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BACKGROUND: Although decompression surgery is the optimal treatment for patients with severe degenerative cervical myelopathy (DCM), some individuals experience no improvement or even a decline in neurological function after surgery, with spinal cord ischemia-reperfusion injury (SCII) identified as the primary cause. Spinal cord compression results in local ischemia and blood perfusion following decompression is fundamental to SCII. However, owing to inadequate perioperative blood flow monitoring, direct evidence regarding the occurrence of SCII after decompression is lacking. The objective of this study was to establish a suitable animal model for investigating the underlying mechanism of spinal cord ischemia-reperfusion injury following decompression surgery for degenerative cervical myelopathy (DCM) and to elucidate alterations in neurological function and local blood flow within the spinal cord before and after decompression. METHODS: Twenty-four Sprague-Dawley rats were allocated to three groups: the DCM group (cervical compression group, with implanted compression material in the spinal canal, n = 8), the DCM-D group (cervical decompression group, with removal of compression material from the spinal canal 4 weeks after implantation, n = 8), and the SHAM group (sham operation, n = 8). Von Frey test, forepaw grip strength, and gait were assessed within 4 weeks post-implantation. Spinal cord compression was evaluated using magnetic resonance imaging. Local blood flow in the spinal cord was monitored during the perioperative decompression. The rats were sacrificed 1 week after decompression to observe morphological changes in the compressed or decompressed segments of the spinal cord. Additionally, NeuN expression and the oxidative damage marker 8-oxoG DNA were analyzed. RESULTS: Following spinal cord compression, abnormal mechanical pain worsened, and a decrease in forepaw grip strength was observed within 1-4 weeks. Upon decompression, the abnormal mechanical pain subsided, and forepaw grip strength was restored; however, neither reached the level of the sham operation group. Decompression leads to an increase in the local blood flow, indicating improved perfusion of the spinal cord. The number of NeuN-positive cells in the spinal cord of rats in the DCM-D group exceeded that in the DCM group but remained lower than that in the SHAM group. Notably, a higher level of 8-oxoG DNA expression was observed, suggesting oxidative stress following spinal cord decompression. CONCLUSION: This model is deemed suitable for analyzing the underlying mechanism of SCII following decompressive cervical laminectomy, as we posit that the obtained results are comparable to the clinical progression of degenerative cervical myelopathy (DCM) post-decompression and exhibit analogous neurological alterations. Notably, this model revealed ischemic reperfusion in the spinal cord after decompression, concomitant with oxidative damage, which plausibly underlies the neurological deterioration observed after decompression.

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BACKGROUND AND OBJECTIVES: To assess the feasibility, accuracy, and safety of 3-dimensional (3D) structure light robot-assisted frameless stereotactic brain biopsy. METHODS: Five consecutive patients (3 males, 2 females) were included in this study. The patients' clinical, imaging, and histological data were analyzed, and all patients received a 3D structure light robot-assisted frameless stereotactic brain biopsy. The raw and/or analyzed data of the study are available from the corresponding author. RESULTS: The statistical results showed a mean age of 59.6 years (range 40-70 years), a mean target depth of 60.9 mm (range 53.5-65.8 mm), a mean radial error of 1.2 ± 0.7 mm (mean ± SD), a mean depth error of 0.7 ± 0.3 mm, and a mean absolute tip error of 1.5 ± 0.6 mm. The calculated Pearson product-moment correlation coefficient ( r = 0.23) revealed no correlation between target depth and absolute tip error. All biopsy needles were placed in line with the planned trajectory successfully, and diagnostic specimens were harvested in all cases. Histopathological analysis revealed lymphoma (2 cases), lung adenocarcinoma (1 case), glioblastoma multiforme (1 case), and oligodendroglioma (1 case). CONCLUSION: Surface registration using the 3D structure light technique is fast and precise because of the achievable million-scale point cloud data of the head and face. 3D structure light robot-assisted frameless stereotactic brain biopsy is feasible, accurate, and safe.

Asunto(s)

Imagenología Tridimensional , Técnicas Estereotáxicas , Humanos , Persona de Mediana Edad , Femenino , Masculino , Adulto , Anciano , Imagenología Tridimensional/métodos , Neoplasias Encefálicas/diagnóstico por imagen , Neoplasias Encefálicas/patología , Procedimientos Quirúrgicos Robotizados/métodos , Procedimientos Quirúrgicos Robotizados/instrumentación , Encéfalo/patología , Encéfalo/diagnóstico por imagen , Estudios de Factibilidad , Biopsia/métodos , Biopsia/instrumentación , Neuronavegación/métodos , Neuronavegación/instrumentación

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Glioma is the most common type of primary intracranial malignant tumor, and because of its high invasiveness and recurrence, its prognosis remains poor. The present study investigated the biological function of piggyBac transportable element derived 5 (PGBD5) in glioma. Glioma and para-cancerous tissues were obtained from five patients. Reverse transcription-quantitative PCR and western blotting were used to detect the expression levels of PGBD5. Transwell assay and flow cytometry were used to evaluate cell migration, invasion, apoptosis and cell cycle distribution. In addition, a nude mouse tumor transplantation model was established to study the downstream pathways of PGBD5 and the molecular mechanism was analyzed using transcriptome sequencing. The mRNA and protein expression levels of PGBD5 were increased in glioma tissues and cells. Notably, knockdown of PGBD5 in vitro could inhibit the migration and invasion of glioma cells. In addition, the knockdown of PGBD5 expression promoted apoptosis and caused cell cycle arrest in the G2/M phase, thus inhibiting cell proliferation. Furthermore, in vivo experiments revealed that knockdown of PGBD5 expression could inhibit Ki67 expression and slow tumor growth. Changes in PGBD5 expression were also shown to be closely related to the peroxisome proliferator-activated receptor (PPAR) signaling pathway. In conclusion, interference with PGBD5 could inhibit the malignant progression of glioma through the PPAR pathway, suggesting that PGBD5 may be a potential molecular target of glioma.

Asunto(s)

Neoplasias Encefálicas , Glioma , Animales , Ratones , Humanos , Receptores Activados del Proliferador del Peroxisoma/metabolismo , Regulación hacia Arriba , Línea Celular Tumoral , Glioma/patología , Factores de Transcripción/genética , Neoplasias Encefálicas/patología , Proliferación Celular/genética , Apoptosis/genética , Movimiento Celular/genética , Regulación Neoplásica de la Expresión Génica , Invasividad Neoplásica/genética , Invasividad Neoplásica/patología , Transposasas/genética , Transposasas/metabolismo

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BACKGROUND: This case series describes the safety and efficacy of superselective intra-arterial (IA) cerebral infusion of teniposide for the treatment of patients with glioma, to provide new ideas and methods for the treatment of high grade gliomas. METHODS: 12 patients with glioma who were previously treated with standard therapy were treated with superselective IA cerebral infusion of teniposide. Patients received at least two cycles of treatment (one cycle: 150 mg/time, used for 1 day, repeated at 28 day intervals) after blood-brain barrier disruption. Patients received individualized treatment on the tumor location. The ophthalmic artery was bypassed during the super-selective arterial infusion. RESULTS: No significant differences in biochemical indexes and Karnofsky performance status (KPS) score were observed before and after treatment, and no evident adverse events occurred (P>0.05). In a recent response evaluation (August 2023), two (8%) patients presented with a complete response (16.7%), four had a partial response (33.3%), four had stable disease (33.3%), and two showed progressive disease (16.7%). The overall response rate and disease control rate were 50.0% and 83.3%, respectively. In addition, we described the detailed course of treatment in two patients. Case No 1 (recurrent tumor) and case No 2 (primary tumor) received six and three cycles of teniposide infusion, respectively. After treatment, the tumors of the patients were significantly reduced without evident adverse effects. CONCLUSION: This small series suggests that superselective IA cerebral infusion of teniposide may be a safe and effective therapy in the multimodal treatment of malignant glioma and warrants further study in larger prospective investigations.

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Acquired brain injury (ABI) is the most common disease of the nervous system, involving complex pathological processes, which often leads to a series of nervous system disorders. The structural destruction and dysfunction of the Neurovascular Unit (NVU) are prominent features of ABI. Therefore, understanding the molecular mechanism underlying NVU destruction and its reconstruction is the key to the treatment of ABI. SUMOylation is a protein post-translational modification (PTM), which can degrade and stabilize the substrate dynamically, thus playing an important role in regulating protein expression and biological signal transduction. Understanding the regulatory mechanism of SUMOylation can clarify the molecular mechanism of the occurrence and development of neurovascular dysfunction after ABI and is expected to provide a theoretical basis for the development of potential treatment strategies. This article reviews the role of SUMOylation in vascular events related to ABI, including NVU dysfunction and vascular remodeling, and puts forward therapeutic prospects.

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Introduction: As a common endovascular treatment for intracranial aneurysms, the pipeline embolization device (PED) is considered a standard treatment option, especially for large, giant, wide-necked, or dissecting aneurysms. A layer of phosphorylcholine biocompatible polymer added to the surface of the PED can substantially improve this technology. This PED with shield technology (pipeline shield) is relatively novel; its early technical success and safety have been reported. We conducted a systematic literature review with the aim of evaluating the efficacy and safety of the pipeline shield. Methods: We searched the PubMed, Embase, and Cochrane databases, following the preferred reporting items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines. Results: We selected five prospective and two retrospective studies for review. A total of 572 aneurysms were included; of these, 506 (88.5%) were unruptured. The antiplatelet regimens were heterogeneous. The rate of perioperative and postoperative complications was 11.1% [95% confidence interval (CI): 6.5-18.9%]. The adequate occlusion rate at 6 months was 73.9% (95% CI: 69.1-78.7%). The adequate occlusion rate of more than 12 months was 80.9% (95% CI: 75.1-86.1%). The mortality rate was 0.7% (95% CI: 0.2-1.5%). Subgroup analyses showed that aneurysm rupture status had no effect on aneurysm occlusion rate, patient morbidity, or mortality. Conclusion: This review demonstrates the safety and efficacy of the pipeline shield for treating intracranial aneurysms. However, direct comparisons of the pipeline shield with other flow diverters are needed to better understand the relative safety and effectiveness of different devices.

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Stroke is a common and devastating disease with an escalating prevalence worldwide. The known secondary injuries after stroke include cell death, neuroinflammation, blood-brain barrier disruption, oxidative stress, iron dysregulation, and neurovascular unit dysfunction. Lipocalin-2 (LCN-2) is a neutrophil gelatinase-associated protein that influences diverse cellular processes during a stroke. The role of LCN-2 has been widely recognized in the peripheral system; however, recent findings have revealed that there are links between LCN-2 and secondary injury and diseases in the central nervous system. Novel roles of LCN-2 in neurons, microglia, astrocytes, and endothelial cells have also been demonstrated. Here, we review the evidence on the regulatory roles of LCN-2 in secondary injuries following a stroke from various perspectives and the pathological mechanisms involved in the modulation of stroke. Overall, our review suggests that LCN-2 is a promising target to promote a better understanding of the neuropathology of stroke.