Find research datasets worth reusing

opencc-by-4.0Feb 2017View details →

Figure 1. from: Acoustic biomarkers of Chronic Obstructive Lung Disease - Research Ideas and Outcomes 2: e9173 (11 May 2016) https://doi.org/10.3897/rio.2.e9173

Figure 1. - Poster as it was presented at the conference. Please see text for details.

opencc-by-4.0Jun 2024View details →

Cross-disease integration of single-cell RNA sequencing data from lung myeloid cells reveals TAM signature in in vitro model

Single cells from a 3D human cell-based model comprising tumor cell line-derived spheroids, cancer-associated fibroblasts and primary monocytes were dissociated and analyzed using scRNAseq. 4 monocyte donors were used in the 3D model, and 3 monocyte donors were used for 2D differentiation of macrophages.

opencc-by-4.0Apr 2024View details →

Transcriptomic atlas reveals organ-specific disease tolerance in sickle cell mice. Dataset for HbSS lung injected or not with heme

The objective of this experiment was to explore the transcriptome of the HbSS Townes mouse model of sickle cell disease.Townes model mice carry several human hemoglobin knock-in genes replacing the endogenous mouse genes and may be useful in studying sickle cell disease.All mice were genotyped, age- and sex-matched littermates. All HbAA (control, normal human hemoglobin) vs HbSS (sickle cell disease, mutated human hemoglobin) mice were used for experimentations at 6-8 weeks of age, to limit intra-group heterogeneity. Hemin (Ferriprotoporphyrin IX) was purchased from Frontiers Scientific and injected intravenously (iv.) in a retroorbital sinus at a concentration of 24 µmol/kg. Control mice received PBS instead. Mice were anesthetized with isoflurane 2-3% for injections, blood collection and sacrifice. All mice were sacrificed by cervical dislocation, 4 hours after injection. The results of lung (indicated poumon) from HbSS mice injected or not with heme are presented here .  The results of lung (indicated poumon) from HbAA mice injected or not with heme can be found at number  10.5281/zenodo.10965912 Thirty μm-thick frozen tissue sections of lungs were cut as above and homogenized in 200μL of 1-Thioglycerol/Homogenization Solution (Maxwell® 16 LEV simplyRNA Tissue Kit Promega AS1280). The quality and quantity of mRNA were evaluated using a 2100 bioanalyzer with TNA 6000 NanoKits (all Agilent Technologies, Palo Alto, CA, USA). RNA Integrity Numbers superior to 7 were eligible for subsequent reverse transcription into cDNA. RNAseq was performed at the GenomIC plateform Cochin Institute INSERM U1016. After RNA extraction, RNA quality (RNA integrity number) was estimated. 1μg of high-quality total RNA sample (RIN &gt;7) was processed to build up the libraries, using TruSeq Stranded mRNA kit (Illumina) according to manufacturer instructions. Briefly, purified poly-A containing mRNA molecules were fragmented and reverse-transcribed using random primers. Replacement of dTTP by dUTP during second strand synthesis allowed us to achieve strand specificity. Addition of a single A base to the cDNA was followed by ligation of Illumina adapters. Libraries were quantified by qPCR using KAPA Library Quantification Kits for Illumina Libraries (KapaBiosystems, Wilmington, MA). Library profiles were assessed using DNA High Sensitivity LabChip kits on an Agilent Bioanalyzer. Libraries were sequenced on an Illumina Nextseq 500 instrument using 75 base-lengths read V2 chemistry in a paired-end mode. After sequencing, primary analysis based on AOZAN software (ENS, Paris), was applied to demultiplex and control the quality of the raw data (based of FastQC modules / version 0.11.5). The dataset here represents 4 groups of mice, 4 mice per group as follows: HbAA PBS, HbAA heme, HbSS PBS, HbSS heme.

opencc-by-4.0Apr 2024View details →

Transcriptomic atlas reveals organ-specific disease tolerance in sickle cell mice. Dataset for HbAA lung injected or not with heme

<div> <div> The objective of this experiment was to explore the transcriptome of the HbSS Townes mouse model of sickle cell disease.Townes model mice carry several human hemoglobin knock-in genes replacing the endogenous mouse genes and may be useful in studying sickle cell disease.All mice were genotyped, age- and sex-matched littermates. All HbAA (control, normal human hemoglobin) vs HbSS (sickle cell disease, mutated human hemoglobin) mice were used for experimentations at 6-8 weeks of age, to limit intra-group heterogeneity. Hemin (Ferriprotoporphyrin IX) was purchased from Frontiers Scientific and injected intravenously (iv.) in a retroorbital sinus at a concentration of 24 µmol/kg. Control mice received PBS instead. Mice were anesthetized with isoflurane 2-3% for injections, blood collection and sacrifice. All mice were sacrificed by cervical dislocation, 4 hours after injection. The results of lung (indicated poumon) from HbAA mice injected or not with heme are presented here .  The results of lung (indicated poumon) from HbSS mice injected or not with heme can be found at number 10.5281/zenodo.10966094 Thirty μm-thick frozen tissue sections of lungs were cut as above and homogenized in 200μL of 1-Thioglycerol/Homogenization Solution (Maxwell® 16 LEV simplyRNA Tissue Kit Promega AS1280). The quality and quantity of mRNA were evaluated using a 2100 bioanalyzer with TNA 6000 NanoKits (all Agilent Technologies, Palo Alto, CA, USA). RNA Integrity Numbers superior to 7 were eligible for subsequent reverse transcription into cDNA. RNAseq was performed at the GenomIC plateform Cochin Institute INSERM U1016. After RNA extraction, RNA quality (RNA integrity number) was estimated. 1μg of high-quality total RNA sample (RIN &gt;7) was processed to build up the libraries, using TruSeq Stranded mRNA kit (Illumina) according to manufacturer instructions. Briefly, purified poly-A containing mRNA molecules were fragmented and reverse-transcribed using random primers. Replacement of dTTP by dUTP during second strand synthesis allowed us to achieve strand specificity. Addition of a single A base to the cDNA was followed by ligation of Illumina adapters. Libraries were quantified by qPCR using KAPA Library Quantification Kits for Illumina Libraries (KapaBiosystems, Wilmington, MA). Library profiles were assessed using DNA High Sensitivity LabChip kits on an Agilent Bioanalyzer. Libraries were sequenced on an Illumina Nextseq 500 instrument using 75 base-lengths read V2 chemistry in a paired-end mode. After sequencing, primary analysis based on AOZAN software (ENS, Paris), was applied to demultiplex and control the quality of the raw data (based of FastQC modules / version 0.11.5). The dataset here represents 4 groups of mice, 4 mice per group as follows: HbAA PBS, HbAA heme, HbSS PBS, HbSS heme.  </div> </div>

opencc-by-4.0Aug 2024View details →

Identification of early genes in the pathophysiology of fibrotic interstitial lung disease in a new model of pulmonary fibrosis

Some interstitial lung diseases involve pulmonary fibrosis, which is a process that is characterized by the excessive and abnormal accumulation of extracellular matrix in the pulmonary interalveolar space. Although the current anti-fibrotic therapy aims at slowing down the progression of pulmonary fibrosis, it does not reverse it, and many of the drugs that were identified in basic-research studies failed in clinical phases, mainly because of the lack of a model that can recapitulate the pathophysiological mechanisms of human pulmonary fibrosis. We developed a novel experimental model of pulmonary fibrosis induced by a cocktail of molecules on an air/liquid interface culture of mouse embryonic lung explants. Histological analyses revealed a pattern of usual interstitial pneumonia, the worst-prognosis form of pulmonary fibrosis. We performed a transcriptomics analysis at the single-cell level after the induction of fibrosis and before any histological signs of fibrosis could be observed. The results revealed increased expression of several gene families that are involved in early inflammation, fibrosis and iron homeostasis, as well as potential new genetic targets. This Zenodo repository includes original datasets of single cell RNA sequencing, analysis R scripts, final dataset/markers, and HTML codes for the interactive 3D UMAP and VolcanoPlot.

dryad36/100

Lung proteome and metabolome endotype in HIV-associated obstructive lung disease

Purpose: Obstructive lung disease is increasingly common among persons with HIV in both smokers and non-smokers. We used aptamer proteomics to identify proteins and associated pathways in HIV-associated obstructive lung disease. Methods: Bronchoalveolar lavage fluid (BALF) samples from 26 persons living with HIV with obstructive lung disease were matched to persons living with HIV without obstructive lung disease based on age, smoking status, and antiretroviral treatment. 6,414 proteins were measured using SomaScan aptamer-based assay. We used sparse distance-weighted discrimination (sDWD) to test for a difference in protein expression and permutation tests to identify univariate associations between proteins and forced expiratory volume in 1s precent predicted (FEV1pp). Significant proteins were entered into a pathway overrepresentation analysis (ORA). We also constructed protein-driven endotypes using K-means clustering and performed ORA on the proteins that were significantly different between clusters. We compared protein-associated clusters to those obtained from BALF and plasma metabolomics data on the same patient cohort. Results: After filtering, we retained 3872 proteins for further analysis. Based on sDWD, protein expression was able to separate cases and controls. We found 575 proteins that were significantly correlated with FEV1pp after multiple comparisons adjustment. We identified two protein-driven endotypes, one of which was associated with poor lung function, and found that insulin and apoptosis pathways were differentially represented. We found similar clusters driven by metabolomics in BALF but not plasma. Conclusion: Protein expression differs in persons living with HIV with and without obstructive lung disease. We were not able to identify specific pathways differentially expressed among patients based on FEV1pp; however, we identified a unique protein endotype associated with insulin and apoptotic pathways.

opencc-zeroDec 2021View details →

Safety and Efficacy of Sildenafil in Cystic Fibrosis (CF) Lung Disease

ClinicalTrials.gov study NCT00659529. IPD Sharing: NO. Countries: 1. Publications: 2.

controlledIPD-YESFeb 2026View details →

The Study of the Use of Nintedanib in Slowing Lung Disease in Patients With Fibrotic or Non-Fibrotic Interstitial Lung Disease Related to COVID-19

ClinicalTrials.gov study NCT04619680. IPD Sharing: YES. Countries: 1. Publications: 1.

To Evaluate the Effect of Inhaled Medication Together With Exercise and Activity Training on Exercise Capacity and Daily Activities in Patients With Chronic Lung Disease With Obstruction of Airways

ClinicalTrials.gov study NCT02085161. IPD Sharing: Not stated. Countries: 11. Publications: 2.

Trial in Extensive-Disease Small Cell Lung Cancer (ED-SCLC) Subjects Comparing Ipilimumab Plus Etoposide and Platinum Therapy to Etoposide and Platinum Therapy Alone

ClinicalTrials.gov study NCT01450761. IPD Sharing: Not stated. Countries: 34. Publications: 1.

Effect of Sildenafil on Diffusion Capacity in Patients With PH and Parenchymal Lung Disease

ClinicalTrials.gov study NCT01948518. IPD Sharing: Not stated. Countries: 1. Publications: 14.

controlledIPD-YESFeb 2026View details →

Tofacitinib in the Treatment of Rheumatoid Arthritis-related Interstitial Lung Disease.

ClinicalTrials.gov study NCT05246293. IPD Sharing: YES. Countries: 1. Publications: 3.

Evaluation of Lung Function and Symptoms in Patients Diagnosed With Chronic Obstructive Pulmonary Disease (COPD) on Long-Acting Bronchodilator Monotherapy

ClinicalTrials.gov study NCT00791518. IPD Sharing: Not stated. Countries: 1. Publications: 1.

Abatacept for the Treatment of Myositis-associated Interstitial Lung Disease

ClinicalTrials.gov study NCT03215927. IPD Sharing: NO. Countries: 1. Publications: 24.

Best Clinical Endpoints That Likely Induce Worse Prognosis in Interstitial Lung Diseases

ClinicalTrials.gov study NCT03400839. IPD Sharing: NO. Countries: 1. Publications: 1.

Comparison of Therapeutic Regimens for Scleroderma Interstitial Lung Disease (The Scleroderma Lung Study II)

ClinicalTrials.gov study NCT00883129. IPD Sharing: NO. Countries: 1. Publications: 31.