Sepsis is a systemic inflammatory response that requires effective macrophage metabolic functions to resolve ongoing inflammation. Previous work showed that the mechanosensitive cation channel, transient receptor potential vanilloid 4 (TRPV4), mediates macrophage phagocytosis and cytokine production in response to lung infection. Here, we show that TRPV4 regulates glycolysis in a stiffness-dependent manner by augmenting macrophage glucose uptake by GLUT1. In addition, TRPV4 is required for LPS-induced phagolysosome maturation in a GLUT1-dependent manner. In a cecal slurry mouse model of sepsis, TRPV4 regulates sepsis-induced glycolysis as measured by BAL fluid (BALF) lactate and sepsis-induced lung injury as measured by BALF total protein and lung compliance. TRPV4 is necessary for bacterial clearance in the peritoneum to limit sepsis-induced lung injury. It is interesting that BALF lactate is increased in patients with sepsis compared with healthy control participants, supporting the relevance of lung cell glycolysis to human sepsis. These data show that macrophage TRPV4 is required for glucose uptake through GLUT1 for effective phagolysosome maturation to limit sepsis-induced lung injury. Our work presents TRPV4 as a potential target to protect the lung from injury in sepsis.

The potential of a biosorbent derived from Arundo donax stem, a readily available agricultural product, was examined to remove Cr(VI) from water. Various techniques such as XRD, FTIR, SEM, and EDX were used for the characterization of the prepared adsorbent. The optimal pH for Cr(VI) biosorption was found to be 2.0. The experimental data best suits the Langmuir isotherm model and pseudosecond-order kinetics. The maximum biosorption capacity (q_max) of the investigated biosorbent for Cr(VI) was evaluated to be 76.92mg/g by the Langmuir model. From the results of the Cr(VI) biosorption using charred Arundo donax stem powder (CADSP), it can be a novel, cost-efficient, and effective material for removing Cr(VI) from water and wastewater.

The complete assessment is appropriate. According to my expertise and education, it requires additional improvements and the addition of certain things before publication. This review paper lacks an adequate introduction and a literature review. The...

Antimicrobial resistance (AMR) is an increasing global health threat that underscores the urgent need for antimicrobial agents with mechanisms of action distinct from those of conventional antibiotics. Gallium (Ga) has emerged as a promising metal-based antimicrobial owing to the chemical similarity of Ga(III) to Fe(III), which enables it to interfere with bacterial iron acquisition and utilization. In contrast to Fe(III), Ga(III) is redox-inactive under physiological conditions and cannot support the redox reactions required for many iron-dependent cellular processes, thereby disrupting bacterial metabolism. This review highlights recent advances in gallium-based antimicrobial strategies, with particular emphasis on the role of ligand coordination in modulating the antibacterial activity of Ga(III) against drug-resistant pathogens. Emerging evidence indicates that coordination with lipophilic ligands can enhance the cellular update and accumulation of Ga(III) and may confer additional antibacterial effects beyond Fe(III) mimicry alone. These findings suggest that ligand design is a key strategy for tuning the physicochemical properties and antimicrobial activity of gallium complexes. Rational development of ligand-coordinated Ga(III) complexes may therefore provide new therapeutic approaches for combating multidrug-resistant bacterial infections.