Influences of hydrodynamics on dissolved inorganic carbon in deep subtropical reservoir: Insights from hydrodynamic model and carbon isotope analysis.

Dam construction significantly impacts river hydrodynamics, subsequently influencing carbon biogeochemical processes. However, the influence of hydrodynamic conditions on the migration and transformation of Dissolved Inorganic Carbon (DIC) remains uncertain. To bridge this knowledge gap, we integrated hydrochemistry, isotopic composition (δ13CDIC), and a hydrodynamic model (CE-QUAL-W2) to examine the distinctions, control mechanisms, and environmental effects of DIC biogeochemical processes in a typical large and deep reservoir (Hongjiadu Reservoir) under different hydrodynamic conditions. We evaluated hydrodynamic alterations through the Schmidt stability index and relative water column stability. The analysis disclosed that during weak hydrodynamics periods, the energy necessary for complete mixing the surface and deep water was 34 times higher (3615.32 J/m2 vs.106.86 J/m2), and stability was 13 times greater (312.96 vs. 24.69) compared to periods of strong hydrodynamics. Additionally, the spatiotemporal heterogeneity of DIC concentrations (1.4 % to -9.1 %) and δ13CDIC (-1.7 % to -19.5 %) from the dry to wet seasons reflected disparities in DIC control mechanisms under varied hydrodynamic conditions. Based on model simulations, our calculations indicate that during weak hydrodynamics periods, the enhancement of the biological carbon pump effect resulted in substantial sequestration of DIC, reaching up to 379.6 t-DIC·d-1 in the water. Conversely, during strong hydrodynamics periods, DIC retention capacity decreased by 69.2 t·d-1, resulting in reservoir CO2 emissions of 22.7 × 104 t, which were more than 7 times higher than during weak hydrodynamics periods (3.2 × 104 t). Our findings emphasize the discernible impact of hydrodynamic conditions on reservoir biogeochemical processes related to DIC. Considering the increasing construction of reservoirs globally, understanding and controlling hydrodynamic conditions are crucial for mitigating CO2 emissions and optimizing reservoir management.

Isolation and characterization of a bacterium able to degrade high concentrations of iprodione.

A bacterial strain CQH-1 capable of mineralizing iprodione was isolated and characterized. On the basis of its morphological, physiological, and biochemical characteristics combined with phylogenetic analysis of its 16S rRNA gene sequence, strain CQH-1 was identified as a Microbacterium sp. CQH-1. It was able to use iprodione and 3,5-dichloroaniline as the sole source of carbon and energy for its growth. It completely degraded 100 mg·L-1 iprodione within 96 h at 30 °C. During the degradation of iprodione by strain CQH-1, 2 compounds were detected in GC-MS analysis and were recognized as N-(3,5-dichlorophenyl)-2,4-dioxoimidazolidine and 3,5-dichloroaniline. So, the biodegradation pathway of iprodione by strain CQH-1 was proposed. This is the first report of an iprodione-mineralizing strain from the genus Microbacterium, and strain CQH-1 might be a promising candidate for application in the bioremediation of iprodione-contaminated environments.

Activation of mPTP-dependent mitochondrial apoptosis pathway by a novel pan HDAC inhibitor resminostat in hepatocellular carcinoma cells.

Over-expression and aberrant activation of histone deacetylases (HDACs) are often associated with poor prognosis of hepatocellular carcinoma (HCC). Here, we evaluated the potential anti-hepatocellular carcinoma (HCC) cell activity by resminostat, a novel pan HDAC inhibitor (HDACi). We demonstrated that resminostat induced potent cytotoxic and anti-proliferative activity against established HCC cell lines (HepG2, HepB3, SMMC-7721) and patient-derived primary HCC cells. Further, resminostat treatment in HCC cells activated mitochondrial permeability transition pore (mPTP)-dependent apoptosis pathway, which was evidenced by physical association of cyclophilin-D and adenine nucleotide translocator 1 (ANT-1), mitochondrial depolarization, cytochrome C release and caspase-9 activation. Intriguingly, the mPTP blockers (sanglifehrin A and cyclosporine A), shRNA knockdown of cyclophilin-D or the caspase-9 inhibitor dramatically attenuated resminostat-induced HCC cell apoptosis and cytotoxicity. Reversely, HCC cells with exogenous cyclophilin-D over-expression were hyper-sensitive to resminostat. Intriguingly, a low concentration of resminostat remarkably potentiated sorafenib-induced mitochondrial apoptosis pathway activation, leading to a profound cytotoxicity in HCC cells. The results of this preclinical study indicate that resminostat (or plus sorafenib) could be further investigated as a valuable anti-HCC strategy.