Patrick Geraghty

ORCID: 0000-0003-1647-5505
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About
Contact & Profiles
Research Areas
  • Chronic Obstructive Pulmonary Disease (COPD) Research
  • Neonatal Respiratory Health Research
  • Protease and Inhibitor Mechanisms
  • Pulmonary Hypertension Research and Treatments
  • Peptidase Inhibition and Analysis
  • S100 Proteins and Annexins
  • Respiratory viral infections research
  • Respiratory Support and Mechanisms
  • Asthma and respiratory diseases
  • Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
  • Pediatric health and respiratory diseases
  • Blood Coagulation and Thrombosis Mechanisms
  • Protein Tyrosine Phosphatases
  • Immune Response and Inflammation
  • Smoking Behavior and Cessation
  • Cystic Fibrosis Research Advances
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Renal and related cancers
  • PI3K/AKT/mTOR signaling in cancer
  • Tumors and Oncological Cases
  • Sarcoma Diagnosis and Treatment
  • Air Quality and Health Impacts
  • Cytokine Signaling Pathways and Interactions
  • Pneumocystis jirovecii pneumonia detection and treatment
  • Cancer Diagnosis and Treatment

SUNY Downstate Health Sciences University
2016-2025

State University of New York
2016-2024

Good Samaritan Hospital
2022

Washington University in St. Louis
2022

Sisters of Charity Hospital
2022

Pulmonary and Critical Care Associates
2018-2019

Columbia University
2011-2016

Mount Sinai Health System
2014-2015

Roosevelt Hospital
2015

Theodore Roosevelt High School
2014-2015

<h3>Background</h3> The use of electronic (e)-cigarettes is increasing rapidly, but their lung health effects are not established. Clinical studies examining the potential long-term impact e-cigarette on will take decades. To address this gap in knowledge, study investigated exposure to aerosolised nicotine-free and nicotine-containing fluid mouse lungs normal human airway epithelial cells. <h3>Methods</h3> Mice were exposed phosphate-buffered saline, or solution, 1-hour daily for 4 months....

10.1136/thoraxjnl-2015-208039 article EN cc-by-nc Thorax 2016-08-24

Chronic Obstructive Pulmonary Disease (COPD) is a complex disease. Genetic, epigenetic, and environmental factors are known to contribute COPD risk disease progression. Therefore we developed systematic approach identify key regulators of that integrates genome-wide DNA methylation, gene expression, phenotype data in lung tissue from control samples. Our integrative analysis identified 126 COPD. We EPAS1 as the only regulator whose downstream genes significantly overlapped with multiple sets...

10.1371/journal.pgen.1004898 article EN cc-by PLoS Genetics 2015-01-08

Circulating levels of fibroblast growth factor (FGF)23 are associated with systemic inflammation and increased mortality in chronic kidney disease. α-Klotho, a co-receptor for FGF23, is downregulated obstructive pulmonary disease (COPD). However, whether FGF23 Klotho-mediated FGF receptor (FGFR) activation delineates pathophysiological mechanism COPD remains unclear. We hypothesised that can potentiate airway via Klotho-independent FGFR4 activation. its effect were studied using plasma...

10.1183/13993003.00236-2018 article EN European Respiratory Journal 2018-05-10

Abstract Neutrophil elastase (NE) activity is increased in many diseases. Other families of proteases, including cathepsins and matrix metalloproteases (MMPs), are also present at elevated levels similar disease conditions. We postulated that NE could induce expression MMPs human macrophages. exposure resulted macrophages, producing significantly greater amounts cathepsin B latent active MMP-2. Cathepsin MMP-2 activities were decreased Pseudomonas-infected knockout mice compared with...

10.4049/jimmunol.178.9.5871 article EN The Journal of Immunology 2007-05-01

Rationale: Augmentation therapy with intravenous AAT (alpha-1 antitrypsin) is the only specific for individuals pulmonary disease from deficiency (AATD). The recommended standard dose (SD; 60 mg/kg/wk) elevates trough serum levels to around 50% of normal; however, outside slowing emphysema progression, its effects in other clinical outcomes have not been rigorously proven.Objectives: To evaluate biological normalizing double-dose (DD) (120 subjects AATD already receiving SD therapy.Methods:...

10.1164/rccm.201901-0010oc article EN cc-by-nc-nd American Journal of Respiratory and Critical Care Medicine 2019-04-09

Smoke exposure is known to decrease total pulmonary surfactant and alter its composition, but the role of in chronic obstructive disease (COPD) remains unknown. We aimed analyze compositional changes lipidome COPD identify specific lipids associated with function decline. Bronchoalveolar lavage (BAL) fluid was obtained from 12 former smokers 5 non-smoking, non-asthmatic healthy control volunteers. Lipids were extracted analyzed by liquid chromatography mass spectrometry. Pulmonary data...

10.1371/journal.pone.0228279 article EN cc-by PLoS ONE 2020-02-06

Cigarette smoke is the major risk factor associated with development of chronic obstructive pulmonary disease and alters expression proteolytic enzymes that contribute to pathology. Previously, we reported exposure leads induction matrix metalloproteinase-1 (MMP-1) through activation ERK1/2, which critical emphysema. To date, upstream signaling pathway by cigarette induces MMP-1 has been undefined. This study demonstrates mediates via TLR4 cascade. In vitro cell culture studies demonstrated...

10.1074/jbc.m111.238824 article EN cc-by Journal of Biological Chemistry 2011-07-06

Rationale Though matrix metalloproteinases (MMPs) are critical in the pathogenesis of COPD, their utility as a disease biomarker remains uncertain. This study aimed to determine whether bronchoalveolar lavage (BALF) or plasma MMP measurements correlated with severity functional decline emphysema. Methods Enzyme-linked immunosorbent assay and luminex assays measured MMP-1, -9, -12 tissue inhibitor metalloproteinase-1 BALF non-smokers, smokers normal lung function moderate-to-severe emphysema...

10.1371/journal.pone.0056352 article EN cc-by PLoS ONE 2013-02-18

Respiratory syncytial virus (RSV) infects the lung epithelium where it stimulates production of numerous host cytokines that are associated with disease burden and acute injury. Characterizing cytokine response to RSV infection, regulation impact neutralizing an RSV-inducible during infection were undertaken in this study. A549, primary human small airway epithelial (SAE) cells wild-type, TIR-domain-containing adapter-inducing interferon-β (Trif) mitochondrial antiviral-signaling protein...

10.1186/s12865-014-0041-4 article EN cc-by BMC Immunology 2014-10-02

Rationale Biomass is the energy source for cooking and heating billions of people worldwide. Despite their prevalent use potential impact on global health, effects these fuels lung biology function remain poorly understood. Methods We exposed human small airway epithelial cells C57BL/6 mice to dung biomass smoke or cigarette compare how exposures impacted signaling inflammatory proteolytic responses that have been linked with disease pathogenesis. Results The in vitro exposure siRNA studies...

10.1371/journal.pone.0052889 article EN cc-by PLoS ONE 2012-12-20

Respiratory syncytial viral (RSV) infections are a frequent cause of chronic obstructive pulmonary disease (COPD) exacerbations, which major factor in progression and mortality. RSV is able to evade antiviral defenses persist the lungs COPD patients. Though infection has been identified COPD, its contribution cigarette smoke-induced airway inflammation lung tissue destruction not established. Here we examine long-term effects smoke exposure, combination with monthly infections, on...

10.1371/journal.pone.0090567 article EN cc-by PLoS ONE 2014-02-28

Rationale: CTSS (cathepsin S) is a cysteine protease that observed at higher concentrations in BAL fluid and plasma of subjects with chronic obstructive pulmonary disease (COPD). Objectives: To investigate whether involved the pathogenesis cigarette smoke-induced COPD determine targeting upstream signaling could prevent disease. Methods: expression was investigated animal human tissue cell models COPD. Ctss-/- mice were exposed to long-term smoke forced oscillation expiratory measurements...

10.1164/rccm.201808-1518oc article EN American Journal of Respiratory and Critical Care Medicine 2019-01-14

Induction of the unfolded protein response by cigarette smoke is primarily an activating transcription factor 4-C/EBP homologous mediated process Patrick Geraghty, Alison Wallace, Jeanine M D&#39;ArmientoDepartment Medicine, Divisions Molecular and Pulmonary Columbia University College Physicians Surgeons, New York, NY, USAPurpose: Cigarette major risk associated with development chronic obstructive pulmonary disease (COPD). Recent studies propose a link between endoplasmic reticulum (ER)...

10.2147/copd.s19599 article EN cc-by-nc International Journal of COPD 2011-06-01

Protein phosphatase 2A (PP2A) is the primary serine-threonine of eukaryotic cells, and changes in its activity have been linked to neoplastic neurodegenerative diseases. However, role PP2A noncancerous lung diseases such as chronic obstructive pulmonary disease (COPD) has not previously examined. This study determined that was significantly increased lungs advanced emphysema subjects compared with age-matched controls. Furthermore, we found cigarette smoke exposure increases mouse vivo human...

10.1093/toxsci/kfr351 article EN Toxicological Sciences 2012-01-05

Chronic inflammation is a hallmark of cystic fibrosis (CF) and associated with increased production transforming growth factor (TGF) β interleukin (IL)-8. α-klotho (KL), transmembrane or soluble protein, functions as co-receptor for Fibroblast Growth Factor (FGF) 23, known pro-inflammatory, prognostic marker in chronic kidney disease. KL downregulated airways from COPD patients. We hypothesized that both FGF23 signaling modulate TGF β-induced IL-8 secretion CF bronchial epithelia. Thus,...

10.1038/s41598-017-14811-0 article EN cc-by Scientific Reports 2017-10-24

Rationale: α1-Antitrypsin (A1AT) was identified as a plasma protease inhibitor; however, it is now recognized multifunctional protein that modulates immunity, inflammation, proteostasis, apoptosis, and cellular senescence. Like A1AT, phosphatase 2A (PP2A), major serine-threonine phosphatase, regulates similar biologic processes plays key role in chronic obstructive pulmonary disease.Objectives: Given their common effects, this study investigated whether A1AT acts via PP2A to alter tumor...

10.1164/rccm.201405-0872oc article EN American Journal of Respiratory and Critical Care Medicine 2014-10-23

Neutrophil elastase (NE) activity is increased in lung diseases such as alpha(1)-antitrypsin (A1AT) deficiency and pneumonia. It has recently been shown to induce expression of cathepsin B matrix metalloprotease 2 (MMP-2) vitro a mouse model. postulated that MMP-2 acute chronic result from high levels extracellular NE these proteases could be inhibited by A1AT augmentation therapy.Cathepsin MMP activities were assessed bronchoalveolar lavage (BAL) fluid patients with deficiency, pneumonia...

10.1136/thx.2007.088559 article EN Thorax 2008-02-05
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