Schlafen genes are conserved regulators of cell proliferation and play a pivotal role in immunity and host defence, yet their function during vertebrate development remains poorly understood. Here, we characterize the expression, phosphorylation dynamics, and function of the single Schlafen ortholog in Xenopus laevis (slfn13) during embryogenesis and in adult tissues. Slfn13 protein levels increase markedly around the mid-blastula transition/late blastula, with unphosphorylated Slfn13 predominating during gastrulation and neurulation, while phosphorylated Slfn13 (p-Slfn13) is more abundant during early cleavage stages. We found that Morpholino-mediated knockdown of Slfn13 in Xenopus laevis causes delayed blastopore lip formation, impaired blastopore closure, and severe gastrulation defects in a dose-dependent manner, indicating a non-redundant requirement for Slfn13 in early morphogenesis. We further analysed Slfn13 expression in adult Xenopus laevis. Slfn13 is enriched in immune tissues and thymic tumour cell lines, with p-Slfn13 specifically detected in proliferative tumour-derived cells. Collectively, our findings reveal a previously unrecognized role for slfn13 in gastrulation and support a conserved immuneassociated expression pattern in adult frogs, expanding the functional landscape of Schlafen proteins across vertebrates.

Influenza-associated encephalopathy (IAE) is a life-threatening complication of influenza. We report a case of a 9-year-old boy diagnosed with fulminant IAE. The patient received life-sustaining support, intensive immunomodulatory therapy, and antiviral therapy. Following an initial single dose of baloxavir marboxil, persistent influenza A (H3N2) RNA detection prompted a multi-targeted antiviral regimen (oseltamivir, baloxavir marboxil, peramivir, and onradivir) as salvage therapy. Nevertheless, influenza A RNA remained detectable for more than 1 month, potentially reflecting severe neurological injury, immunosuppression, and impaired airway clearance.

Agonists of peroxisome proliferator-activated receptor-gamma (PPAR-γ) gained the main interest for managing type-II diabetes mellitus (T2DM) as insulin sensitizers. Serving as 2nd-line therapeutics, glitazones were the first class, influencing PPAR-γ, yet a range of adverse effects were reported regarding the use of PPAR-γ full agonists. Agents having partial PPAR-γ agonistic effect or selectively modulate PPAR-γ transactivity have been introduced. Nonetheless, most of these agents were abandoned at phase II clinical trials for unbalanced supra-therapeutic activation of the multireceptors. Despite clinical attentions towards advers effects, these clinical failures have defined the pharmacological boundaries for safer drug design. The emerging clinical pathway focuses on bifunctional hybridization to achieve glucose homeostasis through synergistic modulation rather than high-dose single-target activation. It was not until 2003 where G-protein-coupled receptor 40 (GPCR40), currently named as free fatty acid receptor-I (FFAR1), was discovered. A plausible FFAR1/PPAR-γ crosstalk has been suggested linking both receptors and insulin secretion. These findings triggered the development of several FFAR1 agonists. Nevertheless, and till the time of writing this review, limited studies proposed the synthesis of such hybrid molecules with only one reaching a regional market. The provided review deals with recent advances of both FFAR1 and PPAR-γ ligands in managing T2DM. Up-to-date medicinal chemistry description of FFAR1 and PPAR-γ modulators as well as each dual agonists have been provided with highlighted structural diversity and activity interlink for each main class.

Lyssaviruses cause rabies in mammals, a viral encephalomyelitis that is almost always fatal once clinical symptoms develop and can be transmitted to humans. Given this high fatality rate, strict biosafety measures are essential during laboratory handling of potentially infectious materials. This review critically assesses current biosafety practices in rabies diagnostic and research laboratories by examining principal risk factors, transmission pathways, and the effectiveness of existing preventive measures. We conducted a comprehensive review of the literature on biosafety risks associated with handling rabies virus and related lyssaviruses, including the use of personal protective equipment, sample handling procedures, and chemical and physical methods for virus inactivation. Particular attention was given to documented cases of laboratory-acquired rabies and their implications for laboratory safety. Although laboratory-acquired infections remain rare, their occurrence highlights important gaps in current biosafety practices. The effectiveness of disinfection and inactivation methods varies widely, especially in resource-limited settings, and key diagnostic procedures, such as the direct fluorescent antibody test, require validation under biosafety constraints. Significant knowledge gaps remain regarding infectious dose, the effectiveness of decontamination methods, and diagnostic standardisation. Strengthening evidence-based biosafety protocols and validating inactivation methods are essential to ensure safer rabies diagnostics and to support effective rabies control, particularly in low-resource settings.