This prospective observational study describes the pharmacokinetic characteristics of favipiravir in adult patients hospitalized for mild to moderate COVID‐19 with a positive RT‐PCR test. Favipiravir was administered for 5 days, with a loading dose of 3200 mg and a maintenance dose of 1200 mg/day. Serial blood samples were collected on Day 2 and Day 4 of the therapy. Laboratory findings of the patients (n = 21) and in‐hospital mortality were recorded. Favipiravir concentrations exhibited substantial variability and a significant decrease during the treatment of COVID‐19. The median favipiravir trough concentration (C_0‐trough) on Day 2 was 21.26 (interquartile range [IQR], 8.37–30.78) μg/mL, whereas it decreased significantly to 1.61 (IQR, 0.00–6.41) μg/mL on Day 4, the area under the concentration–time curve decreased by 68.5%. Day 2 C_0‐trough of female patients was higher than male patients. Our findings indicate that favipiravir concentrations show significant variability during the treatment of COVID‐19 and therapeutic drug monitoring may be necessary to maintain targeted concentrations.

Central nervous system (CNS) tumors represent a heterogeneous group of neoplasms associated with significant morbidity and mortality despite their relatively low incidence. Advances in the fifth edition of the World Health Organization (WHO) classification have emphasized the integration of histopathological, immunohistochemical, and molecular features, fundamentally transforming diagnostic and prognostic frameworks in neuro-oncology. This manuscript aims to provide an overview of CNS tumor biology, focusing on key diagnostic markers, genetic and epigenetic alterations, and emerging therapeutic strategies. It further describes recent advances in multi-omics approaches and artificial intelligence, which enable deeper characterization of tumor heterogeneity and support the development of precision medicine strategies. Finally, current and emerging therapeutic modalities, including combination therapies, targeted treatments, and novel molecular targets, are examined with emphasis on overcoming resistance mechanisms and improving clinical outcomes. Overall, the integration of molecular biology, advanced diagnostics, and innovative therapeutic approaches represents a critical step toward personalized management of CNS tumors and improved patient survival.

This study investigates the effects of a ketogenic diet (KD) on the brain proteome in Genetic Absence Epilepsy Rats from Strasbourg (GAERS), a model of genetic absence epilepsy. The ketogenic diet is a therapeutic intervention for epilepsy, yet its mechanisms remain incompletely understood. Thirty-day-old male GAERS rats were fed a KD (88.8% fat, 10.2% protein, 1% carbohydrate; n = 4) or a normal diet (ND; n = 3), with Wistar rats (n = 3) as healthy controls. A shotgun proteomics approach with data-dependent acquisition was used to analyze the somatosensory cortex (SCx) and hippocampus (Hipp). Data were processed with MaxQuant and Perseus. Compared to Wistars, GAERS-ND rats showed significant alterations in 526 proteins in SCx and 612 in Hipp. KD treatment significantly altered 122 proteins in SCx and 124 in Hipp of GAERS. Notably, KD reversed the expression of 22 proteins in SCx and 32 in Hipp to levels observed in controls. Most KD-affected proteins were synaptic (72% SCx, 76.6% Hipp) and mitochondrial. Pathway analysis indicated KD regulates axon guidance, neurodevelopment, and metabolism in SCx, and autophagy, mitophagy, and Rho GTPase signaling in Hipp. The workflow of the experimental design is provided in Fig. 1.

Purpose: This study investigated the effects of ketogenic diet (KD) intervention on the cortical proteome in genetic absence epilepsy rats from Strasbourg (GAERS), a well‐established model of absence epilepsy. The ketogenic diet is a therapeutic intervention for epilepsy, yet its mechanisms remain incompletely understood. Method: Thirty‐day‐old male GAERS rats were fed a KD (88.8% fat, 10.2% protein, 1% carbohydrate; n = 4) or a normal diet (ND; n = 3), with Wistar rats ( n = 3) as healthy controls. A shotgun proteomics approach with data‐dependent acquisition (DDA) was used to analyze the somatosensory cortex (SCx), a key cortical driver of absence seizures. Data were processed with MaxQuant and Perseus. Findings: Compared to Wistars, GAERS‐ND rats showed significant alterations in 526 proteins in SCx and KD treatment significantly altered 121 proteins in SCx of GAERS. Notably, KD was associated with partial shifts in the expression patterns of 22 proteins toward those observed in Wistar controls. Most KD‐affected proteins were synaptic (72% SCx) and mitochondrial. Pathway analysis indicated that ketogenic diet–associated protein changes were enriched in axon guidance, neurodevelopment, and metabolic pathways in the somatosensory cortex. Conclusion: Together, these results suggest that synaptic and mitochondrial protein alterations in this region are associated with cortical molecular adaptations observed under ketogenic diet administration in absence epilepsy.