erythropoietin (Epocain / Epokine)

Trial of erythropoietin and platelet rich plasma as adjunctive treatment in dogs with paraplegia and absent pan perception after thoracolumbar intervertebral disc extrusion and surgical decompression: A clinical pilot study.

Janzen Madison M, Faissler Dominik D, Rozanski Elizabeth E, Kowaleski Michael P MP

To assess the effectiveness of adjunctive treatment with either systemic erythropoietin or local platelet rich plasma administered at the time of decompressive surgery in dogs with severe spinal cord injury (SCI). Prospective randomized study. A total of 32 client owned dogs presented for acute onset of paraplegia and loss of pain perception after a thoracolumbar disc extrusion. All dogs underwent a standard laminectomy within 24 h after admission and were randomly assigned to one of the following treatment groups: (1) Subarachnoid saline (controls), (2) subarachnoid autologous platelet rich plasma (PRP), or (3) subarachnoid saline plus IV erythropoietin (EPO). Examinations were performed initially at the time of admission, and 1, 3, 7-, 14-, 42-, and 84-days post-surgery. Parameters of interest included return of pain perception, motor or ambulatory function, and fecal or urinary continence. Statistical analysis was performed with SPSS for Windows 30 software with p < .05. The median age of the 32 dogs enrolled was 5 years (3-12.5 years). Dachshunds were the most common breed. One dog (3.1%) developed myelomalacia 4 days post-surgery and was euthanized. Three months post-surgery, 24/32 (75%) dogs regained ambulatory function whereas 7/32 (21.8%) did not. There was no overall difference among groups. Dogs treated with EPO appeared to have a trend towards a reduction in incontinence (Fisher exact test, p = .089) but a larger study is needed to verify this apparent finding. The use of EPO might be beneficial to reduce the likelihood of incontinence, but the low number of patients prohibits definitive conclusions. There was no statistically significant clinical benefit found associated with local application of PRP and systemic injection of EPO at the time of decompressive surgery.

Cinematic Rendering of Brain Magnetic Resonance Imaging: Photorealistic Visualization of Normal Neuroanatomy and Primary Brain Tumors.

Fırat Zeynep Z, Er Füsun F, Di Ieva Antonio A, Ekinci Gazanfer G et al.

Cinematic rendering (CR) is an advanced post-processing technique that generates volumetric 3-dimensional (3D) visualizations from routine clinical magnetic resonance imaging (MRI) data, potentially enhancing anatomical interpretation and spatial understanding. In this retrospective single-center study, 3.0-T MRI datasets from 35 participants (15 healthy controls and 20 patients with histopathologically confirmed primary brain tumors) were analyzed. Cinematic rendering images were generated from precontrast 3D T1-weighted magnetization-prepared rapid acquisition gradient echo (MPRAGE) sequences. Two independent senior observers evaluated image resolution, anatomical detail, lesion depiction, visualization utility, and educational value using a 3-point Likert-type scale. Interobserver agreement was assessed using quadratic weighted Cohen's κ with bootstrap-derived 95% confidence intervals. Statistical analyses were performed using IBM SPSS Statistics for Windows, Version 29.0 (IBM Corp.; Armonk, NY, USA). Cinematic rendering provided consistent, high-fidelity 3D visualization of normal neuroanatomy and tumor-related structural alterations across different primary brain tumor histologies. Image quality ratings were uniformly high (median score: 3), with no significant differences between groups (P ≥ .229). Educational value was rated consistently by both observers across all cases. Interobserver agreement ranged from substantial to almost perfect (κ = 0.65-1.00), with perfect agreement for lesion depiction (κ = 1.00; 100% agreement). Cinematic rendering applied to routine brain MRI provides reproducible, depth-enhanced 3D visualization of normal brain anatomy and tumor-related spatial relationships. The technique demonstrates consistent image quality and interpretability across different tumor types and may serve as a supplementary tool for neuroanatomical education and spatial understanding in clinical practice. Cite this article as: Fırat Z, Er F, Ieva AD, Ekinci G, Türe U. Cinematic rendering of brain magnetic resonance imaging: photorealistic visualization of normal neuroanatomy and primary brain tumors. Eurasian J Med. 2026, 58(4), 1605, doi: 10.5152/ eurasianjmed.2026.261605.

Renal contractile pericytes: When vascular cells choose erythropoietin over renin.

Empitu Maulana A MA, Yasin Muhammad Nabhan MN, Saputra Ketut Wahyu A KWA, Lesmana Jevon Aaron JA

The glycolytic metabolite methylglyoxal drives axon degeneration in vitro and in vivo.

Totta-Griese Gentry G, Enders Jonathan D JD, Madden Trent K TK, Ryals Janelle J et al.

Diabetes impacts 1 in 9 people worldwide, with up to 50% of those patients developing diabetic peripheral neuropathy (DPN). Despite the prevalence of DPN, treatment options for patients remain limited. Methylglyoxal (MGO) is a noxious metabolite elevated in diabetic patients in response to increased glycolytic activity. MGO is thought to participate in complications associated with diabetes, including nociceptive symptoms. Given MGO's known role in driving pain in DPN, we hypothesized that it also contributes to axon degeneration mechanisms. Here, we explore the role of MGO in axon degeneration and its potential contributions to DPN development. We treated primary mouse dorsal root ganglion (DRG) cultures with MGO (5 μM, 10 μM, 500 μM, and 5 mM) and measured neurite length to monitor neurite growth and degeneration. We also administered a single injection of MGO (720 ng) to adult male mice and examined intraepidermal nerve fiber density. Our results reveal that MGO causes axon degeneration in vitro and in vivo. Additionally, at high concentrations (500 μM and 5 mM), MGO reduced the number of somata in primary DRG cultures. Because glyoxalase 1 (GLO1) is the rate-limiting enzyme in the primary pathway that scavenges MGO, we explored a potential role of GLO1 in MGO-induced axon degeneration. To investigate the role of GLO1, we used BALB/cJ and BALB/cByJ mouse substrains, which differ in GLO1 levels due to gene duplication. Increased GLO1 expression was protective in vitro against MGO; however, MGO did not cause fiber loss in vivo. Ultimately, our results demonstrate that MGO is a potential tool for understanding axon degeneration in DPN. Additionally, MGO-driven axon degeneration provides a novel model to further explore the nuanced relationship between axon degeneration and pain.