Acid treatment for enhancing Hg0 removal efficiency of chlorine-loaded biochar: mechanism and kinetic analysis.

Adsorbents modified solely with chlorine have limited effectiveness in removing mercury at high temperatures. This study aims to investigate the influence of various acid (HNO3, H2SO4, and H2O2) loadings on the removal efficiency of mercury from NH4Cl-modified adsorbents. The objective is to develop rice straw carbon adsorbents that are both more efficient and cost-effective. The experiments were conducted on a fixed bed experimental platform, with SEM and BET to observe the physical property changes of the modified char samples. XPS analysis was employed to analyze the effects of oxygen, chlorine, and sulfur functional groups. Additionally, a kinetic model was used to investigate the interaction mechanism between the adsorbent and mercury. The findings demonstrate that co-modification surpasses the use of NH4Cl alone, with the combination of NH4Cl and HNO3 yielding the best results. Co-modification enhances the development of a more refined and compact pore structure on the char surface, promoting the physical adsorption of mercury. Moreover, an increased presence of chlorine and oxygen functional groups is observed on the char surface, particularly in the NH4Cl and HNO3 co-modified samples, further enhancing the chemical adsorption capacity of the char. The results from the kinetic analysis support this conclusion. Furthermore, the adsorption process of Hg0 relies on both external mass transfer and chemical adsorption, with the chemical adsorption process playing a more significant role as the controlling factor.

Silencing circ_0001879 inhibits the proliferation and migration of human retinal microvascular endothelial cells under high-glucose conditions via modulating miR-30-3p.

BACKGROUND AND AIM: Diabetic retinopathy is a severe diabetic complication and a major cause of blindness. In this study, we explored the role of circ_0001879 in retinal vascular dysfunction under diabetic conditions. METHODS: Human retinal microvascular endothelial cells (HRMECs) were divided into normal glucose group (NG, 5.5 mmol/L d-glucose), high glucose group (HG, 25 mmol/L d-glucose), and osmotic control group (5.5 mmol/L d-glucose + 19.5 mmol/L mannitol). The expression of circ_0001879 and miR-30-3p was assessed via qRT-PCR. The circ_0001879/miR-30-3p roles in retinal vascular dysfunction were investigated through Cell Counting Kit-8 and Transwell assay. Bioinformatics analysis and luciferase reporter assays were applied to examine interactions between circ_0001879 and miR-30-3p in HRMECs. RESULTS: The relative circ_0001879 expression was remarkably increased in diabetic retinas group than that in the control group. Silencing circ_0001879 suppressed the proliferation and migration of HRMECs under high-glucose conditions. In addition, circ_0001879 acted as a binding platform and miRNA sponge for miR-30-3p. Circ_0001879 modulated the function of HRMECs via targeting miR-30-3p. CONCLUSION: Silencing circ_0001879 inhibited the proliferation and migration of HRMECs under high-glucose conditions via modulating miR-30-3p, which might shed new light on a novel potentially marker and molecular therapeutic target for diabetic retinopathy.

Circular RNA circ-MAT2B facilitates glycolysis and growth of gastric cancer through regulating the miR-515-5p/HIF-1α axis.

BACKGROUND: Circular RNAs (circRNAs) are a special kind of non-coding RNAs that are implicated in cancer malignant behavior, including glycolysis. However, their contributions to gastric cancer (GC) cell glycolysis are still poorly understood. In the present study, we aimed to investigate the glycolysis-related role of circ-MAT2B in GC. METHODS: Gene expression was determined by qRT-PCR analysis. Protein level was detected by Western blot. The CCK-8, colony and EdU assays were carried out to assess GC cell viability, colony formation and DNA synthesis rate. Glycolysis was determined by glucose uptake and lactate production. The positive regulatory network of circ-MAT2B/miR-515-5p/HIF-1α was identified by RNA pull-down, RIP, ChIP and luciferase reporter assays. The in vivo role of circ-MAT2B was evaluated by using xenograft tumor model. RESULTS: Circ-MAT2B was notably increased in GC and could be used as a sensitive and specific indicator of GC diagnosis and prognosis. Stable knockdown of circ-MAT2B dramatically inhibited GC cell viability, colony formation, DNA synthesis, glucose uptake and lactate production in vitro, and retarded tumor growth in vivo. Mechanistically, circ-MAT2B was dominantly located in the cytoplasm and acted as a ceRNA to sponge miR-515-5p and increase HIF-1α expression. Silencing of miR-515-5p or overexpression of HIF-1α could evidently rescue the attenuated aggressive phenotype of GC cells caused by circ-MAT2B knockdown. Importantly, HIF-1α was able to directly bind to circ-MAT2B promoter and transcriptionally activate circ-MAT2B, thus forming a positive feedback loop. CONCLUSION: Our data suggest that circ-MAT2B is a oncogenic circRNA in GC and provide a promising therapeutic target for GC patients.

DRIFT studies on promotion mechanism of H3PW12O40 in selective catalytic reduction of NO with NH3.

Heteropoly acids (HPAs) have been effectively utilized in selective catalytic reduction (SCR) of NO to improve the NH3 absorption capacity and alkaline/alkali metal resistance for SCR catalysts. However, despite the promise on super-acidities, their other properties that would work on SCR process are still lack of exploration. In this study, a 12-tungstaphosphoric acid (H3PW12O40, HPW) was selected to modify a well-reported CeO2 catalyst. The resulted CeO2/HPW catalyst was subsequently utilized for SCR of NO with excess NH3, which revealed a significantly promoted performance in SCR reaction. DRIFT analyses showed that the unique NO2 absorption capacity of HPW could prevent the NO2 being further oxidized into nitrate species and the abundant Brønsted acid sites could effectively retain the NH3, avoiding them being over-oxidized at evaluated temperatures. The presence of NO2 was demonstrated able to induce a so called "fast SCR" reaction over the CeO2/HPW catalyst, which effectively facilitated the SCR reaction. Furthermore, we have also constructed a CeO2@HPW catalyst, which showed an enhanced SO2 poisoning resistance in SCR reaction.