cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.15468/dl.42xdvj
title: Occurrence Download

description: A dataset containing 58 species occurrences available in GBIF matching the query:
{
 "and" : [
 "TaxonKey is one of (Parambassis lala)",
 "BasisOfRecord is one of (Specimen, Literature Occurrence, Human Observation, Observation)",
 "HasCoordinate is true",
 "HasGeospatialIssue is false",
 "Year is greater than or equal to 1991",
 "Year is less than or equal to 2025"
 ]
}

 The dataset includes 58 records from 10 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0015362-250914085247600/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.5jzntt
title: Occurrence Download

description: A dataset containing 3735 species occurrences available in GBIF matching the query:
{
 "and" : [
 "OccurrenceStatus is Present",
 "StateProvince is Idaho",
 "TaxonKey is Andrenidae"
 ]
}

 The dataset includes 3735 records from 33 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0015363-250914085247600/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.6084/m9.figshare.28571996
title: Venous thromboembolism associated with severe dyspnea and asthma in 21,205 adults from the Danish population

description: Long-term consequences after a pulmonary embolism include lung function deficits, dyspnea, and chronic thromboembolic pulmonary hypertension. Recent studies suggest patients who experience pulmonary embolism may also be at increased risk of asthma. We tested the hypothesis that individuals with pulmonary embolism or deep vein thrombosis (venous thromboembolism) have lower lung function, or higher risks of dyspnea and asthma using data from 21,205 random adults from the Danish General Suburban Population Study. Prevalences of pulmonary embolism, deep vein thrombosis, and venous thromboembolism were 0.60%, 1.7%, and 1.9%, respectively. Individuals with pulmonary embolism or deep vein thrombosis had FEV<sub>1</sub>% predicted of 86% and 89% compared with 95% in individuals without venous thromboembolism (<i>t</i>-test: <i>p</i> &lt; .001). Corresponding values for FVC% predicted were 92% and 94% versus 99% (<i>p</i> &lt; .001). Individuals with versus without venous thromboembolism had adjusted odds ratios for light, moderate, and severe dyspnea of 1.6 (95% CI: 1.1–2.2), 1.8 (1.2–2.6), and 2.6 (1.8–3.8), respectively. Individuals with versus without venous thromboembolism had adjusted odds ratios for asthma and use of asthma medication of 1.6 (1.2–2.2) and 1.9 (1.4–2.6), respectively. The adjusted odds ratio for asthma in individuals with versus without venous thromboembolism was increased among individuals who received no treatment with anticoagulants (2.0, 1.4–3.0) compared to those who received treatment (1.0, 0.6–1.6) (<i>p</i> for interaction = .02). Individuals with venous thromboembolism have lower lung function, 2.6-fold higher risk of severe dyspnea, and 1.6-fold higher risk of asthma in the Danish population.
DOI: 10.6084/m9.figshare.28571996.v2
title: Venous thromboembolism associated with severe dyspnea and asthma in 21,205 adults from the Danish population

description: Long-term consequences after a pulmonary embolism include lung function deficits, dyspnea, and chronic thromboembolic pulmonary hypertension. Recent studies suggest patients who experience pulmonary embolism may also be at increased risk of asthma. We tested the hypothesis that individuals with pulmonary embolism or deep vein thrombosis (venous thromboembolism) have lower lung function, or higher risks of dyspnea and asthma using data from 21,205 random adults from the Danish General Suburban Population Study. Prevalences of pulmonary embolism, deep vein thrombosis, and venous thromboembolism were 0.60%, 1.7%, and 1.9%, respectively. Individuals with pulmonary embolism or deep vein thrombosis had FEV<sub>1</sub>% predicted of 86% and 89% compared with 95% in individuals without venous thromboembolism (<i>t</i>-test: <i>p</i> &lt; .001). Corresponding values for FVC% predicted were 92% and 94% versus 99% (<i>p</i> &lt; .001). Individuals with versus without venous thromboembolism had adjusted odds ratios for light, moderate, and severe dyspnea of 1.6 (95% CI: 1.1–2.2), 1.8 (1.2–2.6), and 2.6 (1.8–3.8), respectively. Individuals with versus without venous thromboembolism had adjusted odds ratios for asthma and use of asthma medication of 1.6 (1.2–2.2) and 1.9 (1.4–2.6), respectively. The adjusted odds ratio for asthma in individuals with versus without venous thromboembolism was increased among individuals who received no treatment with anticoagulants (2.0, 1.4–3.0) compared to those who received treatment (1.0, 0.6–1.6) (<i>p</i> for interaction = .02). Individuals with venous thromboembolism have lower lung function, 2.6-fold higher risk of severe dyspnea, and 1.6-fold higher risk of asthma in the Danish population.
DOI: 10.6084/m9.figshare.28571996.v1
title: Venous thromboembolism associated with severe dyspnea and asthma in 21,205 adults from the Danish population

description: Long-term consequences after a pulmonary embolism include lung function deficits, dyspnea, and chronic thromboembolic pulmonary hypertension. Recent studies suggest patients who experience pulmonary embolism may also be at increased risk of asthma. We tested the hypothesis that individuals with pulmonary embolism or deep vein thrombosis (venous thromboembolism) have lower lung function, or higher risks of dyspnea and asthma using data from 21,205 random adults from the Danish General Suburban Population Study. Prevalences of pulmonary embolism, deep vein thrombosis, and venous thromboembolism were 0.60%, 1.7%, and 1.9% respectively. Individuals with pulmonary embolism or deep vein thrombosis had FEV<sub>1</sub>% predicted of 86% and 89% compared with 95% in individuals without venous thromboembolism (t-test: P &lt; 0.001). Corresponding values for FVC% predicted were 92% and 94% versus 99% (P &lt; 0.001). Individuals with versus without venous thromboembolism had adjusted odds ratios for light, moderate, and severe dyspnea of 1.6 (95% CI: 1.1-2.2), 1.8 (1.2-2.6), and 2.6 (1.8-3.8), respectively. Individuals with versus without venous thromboembolism had adjusted odds ratios for asthma and use of asthma medication of 1.6 (1.2-2.2) and 1.9 (1.4-2.6), respectively. The adjusted odds ratio for asthma in individuals with versus without venous thromboembolism was increased among individuals who received no treatment with anticoagulants (2.0, 1.4-3.0) compared to those who received treatment (1.0, 0.6-1.6) (P for interaction = 0.02). Individuals with venous thromboembolism have lower lung function, 2.6 fold higher risk of severe dyspnea, and 1.6 fold higher risk of asthma in the Danish population.
DOI: 10.6084/m9.figshare.28506338
title: Causal relationships between allergic diseases and significant declines in lung function: a multivariable Mendelian randomization study

description: Asthma and other allergic diseases are increasing globally each year, with some patients experiencing the co-occurrence of two or more conditions, significantly impacting their quality of life. While these diseases may share certain immune mechanisms, the independent causal relationships between them and lung function remain unclear. This study aims to investigate the independent and interactive effects of allergic asthma, atopic dermatitis, allergic rhinitis, and allergic conjunctivitis on significant declines in lung function. By elucidating the potential causal relationships between these allergic diseases and reduced lung function, we hope to provide valuable scientific evidence for managing asthma patients who are co-morbid with multiple allergic conditions. In this study, we conducted Mendelian randomization (MR) analysis using data from the FinnGen database and the UK Biobank. We rigorously selected instrumental variables (IVs) based on established criteria and employed both univariable and multivariable MR approaches to investigate the relationship between various allergic diseases and significant declines in lung function. In univariable MR analysis, the inverse variance-weighted (IVW) method or the weighted median approach indicated a causal relationship between allergic conjunctivitis, atopic dermatitis, and allergic asthma with significant declines in lung function. However, in multivariable MR analysis, the independent effects of atopic dermatitis and allergic conjunctivitis on lung function were no longer significant. Only allergic asthma continued to show a significant causal relationship with decreased lung function (OR [95%CI]: 1.019 [1.008–1.030], <i>p</i> &lt; .001). This study suggests that while atopic dermatitis and allergic conjunctivitis may indirectly affect lung function and lead to significant declines, their independent effects are not notable when asthma is well-controlled. Therefore, clinicians should recognize that acute exacerbations of allergic diseases are unlikely to be the primary reason for significant declines in lung function among asthma patients with multiple allergic conditions, provided that their asthma is well-managed.
DOI: 10.6084/m9.figshare.28573165
title: Global research trends and hotspots in mitochondria and asthma: a bibliometric and visualized analysis

description: Asthma is a complex chronic respiratory disease marked by inflammation, bronchoconstriction, and hyperresponsiveness. Mitochondria, key regulators of energy production, ROS, and apoptosis, are increasingly recognized as crucial in asthma pathophysiology. However, a comprehensive analysis of global research trends in this area is lacking. This study aims to perform a bibliometric and visualized analysis of global research on mitochondria and asthma. A bibliometric analysis was conducted using Web of Science Core Collection data from 2004 to June 2024. CiteSpace and VOSviewer software were used to examine co-authorship, co-citation, keyword co-occurrence, and thematic clusters. A total of 669 publications were identified. The number of studies grew significantly after 2015, with the United States, China, and the UK leading research. Co-citation and keyword analyses revealed mitochondrial dysfunction, oxidative stress, apoptosis, and airway inflammation as major themes. Emerging areas of interest include mitochondrial biogenesis, NLRP3 inflammasome, and innate immunity. Collaboration among institutions like Harvard University and the Council of Scientific & Industrial Research was significant, and journals, such as European Respiratory Journal and Nature Medicine were highly influential. This study provides an overview of research on mitochondria and asthma, highlighting emerging trends, such as mitochondrial biogenesis and immune pathways. Future research should focus on these areas and the role of environmental triggers in mitochondrial dysfunction, offering valuable insights for therapeutic strategies targeting mitochondria in asthma.
DOI: 10.6084/m9.figshare.28573165.v2
title: Global research trends and hotspots in mitochondria and asthma: a bibliometric and visualized analysis

description: Asthma is a complex chronic respiratory disease marked by inflammation, bronchoconstriction, and hyperresponsiveness. Mitochondria, key regulators of energy production, ROS, and apoptosis, are increasingly recognized as crucial in asthma pathophysiology. However, a comprehensive analysis of global research trends in this area is lacking. This study aims to perform a bibliometric and visualized analysis of global research on mitochondria and asthma. A bibliometric analysis was conducted using Web of Science Core Collection data from 2004 to June 2024. CiteSpace and VOSviewer software were used to examine co-authorship, co-citation, keyword co-occurrence, and thematic clusters. A total of 669 publications were identified. The number of studies grew significantly after 2015, with the United States, China, and the UK leading research. Co-citation and keyword analyses revealed mitochondrial dysfunction, oxidative stress, apoptosis, and airway inflammation as major themes. Emerging areas of interest include mitochondrial biogenesis, NLRP3 inflammasome, and innate immunity. Collaboration among institutions like Harvard University and the Council of Scientific & Industrial Research was significant, and journals, such as European Respiratory Journal and Nature Medicine were highly influential. This study provides an overview of research on mitochondria and asthma, highlighting emerging trends, such as mitochondrial biogenesis and immune pathways. Future research should focus on these areas and the role of environmental triggers in mitochondrial dysfunction, offering valuable insights for therapeutic strategies targeting mitochondria in asthma.
DOI: 10.6084/m9.figshare.28506338.v1
title: Causal relationships between allergic diseases and significant declines in lung function: a multivariable Mendelian randomization study

description: Asthma and other allergic diseases are increasing globally each year, with some patients experiencing the co-occurrence of two or more conditions, significantly impacting their quality of life. While these diseases may share certain immune mechanisms, the independent causal relationships between them and lung function remain unclear. This study aims to investigate the independent and interactive effects of allergic asthma, atopic dermatitis, allergic rhinitis, and allergic conjunctivitis on significant declines in lung function. By elucidating the potential causal relationships between these allergic diseases and reduced lung function, we hope to provide valuable scientific evidence for managing asthma patients who are co-morbid with multiple allergic conditions. In this study, we conducted Mendelian randomization (MR) analysis using data from the FinnGen database and the UK Biobank. We rigorously selected instrumental variables (IVs) based on established criteria and employed both univariable and multivariable MR approaches to investigate the relationship between various allergic diseases and significant declines in lung function. In univariable MR analysis, the inverse variance-weighted (IVW) method or the weighted median approach indicated a causal relationship between allergic conjunctivitis, atopic dermatitis, and allergic asthma with significant declines in lung function. However, in multivariable MR analysis, the independent effects of atopic dermatitis and allergic conjunctivitis on lung function were no longer significant. Only allergic asthma continued to show a significant causal relationship with decreased lung function (OR [95%CI]: 1.019 [1.008–1.030], <i>p</i> &lt; .001). This study suggests that while atopic dermatitis and allergic conjunctivitis may indirectly affect lung function and lead to significant declines, their independent effects are not notable when asthma is well-controlled. Therefore, clinicians should recognize that acute exacerbations of allergic diseases are unlikely to be the primary reason for significant declines in lung function among asthma patients with multiple allergic conditions, provided that their asthma is well-managed.
DOI: 10.6084/m9.figshare.28573165.v1
title: Global research trends and hotspots in mitochondria and asthma: A bibliometric and visualized analysis

description: Asthma is a complex chronic respiratory disease marked by inflammation, bronchoconstriction, and hyperresponsiveness. Mitochondria, key regulators of energy production, ROS, and apoptosis, are increasingly recognized as crucial in asthma pathophysiology. However, a comprehensive analysis of global research trends in this area is lacking. This study aims to perform a bibliometric and visualized analysis of global research on mitochondria and asthma. A bibliometric analysis was conducted using Web of Science Core Collection data from 2004 to June 2024. CiteSpace and VOSviewer software were used to examine co-authorship, co-citation, keyword co-occurrence, and thematic clusters. A total of 669 publications were identified. The number of studies grew significantly after 2015, with the United States, China, and the UK leading research. Co-citation and keyword analyses revealed mitochondrial dysfunction, oxidative stress, apoptosis, and airway inflammation as major themes. Emerging areas of interest include mitochondrial biogenesis, NLRP3 inflammasome, and innate immunity. Collaboration among institutions like Harvard University and the Council of Scientific & Industrial Research was significant, and journals such as European Respiratory Journal and Nature Medicine were highly influential. This study provides an overview of research on mitochondria and asthma, highlighting emerging trends such as mitochondrial biogenesis and immune pathways. Future research should focus on these areas and the role of environmental triggers in mitochondrial dysfunction, offering valuable insights for therapeutic strategies targeting mitochondria in asthma.
DOI: 10.6084/m9.figshare.28553179
title: Lingganwuweijiangxin Decoction suppresses allergic airway inflammation in Guinea pigs with cough variant asthma by regulating the treg/Th17 balance and the JAK1/STAT6 signaling pathway

description: Lingganwuweijiangxin Decoction (LD) is an effective prescription widely used to treat cough variant asthma (CVA) in traditional Chinese medicine, although its mechanisms remain unclear. This study investigates the therapeutic effects and underlying mechanisms of LD on CVA. A guinea pig CVA model was treated with either LD or budesonide (BUD). Capsaicin aerosol-induced coughs were recorded. Pathological changes were then examined using hematoxylin and eosin staining, transmission electron microscopy, and Wright–Giemsa staining of bronchoalveolar lavage fluid (BALF). Inflammatory cytokines were measured by enzyme-linked immunosorbent assay. mRNA expression levels of transcription factors forkhead box P3 (Foxp3), retinoic acid-related orphan receptor γt (RORγt), Janus kinase 1 (JAK1), signal transducer and activator of transcription 6 (STAT6), the transient receptor potential ankyrin 1 (TRPA1), and transient receptor potential vanilloid 1 (TRPV1) in lung tissue were detected by real-time reverse transcription polymerase chain reaction, and protein levels of these markers were assessed by Western blotting. Compared to the control group, the model group showed significantly more coughs, which were markedly reduced by LD treatment (<i>p</i> = 0.0083 and <i>p</i> = 0.0117). LD treatment also decreased inflammatory cell infiltration, alveolar epithelial hyperplasia, and mitochondrial swelling in ciliated cells, consistent with the lung tissue injury score (<i>p</i> &lt; 0.0001). LD significantly reduced the ovalbumin-induced elevation of TRPA1 (<i>p</i> &lt; 0.01 and <i>p</i> &lt; 0.0001), TRPV1 (<i>p</i> &lt; 0.01 and <i>p</i> &lt; 0.0001), and substance P (SP) levels (<i>p</i> &lt; 0.05). Moreover, LD treatment increased <i>Foxp3</i> mRNA (<i>p</i> = 0.0013) and protein expression (<i>p</i> &lt; 0.0001) and reduced <i>RORγt</i> mRNA (<i>p</i> &lt; 0.0001). LD also decreased <i>JAK1</i> and <i>STAT6</i> transcription (<i>p</i> = 0.0021, <i>p</i> &lt; 0.0001, respectively), with consistent effects observed at the protein level (<i>p</i> &lt; 0.0001). LD significantly reduced coughs and airway inflammation in the CVA guinea pig model by regulating TRPA1, TRPV1, SP, regulatory T cell/T helper 17 cell balance, and the JAK1/STAT6 signaling pathway. These effects were comparable to BUD, suggesting that LD may be a viable alternative treatment for CVA.
DOI: 10.6084/m9.figshare.28553179.v1
title: Lingganwuweijiangxin Decoction suppresses allergic airway inflammation in Guinea pigs with cough variant asthma by regulating the treg/Th17 balance and the JAK1/STAT6 signaling pathway

description: Lingganwuweijiangxin Decoction (LD) is an effective prescription widely used to treat cough variant asthma (CVA) in traditional Chinese medicine, although its mechanisms remain unclear. This study investigates the therapeutic effects and underlying mechanisms of LD on CVA. A guinea pig CVA model was treated with either LD or budesonide (BUD). Capsaicin aerosol-induced coughs were recorded. Pathological changes were then examined using hematoxylin and eosin staining, transmission electron microscopy, and Wright–Giemsa staining of bronchoalveolar lavage fluid (BALF). Inflammatory cytokines were measured by enzyme-linked immunosorbent assay. mRNA expression levels of transcription factors forkhead box P3 (Foxp3), retinoic acid-related orphan receptor γt (RORγt), Janus kinase 1 (JAK1), signal transducer and activator of transcription 6 (STAT6), the transient receptor potential ankyrin 1 (TRPA1), and transient receptor potential vanilloid 1 (TRPV1) in lung tissue were detected by real-time reverse transcription polymerase chain reaction, and protein levels of these markers were assessed by Western blotting. Compared to the control group, the model group showed significantly more coughs, which were markedly reduced by LD treatment (<i>p</i> = 0.0083 and <i>p</i> = 0.0117). LD treatment also decreased inflammatory cell infiltration, alveolar epithelial hyperplasia, and mitochondrial swelling in ciliated cells, consistent with the lung tissue injury score (<i>p</i> &lt; 0.0001). LD significantly reduced the ovalbumin-induced elevation of TRPA1 (<i>p</i> &lt; 0.01 and <i>p</i> &lt; 0.0001), TRPV1 (<i>p</i> &lt; 0.01 and <i>p</i> &lt; 0.0001), and substance P (SP) levels (<i>p</i> &lt; 0.05). Moreover, LD treatment increased <i>Foxp3</i> mRNA (<i>p</i> = 0.0013) and protein expression (<i>p</i> &lt; 0.0001) and reduced <i>RORγt</i> mRNA (<i>p</i> &lt; 0.0001). LD also decreased <i>JAK1</i> and <i>STAT6</i> transcription (<i>p</i> = 0.0021, <i>p</i> &lt; 0.0001, respectively), with consistent effects observed at the protein level (<i>p</i> &lt; 0.0001). LD significantly reduced coughs and airway inflammation in the CVA guinea pig model by regulating TRPA1, TRPV1, SP, regulatory T cell/T helper 17 cell balance, and the JAK1/STAT6 signaling pathway. These effects were comparable to BUD, suggesting that LD may be a viable alternative treatment for CVA.