Quercetin, a dietary flavonoid, contributes to bowel regulation and anti-inflammatory effects. Enterochromaffin (EC) cells express transient receptor potential ankyrin1 (TRPA1) and significantly contribute to gastrointestinal motility and secretion via 5-hydroxytryptamine (5-HT) release. A recent study reported that flavonoids, including quercetin, activate heterogeneously expressed TRPA1. We here evaluated the effects of quercetin and its analogs (kaempferol and galangin) on TRPA1 channels using RIN-14B, an EC model cell line. To elucidate the function of these flavonoids, intracellular Ca2+ concentration ([Ca2+]i) was measured, and 5-HT release from RIN-14B cells was analyzed. Quercetin- and kaempferol-induced [Ca2+]i increases, which were abolished by extracellular Ca2+ removal. The [Ca2+]i responses to quercetin and kaempferol were partially suppressed by TRPA1 antagonists and nearly completely abolished by L-type voltage-dependent Ca2+ (Cav) channel inhibitors. Reverse transcription-polymerase chain reaction analysis confirmed the expression of both TRPA1 and L-type Cav channels in RIN-14B cells. Quercetin- and kaempferol-induced 5-HT release from RIN-14B cells was inhibited by TRPA1 antagonists and L-type Cav channel inhibitors. Along with the activation effects, flavonoids inhibited the [Ca2+]i responses to TRPA1 agonists, with the inhibitory potency ranking as follows: quercetin, kaempferol, and galangin. Moreover, these flavonoids demonstrated inhibitory effects on heterogeneously expressed TRPA1. Furthermore, flavonoids inhibited TRPA1 agonist-induced 5-HT release from RIN-14B cells. These results suggest that flavonoids can regulate 5-HT secretion through TRPA1 and L-type Cav channels. Dietary flavonoids may hold therapeutic potential for gastrointestinal functions and disorders.

The growing challenge of antimicrobial resistance has necessitated the development of new antibiotics with novel mechanisms of action. Gepotidacin is a first-in-class triazaacenaphthylene antibiotic developed for the treatment of uncomplicated urinary tract infections (uUTIs) in female adults and adolescents. It inhibits bacterial DNA replication by targeting both DNA gyrase and topoisomerase IV at a distinct binding site, differing from fluoroquinolones and therefore presenting a novel mechanism of action. However, resistance-associated mutations affecting susceptibility have been documented, emphasizing the need for ongoing monitoring. Pharmacokinetic studies indicate predictable, dose-dependent oral absorption suitable for twice- or thrice-daily dosing, with minimal accumulation and comparable profiles across populations. In terms of therapeutic success for the treatment of uUTIs, phase III clinical trials (EAGLE-2 and EAGLE-3) have demonstrated that gepotidacin was non‑inferior to the broad-spectrum antibiotic nitrofurantoin in EAGLE-2 and even superior to nitrofurantoin in EAGLE-3, with a tolerability profile comparable to other antibiotics of its class. Studies also suggest potential efficacy against uncomplicated gonorrhea (GC), including strains resistant to current therapies. Adverse events were generally mild to moderate, predominantly gastrointestinal, and caution is advised in patients with QT prolongation risk. While gepotidacin represents an important addition to the limited pool of oral antibiotics for these infections, its long-term clinical utility will depend on careful stewardship, resistance surveillance, and further evaluation in broader indications and combination regimens.

Ex vivo lung perfusion (EVLP) is now an established normothermic machine-perfusion strategy in lung transplantation, primarily enabling structured donor lung assessment, short-term preservation, and selective rehabilitation outside the recipient. Because the supply of transplantable lungs remains limited, clinically implemented EVLP protocols have increased donor-lung utilization by allowing transplant teams to evaluate marginal grafts under near-physiological ventilation and perfusion rather than relying exclusively on static cold storage. The perfusate is central to this process because it stabilizes colloid osmotic pressure, electrolytes, buffering capacity, metabolic substrates, and oxygen transport according to protocol requirements. This review critically summarizes the development of EVLP perfusates and separates clinically validated roles from experimental repair strategies. We first distinguish EVLP perfusates from cold preservation solutions and compare acellular, red blood cell-containing, and whole-blood approaches with attention to their physiological rationale, logistical constraints, and level of evidence. We then discuss protocol-specific additives, including anti-inflammatory agents, antioxidants, antimicrobials, anticoagulants, hormones, nutritional substrates, and cellular or gene-based therapies. Emerging interventions such as polymerized hemoglobin, cytokine adsorption, mesenchymal stromal cell-derived products, CRISPR-Cas-mediated interleukin-10 modulation, and prolonged or intermittent EVLP illustrate the expanding therapeutic potential of the platform. However, most of these strategies remain preclinical or early translational. Future perfusate development should therefore prioritize standardized outcome measures, evidence-based component selection, and careful separation of organ preservation, organ assessment, and organ rehabilitation.

The article "Hypoxia-Treated Adipose Mesenchymal Stem Cells Derived Exosomes Enhance the Therapeutic Effects on Unilateral Ureteral Obstruction Mice" [Pharmacology. 2025;110(3):165-177; https://doi.org/10.1159/000542609] by Chi Zhang, Longjun Cai, Meimei Ma, Xiaohui Xie, Junsheng Wang and Yuanyuan Zhang has been retracted by the Publisher and the Editor.After the publication of this article, it was identified that Figure S1c in this article, depicting confirmation of the capability of the AMSCs for adipogenic differentiation, had been previously published as Figure 1C by a different author group depicting the capability of primary mouse BMSCs to differentiate to adipocytes [1].When asked to comment on the above, the authors stated that the image in question was provided by the stem cell distributor and that they did not conduct the differentiation experiments depicted in Figure S1, which was not disclosed in the article. As the authors did not disclose the source of the experiments and images in the figure in question and did not independently characterise the cell population before the study was conducted, the Editor concluded that the concerns undermined the results of the article and, therefore, the article has been retracted.The authors agreed to this retraction.