Robert Foronjy

ORCID: 0000-0003-3964-5335
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Chronic Obstructive Pulmonary Disease (COPD) Research
  • Neonatal Respiratory Health Research
  • Pulmonary Hypertension Research and Treatments
  • Protease and Inhibitor Mechanisms
  • Respiratory Support and Mechanisms
  • Respiratory viral infections research
  • Asthma and respiratory diseases
  • Pneumocystis jirovecii pneumonia detection and treatment
  • Air Quality and Health Impacts
  • S100 Proteins and Annexins
  • Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
  • Protein Tyrosine Phosphatases
  • HIV-related health complications and treatments
  • Peptidase Inhibition and Analysis
  • Pediatric health and respiratory diseases
  • RNA modifications and cancer
  • Heme Oxygenase-1 and Carbon Monoxide
  • Redox biology and oxidative stress
  • Sepsis Diagnosis and Treatment
  • Phytochemicals and Antioxidant Activities
  • Antioxidant Activity and Oxidative Stress
  • Inflammation biomarkers and pathways
  • Sinusitis and nasal conditions
  • Hydrogen's biological and therapeutic effects
  • COVID-19 Clinical Research Studies

SUNY Downstate Health Sciences University
2016-2024

State University of New York
2016-2024

Minneapolis VA Health Care System
2024

Pulmonary and Critical Care Associates
2018-2019

Vanderbilt University
2017

Roosevelt Hospital
2015

Mount Sinai Health System
2014-2015

St. Luke's-Roosevelt Hospital Center
2012-2014

Theodore Roosevelt High School
2014

Sinai Health System
2014

<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

Lung injury after cigarette smoking is related to particle retention. Iron accumulates with the deposition of these particles.We tested postulate that (1) correlates exposure particulate fraction smoke, (2) particles alter iron homeostasis, triggering metal accumulation, and (3) this alteration in homeostasis affects oxidative stress inflammation.Rats human respiratory epithelial cells were exposed filtered smoke condensate (the smoke), indices stress, inflammatory determined. Comparable...

10.1164/rccm.200802-334oc article EN American Journal of Respiratory and Critical Care Medicine 2008-08-22

Background— Left ventricular assist devices (LVADs) induce reverse remodeling of the failing heart except for extracellular matrix, which exhibits additional pathophysiological changes, although their mechanisms and functional consequences are unknown. Methods Results— Hearts were obtained at transplant from patients with idiopathic dilated cardiomyopathy (DCM) not requiring LVAD support (n=30), (n=16; duration, 145±33 days), 5 nonfailing hearts. (LV) right (RV) ex vivo pressure-volume...

10.1161/circulationaha.104.515106 article EN Circulation 2005-07-06

Rationale: Oxidants are believed to play a major role in the development of emphysema.Objectives: This study aimed determine if expression human copper–zinc superoxide dismutase (CuZnSOD) within lungs mice protects against emphysema.Methods: Transgenic CuZnSOD and littermate were exposed cigarette smoke (6 h/d, 5 d/wk, for 1 yr) compared with nonexposed mice. A second group was treated intratracheal elastase induce emphysema.Measurements: Lung inflammation measured by cell counts...

10.1164/rccm.200506-850oc article EN American Journal of Respiratory and Critical Care Medicine 2005-12-31

Matrix metalloproteinase (MMP)-9 has been consistently identified in the lungs of patients with chronic obstructive pulmonary disease (COPD). However, its role development remains undefined. Mice that specifically express human MMP-9 their macrophages were generated, and morphometric, biochemical, histological analyses conducted on transgenic littermate control mice over 1 yr to determine effect macrophage expression emphysema formation lung matrix content. Lung morphometry was normal at 2...

10.1152/ajplung.00481.2007 article EN AJP Lung Cellular and Molecular Physiology 2008-04-12

Arsenic from drinking water has been associated with malignant and nonmalignant respiratory illnesses. The association illnesses not well established because the assessments of symptoms may be influenced by recall bias or interviewer participants had visible skin lesions.We examined relationship serum level Clara cell protein CC16--a novel biomarker for illnesses--with As, total urinary As methylation indices.We conducted a cross-sectional study in nonsmoking individuals (n = 241) selected...

10.1289/ehp.9507 article EN public-domain Environmental Health Perspectives 2007-11-06

Tissue resident mesenchymal stem cells (MSCs) are important regulators of tissue repair or regeneration, fibrosis, inflammation, angiogenesis and tumor formation. Bone marrow derived (BM-MSCs) endothelial progenitor (EPC) currently being considered tested in clinical trials as a potential therapy patients with such inflammatory lung diseases including, but not limited to, chronic disease, pulmonary arterial hypertension (PAH), fibrosis (PF), obstructive disease (COPD)/emphysema asthma....

10.3390/cells1040874 article EN Cells 2012-10-19

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

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

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

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

Mice with lung-specific expression of human matrix metalloproteinase-1 (MMP-1) develop emphysematous changes similar to those seen in smoking-induced emphysema humans. Morphometric analyses three transgenic lines [homozygous colony ( Col) 34, Col 50, and 64] varying temporal MMP-1 were undertaken determine the validity this animal as a model adult-onset emphysema. Line 50 mice, which have early (14 days postconception), exhibited morphometric by 5 age. In contrast, homozygous line 34 64...

10.1152/ajplung.00349.2002 article EN AJP Lung Cellular and Molecular Physiology 2003-05-01

The murine smoke-induced model produces histologic emphysema. authors sought to assess whether the structural emphysema that occurred correlated with development of compliance changes. study exposed 2 strains mice (CBA/J/J × C57BL/6J and A/J) chronic cigarette smoke. Lung morphometry were measured. smoking generated significant in A/J absence changes compliance, lung matrix, or apoptosis. Importantly, there was no correlation between measured by pulmonary compliance. This lack suggests...

10.1080/019021490951522 article EN Experimental Lung Research 2005-01-01

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

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
Coming Soon ...