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As a key component of meridional overturning circulation, mid-deep circulation plays a crucial role in the vertical and meridional distribution of heat. However, due to a lack of observation data, current knowledge of the dynamics of mid-deep circulation currents moving through basin boundaries and complicated seabed topographies is severely limited. In this study, we combined oceanic observation data, bathymetric data, and numerical modeling of the northwest continental margin of the South China Sea to investigate (i) the main features of mid-deep circulation currents traveling through the central depression belt and (ii) how atmospheric-forcing (winds) mesoscale oceanic processes such as eddies and current–topography interactions modulate the mid-deep circulation patterns. Comprehensive results suggest that the convergence of different water masses and current–topography interactions take primary responsibility for the generation of instability and enhanced mixing within the central depression belt. By contrast, winds and mesoscale eddies have limited influence on the development of local circulation patterns at mid-deep depths (>400 m). This study emphasizes that the intensification and bifurcation of mid-deep circulation; specifically, those induced by a large depression belt morphology determine the local material cycle (temperature, salinity, etc.) and energy distribution. These findings provide insights for a better understanding of mid-deep circulation structures on the western boundary of ocean basins such as the South China Sea. [ABSTRACT FROM AUTHOR]

Sepsis-induced acute lung injury (ALI) is a life-threatening medical condition with high mortality and morbidity. Autophagy is involved in the pathophysiological process of sepsis-induced ALI, including inflammation, which indicates that regulating autophagy may be beneficial for this disease. Tomatidine, a natural compound abundant in unripe tomatoes, has been reported to have anti-inflammatory, anti-tumorigenic, and lipid-lowering effects. However, the biological functions and mechanisms of tomatidine in sepsis-induced ALI remain unknown. The principal objective of this study was to investigate the effect of tomatidine on sepsis-induced ALI. Cecal ligation and puncture (CLP) was used to induce septic lung injury in mice, and 10 mg/kg tomatidine was intraperitoneally injected into mice 2 h after the operation. The results of hematoxylin and eosin staining and assessment of lung edema and total protein levels in bronchoalveolar lavage fluid (BALF) demonstrated that tomatidine alleviated CLP-induced severe lung injuries such as hemorrhage, infiltration of inflammatory cells, and interstitial and alveolar edema in mice. Additionally, the levels of proinflammatory cytokines in BALF and lung tissues were measured by enzyme-linked immunosorbent assay (ELISA), and the results showed that tomatidine inhibited CLP-induced inflammatory damage to lungs. Moreover, the results of western blotting showed that tomatidine promoted autophagy during CLP-induced ALI. Mechanistically, immunofluorescence staining and western blotting were used to measure the protein levels of TLR4, phosphorylated NF-κB, phosphorylated IκBα, and phosphorylated MAPKs, showing that tomatidine inactivated NF-κB and MAPK signaling in lung tissues of CLP-induced ALI mice. In conclusion, tomatidine exerts protective effects against sepsis-induced severe damage to the lungs by inhibiting inflammation and activating autophagy in CLP-treated mice through inactivating the NF-κB and MAPK pathways, which may be an effective candidate for treating septic ALI. [ABSTRACT FROM AUTHOR]