Human OSM(Oncostatin-M) ELISA Kit

OpenStreetMap (OSM) is a free, open-access Volunteered geographic information (VGI) platform that has been widely used over the last decade as a source for Land Use Land Cover (LULC) mapping and visualization. However, it is known that the spatial coverage and accuracy of OSM data are not evenly distributed across all regions, with urban areas being likelier to have promising contributions (in both quantity and quality) than rural areas. The present study used OSM data history to generate LULC datasets with one-year timeframes as a way to support regional and rural multi-temporal LULC mapping. We evaluated the degree to which the different OSM datasets agreed with two existing reference datasets (CORINE Land Cover and the official Portuguese Land Cover Map). We also evaluated whether our OSM dataset was of sufficiently high quality (in terms of both completeness accuracy and thematic accuracy) to be used as a sampling data source for multi-temporal LULC maps. In addition, we used the near boundary tag accuracy criterion to assesses the fitness of the OSM data for producing training samples, with promising results. For each annual dataset, the completeness ratio of the coverage area for the selected study area was low. Nevertheless, we found high thematic accuracy values (ranged from 77.3% to 91.9%). Additionally, the training samples thematic accuracy improved as they moved away from the features' boundaries. Features with larger areas (>10 ha), e.g., Agriculture and Forest, had a steadily positive correlation between training samples accuracy and distance to feature boundaries.

Background: A key cause of the high mortality of cardiovascular diseases is the cardiomyocyte inability to renew after cardiac injury. As a promising strategy to supplement functional myocytes for cardiac repair, there is a pressing need to understand the cellular and molecular mechanisms of heart regeneration. Methods: Seven genetic mouse lines were used: global OSM (oncostatin M) knockout, monocyte-/macrophage-specific OSM deletion, cardiomyocyte-specific lines, including OSM receptor deletion, gp130 (glycoprotein 130) deletion, gp130 activation, and Yap (yes-associated protein) ablation with gp130 activation mice. A series of molecular signaling experiments, including RNA sequencing, immunostaining, coimmunoprecipitation, and imaging flow cytometry, were conducted. Two models of cardiac injury, apical resection and myocardial infarction operation, were performed in neonatal, juvenile, and adult mice. Heart regeneration and cardiac function were evaluated by Masson staining and echocardiography, respectively. Gene recombinant adenovirus-associated virus was constructed and infected myocardial-infarcted mice as a gene therapy. Results: OSM was identified by RNA sequencing as a key upstream regulator of cardiomyocyte proliferation during neonatal heart regeneration in mice. Cardiomyocyte proliferation and heart regeneration were suspended in neonatal mice after cardiac injury when OSM was conditionally knockout in macrophages. The cardiomyocyte-specific deficiency of the OSM receptor heterodimers, OSM receptor and gp130, individually in cardiomyocytes reduced myocyte proliferation and neonatal heart regeneration. Conditional activation of gp130 in cardiomyocytes promoted cardiomyocyte proliferation and heart regeneration in juvenile and adult mice. Using RNA sequencing and functional screening, we found that Src mediated gp130-triggered cardiomyocyte proliferation by activating Yap (yes-associated protein) with Y357 phosphorylation independently of the Hippo pathway. Cardiomyocyte-specific deletion of Yap inMyh6-gp130(ACT)mice blocked the effect of gp130 activation-induced heart regeneration in juvenile mice. Gene therapy with adenovirus-associated virus encoding constitutively activated gp130 promoted cardiomyocyte proliferation and heart regeneration in adult mice after myocardial infarction. Conclusions: Macrophage recruitment is essential for heart regeneration through the secretion of OSM, which promotes cardiomyocyte proliferation. As the coreceptor of OSM, gp130 activation is sufficient to promote cardiomyocyte proliferation by activating Yap through Src during heart regeneration. gp130 is a potential therapeutic target to improve heart regeneration after cardiac injury.