Article in Science advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
17 authors.
Nicolas L PereiraLung and Vascular Inflammation Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0003-3654-4029
Niccole SchaibleCenter for Vascular Biology Research, Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA.ORCID 0000-0002-4765-5966
Abhishek DesaiLung and Vascular Inflammation Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Eunice C ChanLung and Vascular Inflammation Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Ararat J AbloogluLung and Vascular Inflammation Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0009-0002-8692-4572
Jacqueline CapuanoCenter for Vascular Biology Research, Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA.
Erika LinCenter for Vascular Biology Research, Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA.ORCID 0000-0001-9775-0868
Zheming AnDivision of Genetics and Genomics, Manton Center for Cell Discovery Research, Department of Pediatrics, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.ORCID 0000-0002-6325-1494
Eric GebskiRutgers Institute for Translational Medicine and Science, Child Health Institute of New Jersey, Rutgers, the State University of New Jersey, New Brunswick, NJ 08901, USA.ORCID 0009-0007-2748-5975
William JesterRutgers Institute for Translational Medicine and Science, Child Health Institute of New Jersey, Rutgers, the State University of New Jersey, New Brunswick, NJ 08901, USA.ORCID 0000-0002-2872-6095
Sundar GanesanBiological Imaging Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Nariman BalengaLung and Vascular Inflammation Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0002-2741-9595
Cynthia Koziol-WhiteRutgers Institute for Translational Medicine and Science, Child Health Institute of New Jersey, Rutgers, the State University of New Jersey, New Brunswick, NJ 08901, USA.ORCID 0000-0003-1101-2747
Reynold A PanettieriRutgers Institute for Translational Medicine and Science, Child Health Institute of New Jersey, Rutgers, the State University of New Jersey, New Brunswick, NJ 08901, USA.ORCID 0000-0003-0834-4636
Sangita ChoudhuryDivision of Genetics and Genomics, Manton Center for Cell Discovery Research, Department of Pediatrics, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.ORCID 0000-0001-7357-1988
Ramaswamy KrishnanCenter for Vascular Biology Research, Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA.ORCID 0000-0003-4994-0709
Kirk M DrueyLung and Vascular Inflammation Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.ORCID 0000-0002-5834-6501
Funding
Translational Research Support CoreP30ES005022 · NIEHS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI BRIAN T BUCKLEY · 1988 to 2026
$47.4M
Studies in the Pathogenesis of Systemic Capillary Leak SyndromeZIAAI001083 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI DRUEY, KIRK M · 2009 to 2025
$11.5M
Screening for inhibitors of allergen-associated airway smooth muscle contractionR21AI151695 · NIAID · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KRISHNAN, RAMASWAMY · 2020 to 2021
Severe asthma induces substantial mortality and chronic disability due to intractable airway obstruction, which may become resistant to currently available therapies including corticosteroids and β-adrenergic agonist bronchodilators. A key effector of these changes is exaggerated airway smooth muscle (ASM) cell contraction to spasmogens. No drugs in clinical use effectively prevent ASM hyperresponsiveness in asthma across all severities. We find that N-cadherin, a membrane cell-cell adhesion protein up-regulated in ASM from patients with severe asthma, is required for the development of airway obstruction induced by allergic airway inflammation in mice. Inhibition of N-cadherin by ADH-1 reduced airway hyperresponsiveness independent of allergic inflammation, prevented bronchoconstriction, and actively promoted bronchodilation of airways ex vivo. ADH-1 inhibited ASM contraction by disrupting N-cadherin-δ-catenin interactions, which decreased intracellular actin remodeling. These data provide evidence for an intercellular communication pathway mediating ASM contraction and identify N-cadherin as a potential therapeutic target for inhibiting bronchoconstriction in asthma.
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.
N-cadherin antagonism is bronchoprotective in severe asthma models. · full record | OpenQuestion