Background: The first instance of a robotic-assisted surgery occurred in neurosurgery; however, it is now more common in other fields such as urology and gynecology. This study aims to characterize the prevalence of robotic surgery among current neurosurgery programs as well as identify trends in clinical trials pertaining to robotic neurosurgery. Methods: Each institution’s website was analyzed for the mention of a robotic neurosurgery program and procedures. The future potential of robotics in neurosurgery was assessed by searching for current clinical trials pertaining to neurosurgical robotic surgery. Results: Of the top 100 programs, 30 offer robotic cranial and 40 offer robotic spinal surgery. No significant differences were observed with robotic surgical offerings between geographic regions in the US. Larger programs (faculty size 16 or over) had 20 of the 30 robotic cranial programs (66.6%), whereas 21 of the 40 robotic spinal programs (52.5%) were at larger programs. An initial search of clinical trials revealed 223 studies, of which only 13 pertained to robotic neurosurgery. Spinal fixation was the most common intervention (six studies), followed by Deep Brain Stimulation (DBS, two studies), Cochlear implants (two studies), laser ablation (LITT, one study), and endovascular embolization (one study). Most studies had industry sponsors (9/13 studies), while only five studies had hospital sponsors. Conclusion: Robotic neurosurgery is still in its infancy with less than half of the top programs offering robotic procedures. Future directions for robotics in neurosurgery appear to be focused on increased automation of stereotactic procedures such as DBS and LITT and robot-assisted spinal surgery.
Background: Stroke is the third leading cause of disability and mortality in the world. The c omplement C3a receptor plays a prominent role in post stroke brain inflammation. We and others have reported that either genetic deficiency of complement C3a receptor (C3aR) or its pharmacological inhibition in rodents protect against cerebral ischemia. The existing C3aR antagonist (SB290157) is limited by its reported agonist effect in different model systems. Hypothesis: The novel highly-selective C3aR antagonist JR14a confers robust neuroprotection in stroke Methods: Mouse primary brain endothelial cells (cell biologics Inc. IL, USA) were seeded at a density of 5000 cells/well in 96-well plates and cultured until 80-90% confluency. Endothelial cytotoxicity was tested using an LDH assay following 24 hours of exposure to JR14a. Oxygen-glucose deprivation (OGD) was followed by reperfusion to compare the in-vitro effects of JR14a and SB290157, using ELISA performed for TNF-α and IL-6 and immunofluorescence for ICAM-1 expression. We also compared JR14a and SB290157 in the middle cerebral artery occlusion (MCAO, C57BL/6) stroke model, evaluating infarct volume. Results: JR14a treated endothelial cells exhibited reduced LDH release (Fig.1) and more potent anti-inflammatory response following OGD/R compared to SB290157. We found that JR14a treatment significantly reduced endothelial TNF-α, IL-6 and ICAM-1 expression. JR14a also significantly reduced brain infarction and microglial activation relative to SB290157 following MCAO in C57BL/6 mice (Fig 2). Conclusion: We conclude that the novel C3aR inhibitor JR14a attenuates inflammation and endothelial dysfunction in stroke and may confer a more potent neuroprotective effect than SB290157. Further work is warranted to explore the mechanisms underlying JR14a-mediated neuroprotection
Background: Stroke is one of the leading causes of death and disability. Some aspects of inflammation are known to be detrimental and arresting these aspects may improve stroke outcomes. Neutrophils are critical neuroinflammatory mediators and among the first immune cells to respond to the onset of stroke. As the stroke evolves, neutrophils may expel their intracellular contents, referred to as Neutrophil Extracellular Traps (NETs), in a process called NETosis. NETs increase microvascular occlusion and lead to further progression of stroke. However, the interaction of NETs with the cerebral microvascular endothelial cells and the effect of this interaction on stroke outcomes is poorly understood. This project aims to investigate this relationship. Methods: Leukocytes and plasma from C57BL/6 wildtype mice were isolated from whole blood. The leukocytes were then plated in 24-well plates and divided into control and Oxygen Glucose Deprivation (OGD) simulating a stroke environment in vitro. Thereafter, leukocytes were subjected to immunofluorescent staining for neutrophils (Ly6G), and the NETosis markers citrullinated histones (CitH3) and dsDNA. Media from both groups was assayed for Neutrophil Elastase, IL-6, TNF-α, and lactate dehydrogenase (LDH). The remaining media was used to treat primary microvascular endothelial cells to assess inflammation and cell death. Results: Ly6G antibody staining verified that most of the leukocytes plated were neutrophils. The CitH3 and dsDNA immunostaining confirmed induction of NETosis in the OGD group. We also found a significant increase in IL-6 and LDH levels suggesting significant inflammation and cell death in OGD treated leukocytes. Exposure of endothelial cells with NETs enriched media obtained from OGD exposed leukocytes resulted in significant decrease in cell count and increase in IL-6 and LDH levels, suggesting that NETs promoted inflammation and death in the endothelial cells. Nuclear staining of the endothelial cells also exhibited significant decrease in cell count in cohorts treated with the OGD exposed leukocyte media. Conclusion: These pilot data suggest that NETosis may contribute to the cytotoxicity of cerebral endothelial cells during stroke and serve as a potential therapeutic target.
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