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246 results for “ROS”
It Takes a Village to Build a Robot: An Empirical Study of The ROS Ecosystem - Replication Package
<p>Over the past eleven years, the Robot Operating System (ROS), has grown from a small research project into the most popular framework for robotics development. Composed of packages released on the Rosdistro package manager, ROS aims to simplify development by providing reusable libraries, tools and conventions for building a robot. Still, developing a complete robot is a difficult task that involves bridging many technical disciplines. Experts who create computer vision packages, for instance, may need to rely on software designed by mechanical engineers to implement motor control. As building a robot requires domain expertise in software, mechanical, and electrical engineering, as well as artificial intelligence and robotics, ROS faces knowledge based barriers to collaboration.</p> <p>In this paper, we examine how the necessity of domain specific knowledge impacts the open source collaboration model. We create a comprehensive corpus of package metadata and dependencies over three years in the ROS ecosystem, analyze how collaboration is structured, and study the dependency network evolution. We find that the most widely used ROS packages belong to a small cluster of foundational working groups (FWGs), each organized around a different domain in robotics. We show that the FWGs are growing at a slower rate than the rest of the ecosystem, in terms of their membership and number of packages, yet the number of dependencies on FWGs is increasing at a faster rate. In addition, we mined all ROS packages on GitHub, and showed that 82% rely exclusively on functionality provided by FWGs. Finally, we investigate these highly influential groups and describe the unique model of collaboration they support in ROS.</p>
Data from: Hyperandrogenism and insulin resistance induce gravid uterine defects in association with mitochondrial dysfunction and aberrant ROS production
Women with polycystic ovary syndrome (PCOS) are at increased risk of miscarriage, which often accompanies the hyperandrogenism and insulin resistance seen in these patients. However, neither the combinatorial interaction between these two PCOS-related etiological factors nor the mechanisms of their actions in the uterus during pregnancy are well understood. We hypothesised that hyperandrogensim and insulin resistance exert a causative role in miscarriage by inducing defects in uterine function that are accompanied by mitochondrial-mediated oxidative stress, inflammation and perturbed gene expression. Here we tested this hypothesis by studying the metabolic, endocrine and uterine abnormalities in pregnant rats after exposure to daily injection of 5α-dihydrotestosterone (DHT, 1.66 mg/kg body weight/day) and/or insulin (6.0 IU/day) from gestational day 7.5 to 13.5. We showed that while DHT-exposed and insulin-exposed pregnant rats presented impaired insulin sensitivity, DHT+insulin-exposed pregnant rats exhibited hyperandrogenism and peripheral insulin resistance, which mirrors pregnant PCOS patients. Compared to controls, hyperandrogenism and insulin resistance in the dam was associated with alterations in uterine morphology and aberrant expression of genes responsible for decidualization (Prl8a2, Fxyd2, and Mt1g), placentation (Fcgr3 and Tpbpa), angiogenesis (Flt1, Angpt1, Angpt2, Ho1, Ccl2, Ccl5, Cxcl9, and Cxcl10) and insulin signaling (Akt, Gsk3 and Gluts). Moreover, we observed changes in uterine mitochondrial function and homeostasis (i.e. mitochondrial DNA copy number and the expression of genes responsible for mitochondrial fusion, fission, biogenesis, and mitophagy) and suppression of both oxidative and antioxidative defenses (i.e. reactive oxygen species, Nrf2 signaling, and interactive networks of antioxidative stress responses) in response to the hyperandrogenism and insulin resistance. These findings demonstrate that hyperandrogenism and insulin resistance induce mitochondria-mediated damage and a resulting imbalance between oxidative and antioxidative stress responses in the gravid uterus.
Data from: Hyperandrogenism and insulin resistance-induced fetal loss: evidence for placental mitochondrial abnormalities and elevated ROS production in pregnant rats that mimic the clinical features of PCOS
Women with polycystic ovary syndrome (PCOS) commonly suffer from miscarriage, but the underlying mechanism of PCOS‐induced fetal loss during pregnancy remains obscure and specific therapies are lacking. We used pregnant rats treated with 5α‐dihydrotestosterone (DHT) and insulin to investigate the impact of hyperandrogenism and insulin resistance on fetal survival and to determine the molecular link between PCOS conditions and placental dysfunction during pregnancy. Our study shows that pregnant rats chronically treated with a combination of DHT and insulin exhibited endocrine aberrations such as hyperandrogenism and insulin resistance that are strikingly similar to those in pregnant PCOS patients. Of pathophysiological significance, DHT+insulin‐treated pregnant rats had greater fetal loss and subsequently decreased litter sizes compared to normal pregnant rats. This negative effect was accompanied by impaired trophoblast differentiation, increased glycogen accumulation, and decreased angiogenesis in the placenta. Mechanistically, we report that over‐production of reactive oxygen species (ROS) in the placenta, mitochondrial dysfunction, and disturbed SOD1 and Keap1/Nrf2 antioxidant responses constitute important contributors to fetal loss in DHT+insulin‐treated pregnant rats. Many of the molecular pathways leading to placental abnormalities and fetal loss in DHT+insulin treatment were also seen in pregnant rats treated with DHT alone, whereas pregnant rats treated with insulin alone often exerted distinct effects on placental gene expression compared to insulin treatment in combination with DHT. We also found that treatment with the antioxidant N‐acetylcysteine (NAC) improved fetal survival in DHT+insulin‐treated pregnant rats, an effect related to changes in Keap1/Nrf2 and NFκB signaling. However, NAC administration resulted in fetal loss in normal pregnant rats, most likely due to PCOS‐like endocrine abnormality induced by the treatment. Our results suggest that the deleterious effects of hyperandrogenism and insulin resistance on fetal survival are related to a constellation of mitochondrial‐ROS‐SOD1/Nrf2 changes in the placenta. Our findings also suggest that physiological levels of ROS are required for normal placental formation and fetal survival during pregnancy.
ROS-specific Huntingtin Interactions: Oxidative Stress Optimization 3NP
<p>Optimization step in the lead up to mass spec identification of ROS-specific huntingtin protein-protein interactions.</p>
Supplementary material 1 from: Zamora-Marín JM, Ruiz-Navarro A, Oficialdegui FJ, Anastácio PM, Miranda R, García-Murillo P, Cobo F, Ribeiro F, Gallardo B, García-Berthou E, Boix D, Medina L, Morcillo F, Oscoz J, Guillén A, Herrero-Reyes AA, Aguiar FC, Almeida D, Arias A, Ayres C, Banha F, Barca S, Biurrun I, Cabezas MP, Calero S, Campos JA, Capdevila-Argüelles L, Capinha C, Carapeto A, Casals F, Chainho P, Cirujano S, Clavero M, Cuesta JA, Deltoro V, Encarnação J, Fernández-Delgado C, Franco J, García-Meseguer AJ, Guareschi S, Guerrero-Gómez A, Hermoso V, López-Cañizares C, López-Soriano J, Machordom A, Martelo J, Mellado-Díaz A, Moreno JC, Olivo del Amo R, Otero JC, Perdices A, Pou-Rovira Q, Quiñonero-Salgado S, Rodríguez-Merino A, Ros M, Sánchez-Gullón E, Sánchez MI, Sánchez-Fernández D, Sánchez-González JR, Soriano O, Teodósio MA, Torralva M, Vieira-Lanero R, Zamora-López A, Oliva-Paterna FJ (2023) A multi-taxa assessment of aquatic non-indigenous species introduced into Iberian freshwater and transitional waters. NeoBiota 89: 17-44. https://doi.org/10.3897/neobiota.89.105994
All data of the recorded NIS
Supplementary material 2 from: Zamora-Marín JM, Ruiz-Navarro A, Oficialdegui FJ, Anastácio PM, Miranda R, García-Murillo P, Cobo F, Ribeiro F, Gallardo B, García-Berthou E, Boix D, Medina L, Morcillo F, Oscoz J, Guillén A, Herrero-Reyes AA, Aguiar FC, Almeida D, Arias A, Ayres C, Banha F, Barca S, Biurrun I, Cabezas MP, Calero S, Campos JA, Capdevila-Argüelles L, Capinha C, Carapeto A, Casals F, Chainho P, Cirujano S, Clavero M, Cuesta JA, Deltoro V, Encarnação J, Fernández-Delgado C, Franco J, García-Meseguer AJ, Guareschi S, Guerrero-Gómez A, Hermoso V, López-Cañizares C, López-Soriano J, Machordom A, Martelo J, Mellado-Díaz A, Moreno JC, Olivo del Amo R, Otero JC, Perdices A, Pou-Rovira Q, Quiñonero-Salgado S, Rodríguez-Merino A, Ros M, Sánchez-Gullón E, Sánchez MI, Sánchez-Fernández D, Sánchez-González JR, Soriano O, Teodósio MA, Torralva M, Vieira-Lanero R, Zamora-López A, Oliva-Paterna FJ (2023) A multi-taxa assessment of aquatic non-indigenous species introduced into Iberian freshwater and transitional waters. NeoBiota 89: 17-44. https://doi.org/10.3897/neobiota.89.105994
Supplementary images
Supplementary material 2 from: Dahms C, Roch S, Elmer KR, Ros A, Brinker A, Jacobs A (2024) Intra-lake origin and rapid expansion of invasive pelagic three-spined stickleback in Lake Constance. NeoBiota 92: 259-280. https://doi.org/10.3897/neobiota.92.117430
Sample information
Supplementary material 1 from: Dahms C, Roch S, Elmer KR, Ros A, Brinker A, Jacobs A (2024) Intra-lake origin and rapid expansion of invasive pelagic three-spined stickleback in Lake Constance. NeoBiota 92: 259-280. https://doi.org/10.3897/neobiota.92.117430
Supplementary methods and results
Association between Dysregulated Expression of Ca2+ and ROS-Related Gene Pairs and Breast Cancer Patient Survival
<p>This file is composed by two documents:</p> <ul> <li>Supplementary Table 1 containing an Excel file with data on gene expression, differential gene expression (tumoral versus normal), and survival outcomes related to redox (sheet 1) and calcium-related (sheet 2) genes.</li> <li>Suplementary Table 2 including a table summarizing the primary functions of selected redox- and calcium-related genes and various studies reporting their impact on breast cancer</li> </ul> <p>Both supplementary tables belongs to the study <strong><strong>Association between Dysregulated Expression of Ca2+ and ROS-Related Gene Pairs and Breast Cancer Patient Survival</strong></strong>, published in <strong>Molecular Diagnosis and therapy </strong></p>
Figure 3 from: Ros-Candeira A, Pérez-Luque AJ, Suárez-Muñoz M, Bonet-García FJ, Hódar JA, Giménez de Azcárate F, Ortega-Díaz O (2019) Dataset of occurrence and incidence of pine processionary moth in Andalusia, south Spain. ZooKeys 852: 125-136. https://doi.org/10.3897/zookeys.852.28567
Figure 3 Number of monitoring stands per year according to defoliation degree. Gray area represents the total number of monitored stands per year.
Figure 2 from: Ros-Candeira A, Pérez-Luque AJ, Suárez-Muñoz M, Bonet-García FJ, Hódar JA, Giménez de Azcárate F, Ortega-Díaz O (2019) Dataset of occurrence and incidence of pine processionary moth in Andalusia, south Spain. ZooKeys 852: 125-136. https://doi.org/10.3897/zookeys.852.28567
Figure 2 Number of publications per year about Thaumetopoeapityocampa in Web of Science (search date 2017-10-05) since the first publication registered.
Figure 1 from: Ros-Candeira A, Pérez-Luque AJ, Suárez-Muñoz M, Bonet-García FJ, Hódar JA, Giménez de Azcárate F, Ortega-Díaz O (2019) Dataset of occurrence and incidence of pine processionary moth in Andalusia, south Spain. ZooKeys 852: 125-136. https://doi.org/10.3897/zookeys.852.28567
Figure 1 Distribution of Thaumetopoeapityocampa records from GBIF in Spain and records provided in this dataset. Records from GBIF were downloaded on 2018-03-16 using the R package "rgbif" (Chamberlain et al. 2016).
Supplementary material 3 from: Cabezas MP, Ros M, Santos AM, Martínez-Laiz G, Xavier R, Montelli L, Hoffman R, Fersi A, Dauvin JC, Guerra-García JM (2019) Unravelling the origin and introduction pattern of the tropical species Paracaprella pusilla Mayer, 1890 (Crustacea, Amphipoda, Caprellidae) in temperate European waters: first molecular insights from a spatial and temporal perspective. NeoBiota 47: 43-80. https://doi.org/10.3897/neobiota.47.32408
: Data type: molecular data
Supplementary material 4 from: Cabezas MP, Ros M, Santos AM, Martínez-Laiz G, Xavier R, Montelli L, Hoffman R, Fersi A, Dauvin JC, Guerra-García JM (2019) Unravelling the origin and introduction pattern of the tropical species Paracaprella pusilla Mayer, 1890 (Crustacea, Amphipoda, Caprellidae) in temperate European waters: first molecular insights from a spatial and temporal perspective. NeoBiota 47: 43-80. https://doi.org/10.3897/neobiota.47.32408
: Data type: molecular data
Supplementary material 1 from: Cabezas MP, Ros M, Santos AM, Martínez-Laiz G, Xavier R, Montelli L, Hoffman R, Fersi A, Dauvin JC, Guerra-García JM (2019) Unravelling the origin and introduction pattern of the tropical species Paracaprella pusilla Mayer, 1890 (Crustacea, Amphipoda, Caprellidae) in temperate European waters: first molecular insights from a spatial and temporal perspective. NeoBiota 47: 43-80. https://doi.org/10.3897/neobiota.47.32408
: Data type: molecular data
Supplementary material 2 from: Cabezas MP, Ros M, Santos AM, Martínez-Laiz G, Xavier R, Montelli L, Hoffman R, Fersi A, Dauvin JC, Guerra-García JM (2019) Unravelling the origin and introduction pattern of the tropical species Paracaprella pusilla Mayer, 1890 (Crustacea, Amphipoda, Caprellidae) in temperate European waters: first molecular insights from a spatial and temporal perspective. NeoBiota 47: 43-80. https://doi.org/10.3897/neobiota.47.32408
: Data type: phylogenetic tree
ROS-Specific Huntingtin Interactions: Testing PARP activity in HD patient fibroblasts
<p>Comparison of nuclear PAR levels in wild type and HD (TruHD) fibroblasts in response to a PARP inhibitor concentration gradient (as a measure of PARP activity).</p>
Supproting Materials for "Cross-Linked Selenoctanoic Acid Nanoplatform Enables Bidirectional Regulation of Intra- and Extracellular ROS: A New Avenue for Enhanced Cancer Immunotherapy" - section B
<h1><strong>Table of Content</strong></h1> <h1>1. Synthesis and characterization</h1> <h2> 1.1. SeLA</h2> <h3> 1.1.0. Lab book pages</h3> <h3> 1.1.1. NMR</h3> <h3> 1.1.2. HR-MS</h3> <h3> 1.1.3. UV</h3> <h3> 1.1.4. IR</h3> <h2> 1.2. cSeLAN</h2> <h3> 1.2.0. Lab book pages</h3> <h3> 1.2.1. NMR</h3> <h3> 1.2.2. UV</h3> <h3> 1.2.3. IR</h3> <h3> 1.2.4. GPC</h3> <h3> 1.2.5. MALDI-TOF-MS</h3> <h3> 1.2.6. DLS</h3> <h3> 1.2.7. Critical melle cncentration</h3> <h3> 1.2.8. ICP-MS</h3> <h3> 1.2.9. TEM</h3> <h2> 1.3. cLAN</h2> <h3> 1.3.0. Lab book pages</h3> <h3> 1.3.1. NMR</h3> <h3> 1.3.2. UV</h3> <h3> 1.3.3. DLS</h3> <h3> 1.3.4. GPC</h3> <h1>2. <em>In vitro</em> intra- and extracellular ROS regulation</h1> <h2> 2.0. Lab book pages</h2> <h2> 2.1. Raman scattering spectra</h2> <h2> 2.2. HPLC</h2> <h3> 2.2.1. Standard peaking</h3> <h3> 2.2.2. HPLC analysis</h3> <h2> 2.3. ICP-MS</h2> <h2> 2.4. MTT</h2> <h2> 2.5. Intracellular ROS generation</h2> <h3> 2.5.1. Fluorescence images</h3> <h3> 2.5.2. Flow fluorescence quantification</h3> <h2> 2.6. Intracellular pro-oxidation mechanism</h2> <h3> 2.6.1. Quantification of intracellular ATP</h3> <h3> 2.6.2. Quantification of intracellular NADH</h3> <h3> 2.6.3. Quantification of intracellular <strong>·</strong>OH</h3> <h3> 2.6.4. Quantification of intracellular ROS</h3> <h2> 2.7. Quantification of extracellular ROS</h2> <h1>3. <em>In vitro</em> ICD-inducing ability</h1> <h2> 3.0. Lab book pages</h2> <h2> 3.1. ATP release</h2> <h2> 3.2. HMGB1</h2> <h2> 3.3. CRT</h2> <h1>4. T cell proliferation and activation</h1> <h2> 4.0. Lab book pages</h2> <h2> 4.1. Flow cytometry analysis of the T cell proliferation</h2> <h2> 4.2. Quantification of IFN-γ secretions</h2> <h1>5. Biosafety evaluation of cSeLAN</h1> <h2> 5.0. Lab book pages</h2> <h2> 5.1. Hemolytic and hemagglutination assay</h2> <h3> 5.1.1. Hemolytic assay</h3> <h3> 5.1.2. Hemagglutination assay</h3> <h2> 5.2. Acute toxicity test</h2> <h3> 5.2.1. The amounts of dead mice</h3> <h3> 5.2.2. Body weight of mice</h3> <h3> 5.2.3. Hematological assay</h3> <h3> 5.2.4. Blood biochemistry</h3> <h3> 5.2.5. H&E staining of main organs</h3> <h1>6. Pharmacokinetic evaluation of cSeLAN</h1> <h2> 6.0. Lab book pages</h2> <h2> 6.1 Pharmacokinetic evaluation of cSeLAN</h2> <h1>7. <em>In vivo</em> anti-tumor immune response</h1> <h2> 7.0. Lab book pages</h2> <h2> 7.1. Chemiluminescence images</h2> <h3> 7.1.1. Chemiluminescence images of isoluminol</h3> <h3> 7.1.2. Chemiluminescence images of luminol</h3> <h3> 7.1.3. Related quantifications upon various treatments</h3> <h2> 7.2. Immunofluorescence images</h2> <h2> 7.3. T cell proliferation</h2> <h2> 7.4. DC proliferation</h2> <h1>8. <em>In vivo</em> anti-tumor efficacy</h1> <h2> 8.0. Lab book pages</h2> <h2> 8.1. Tumor growth</h2> <h3> 8.1.1. Tumor volume</h3> <h3> 8.1.2. Tumor weight</h3> <h3> 8.1.3. Tumor images</h3> <h2> 8.2. Body weight</h2> <h2> 8.3. Lung tissues with metastatic nodules</h2> <h3> 8.3.1. Lung tissues images</h3> <h3> 8.3.2. Number of pulmonary metastatic nodules</h3> <h3> 8.3.3. H&E</h3> <h2> 8.4. H&E of tumor and main organs</h2> <h2> 8.5. Cytokine secretions</h2> <h2> 8.6. Kaplan−Meier survival curves</h2> <h1>9. <em>In vitro</em> NK cytotoxicity and activity</h1> <h2> 9.0. Lab book pages</h2> <h2> 9.1. NK cytotoxicity</h2> <h2> 9.2. NK activity</h2>
HYPEROXIA Responses and ROS
ClinicalTrials.gov study NCT05958303. IPD Sharing: NO. Countries: 1. Publications: 0.
Data from: Hyperandrogenism and insulin resistance-induced fetal loss: evidence for placental mitochondrial abnormalities and elevated ROS production in pregnant rats that mimic the clinical features of PCOS
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