The present study is aimed at the development of compositional simulation models of the co-injection of CO₂ and CH₄ during the water-alternating-gas (WAG) process in order to assess the efficiency of carbon capture and storage in combination with enhanced oil recovery (CCS-EOR). The co-injection of CO₂ and CH₄ occupies more reservoir pore volume and causes higher reservoir pressure than CO₂ WAG, thus leading to an enhanced early EOR performance. However, the overall EOR performance of the co-injection method becomes lower than that of CO₂ WAG due to the reduced miscibility and sweep efficiency upon further CH₄ addition. The decrease in gas displacement and sweep efficiency weaken the hysteresis effects upon the residual trapping mechanism. However, the solubility trapping mechanism takes effect because the co-injection generates higher average reservoir pressure than does the CO₂ WAG. The index of global warming potential (GWP) in a mole unit is employed to quantify the carbon storage effects of CO₂ and co-injection WAG cases. According to the index, 1 mole of CH₄ sequestration has the same effects as that of 10 moles of CO₂ for global warming mitigation. In conclusion, the carbon storage effects are enhanced as CH₄ concentration in the WAG increases.

Thymosin beta-4 (Tβ4) is an actin-sequestering peptide that plays important roles in regeneration and remodeling of injured tissues. However, its function in a naturally occurring pathogenic bacterial infection model has remained elusive. We adopted Tβ4-overexpressing transgenic (Tg) mice to investigate the role of Tβ4 in acute pulmonary infection and systemic sepsis caused by Legionella pneumophila. Upon infection, Tβ4-Tg mice demonstrated significantly lower bacterial loads in the lung, less hyaline membranes and necrotic abscess, with lower interstitial infiltration of neutrophils, CD4⁺, and CD8⁺ T cells. Bronchoalveolar lavage fluid of Tβ4-Tg mice possessed higher bactericidal activity against exogenously added L. pneumophila, suggesting that constitutive expression of Tβ4 could efficiently control L. pneumophila. Furthermore, qPCR analysis of lung homogenates demonstrated significant reduction of interleukin 1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α), which primarily originate from lung macrophages, in Tβ4-Tg mice after pulmonary infection. Upon L. pneumophila challenge of bone marrow-derived macrophages (BMDM) in vitro, secretion of IL-1β and TNF-α proteins was also reduced in Tβ4-Tg macrophages, without affecting their survival. The anti-inflammatory effects of BMDM in Tβ4-Tg mice on each cytokine were affected when triggering with tlr2, tlr4, tlr5, or tlr9 ligands, suggesting that anti-inflammatory effects of Tβ4 are likely mediated by the reduced activation of Toll-like receptors (TLR). Finally, Tβ4-Tg mice in a systemic sepsis model were protected from L. pneumophila-induced lethality compared to wild-type controls. Therefore, Tβ4 confers effective resistance against L. pneumophila via two pathways, a bactericidal and an anti-inflammatory pathway, which can be harnessed to treat acute pneumonia and septic conditions caused by L. pneumophila in humans.