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116 results for “galectin”
An annotated high-content fluorescence microscopy dataset with EGFP-Galectin-3-stained cells and manually labelled outlines
<p>Here we present a benchmarking dataset of fluorescence microscopy images with EGFP-Galectin-3-stained cells together with annotations of their outlines. Images were randomly selected from an RNA interference screen with a modified U2OS osteosarcoma cell line, acquired on a Thermo Fischer CX7 high-content imaging system at 20x magnification. </p> <p>The dataset contains 60 images showing over 2000 labelled nuclear objects in total, which is sufficiently large to train well-performing neural networks for instance or semantic segmentation. It is pre-split into training, development and test set, each in a zip file. The dataset should be referred to as Aitslab_bioimaging2.</p> <p>For most of the images, nuclear staining and annotations have been published previously in the dataset Aitslab_bioimaging1 (https://doi.org/10.5281/zenodo.6657260). The conversion script to produce the png images from the C01 images was published together with this dataset.</p>
Dataset: Galectin Therapeutics Inc. (GALT) Stock Performance
This dataset provides historical stock market performance data for specific companies. It enables users to analyze and understand the past trends and fluctuations in stock prices over time. This information can be utilized for various purposes such as investment analysis, financial research, and market trend forecasting.
Рис. 2. Варианты преΑсказанной Αоменной структуры патогенраспознающих моΛекуΛ гемоцитов моΛΛюсков Planorbarius corneus. a — фибриногенпоΑобные беΛки, b — гаΛектины, c — F-Λектины. УсΛовные обозначения и сокращения, зΑесь и ΑаΛее: горизонтаΛьные красные поΛоски — сигнаΛьный пептиΑ, горизонтаΛьные розовые — обΛасть низкой сΛожности, вертикаΛьные синие поΛоски — трансмембранная обΛасть, FBG — фибриногеновый Αомен, FTP — Αомен фукоΛектина, EGF — Αомен эпиΑермаΛьного фактора роста, EGF_CA — каΛьцийсвязывающий EGF-поΑобный Αомен, PAN_AP — APPLE-поΑобный Αомен, SCAN — обΛасть, богатая Λейцином, GLECT — гаΛактозосвязывающий Λектин, CLECT — Λектин C-типа, Gal-bind — гаΛактозиΑ–связывающий Λектин, ML — MD-2- поΑробный Αомен распознавания ΛипиΑов Fig. 2. Variants of the predicted domain structure of pattern recognition molecules from hemocytes of Planorbarius corneus molluscs. a — fibrinogen-related proteins, b — galectins, c — F-lectins. Symbols and abbreviations (here and further): horizontal red stripes — signal peptide, horizontal pink stripes — a low complexity region, vertical blue stripes — transmembrane region, FBG — fibrinogen-related domain, FTP — fucolectin domain, EGF — epidermal growth factor-like domain, EGF_CA — calcium-binding EGF-like domain, PAN_AP — APPLE-like domain, SCAN — leucine rich region, Apple — APPLE domain, GLECT — galactose-binding lectin, CLECT — C-type lectin, Gal-bind — galactoside-binding lectin, ML — MD-2-related lipid-recognition domain in Pathogen recognition molecules from hemocytes of Planorbarius corneus molluscs (Planorbidae, Pulmonata)
Рис. 2. Варианты преΑсказанной Αоменной структуры патогенраспознающих моΛекуΛ гемоцитов моΛΛюсков Planorbarius corneus. a — фибриногенпоΑобные беΛки, b — гаΛектины, c — F-Λектины. УсΛовные обозначения и сокращения, зΑесь и ΑаΛее: горизонтаΛьные красные поΛоски — сигнаΛьный пептиΑ, горизонтаΛьные розовые — обΛасть низкой сΛожности, вертикаΛьные синие поΛоски — трансмембранная обΛасть, FBG — фибриногеновый Αомен, FTP — Αомен фукоΛектина, EGF — Αомен эпиΑермаΛьного фактора роста, EGF_CA — каΛьцийсвязывающий EGF-поΑобный Αомен, PAN_AP — APPLE-поΑобный Αомен, SCAN — обΛасть, богатая Λейцином, GLECT — гаΛактозосвязывающий Λектин, CLECT — Λектин C-типа, Gal-bind — гаΛактозиΑ–связывающий Λектин, ML — MD-2- поΑробный Αомен распознавания ΛипиΑов Fig. 2. Variants of the predicted domain structure of pattern recognition molecules from hemocytes of Planorbarius corneus molluscs. a — fibrinogen-related proteins, b — galectins, c — F-lectins. Symbols and abbreviations (here and further): horizontal red stripes — signal peptide, horizontal pink stripes — a low complexity region, vertical blue stripes — transmembrane region, FBG — fibrinogen-related domain, FTP — fucolectin domain, EGF — epidermal growth factor-like domain, EGF_CA — calcium-binding EGF-like domain, PAN_AP — APPLE-like domain, SCAN — leucine rich region, Apple — APPLE domain, GLECT — galactose-binding lectin, CLECT — C-type lectin, Gal-bind — galactoside-binding lectin, ML — MD-2-related lipid-recognition domain
Data described in the article "Glycopolymer Inhibitors of Galectin-3 Suppress the Markers of Tissue Remodeling in Pulmonary Hypertension"
<p>The dataset includes supplementary data, i.e. experimental data, tables, and figures detailing the synthetic procedures, compound characterization, binding assays, and cell culture studies of the study titled "Glycopolymer Inhibitors of Galectin‑3 Suppress the Markers of Tissue Remodeling in Pulmonary Hypertension" available here: https://doi.org/10.1021/acs.jmedchem.4c00341</p>
A pro-inflammatory stem cell niche drives myelofibrosis through a targetable galectin-1 axis
<p><span>Myeloproliferative neoplasms are stem cell-driven cancers associated with a large burden of morbidity and mortality. The majority of <a>patients p</a></span><span>resent with early-stage disease, but a substantial proportion progress to myelofibrosis and/or secondary leukemia, advanced cancers with a poor prognosis and high symptom burden. Currently, it remains difficult to predict progression, and therapies that reliably prevent or reverse fibrosis are lacking. A major bottleneck to the discovery of disease-modifying therapies has been an incomplete understanding of the interplay between perturbed cellular and molecular states. </span><span>Several cell types have individually been implicated, but a comprehensive analysis of myelofibrotic bone marrow is lacking. We therefore mapped the crosstalk between bone marrow cell types in myelofibrotic bone marrow. We found that inflammation and fibrosis are orchestrated by a ‘quartet’ of immune and stromal cell lineages – with basophils and mast cells creating a TNF signaling hub, communicating with megakaryocytes, mesenchymal stromal cells and pro-inflammatory fibroblasts. We identified the </span><span>b</span><span>-galactoside binding protein galectin-1 as a striking biomarker of progression to myelofibrosis and poor survival in multiple patient cohorts, and as a promising therapeutic target, with reduced myeloproliferation and fibrosis </span><a><span>in vitro</span></a><span> and </span><span>in vivo </span><span>and improved survival following galectin-1 inhibition. In human bone marrow organoids, TNF increased galectin-1 expression, suggesting a feedback loop wherein the pro-inflammatory MPN clone creates a self-reinforcing niche, fueling progression to advanced disease. This study pr</span><span>ovides a valuable resource for studying hematopoietic cell-niche interactions, with broad relevance for cancer-associated inflammation and disorders of tissue fibrosis. </span></p>
Assessment of the association of new biomarkers (GDF15, ST2, galectin-3, TIMP-1, MMP-9, NfL) and plasma prothrombotic potential in the course of cardiac transthyretin amyloidosis.
<p><span>The development of cardiac amyloidosis (ATTR) is caused by the deposition of misfolded, insoluble proteins in the extracellular matrix of tissues. An important element of the clinical presentation of the disease is the increased risk of thromboembolic complications. Currently, there is limited published data on the potential role of new heart failure biomarkers in the assessment of ATTR cardiomyopathy, particularly in the assessment of asymptomatic carriers of pathogenic transthyretin (TTR) variants.</span></p> <p><span>Purpose of the study: To assess the diagnostic value of biomarkers related to heart failure (growth differentiation factor-15 (GDF15), soluble suppression of tumorigenicity-2 (ST2), galectin-3), amyloidosis ( retinol binding protein 4 (RBP4, transthyretin) , tissue inhibitor of metalloproteinase-1 (TIMP-1), matrix metalloproteinase-9 (MMP-9, matrix metalloproteinase-9), neurofilament light chain (NfL)) and the generation potential thrombin as a marker of the prothrombotic state in the course of ATTR.</span></p> <p><span>Methods: This prospective, single-center study included consecutive patients diagnosed with ATTR, asymptomatic carriers of pathogenic TTR variants, and a matched control group of healthy volunteers. The values of these biomarkers were evaluated using the ELISA method from peripheral blood (enzyme-linked immunosorbent assay) GDF15, ST2, RBP4 (TTR), TIMP-1, MMP-9, galectin-3, NfL. Additionally, the prothrombotic potential of plasma was tested using the calibrated automatic thrombogram (CAT) method. Results are presented in Table 1. </span><span>The demographic and clinical characteristics of the study population are presented in Table 2 and Table 3.</span></p> <p><span>Conclusions: The project provides information on the value of novel biomarkers in the assessment of ATTR cardiomyopathy, especially in the assessment of asymptomatic carriers of pathogenic TTR variants. Moreover, it evaluated prothrombotic state in the course of ATTR.</span></p>
The transcriptomic landscape of Galectin-3-treated versus vehicle-treated Tregs
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Mass spectrometry data from: Deficiency in Galectin-3, -8, and -9 impairs immunity to chronic Mycobacterium tuberculosis infection but not acute infection with multiple intracellular pathogens
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Association between Galectin-1 gene expression and acute myeloid leukemia patient survival in The Cancer Genome Atlas
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Predicting Prognosis and Recurrence of Thyroid Cancer Via New Biomarkers, Urinary Exosomal Thyroglobulin and Galectin-3
ClinicalTrials.gov study NCT03488134. IPD Sharing: NO. Countries: 1. Publications: 2.
Galectin-3 in Patients With Endometriosis
ClinicalTrials.gov study NCT03212612. IPD Sharing: UNDECIDED. Countries: 1. Publications: 1.
Galectin Role in Periodontal Disease
ClinicalTrials.gov study NCT06038812. IPD Sharing: NO. Countries: 1. Publications: 1.
Galectin-3 Blockade in Patients With High Blood Pressure
ClinicalTrials.gov study NCT01960946. IPD Sharing: NO. Countries: 1. Publications: 1.
A Serum Galectin-3 Levels in Placenta Accreta Spectrum Pregnancies
ClinicalTrials.gov study NCT05945446. IPD Sharing: NO. Countries: 1. Publications: 2.
Galectin-3 as a Biomarker in Patients With Chagas Disease
ClinicalTrials.gov study NCT01842854. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Serum Galectin-3 as a Marker of Human Papillomavirus Infection
ClinicalTrials.gov study NCT06005389. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Evaluation of Salivary Galectin-8, Galectin-9 and RANKL Levels of Individuals With Different Periodontal Diseases
ClinicalTrials.gov study NCT06404476. IPD Sharing: YES. Countries: 1. Publications: 1.
Data from: Deep phylogenomics of a tandem-repeat galectin regulating appendicular skeletal pattern formation
Background: A multiscale network of two galectins Galectin-1 (Gal-1) and Galectin-8 (Gal-8) patterns the avian limb skeleton. Among vertebrates with paired appendages, chondrichthyan fins typically have one or more cartilage plates and many repeating parallel endoskeletal elements, actinopterygian fins have more varied patterns of nodules, bars and plates, while tetrapod limbs exhibit tandem arrays of few, proximodistally increasing numbers of elements. We applied a comparative genomic and protein evolution approach to understand the origin of the galectin patterning network. Having previously observed a phylogenetic constraint on Gal-1 structure across vertebrates, we asked whether evolutionary changes of Gal-8 could have critically contributed to the origin of the tetrapod pattern. Results: Translocations, duplications, and losses of Gal-8 genes in Actinopterygii established them in different genomic locations from those that the Sarcopterygii (including the tetrapods) share with chondrichthyans. The sarcopterygian Gal-8 genes acquired a potentially regulatory non-coding motif and underwent purifying selection. The actinopterygian Gal-8 genes, in contrast, did not acquire the non-coding motif and underwent positive selection. Conclusion: These observations interpreted through the lens of a reaction-diffusion-adhesion model based on avian experimental findings can account for the distinct endoskeletal patterns of cartilaginous, ray-finned, and lobe-finned fishes, and the stereotypical limb skeletons of tetrapods.
Data from: Protective effect of Galectin-9 in murine model of lung emphysema: involvement of neutrophil migration and MMP-9 production
Purpose: Chronic obstructive pulmonary disease (COPD) is characterized by irreversible airflow obstruction and pulmonary emphysema. Persistent inflammation and remodeling of the lungs and airways result in reduced lung function and a lower quality of life. Galectin (Gal)-9 plays a crucial role as an immune modulator in various diseases. However, its role in the pathogenesis of pulmonary emphysema is unknown. This study investigates whether Gal-9 is involved in pulmonary inflammation and changes in emphysema in a porcine pancreatic elastase (PPE)-induced emphysema model. Materials and Methods: Gal-9 was administered to mice subcutaneously once daily from 1 day before PPE instillation to day 5. During the development of emphysema, lung tissue and bronchoalveolar lavage fluid (BALF) were collected. Histological and cytological findings, concentrations of chemokines and matrix metalloproteinases (MMPs) in the BALF, and the influence of Gal-9 treatment on neutrophils were analyzed. Results: Gal-9 suppressed the pathological changes of PPE-induced emphysema. The mean linear intercept (Lm) of Gal-9-treated emphysema mice was significantly lower than that of PBS-treated emphysema mice (66.1 ± 3.3 µm vs. 118.8 ± 14.8 µm, respectively; p < 0.01). Gal-9 decreased the number of neutrophils and levels of MMP-9, MMP-2 and tissue inhibitor of metalloproteinases (TIMP)-1 in the BALF. The number of neutrophils in the BALF correlated significantly with MMPs levels. Interestingly, Gal-9 pretreatment in vitro inhibited the chemotactic activity of neutrophils and MMP-9 production from neutrophils. Furthermore, in Gal-9-deficient mice, PPE-induced emphysema progressed significantly compared with that in wild–type (WT) mice (108.7 ± 6.58 µm vs. 77.19 ± 6.97 µm, respectively; p < 0.01). Conclusions: These results suggest that Gal-9 protects PPE-induced inflammation and emphysema by inhibiting the infiltration of neutrophils and decreasing MMPs levels. Exogenous Gal-9 could be a potential therapeutic agent for COPD.
The Role of Galectins in the Non-invasive Diagnosis of Endometriosis
ClinicalTrials.gov study NCT04401592. IPD Sharing: NO. Countries: 0. 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.