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Salt cavern flow batteries (SCFBs) are an energy storage technology that utilize salt caverns to store electrolytes of flow batteries with a saturated NaCl solution as the supporting electrolyte. However, the geological characteristics of salt caverns differ significantly from above-ground storage tanks, leading to complex issues in storing electrolytes within salt caverns. Therefore, investigating and summarizing these issues is crucial for the advancement of SCFB technology. This paper's innovation lies in its comprehensive review of the current state and development trends in SCFBs both domestically and internationally. First, the current development status of SCFB energy storage technology both domestically and internationally is summarized. Then, eight main issues are proposed from the perspectives of salt cavern geological characteristics (tightness, conductivity, ions, and temperature) and electrolyte properties (selection, permeability, corrosion, and concentration). Finally, a novel SCFB system is proposed to address the most critical issue, which is the low concentration and uneven distribution of active materials in the current SCFB system. The review in this paper not only comprehensively summarizes the development status of SCFBs both domestically and internationally, but also points out the direction for the future research focussing on SCFBs. [ABSTRACT FROM AUTHOR]

Hydrophobic surfaces exhibit unique surface effects and hold broad potential across numerous domains, including anti-icing, condensation, and self-cleaning. Conventionally, droplets on hydrophobic surfaces have been conceptualized as spherical segments to predict contact angles. However, a droplet deposited on hydrophobic surfaces tends to be flattened at the bottom due to gravity, leading to a discrepancy between the experimental observation and prediction derived from the Cassie–Baxter equation. Here, we propose an approximation that divides the distorted droplet into upper and lower segments, i.e., simplifying its morphology into a double-radius contour. This approach leads to a more accurate prediction of the contact angle on hydrophobic structured surfaces. The deviation between experiment and our model is less than 1.7%. Further water evaporation was conducted to investigate the transition condition from the Cassie–Baxter state to the Wenzel state, and we show that the critical transition radius for substrates with varied microstructural geometry parameters consistently falls slightly below the theoretical prediction, which is attributed to an inaccurate assessment of the structure angle. Finally, we demonstrate that the stability of the Cassie–Baxter state can be enhanced by employing hierarchical micro-/nanostructures on the surface. This research advances our foundational comprehension of wetting phenomenon and the stability of the Cassie–Baxter state. [ABSTRACT FROM AUTHOR]

Hyperglycemia mediates oxidative stress, thus inducing transcription factor nuclear factor kappa B (NF-[kappa]B) activation, increasing endothelial adhesion molecule expression and monocyte/endothelial interaction, and resulting in endothelial injury. Ketamine was reported to attenuate oxidative stress in many cases. In this research, we determined whether and how ketamine protects against high-glucose-mediated augmentation of monocyte/endothelial interaction and endothelial adhesion molecule expression in human umbilical vein endothelial cells. High glucose augmented monocyte/endothelial adhesion and endothelial adhesion molecule expression. High glucose induced reactive oxygen species (ROS) production and augmented phospho-protein kinase C (p-PKC) [beta]II expression and PKC activity. Moreover, high glucose inhibited the inhibitory subunit of nuclear factor-[kappa]B[alpha] (I[kappa]B[alpha]) expression in the cytoplasm and induced NF-[kappa]B nuclear translocation. Importantly, the effects induced by high glucose were counteracted by ketamine treatment. Further, CGP53353, a PKC [beta]II inhibitor, inhibited high-glucose- mediated NF-[kappa]B nuclear translocation, attenuated adhesion molecule expression, and reduced monocyte/endothelial interaction. Further, these effects of ketamine against high-glucose-induced endothelial injury were inhibited by phorbol 12-myristate 13- acetate, a PKC [beta]II activator. In conclusion, ketamine, via reducing ROS accumulation, inhibited PKC [beta]II Ser660 phosphorylation and PKC and NF-[kappa]B activation and reduced high-glucose-induced expression of endothelial adhesion molecules and monocyte/endothelial interaction. Key words: ketamine, high glucose, endothelial, inflammation. L'hyperglycemie participe a la mediation du stress oxydatif, ce qui comprend de fait l'activation du facteur de transcription du facteur nucleaire kappa B (NF-[kappa]B), l'augmentation de l'expression des molecules d'adherence endotheliale, ainsi que l'interaction entre les monocytes et l'endothelium, avec des lesions endotheliales resultantes. On a rapporte que la ketamine permet d'attenuer le stress oxydatif dans bien des cas. Dans cette etude, nous avons cherche a etablir si la participation de la ketamine a la protection contre l'augmentation de l'interaction entre les monocytes et l'endothelium et a l'expression des molecules d'adherence endotheliale mediees par l'hyperglycemie dans les cellules endotheliales de veine ombilicale humaine, ainsi que les modes d'action, le cas echeant. L'hyperglycemie entramait une augmentation de l'adherence entre les monocytes et l'endothelium, ainsi que de l'expression des molecules d'adherence de l'endothelium. L'hyperglycemie entramait la production de derives reactifs de l'oxygene et une augmentation de l'expression de la phospho-proteine kinase C (p-PKC) [beta]II et de l'activite de la PKC. En outre, l'hyperglycemie entramait une inhibition de l'expression de la sous-unite inhibitrice du facteur nucleaire [kappa]B[alpha] (I[kappa]B[alpha]) dans le cytoplasme, ainsi que la stimulation de la translocation nucleaire du NF-[kappa]B. Il est important de noter que l'administration de ketamine contrait les effets engendres par l'hyperglycemie. De plus, le CGP53353, un inhibiteur de la PKC [beta]II, permettait d'inhiber la translocation nucleaire du NF-[kappa]B mediee par l'hyperglycemie, d'attenuer l'expression des molecules d'adherence et d'inhiber l'interaction entre les monocytes et l'endothelium. Enfin, ces effets de la ketamine contre les lesions endotheliales engendrees par l'hyperglycemie etaient inhibes par le phorbol 12-myristate 13-acetate, un activateur de la PKC [beta]II. En conclusion, la ketamine, par l'intermediaire de la diminution de l'accumulation des derives reactifs de l'oxygene, de l'inhibition de la phosphorylation de la PKC [beta]II en Ser660, de l'activation de la PKC et du NF-[kappa]B entramait une diminution de l'expression des molecules d'adherence endotheliale et de l'interaction entre les monocytes et l'endothelium engendrees par l'hyperglycemie. [Traduit par la Redaction] Mots-cles: ketamine, hyperglycemie, endothelial, inflammation., Introduction Perioperative hyperglycemia is often seen in both nondiabetic patients (Werb et al. 1989) and diabetic patients (Walts et al. 1981). Hyperglycemia increases the expression of endothelial adhesion molecules, including [...]