Relevance.The search for new methods of effective therapy for traumatic brain injury is one of the important tasks of modern biomedicine. One promising approach for treating traumatic brain injury is cell therapy. The aim of the work is to study the therapeutic effect of glial progenitor cells derived from induced pluripotent stromal cells in an experimental model of traumatic brain injury.Materials and Methods.Modeling of traumatic brain injury was carried out on mature male Wistar rats. The therapeutic group was administered asingle dose of 750*103cells/ml glial progenitor cells with avolume of 1 ml, and the control group — 1 ml of phosphate-­buffered saline. Administration was carried out intra-­arterially 24 hours after injury. To analyze the therapeutic effectiveness, an MRI study was performed on the 14th day, as well as alimb-placing test on the 1st, 3rd, 7th and 14th days. Histological examination was carried out on days 1, 3 and 7 after administration to assess the migration and distribution of stained cells (concentration 750*103cells/ml) by lipophilic dye PKH26 (Sigma, USA) at the rat’s brain tissues after traumatic brain injury. Measurements of injury volume and counts of PKH26-stained cells were performed using ImageJ software (Wayne Rasband, National Institute of Mental Health, Bethesda, MD, USA). The statistical analysis was carried out using GraphPad Prism 8.2.0 program (GraphPad Software, Inc., USA).Results and Discussion.Administration of GPCs led to decreasing the damage volume. Significant decrease in sensorimotor deficit was observed on days 3, 7 and 14 after injury compared with the control group. Intra-arterial administration resulted in successful delivery of glial progenitor cells to brain tissue. Cells were detected in the cerebral cortex, hippocampus, and striatum on day 1, and were not observed on days 3 and 7 after administration.Conclusion.Intra-arterial administration of GPCs leads to efficient migration of cells into brain tissue. Glial progenitor cells therapy promotes neurorecovery processes after traumatic brain injury. This therapy is apromising treatment for traumatic brain injury.

Object-based tasks are widely used in rodent behavioral research, yet object selection remains largely unsystematic. We present a paired-object validation protocol in which objects differ along one researcher-defined feature, allowing assessment of whether that feature is salient to the animal. Using six object pairs varying in height, color, shape, or aperture presence, we tested two wild-caught mice species with contrasting ecologies. Wood mice ( Sylvaemus uralensis ) and striped field mice ( Apodemus agrarius ) showed equal preference for both objects in most pairs, indicating that color, apertures, and apex shape differences are not salient under the tested conditions and can be used interchangeably in object recognition tasks. Height, however, produced ecology-predicted responses: arboreal wood mice avoided the shortest object while open-habitat striped field mice did not. These results demonstrate that the protocol successfully detects feature salience when present and that ecological background predicts which features matter. Summary Statement: A systematic paired-object protocol reveals that most researcher-defined features (color, holes, shape) do not affect rodent exploration, but height preferences emerge in ecology-predicted patterns, demonstrating that feature salience is species-specific.

Introduction/Objective: Traumatic Brain Injury (TBI) causes substantial neurological deficits and remains a major therapeutic challenge. This study aimed to evaluate the neuroprotective properties of Vindeburnol (VIND), a semi-synthetic derivative of vincamine, and to identify its potential molecular targets and optimal dosing regimen for post-traumatic treatment. Methods: Radioligand binding assays were used to determine VIND affinity for 22 CNS receptors, 7 ion channels, and 1 enzyme at a concentration of 10 μM. The in vivo neuroprotective effect was studied in a rat model of TBI induced by controlled cortical impact. VIND was administered intraperitoneally at doses of 10 or 20 mg/kg daily or every other day for 10 days. Neurological recovery was assessed using the beam-walking and limb-placement tests, and brain lesion volume was quantified by MRI on day 14. Results: VIND showed strong inhibition of radioligand binding at α1- and α2-adrenergic receptors (74% and 84.1%, respectively). In vivo, the most pronounced neuroprotective effect was observed at 20 mg/kg every other day, resulting in approximately a twofold reduction in lesion volume (88.7 ± 6.5 mm3 vs 179.4 ± 19.3 mm3 in saline-treated TBI rats, p < 0.001) and a significant improvement in neurological outcomes. The 10 mg/kg dose showed a non-significant trend towards neuroprotection. Discussion: The neuroprotective effect of VIND is likely mediated by the inhibition of excessive adrenergic receptor activation, resulting in improved neuronal survival and functional recovery. These findings highlight adrenergic modulation as a promising therapeutic mechanism for mitigating post-traumatic brain damage. Conclusion: Vindeburnol demonstrated significant neuroprotective efficacy in a rat model of TBI and may represent a promising pharmacological candidate for post-traumatic neuroprotection.

Human papillomavirus (HPV)-associated cervical lesions remain a significant disease burden and minimally invasive blood-based biomarkers could complement cytology and HPV testing. This study aimed to characterize the proteomic composition of plasma-derived CD9⁺ small extracellular vesicles (sEVs) across the morphological spectrum of HPV-associated cervical disease, from histologically normal (NILM) through low-grade (LSIL) and high-grade (HSIL) lesions to invasive squamous cell carcinoma (SCC). Plasma samples from 34 women (NILM, LSIL, HSIL, SCC) were pooled per group, and CD9⁺ sEVs were isolated using an electrochemically controlled immunoaffinity capture method, followed by nanoparticle tracking analysis, transmission electron microscopy, Western blotting, and label-free LC–MS/MS proteomic profiling. The core sEV proteome comprised 258 shared proteins. LSIL showed the most pronounced changes with broad enrichment of complement and coagulation components and acute-phase reactants alongside depletion of immunoglobulin chains and complement C1r-like protein (C1RL). HSIL exhibited few differential proteins, dominated by neutrophil degranulation and retinoid metabolism pathways. SCC demonstrated extensive cargo depletion (22 downregulated proteins) and a nearly sevenfold upregulation of C1RL. Five proteins (including immunoglobulin chains and GPLD1) correlated positively with lesion severity. Pathway analysis consistently implicated platelet activation, lipoprotein remodeling, and insulin-like growth factor signaling. We conclude that plasma CD9⁺ sEVs carry stage-specific proteomic signatures distinguishing HPV-associated cervical lesions, with C1RL emerging as a candidate biphasic marker warranting further validation.