Sorption of Soil Carbon Dioxide by Biochar and Engineered Porous Carbons.

CO2 is 45 to 50 times more concentrated in soil than in air, resulting in global diffusive fluxes that outpace fossil fuel combustion by an order of magnitude. Despite the scale of soil CO2 emissions, soil-based climate change mitigation strategies are underdeveloped. Existing approaches, such as enhanced weathering and sustainable land management, show promise but continue to face deployment barriers. We introduce an alternative approach: the use of solid adsorbents to directly capture CO2 in soils. Biomass-derived adsorbents could exploit favorable soil CO2 adsorption thermodynamics while also sequestering solid carbon. Despite this potential, previous study of porous carbon CO2 adsorption is mostly limited to single-component measurements and conditions irrelevant to soil. Here, we probe sorption under simplified soil conditions (0.2 to 3% CO2 in balance air at ambient temperature and pressure) and provide physical and chemical characterization data to correlate material properties to sorption performance. We show that minimally engineered pyrogenic carbons exhibit CO2 sorption capacities comparable to or greater than those of advanced sorbent materials. Compared to textural features, sorbent carbon bond morphology substantially influences low-pressure CO2 adsorption. Our findings enhance understanding of gas adsorption on porous carbons and inform the development of effective soil-based climate change mitigation approaches.

MicroRNA-126-3p Inhibits Angiogenic Function of Human Lung Microvascular Endothelial Cells via LAT1 (L-Type Amino Acid Transporter 1)-Mediated mTOR (Mammalian Target of Rapamycin) Signaling.

OBJECTIVE: MicroRNA-126-3p (miR-126) is required for angiogenesis during organismal development or the repair of injured arterial vasculature. The role of miR-126 in lung microvascular endothelial cells, which are essential for gas exchange and for lung injury repair and regeneration, remains poorly understood. Considering the significant heterogeneity of endothelial cells from different vascular beds, we aimed to determine the role of miR-126 in regulating lung microvascular endothelial cell function and to elucidate its downstream signaling pathways. Approach and Results: Overexpression and knockdown of miR-126 in primary human lung microvascular endothelial cells (HLMVEC) were achieved via transfections of miR-126 mimics and antisense inhibitors. Increasing miR-126 levels in HLMVEC reduced cell proliferation, weakened tube formation, and increased cell apoptosis, whereas decreased miR-126 levels stimulated cell proliferation and tube formation. Whole-genome RNA sequencing revealed that miR-126 was associated with an antiangiogenic and proapoptotic transcriptomic profile. Using validation assays and knockdown approaches, we identified that the effect of miR-126 on HLMVEC angiogenesis was mediated by the LAT1 (L-type amino acid transporter 1), via regulation of mTOR (mammalian target of rapamycin) signaling. Furthermore, downregulation of miR-126 in HLMVEC inhibited cell apoptosis and improved endothelial tube formation during exposure to environmental insults such as cigarette smoke. CONCLUSIONS: miR-126 inhibits HLMVEC angiogenic function by targeting the LAT1-mTOR signaling axis, suggesting that miR-126 inhibition may be useful for conditions associated with microvascular loss, whereas miR-126 augmentation may help control unwanted microvascular angiogenesis.