ABSTRACT
Overuse of sulfonamides in aquaculture and agriculture leads to residual drugs that cause serious pollution of the environment. However, the residues of sulfonamides in the environment are not unique, and the existing microbial degradation technology has a relatively low degradation rate of sulfonamides. Therefore, in this study, a Pseudomonas stutzeri strain (DLY-21) with the ability to degrade four common SAs was screened and isolated from aerobic compost. Under optimal conditions, the DLY-21 strain degraded four sulfonamides simultaneously within 48 h, and the degradation rates were all over 90%, with the average degradation rates of SAs being sulfoxide (SDM) ≈ sulfachloropyridazine (SCP) > sulfa quinoxaline (SQ) > sulfadiazine (SQ). In addition, the main compounds of the strain DLY-21-degrading SAs were identified by LC-MS analysis. On this basis, four detailed reaction pathways for SA degradation were deduced. This is the first report of the use of a P. stutzeri strain to degrade four sulfonamide antibiotics (SQ, SDM, SCP, and SM1), which can improve the removal efficiency of sulfonamide antibiotic pollutants and thus ameliorate environmental pollution. The results showed that DLY-21 had a good degradation effect on four SAs (SQ, SDM, SCP, and SM1).
ABSTRACT
In this study, a pilot-scale integrated process was developed, which combined the integrated biological contact oxidation technology (AO) and the improved constructed wetland technology. The results showed significant removal efficiency for both conventional and trace organic pollutants. The average removal efficiencies for COD, NH4+-N, and TP were 78.52, 85.95, and 49.47%, respectively. For trace organic pollutants, triclocarban, triclosan, and sulfadiazine, the removal efficiencies reached 60.14, 57.42, and 84.29%, respectively. The AO stage played a crucial role in removing trace organic pollutants, achieving removal efficiencies of 37.28, 43.44, and 83.82% for triclocarban, triclosan, and sulfadiazine, respectively. Subsequent treatment using improved constructed wetland technology with coal slag + gravel fillers demonstrated the highest removal efficiency, with average efficiencies of 68.66, 63.38, and 81.32% for triclocarban, triclosan, and sulfadiazine, respectively. Correlation analysis revealed positive correlations between temperature, precipitation, and the removal efficiency of COD, NH4+-N, and TP, while negative correlations were observed with the removal efficiency of triclocarban, triclosan, and sulfadiazine. Furthermore, the influent concentrations of triclocarban and triclosan were significantly negatively correlated with the removal efficiency of COD and TP. The presence of triclocarban and triclosan potentially reduced the microbial diversity and hindered sludge sedimentation performance.
ABSTRACT
The resistance of synovial sublining macrophages to apoptosis has a crucial role in joint inflammation and destruction in rheumatoid arthritis (RA). However, the underlying mechanism is incompletely understood. Here we report that inactivation of the pro-apoptotic BCL-2 family protein BAD is essential for survival of synovial sublining macrophage in RA. Genetic disruption of Bad leads to more severe joint inflammation and cartilage and bone damage with reduced apoptosis of synovial sublining macrophages in collagen-induced arthritis (CIA) and TNFα transgenic (TNF-Tg) mouse models. Conversely, Bad3SA/3SA mice, in which BAD can no longer be inactivated by phosphorylation, are protected from collagen-induced arthritis. Mechanistically, phosphorylation-mediated inactivation of BAD specifically protects synovial sublining macrophages from apoptosis in highly inflammatory environment of arthritic joints in CIA and TNF-Tg mice, and in patients with RA, thereby contributing to RA pathology. Our findings put forward a model in which inactivation of BAD confers the apoptosis resistance on synovial sublining macrophages, thereby contributing to the development of arthritis, suggesting that BAD may be a potential therapeutic target for RA.
