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It is significant to investigate the calcium carbonate (CaCO3) precipitation mechanism during the carbon capture process; nevertheless, CaCO3 precipitation is not clearly understood yet. Understanding the carbonation mechanism at the atomic level can contribute to the mineralization capture and utilization of carbon dioxide, as well as the development of new cementitious materials with high-performance. There are many factors, such as temperature and CO2 concentration, that can influence the carbonation reaction. In order to achieve better carbonation efficiency, the reaction conditions of carbonation should be fully verified. Therefore, based on molecular dynamics simulations, this paper investigates the atomic-scale mechanism of carbonation. We investigate the effect of carbonation factors, including temperature and concentration, on the kinetics of carbonation (polymerization rate and activation energy), the early nucleation of calcium carbonate, etc. Then, we analyze the local stresses of atoms to reveal the driving force of early stage carbonate nucleation and the reasons for the evolution of polymerization rate and activation energy. Results show that the higher the calcium concentration or temperature, the higher the polymerization rate of calcium carbonate. In addition, the activation energies of the carbonation reaction increase with the decrease in calcium concentrations. 

The precipitation of calcium carbonate (CaCO3) is a key mechanism in carbon capture applications relying on mineralization. In that regard, Ca-rich cementitious binders offer a unique opportunity to act as a large-scale carbon sink by immobilizing CO2 as calcium carbonate by mineralization. However, the atomistic mechanism of calcium carbonate formation is still not fully understood. Here, we study the atomic scale nucleation mechanism of an early stage amorphous CaCO3 gel based on reactive molecular dynamics (MD) simulations. We observe that reactive MD offers a notably improved description of this reaction as compared to classical MD, which allows us to reveal new insights into the structure of amorphous calcium carbonate gels and formation kinetics thereof. 

Meniscal tears are associated with a high risk of osteoarthritis but currently have no disease-modifying therapies. Using a Gli1 reporter line, we found that Gli1 + cells contribute to the development of meniscus horns from 2 weeks of age. In adult mice, Gli1 + cells resided at the superficial layer of meniscus and expressed known mesenchymal progenitor markers. In culture, meniscal Gli1 + cells possessed high progenitor activities under the control of Hh signal. Meniscus injury at the anterior horn induced a quick expansion of Gli1-lineage cells. Normally, meniscal tissue healed slowly, leading to cartilage degeneration. Ablation of Gli1 + cells further hindered this repair process. Strikingly, intra-articular injection of Gli1 + meniscal cells or an Hh agonist right after injury accelerated the bridging of the interrupted ends and attenuated signs of osteoarthritis. Taken together, our work identified a novel progenitor population in meniscus and proposes a new treatment for repairing injured meniscus and preventing osteoarthritis. 

ObjectiveTo elucidate the role of decorin, a small leucine‐rich proteoglycan, in the degradation of cartilage matrix during the progression of post‐traumatic osteoarthritis (OA). MethodsThree‐month–old decorin‐null (Dcn^−/−) and inducible decorin‐knockout (Dcn^iKO) mice were subjected to surgical destabilization of the medial meniscus (DMM) to induce post‐traumaticOA. TheOAphenotype that resulted was evaluated by assessing joint morphology and sulfated glycosaminoglycan (sGAG) staining via histological analysis (n = 6 mice per group), surface collagen fibril nanostructure via scanning electron microscopy (n = 4 mice per group), tissue modulus via atomic force microscopy–nanoindentation (n = 5 or more mice per group) and subchondral bone structure via micro–computed tomography (n = 5 mice per group). Femoral head cartilage explants from wild‐type and Dcn^−/−mice were stimulated with the inflammatory cytokine interleukin‐1β (IL‐1β) in vitro (n = 6 mice per group). The resulting chondrocyte response toIL‐1β and release ofsGAGs were quantified. ResultsIn both Dcn^−/−and Dcn^iKOmice, the absence of decorin resulted in acceleratedsGAGloss and formation of highly aligned collagen fibrils on the cartilage surface relative to the control (P< 0.05). Also, Dcn^−/−mice developed more salient osteophytes, illustrating more severeOA. In cartilage explants treated withIL‐1β, loss of decorin did not alter the expression of either anabolic or catabolic genes. However, a greater proportion ofsGAGs was released to the media from Dcn^−/−mouse explants, in both live and devitalized conditions (P< 0.05). ConclusionIn post‐traumaticOA, decorin delays the loss of fragmented aggrecan and fibrillation of cartilage surface, and thus, plays a protective role in ameliorating cartilage degeneration.