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16,682 results for “Lung.”
Discovery proteomics by mass spectrometry comparing secreted proteins from young and old mouse lung mesenchymal stromal cells
<p>Lung mesenchymal stromal cells (L-MSCs) were isolated from the young ( 3 months) and old (22-24 months) mice (N = 4 each) following collagenase digestion of the lungs and anchorage-dependent growth. Culture media was collected from young and old L-MSCs (10^6 cells) grown in culture for 24 hrs in serum-free condition. Culture media was then centrifuged to remove any cellular debris. Five (5) ml of supernatants were concentrated using 3kDa Molecular weight cut-off filters, and 10 micrograms of proteins were <span><span><span><span><span>run as multiple MW 1D PAGE fractions using a standard </span><span>GeLC</span><span> approach with a </span><span>nano</span><span>-HPLC in-line with a </span><span>Velos</span><span> Pro Orbitrap MS. </span></span></span></span></span><span><span><span><span><span>Individual data files were searched using </span><span>Sequest</span><span>, the results were then combined for each sample, followed by grouping, filtering, and quantifying by normalized spectral counts. </span></span></span></span></span></p> <p> </p>
Innate immune activation by checkpoint inhibition in patient-derived lung cancer tissues
<p><span>Although Pembrolizumab-based immunotherapy has significantly improved lung cancer patient survival, many patients show variable efficacy and resistance development. A better understanding of the drug's action is needed to improve patient outcomes. Functional heterogeneity of the tumor microenvironment (TME) is crucial to modulating drug resistance; understanding of individual patients' TME that impacts drug response is hampered by lack of appropriate models. </span></p> <p><span>Lung organotypic tissue slice cultures (OTC) with patients' native TME procured from primary and brain-metastasized (BM) non-small cell lung cancer (NSCLC) patients were treated with Pembrolizumab and/or beta-glucan (WGP, an innate immune activator). Metabolic tracing with<sup> 13</sup>C<sub>6</sub>-Glc/<sup>13</sup>C<sub>5,</sub><sup>15</sup>N<sub>2</sub>-Gln, multiplex immunofluorescence (mIF), and digital spatial profiling (DSP) were employed to interrogate metabolic and functional responses to Pembrolizumab and/or WGP.</span></p> <p><span>Primary and BM PD-1<sup>+</sup> lung cancer OTC responded to Pembrolizumab and Pembrolizumab + WGP treatments, respectively. Pembrolizumab activated innate immune metabolism and functions in primary OTC, which were accompanied by tissue damage. DSP analysis indicated an overall decrease in immunosuppressive macrophages and T cells but revealed microheterogeneity in immune responses and tissue damage. Two TMEs with altered cancer cell properties showed resistance. Pembrolizumab or WGP alone had negligible effects on BM-lung cancer OTC but Pembrolizumab + WGP blocked central metabolism with increased pro-inflammatory effector release and tissue damage.</span></p> <p><span>In depth metabolic analysis and multiplex TME imaging of lung cancer OTC demonstrated overall innate immune activation by Pembrolizumab but heterogeneous responses in the native TME of a patient with primary NSCLC. Metabolic and functional analysis also revealed synergistic action of Pembrolizumab and WGP in OTC of metastatic NSCLC.</span></p>
A tunable physiomimetic stretch system evaluated with precision cut lung slices and recellularized human lung scaffolds
<p>Datasets (excel files with raw data) to the publication Rosmark O, Ibáñez-Fonseca A, Thorsson J, Dellgren G, Hallgren O, Larsson Callerfelt A-K, Elowsson L and Westergren-Thorsson G (2022), A tunable physiomimetic stretch system evaluated with precision cut lung slices and recellularized human lung scaffolds. Front. Bioeng. Biotechnol. 10:995460. doi: 10.3389/fbioe.2022.995460</p>
Lung proteome and metabolome endotype in HIV-associated obstructive lung disease
<p><span><strong>Purpose</strong>: 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.</span></p> <p><span><strong>Methods</strong>: 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.</span></p> <p><span><strong>Results</strong>: After filtering, we retained 3872 proteins for further analysis. Based on sDWD, protein expression was able to separate cases and controls. We found </span><span>575 </span><span>proteins that were significantly correlated with FEV1pp </span><span>after multiple comparisons adjustment</span><span>. We identified </span><span>two protein-driven endotypes, one of which was</span><span> 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.</span></p> <p><span><strong>Conclusion</strong>: 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. </span></p>
Lung microbiota analyses in asthma mouse model
<p class="MsoNormal"><span class="Titre2Car"><span>Background:</span></span><span> Asthma is a frequent chronic inflammatory bronchial disease affecting more than 300 million </span><span>patients worldwide, 70% of whom secondary to</span><span> allergy. The diversity of asthmatic endotypes contributes to </span><span>their</span><span> complexity. Many factors, </span><span>such </span><span>as </span><span>the </span><span>environment, allergen sensitization pathways associate with microbiota, influence asthma natural course and explain its phenotypic heterogeneity. Here</span><span>,</span><span> we compared </span><span>a </span><span>mouse model of house dust mite (HDM)-induced allergic asthma sensitized via various routes for </span><span>the </span><span>clinical features of asthma, immune responses, the lung barrier and dysbiosis.</span></p> <p class="MsoNormal"><span class="Titre2Car"><span>Method:</span></span><span> Mice were sensitized HDM by</span> <span>oral, nasal or percutaneous routes. Lung function, barrier integrity, immune response and microbiota composition were analyzed.</span></p> <p class="MsoNormal"><span>Results: </span><span>Severe </span><span>impairment of respiratory function </span><span>was</span><span> observed </span><span>in</span><span> the mice sensitized by the nasal and cutaneous paths. It was associated with epithelial dysfunction characterized by an increased permeability secondary to junction protein disruption. Conversely, </span><span>such sensitization paths induced</span><span> a </span><span>mixed</span><span> eosinophilic and neutrophilic inflammatory response with high IL-17 airways secretion. </span><span>In contrast, oral </span><span>sensitized mice showed a mild impairment of respiratory function. Epithelial dysfunction was lighter with increased mucus production but conserved epithelial junctions. Lung Th2 and eosinophilic inflammation </span><span>were observed</span><span>. Considering lung microbiota, sensitization provoked a significant loss diversity. </span><span>At</span><span> the genus level, </span><span>Cutibacterium, Acinetobacter, Streptococcus and Lactobacillus</span><span> were found to be modulated according to the sensitization pathway. An increase </span><span>in</span><span> anti-inflammatory microbiota metabolites </span><span>was</span><span> observed in the </span><span>oral group</span><span>. </span></p> <p class="MsoNormal"><span>Conclusion: Our study highlights the strong involvement of the sensitization route in allergic asthma physiopathology and the critical </span><span>phenotypic</span><span> diversity in a mouse model.</span></p>
Potential new species of pseudaliid lung nematode (Metastrongyloidea) from two stranded neonatal orcas (Orcinus orca) characterised by ITS-2 and COI sequences
<p class="MsoNormal"><span>Knowledge about parasite species of orcas, their prevalence and impact on the health status is scarce. Only two records of lungworm infections in orca exist from male neonatal orcas stranded in Germany and Norway. The nematodes were identified as <em>Halocercus</em> sp. (Pseudaliidae), which have been described in the respiratory tract of multiple odontocete species, but morphological identification to species level remained impossible due to the fragile structure and ambiguous morphological features. Pseudaliid nematodes (Metastrongyloidea) are specific to the respiratory tract of toothed whales and are hypothesized to have become almost extinct in terrestrial mammals. Severe lungworm infections can cause secondary bacterial infections and bronchopneumonia and are a common cause of mortality in odontocetes. DNA isolations and subsequent sequencing of the rDNA ITS-2 and mtDNA COI revealed nucleotide differences between previously described <em>Halocercus</em> species from common dolphin (<em>H. delphini</em>) and harbour porpoises (<em>H. invaginatus</em>) that were comparatively analysed, pointing towards a potentially new species of pseudaliid lungworm in orcas. New COI sequences of six additional metastrongyloid lungworms of seals and porpoises were derived to elucidate phylogenetic relationships and differences between nine species of Metastrongyloidea.</span></p>
Integrated multi-omics analysis of early lung adenocarcinoma links tumor biological features with predicted indolence or aggressiveness
<p>This is a collection of datasets presented in the manuscript "Multi-omics data analysis identifies correlations between tumor biology features and predicted behaviors in early lung adenocarcinoma". This study provides a comprehensive profiling of LUAD indolence and aggressiveness at the biological bulk and single cell levels, as well as at the clinical and radiomics levels. This hypothesis generating study uncovers several potential future research avenues. It also highlights the importance and power of data integration to improve our systemic understanding of LUAD and to help reduce the gap between basic science research and clinical practice.</p>
Risk factors modifying familial aggregation for lung cancer in affected individuals
<p>Base de Datos</p>
Learn2Reg Challenge: CT Lung Registration
<p>learn2reg_lungData_OriginalSize.zip contains the images used in the Learn2Reg challenge in the Lung CT task in the original resolution.</p> <p>For more information about this dataset go to: https://learn2reg.grand-challenge.org/</p> <p> </p>
Antimicrobial peptides modulate lung injury by altering the intestinal microbiota
<p>This repository contains the OTU tables for "Antimicrobial peptides modulate pulmonary inflammation by altering the intestinal microbiota" by Abdelgawad and Nicola et al., an analysis of the role of antimicrobial peptide in the gut-lung axis during hyperoxia-induced lung injury. This work was supported by the National Heart, Lung, and Blood Institute of the U.S. National Institutes of Health, K NIH: K08 HL151907 (KW), K08 HL141652 (CL), K08 DK120871 (AO); the Kaul Pediatric Research Institute at Children’s of Alabama (KW), and the Microbiome Center at UAB (KW). The funding agencies had no role in the design, conduct, and analysis of the study or in the decision to submit the manuscript for publication. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH. All data in this repository is the intellectual property of the authors and may be utilized for academic publication only with prior written permission.</p>
Cystic fibrosis autoantibody signatures associate with Staphylococcus aureus lung infection or cystic fibrosis-related diabetes
<p>While cystic fibrosis (CF) lung disease is characterized by persistent inflammation and infections, and chronic inflammatory diseases are often accompanied by autoimmunity, autooimmune reactivity in CF has not been studied in depth. In this work, we undertook an unbiased approach to explore the systemic autoantibody repertoire in CF. Our results show higher levels of several new autoantibodies in the blood of people with CF (PwCF) compared to control subjects. Some of these are IgA autoantibodies targeting neutrophil components or autoantigens linked to neutrophil-mediated tissue damage in CF. We also found that PwCF with higher systemic IgM autoantibody levels have lower prevalence of <em>S. aureus</em> infection. On the other hand, IgM autoantibody levels in <em>S. aureus</em>-infected PwCF correlate with lung disease severity. Diabetic PwCF have significantly higher levels of IgA autoantibodies in their circulation compared to nondiabetic PwCF, and several of their IgM autoantibodies are associated with worse lung disease. In contrast, in nondiabetic PwCF blood levels of IgA autoantibodies correlate with lung disease. We have also identified other autoantibodies in CF that are associated with <em>P. aeruginosa</em> airway infection. In summary, we have identified several new autoantibodies and associations of autoantibody signatures with specific clinical features in CF.</p>
High prevalence of lipopolysaccharide mutants and R2-Pyocin susceptible variants in Pseudomonas aeruginosa populations sourced from cystic fibrosis lung infections
<p>Chronic, highly antibiotic-resistant infections in cystic fibrosis (CF) lungs contribute to increasing morbidity and mortality. <em>Pseudomonas</em> <em>aeruginosa</em>, a common CF pathogen, exhibits resistance to multiple antibiotics, contributing to antimicrobial resistance (AMR). These bacterial populations display genetic and phenotypic diversity, but it is unclear how this diversity affects susceptibility to bacteriocins. R-pyocins, i.e. bacteriocins produced by <em>P. aeruginosa</em>, are phage-tail-like antimicrobials. R-pyocins have potential as antimicrobials, however, recent research suggests the diversity of <em>P. aeruginosa</em> variants within CF lung infections leads to varying susceptibility to R-pyocins. This variation may be linked to changes in lipopolysaccharide (LPS), acting as the R-pyocin receptor. Currently, it is unknown how frequently R-pyocin-susceptible strains are in chronic CF lung infection, particularly when considering the heterogeneity within these strains. In this study, we tested R2-pyocin susceptibility of 139 <em>P. aeruginosa</em> variants from 17 sputum samples of seven CF patients and analyzed LPS phenotypes. We found that 83% of sputum samples did not have R2-pyocin-resistant variants, while nearly all samples contained susceptible variants. There was no correlation between LPS phenotype and R2-pyocin susceptibility, though we estimate that about 76% of sputum-derived variants lack an O-specific antigen, 40% lack a common antigen, and 24% have altered LPS cores. The absence of a correlation between LPS phenotype and R-pyocin susceptibility suggests LPS packing density may play a significant role in R-pyocin susceptibility among CF variants. Our research supports the potential of R-pyocins as therapeutic agents, as many infectious CF variants are susceptible to R2-pyocins, even within diverse bacterial populations.</p>
Millions of lung tumors harboring KRAS, BRAF, EGFR, and tumor suppressor alterations from genetically engineered mouse models
<p><span>Tumors acquire alterations in oncogenes and tumor suppressor genes in an adaptive walk through the fitness landscape of tumorigenesis. However, the <a>interactions </a></span><span>between oncogenes and tumor suppressor genes that shape this landscape remain poorly resolved and cannot be revealed by human cancer genomics alone. Here, we use a multiplexed, autochthonous mouse platform to model and quantify the initiation and growth of more than one hundred genotypes of lung tumors across four oncogenic contexts: KRAS G12D, KRAS G12C, BRAF V600E, and EGFR L858R. We show that the fitness landscape is rugged—the effect of tumor suppressor inactivation often switches between beneficial and deleterious depending on the oncogenic context—and shows no evidence of diminishing-returns epistasis within variants of the same oncogene. These findings argue against a simple linear signaling relationship amongst these three oncogenes and imply a critical role for off-axis signaling in determining the fitness effects of inactivating tumor suppressors.</span></p>
Artificial space weathering to mimic solar wind enhances the toxicity of lunar dust simulants in human lung cells
<p>During NASA's Apollo missions, inhalation of dust particles from lunar regolith was identified as a potential occupational hazard for astronauts. These fine particles adhered tightly to spacesuits and were unavoidably brought into the living areas of the spacecraft. Apollo astronauts reported that exposure to the dust caused intense respiratory and ocular irritation. This problem is a potential challenge for the Artemis Program, which aims to return humans to the Moon for extended stays in this decade. Since lunar dust is "weathered" by space radiation, solar wind, and the incessant bombardment of micrometeorites, we investigated whether treatment of lunar regolith simulants to mimic space weathering enhanced their toxicity. Two such simulants were employed in this research, Lunar Mare Simulant-1 (LMS-1), and Lunar Highlands Simulant-1 (LHS-1), which were added to cultures of human lung epithelial cells (A549) to simulate lung exposure to the dusts. In addition to pulverization, previously shown to increase dust toxicity sharply, the simulants were exposed to hydrogen gas at high temperature as a proxy for solar wind exposure. This treatment further increased the toxicity of both simulants, as measured by the disruption of mitochondrial function, and damage to DNA both in mitochondria and in the nucleus. By testing the effects of supplementing the cells with an antioxidant (N-acetylcysteine), we showed that a substantial component of this toxicity arises from free radicals. It remains to be determined to what extent the radicals arise from the dust itself, as opposed to their active generation by inflammatory processes in the treated cells.</p>
Combining graph neural networks and computer vision methods for cell nuclei classification in lung tissue
<p>Database of the article "Combining graph neural networks and computer vision methods for cell nuclei classification in lung tissue ".</p>
Transcriptome of Peromyscus leucopus lungs infected with SARS-CoV-2
<p><em>Peromyscus leucopus</em> is a reservoir for numerous zoonoses and one of the most abundant mammals in North America. Since they live near humans we are interested in the possibility of SARS-CoV-2 infection in this animal model from a zoonoses standpoint. The experimental design for the first trial involves using adult male and female <em>P. leucopus</em> LL stock. Animals were dosed with nasal inhalation of either tissue culture medium (DMEM) alone (controls) or alpha variant, WA1 strain of SARS-CoV-2 virus. We dosed 8 animals with a virus (titer 2x104) and 6 with DMEM alone. Animals were euthanized at either 3 or 6 days post-infection. For a second trial, <em>P. leucopus</em> animals were 1-3 years old and we had 3 groups: control animals with nasal inhalation of media, control animals with nasal inhalation of the heat-treated virus, and infected animals. Each group has 4 animals euthanized on 3- or 6-days post-infection (DPI). Lung tissue was used for RNA isolation and further sequencing to obtain 40 x 106 PE150 reads.</p>
Multimodal Fusion of Liquid Biopsy and CT Enhances Differential Diagnosis of Early-stage Lung Adenocarcinoma
<p>This research explores the potential of multimodal fusion for the differential diagnosis of early-stage lung adenocarcinoma (LUAD) (tumor sizes < 2 cm). It combines liquid biopsy biomarkers, specifically extracellular vesicle long RNA (evlRNA) and the computed tomography (CT) attributes.</p><p>It includes 4 files:</p><p>1. gene expression matrix : gene expression matrix for all samples (normalized read counts) .</p><p>2. evlRNA Rad features: 6 image features, 17 evlRNA features and labels</p><p>3. differentially expressed genes: Differentially expressed genes in LUAD patients compared with Benign individuals.</p><p>4. raw data: raw data used to for figure and table.</p>
Lung Volume Reduction for Severe Emphysema by Stereotactic Ablative Radiation Therapy
ClinicalTrials.gov study NCT03673176. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Rovalpituzumab Tesirine (SC16LD6.5) in Recurrent Small Cell Lung Cancer
ClinicalTrials.gov study NCT01901653. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Sorafenib in Treating Patients With Extensive Stage Small Cell Lung Cancer
ClinicalTrials.gov study NCT00182689. IPD Sharing: Not stated. Countries: 1. Publications: 1.
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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.