinical prognostic features. The Nomogram can accurately predict the 1-, 3-, and 5-year survival rates of patients with OC. Functional analysis revealed immune-related pathways and differences in immune status between the two risk groups. Furthermore, three core prognostic genes involved in model construction were overexpressed in OC versus those in normal ovarian tissues. Patients in the low-risk group were more sensitive to cisplatin and docetaxel. In consensus clustering analysis, OC patients were separated into two subtypes and the survival rate in cluster 1 was better than in cluster 2. Conclusion: A necroptosis-related model based on three core prognostic DEGs can be used to predict OC prognosis.

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