Fubuki XF Long Sheath guide catheter use in neuroendovascular procedures: Institutional experience in 60 cases.

BACKGROUND: Endovascular treatment devices require compatible guide catheters to navigate complex vessels and anatomy. The Fubuki XF Long Sheath guide catheter (Fubuki XF) was developed with a 0.090-inch internal diameter with hydrophilic coating, an atraumatic rounded tip, and enhanced trackability and support with gradual shaft transition zones. METHODS: We retrospectively analyzed a prospectively maintained database of neuroendovascular patients treated using Fubuki XF at our center (July 2022─May 2023). Baseline/procedural characteristics were collected. Outcomes of interest included technical success (procedure completion with Fubuki XF without alternative guide catheter use) and peri-procedural complications. RESULTS: This study included 60 patients (43.3% [26/60] female; mean age: 69.6 ± 9.7) presenting with stenosis (45.0% [27/60]), unruptured aneurysms (31.7% [19/60]), ruptured aneurysm (1.7% [1/60]), arteriovenous fistula (5.0% [3/60]), arteriovenous malformation (3.3% [2/60]), chronic subdural hematoma (3.3% [2/60]), stroke/emboli (6.7% [4/60]), vasospasm (1.7% [1/60]), or carotid web (5.0% [1/60]). Fubuki XF was used to deliver endovascular treatment devices for stenting (43.3% [26/60]), flow diversion (23.3% [14/60]), embolization (11.7% [7/60]), coiling (10.0% [6/60]), balloon angioplasty (10.0% [6/60]), and mechanical thrombectomy (1.7% [1/60]). The Fubuki XF tip was placed in the internal carotid artery in 38.3% (23/60) of cases. Technical success was achieved in all cases. One V1 non-flow-limiting dissection (not related to Fubuki XF) and one failed closure occurred (1.7% [1/60] each). No iatrogenic strokes or intraprocedural ruptures occurred. CONCLUSION: We used Fubuki XF to safely and effectively deliver a variety of compatible neuroendovascular devices. Fubuki XF was stable in all cases and locations, and there were no device-related complications or dissections.

Transcriptome Analysis of Chemically-Induced Sensory Neuron Ablation in Zebrafish.

Peripheral glia are known to have a critical role in the initial response to axon damage and degeneration. However, little is known about the cellular responses of non-myelinating glia to nerve injury. In this study, we analyzed the transcriptomes of wild-type and mutant (lacking peripheral glia) zebrafish larvae that were treated with metronidazole. This treatment allowed us to conditionally and selectively ablate cranial sensory neurons whose axons are ensheathed only by non-myelinating glia. While transcripts representing over 27,000 genes were detected by RNAseq, only a small fraction (~1% of genes) were found to be differentially expressed in response to neuronal degeneration in either line at either 2 hrs or 5 hrs of metronidazole treatment. Analysis revealed that most expression changes (332 out of the total of 458 differentially expressed genes) occurred over a continuous period (from 2 to 5 hrs of metronidazole exposure), with a small number of genes showing changes limited to only the 2 hr (55 genes) or 5 hr (71 genes) time points. For genes with continuous alterations in expression, some of the most meaningful sets of enriched categories in the wild-type line were those involving the inflammatory TNF-alpha and IL6 signaling pathways, oxidoreductase activities and response to stress. Intriguingly, these changes were not observed in the mutant line. Indeed, cluster analysis indicated that the effects of metronidazole treatment on gene expression was heavily influenced by the presence or absence of glia, indicating that the peripheral non-myelinating glia play a significant role in the transcriptional response to sensory neuron degeneration. This is the first transcriptome study of metronidazole-induced neuronal death in zebrafish and the response of non-myelinating glia to sensory neuron degeneration. We believe this study provides important insight into the mechanisms by which non-myelinating glia react to neuronal death and degeneration in sensory circuits.

Peripheral glia have a pivotal role in the initial response to axon degeneration of peripheral sensory neurons in zebrafish.

Axon degeneration is a feature of many peripheral neuropathies. Understanding the organismal response to this degeneration may aid in identifying new therapeutic targets for treatment. Using a transgenic zebrafish line expressing a bacterial nitroreductase (Ntr)/mCherry fusion protein in the peripheral sensory neurons of the V, VII, IX, and X cranial nerves, we were able to induce and visualize the pathology of axon degeneration in vivo. Exposure of 4 days post fertilization Ntr larvae to the prodrug metronidazole (Met), which Ntr metabolizes into cytotoxic metabolites, resulted in dose-dependent cell death and axon degeneration. This was limited to the Ntr-expressing sensory neurons, as neighboring glia and motor axons were unaffected. Cell death was rapid, becoming apparent 3-4 hours after Met treatment, and was followed by phagocytosis of soma and axon debris by cells within the nerves and ganglia beginning at 4-5 hours of exposure. Although neutrophils appear to be activated in response to the degenerating neurons, they did not accumulate at the sites of degeneration. In contrast, macrophages were found to be attracted to the sites of the degenerating axons, where they phagocytosed debris. We demonstrated that peripheral glia are critical for both the phagocytosis and inflammatory response to degenerating neurons: mutants that lack all peripheral glia (foxD3-/-; Ntr) exhibit a much reduced reaction to axonal degeneration, resulting in a dramatic decrease in the clearance of debris, and impaired macrophage recruitment. Overall, these results show that this zebrafish model of peripheral sensory axon degeneration exhibits many aspects common to peripheral neuropathies and that peripheral glia play an important role in the initial response to this process.