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Dataset results
348 results for “vagus nerve”
Non-invasive TRanscutaneous Cervical Vagus Nerve Stimulation as a Treatment for Acute Stroke; Safety and Feasibility Study
ClinicalTrials.gov study NCT03733431. IPD Sharing: UNDECIDED. Countries: 1. Publications: 1.
Transcutaneous Auricular Vagus Nerve Stimulation in Patients With Stroke
ClinicalTrials.gov study NCT06895005. IPD Sharing: Not stated. Countries: 1. Publications: 9.
Effects of Transcutaneous Vagus Nerve Stimulation (taVNS) in Individuals With Primary Dysmenorrhea
ClinicalTrials.gov study NCT06146569. IPD Sharing: NO. Countries: 1. Publications: 11.
Stimulating Compassion UsingTranscutaneous Vagus Nerve Stimulation
ClinicalTrials.gov study NCT05441774. IPD Sharing: YES. Countries: 1. Publications: 1.
BabyStrong Transcutaneous Auricular Vagus Nerve Stimulation (taVNS) Paired Bottle Feeding to Improve Oral Feeding
ClinicalTrials.gov study NCT04849507. IPD Sharing: YES. Countries: 1. Publications: 0.
Safety and Efficacy of Vagus Nerve Stimulator in Patients With Rheumatoid Arthritis (RA)
ClinicalTrials.gov study NCT03437473. IPD Sharing: NO. Countries: 1. Publications: 1.
Transcutaneous Vagus Nerve Stimulation in Heart Failure
ClinicalTrials.gov study NCT05789147. IPD Sharing: Not stated. Countries: 1. Publications: 12.
Pilot Study: Anti-inflammatory Effect of Peroperative Stimulation of the Vagus Nerve
ClinicalTrials.gov study NCT01572155. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Data from: Blood-brain barrier deterioration and hippocampal gene expression in polymicrobial sepsis: an evaluation of endothelial MyD88 and the vagus nerve
Systemic infection can initiate or exacerbate central nervous system (CNS) pathology, even in the absence of overt invasion of bacteria into the CNS. Recent epidemiological studies have demonstrated that human survivors of sepsis have an increased risk of long-term neurocognitive decline. There is thus a need for improved understanding of the physiological mechanisms whereby acute sepsis affects the CNS. In particular, MyD88-dependent activation of brain microvascular endothelial cells and a resulting loss of blood-brain barrier integrity have been proposed to play an important role in the effects of systemic inflammation on the CNS. Signaling through the vagus nerve has also been considered to be an important component of CNS responses to systemic infection. Here, we demonstrate that blood-brain barrier permeabilization and hippocampal transcriptional responses during polymicrobial sepsis occur even in the absence of MyD88-dependent signaling in cerebrovascular endothelial cells. We further demonstrate that these transcriptional responses can occur without vagus nerve input. These results suggest that redundant signals mediate CNS responses in sepsis. Either endothelial or vagus nerve activation may be individually sufficient to transmit systemic inflammation to the central nervous system. Transcriptional activation in the forebrain in sepsis may be mediated by MyD88-independent endothelial mechanisms or by non-vagal neuronal pathways.
Data from: Gut mucosal cells transfer α-synuclein to the vagus nerve
<p>Tabular raw data corresponding to figure sets used in the study. </p><p><strong>Figure 1. α-Synuclein expression and seeding activity in SNCAA53T mice.</strong> ELISA quantification of human α-synuclein in (C) duodenum (α-synuclein quantification in ng/mg of nodose tissue), (D) nodose ganglia (α-synuclein quantification in pg/mg of nodose tissue), and (E) hindbrain (α-synuclein quantification in ng/mg of nodose tissue), from Snca–/– and SNCAA53T mice. RT-QuIC analysis of (F) duodenum, (G) nodose ganglia, and (H) hindbrain of Snca–/– and SNCAA53T mice. </p><p><strong>Figure 3. Conditional human α-synuclein expression induces α-synuclein seeding activity in gut organoids.</strong> (C) A representative ThT fluorescence profile for these genotypes is provided. (D) Endpoint values were collected after 100 hours of RT-QuIC relative to negative controls.</p><p><strong>Figure 4. Conditional human α-synuclein expression in gut mucosal cells produces in α-synuclein seeding activity in nodose ganglia.</strong> (C) ELISA quantification of human α-synuclein protein in nodose ganglia of nontransgenic, Snca–/–, and SNCAbow mice. (D) A representative ThT fluorescence profile (RT-QuIC) and endpoint analysis of nodose ganglia from nontransgenic (nTg), Snca–/–, and SNCAbow mice at 1 month of age. (E) RT-QuIC analysis of nodose ganglia from 6-month-old nTg, Snca–/–, and SNCAbow mice.</p><p><strong>Figure 5. Vagotomy spares the nodose ganglia from α-synuclein seeding activity and prevents spread to the hindbrain. </strong>(C) ELISA measurements of α-synuclein protein in the gut 3 months after tamoxifen treatment. RT-QuIC analysis of (D and E) vagal nodose ganglia and (F and G) hindbrain analyzed 3 months after tamoxifen treatment. Representative ThT fluorescence profiles are shown in D and F.</p><p>Epidemiological and histopathological findings have raised the possibility that misfolded α-synuclein protein might spread from the gut to the brain and increase the risk of Parkinson's disease. Although past experimental studies in mouse models have relied on gut injections of exogenous recombinant α-synuclein fibrils to study gut-to-brain α-synuclein transfer, the possible origins of misfolded α-synuclein within the gut have remained elusive. We recently demonstrated that sensory cells of intestinal mucosa express α-synuclein. Here, we employed mouse intestinal organoids expressing human α-synuclein to observe the transfer of α-synuclein protein from epithelial cells in organoids to cocultured nodose neurons devoid of α-synuclein. In mice expressing human α-synuclein, but no mouse α-synuclein, α-synuclein fibril-templating activity emerged in α-synuclein–seeded fibril aggregation assays in intestine, vagus nerve, and dorsal motor nucleus. In newly engineered transgenic mice that restrict pathological human α-synuclein expression to intestinal epithelial cells, α-synuclein fibril-templating activity transfered to the vagus nerve and dorsal motor nucleus. Subdiaphragmatic vagotomy prior to induction of α-synuclein expression in intestinal epithelial cells effectively protected the hindbrain from emergence of α-synuclein fibril-templating activity. Overall, these findings highlight a potential non-neuronal source of fibrillar α-synuclein protein that might arise in gut mucosal cells.</p>
Vagus Nerve Stimulation and Stress Reduction Training for Migraine
ClinicalTrials.gov study NCT03592329. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Extra-cochlear Electrode Placement at the Post-auricular Vagus Nerve in Cochlear Implantation
ClinicalTrials.gov study NCT07011927. IPD Sharing: YES. Countries: 1. Publications: 0.
Transcutaneous Auricular Vagus Nerve Stimulation (taVNS) in Chronic Kidney Disease (CKD)
ClinicalTrials.gov study NCT06927024. IPD Sharing: YES. Countries: 1. Publications: 0.
Transcutaneous Cervical Vagus Nerve Stimulation (tcVNS) in JIA
ClinicalTrials.gov study NCT05710640. IPD Sharing: YES. Countries: 1. Publications: 0.
Transcutaneous Auricular Vagus Nerve Stimulation for Insomnia in Survivors of Childhood Acute Lymphoblastic Leukemia
ClinicalTrials.gov study NCT07191119. IPD Sharing: YES. Countries: 1. Publications: 0.
Paired Vagus Nerve Stimulation Mechanisms
ClinicalTrials.gov study NCT06716112. IPD Sharing: YES. Countries: 1. Publications: 0.
Study Assessing Vagus Nerve Stimulation in CoViD-19 Respiratory Symptoms
ClinicalTrials.gov study NCT04382391. IPD Sharing: NO. Countries: 1. Publications: 0.
Transcutaneous Auricular Vagus Nerve Stimulation on Post-Herpetic Neuralgia
ClinicalTrials.gov study NCT07123987. IPD Sharing: NO. Countries: 1. Publications: 0.
Blinding and Adverse Effects of Ultrasonic Vagus Nerve Stimulation (U-VNS)
ClinicalTrials.gov study NCT07091812. IPD Sharing: YES. Countries: 1. Publications: 0.
Vagus Nerve Stimulation: Treatment for Gulf Veterans With Gulf War Illness
ClinicalTrials.gov study NCT02791893. IPD Sharing: NO. Countries: 1. Publications: 0.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.