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1,235
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ShareScore release 0.7.1
Dataset results
1,235 results for “pulmonary hypertension”
Clinical Study to Assess the Efficacy and Safety of Macitentan in Patients With Pulmonary Hypertension After Left Ventricular Assist Device Implantation
ClinicalTrials.gov study NCT02554903. IPD Sharing: UNDECIDED. Countries: 1. Publications: 1.
A Study of the Efficacy and Safety of Frespaciguat (MK-5475) in Participants With Pulmonary Arterial Hypertension (INSIGNIA-PAH: Phase 2/3 Study of an Inhaled sGC Stimulator in PAH) (MK-5475-007)
ClinicalTrials.gov study NCT04732221. IPD Sharing: YES. Countries: 18. Publications: 1.
Investigation of H01 in Adults With Pulmonary Hypertension Including Interstitial Lung Disease (The SATURN Study).
ClinicalTrials.gov study NCT05128929. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Sildenafil in Heart Failure With Reactive Pulmonary Hypertension
ClinicalTrials.gov study NCT02304705. IPD Sharing: NO. Countries: 1. Publications: 1.
A Randomized, Double-Blind, Placebo-Controlled Study of Sildenafil in Children With Pulmonary Arterial Hypertension.
ClinicalTrials.gov study NCT00159913. IPD Sharing: Not stated. Countries: 17. Publications: 5.
L-citrulline and Pulmonary Hypertension Associated With Bronchopulmonary Dysplasia
ClinicalTrials.gov study NCT03542812. IPD Sharing: NO. Countries: 1. Publications: 3.
Clinical Study to Assess the Efficacy, Safety and Tolerability of Macitentan in Subjects With Inoperable Chronic Thromboembolic Pulmonary Hypertension
ClinicalTrials.gov study NCT02021292. IPD Sharing: Not stated. Countries: 16. Publications: 3.
An Open-Label, Long-Term Study of Oral Treprostinil in Subjects With Pulmonary Arterial Hypertension
ClinicalTrials.gov study NCT01560637. IPD Sharing: Not stated. Countries: 23. Publications: 1.
Effects of the oral angiotensin II type 2 receptor agonist C21 in Sugen-hypoxia induced pulmonary hypertension in rats
Open the record for dataset details and reuse information.
Right ventricular contractility and load in HIV associated pulmonary hypertension
<p class="Body"><span><span><span><span><span><span><span><span><span><span><span>Background: People living with human immunodeficiency virus (PLWH) are at risk of developing pulmonary hypertension (PH) and right ventricular (RV) dysfunction, but understanding of the relationship of RV function to afterload (RV-PA coupling) is limited. We evaluated the clinical and hemodynamic characteristics of human immunodeficiency virus (HIV)-associated PH.</span></span></span></span></span></span></span></span></span></span></span></p> <p class="Body"><span><span><span><span><span><span><span><span><span><span><span>Methods: We performed a retrospective review of patients with a diagnosis of HIV undergoing right heart catheterization (RHC) from 2000-2016 in a tertiary care center. Inclusion criteria were diagnosis of HIV, age ≥ 18 years and availability of RHC data. PH was classified as either pulmonary arterial hypertension (PAH; mean pulmonary arterial pressure [mPAP] ≥ 25mmHg with pulmonary artery wedge pressure [PAWP] ≤ 15mmHg) or pulmonary venous hypertension (PVH; mPAP ≥ 25mmHg with PAWP > 15). We collected demographics, CD4 cell count, HIV viral load, RHC and echocardiographic data. The single beat method was used to calculate RV-PA coupling from RHC.</span></span></span></span></span></span></span></span></span></span></span></p> <p class="Body"><span><span><span><span><span><span><span><span><span><span><span>Results: Sixty-two PLWH with a clinical likelihood for PH underwent RHC. Thirty-two (52%) met PH criteria (15 with PAH, 17 with PVH). Average time from diagnosis of HIV to diagnosis of PH was 11 years. Eleven of 15 individuals with PAH were on antiretroviral therapy (ART) while all 17 patients with PVH were on ART. Compared to PLWH without PH, those with PH had an increased likelihood of having a detectable HIV viral load and lower CD4 cell counts. PLWH with PAH or PVH had increased RV afterload with normal RV contractility, and preserved RV-PA coupling. </span></span></span></span></span></span></span></span></span></span></span></p> <p class="Body"><span class="None"><span><span><span><span><span><span><span><span><span><span>Conclusion: PLWH with PH (PAH or PVH) were more likely to have a detectable HIV viral load and lower CD4 count at the time of RHC. PLWH with PAH or PVH had increased RV afterload, normal RV contractility, with preserved RV-PA coupling suggestive of an early onset, mild, and compensated form of PH. These results should be confirmed in larger studies.</span></span></span></span></span></span></span></span></span></span></span></p>
Data from: Self-reported functional status predicts post-operative outcomes in non-cardiac surgery patients with pulmonary hypertension
BACKGROUND: Pulmonary hypertension (PHTN) is associated with increased post-procedure morbidity and mortality. Pre-procedure echocardiography (ECHO) is a widely used tool for evaluation of these patients, but its accuracy in predicting post-procedure outcomes is unproven. Self-reported exercise tolerance has not been evaluated for operative risk stratification of PHTN patients. OBJECTIVE: We analyzed whether self-reported exercise tolerance predicts outcomes (hospi-tal length-of-stay [LOS], mortality and morbidity) in PHTN patients (WHO Class I - V) under-going anesthesia and surgery. METHODS AND FINDINGS: We reviewed 550 non-cardiac, non-obstetric procedures per-formed on 370 PHTN patients at a single institution between 2007 and 2013. All patients had cardiac ECHO documented within 1 year prior to the procedure. Pre-procedure comorbidities and ECHO data were collected. Functional status (< or ? 4 metabolic equivalents of task [METs]) was assigned based on responses to standard patient interview questions during the pre-anesthesia clinic visit. Multiple logistic regression was used to develop a risk score model (Pul-monary Hypertension Outcome Risk Score; PHORS) and determine its value in predicting post-procedure outcomes. In an adjusted model, functional status <4 METs was independently associ-ated with a LOS >7 days (p < .003), as were higher ASA class (p < .002), open surgical approach (p < .002), procedure duration > 2 hours (p < .001), and the absence of systemic hypertension (p = .012). PHORS Score ?2 was associated with an increased 30-day major complication rate (28.7% vs. 19.2%; p < 0.001) and ICU admission rate (8.6% s 2.8%; p = .007), but no statistical difference in hospital readmissions rate (17.6% vs. 14.0%; p = .29), or mortality (3.5% vs. 1.4%; p = .75). Similar ECHO findings did not further improve outcome prediction. CONCLUSIONS: Poor functional status is associated with severe PHTN and predicts increased LOS and post-procedure complications in patients with moderate to severe pulmonary hyperten-sion with different etiologies. A risk assessment model predicts increased LOS with fair accura-cy. A thorough evaluation of underlying etiologies of PHTN should be undertaken in every pa-tient.
Expression Data from "A novel multi-network approach reveals tissue-specific cellular modulators of fibrosis in systemic sclerosis, pulmonary fibrosis, and pulmonary arterial hypertension"
<p>Normalized expression data (PCL files) and labeled PCL files (LPCL) that contain the WGCNA coexpression module assignment from Taroni, et al. A novel multi-network approach reveals tissue-specific cellular modulators of fibrosis in systemic sclerosis, pulmonary fibrosis, and pulmonary arterial hypertension. <em>bioRxiv</em>. doi: 10.1101/038950</p> <p>See also Gene Expression Omnibus under the following accession numbers: GSE9285, GSE32413, GSE45485, GSE59785, GSE76806, GSE76807, GSE76808, GSE48149, GSE68698, GSE19617, and GSE22356. </p>
Maternal and perinatal obesity induce bronchial obstruction and pulmonary hypertension via IL-6-FoxO1-axis in later life
<p>Obesity is a pre-disposing condition for chronic obstructive pulmonary disease, asthma, and pulmonary arterial hypertension. Accumulating evidence suggests that metabolic influences during development can determine chronic lung diseases (CLD). We demonstrate that maternal obesity causes early metabolic disorder in the offspring. Here, interleukin-6 induced bronchial and microvascular smooth muscle cell (SMC) hyperproliferation and increased airway and pulmonary vascular resistance. The key anti-proliferative transcription factor FoxO1 was inactivated via nuclear exclusion. These findings were confirmed using primary SMC treated with interleukin-6 and pharmacological FoxO1 inhibition as well as genetic FoxO1 ablation and constitutive activation. In vivo, we reproduced the structural and functional alterations in offspring of obese dams via the SMC-specific ablation of FoxO1. The reconstitution of FoxO1 using IL-6-deficient mice and pharmacological treatment did not protect against metabolic disorder but prevented SMC hyperproliferation. In human observational studies, childhood obesity was associated with reduced forced expiratory volume in 1s/forced vital capacity ratio Z-score (used as proxy for lung function) and asthma. We conclude that the interleukin-6-FoxO1 pathway in SMC is a molecular mechanism by which perinatal obesity programs the bronchial and vascular structures and functions, thereby driving CLD development. Thus, FoxO1 reconstitution provides a potential therapeutic option for preventing this metabolic programming of CLD.</p>
Calf Pulmonary Hypertension Supp FIgures
<p>Supp Figues for proteomic results for three vascular locations. Samples are provided from control calves and and matched animals undergoing two weeks of hypoxyia exposure. </p>
Calf Pulmonary Hypertension Protein Identifications
<p>Proteomic results for three vascular locations. Samples are provided from control calves and and matched animals undergoing two weeks of hypoxyia exposure. Accessions are from the Uniprot protein sequence database and values are area under the curve measurements of peptides assigned to a protein.</p>
Safety and Efficacy of Pulmonary Artery Denervation in Patients With Pulmonary Arterial Hypertension
ClinicalTrials.gov study NCT03282266. IPD Sharing: NO. Countries: 1. Publications: 3.
Biomarkers in Pulmonary Arterial Hypertension Treated With Nilotinib
ClinicalTrials.gov study NCT01320865. IPD Sharing: Not stated. Countries: 1. Publications: 5.
Safety and Efficacy of Bosentan in Patients With Diastolic Heart Failure and Secondary Pulmonary Hypertension
ClinicalTrials.gov study NCT00820352. IPD Sharing: Not stated. Countries: 1. Publications: 20.
Pharmacokinetic Study of Sub-q and IV Treprostinil in Kids With Pulmonary Arterial Hypertension (PAH)
ClinicalTrials.gov study NCT02318186. IPD Sharing: YES. Countries: 1. Publications: 3.
Prevalence, Phenotypes, Predictors and Prognostic Implication of Obstructive Sleep Apnea in Pulmonary Hypertension
ClinicalTrials.gov study NCT05595200. IPD Sharing: UNDECIDED. Countries: 1. Publications: 4.
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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.