HBA-USA members that conduct research on "Lung Diseases"
- Biophysics
Sotirios Zarogiannis
University of California San Francisco, Postdoctoral Scholar
Matrix Biology, Physiology, Lung Disease, Biophysiscs
Sotirios.Zarogiannis@ucsf.edu
- Gene Therapy
Maria Limberis
Univ of Pennsylvania, Post-doctoral fellow
Gene therapy for lung diseases
limberis@mail.med.upenn.edu
- Hypoxia & Pulmonary Hypertension
David G Kalergis
Diffusion Pharmaceuticals LLC, CEO
Developing novel small molecules for the treatment of hypoxia related to ischemic conditions
dkalergis@diffusionpharma.com
Stella Kourembanas
Children's Hospital Boston, Harvard Medical School, Clement A. Smith Associate Professor of Pediatrics
Lung vascular biology; Hypoxic signaling and pulmonary hypertension; Developmental lung biology
stella.kourembanas@ childrens.Harvard.edu
- Lung injury & Cancer
Joanna Floros, PhD
Pennsylvania State University College of Medicine, Evan Pugh Professor of Pediatrics and Obstetrics & Gynecology, Director of The Penn State Center for Host defense,
Inflammation and Lung Disease (CHILD) Research
a) Cancer: DNA methylation of host defense molecules
b) Pulmonary Disease: Study of the molecular basis of individual variability to disease susceptibility with special emphasis on molecules and mechanisms involved in host
defense and inflammation. Genome wide SNP analysis of several hundred candidate genes will be performed using the Illumina Infinium Platform
jfloros@psu.edu
Nicholas E. Vlahakis
Mayo Clinic College of Medicine, Assistant Professor of Medicine
Our current research projects focus on the role of growth factors and integrins in the pathogenesis of the lung injury associated with ventilator associated
lung injury, lung cancer and lymphangioleiomyomatosis (LAM). Specifically our work uses molecular biologic, in vitro cell and chick CAM assays to
investigate the biology of endothelial and vascular smooth muscle cells as it relates to angiogenesis and lymphangiogenesis. New vessel formation plays a
key role in lung cancer, cancer metastasis and LAM and the study of VEGF and integrins lends itself to the discovery of novel therapeutic peptides for
treatment.
In separate projects we are investigating the role of growth factors, integrins and lipids in lung cell injury resulting from mechanical deformation and
subsequent repair mechanisms. These studies are performed in both cells and animals using cell stretchers, confocal microscopy and mechanical
ventilators respectively.
vlahakis.nicholas@mayo.edu
- Lung innate host defense
Zissis C. Chroneos
University of Texas Health Center at Tyler, Assistant Professor
Lung innate host defense as mediated by surfactant proteins A and D in alveolar macrophages and
Type II epithelial cells via the receptor SP-R210/Myo18A. We study SP-R210/Myo18A-mediated mechanisms
of phagocytosis and signaling responses in mycobacterial and staphylococcal infections
Zissis.Chroneos@uthct.edu
Joanna Floros, PhD
Pennsylvania State University College of Medicine, Evan Pugh Professor of Pediatrics and Obstetrics & Gynecology, Director of The Penn State Center for Host
defense, Inflammation and Lung Disease (CHILD) Research
Innate host defense variability in response to environmental pollutants and/or infection. Humanized transgenic mice expressing different human variants of the innate
host defense molecule, surfactant protein A or SP-A, are used for study.
jfloros@psu.edu
- Oxidative stress
Alex Mitsialis
Harvard Medical School, Assistant Professor of Pediatrics
Alex Mitsialis and his colleagues are focusing on oxygen-regulated genes and on gene families that are essential in mounting lung responses to
injury, repair, tissue remodeling, and oxygen homeostasis. Dr. Mitsialis is examining gene expression associated with the activity of the enzyme
Heme Oxygenase-1 (HO-1). When oxygen levels are low, the gene for HO-1 is turned on. The induction of HO-1 stimulates the production of carbon
monoxide and biliverdin (the precursor of the antioxidant bilirubin), both of which may help prevent lung damage. If researchers can establish a
correlation between specific versions of the HO-1 gene and clinical responses to treatment, it might be possible to predict which preterm infants
would be more likely to benefit from a specific therapy.
alex.mitsialis@childrens.harvard.edu
- Biophysics
Sotirios Zarogiannis
University of California San Francisco, Postdoctoral Scholar
Matrix Biology, Physiology, Lung Disease, Biophysiscs
Sotirios.Zarogiannis@ucsf.edu
- Gene Therapy
Maria Limberis
Univ of Pennsylvania, Post-doctoral fellow
Gene therapy for lung diseases
limberis@mail.med.upenn.edu
- Hypoxia & Pulmonary Hypertension
David G Kalergis
Diffusion Pharmaceuticals LLC, CEO
Developing novel small molecules for the treatment of hypoxia related to ischemic conditions
dkalergis@diffusionpharma.com
Stella Kourembanas
Children's Hospital Boston, Harvard Medical School, Clement A. Smith Associate Professor of Pediatrics
Lung vascular biology; Hypoxic signaling and pulmonary hypertension; Developmental lung biology
stella.kourembanas@ childrens.Harvard.edu
- Lung injury & Cancer
Joanna Floros, PhD
Pennsylvania State University College of Medicine, Evan Pugh Professor of Pediatrics and Obstetrics & Gynecology, Director of The Penn State Center for Host defense,
Inflammation and Lung Disease (CHILD) Research
a) Cancer: DNA methylation of host defense molecules
b) Pulmonary Disease: Study of the molecular basis of individual variability to disease susceptibility with special emphasis on molecules and mechanisms involved in host
defense and inflammation. Genome wide SNP analysis of several hundred candidate genes will be performed using the Illumina Infinium Platform
jfloros@psu.edu
Nicholas E. Vlahakis
Mayo Clinic College of Medicine, Assistant Professor of Medicine
Our current research projects focus on the role of growth factors and integrins in the pathogenesis of the lung injury associated with ventilator associated
lung injury, lung cancer and lymphangioleiomyomatosis (LAM). Specifically our work uses molecular biologic, in vitro cell and chick CAM assays to
investigate the biology of endothelial and vascular smooth muscle cells as it relates to angiogenesis and lymphangiogenesis. New vessel formation plays a
key role in lung cancer, cancer metastasis and LAM and the study of VEGF and integrins lends itself to the discovery of novel therapeutic peptides for
treatment.
In separate projects we are investigating the role of growth factors, integrins and lipids in lung cell injury resulting from mechanical deformation and
subsequent repair mechanisms. These studies are performed in both cells and animals using cell stretchers, confocal microscopy and mechanical
ventilators respectively.
vlahakis.nicholas@mayo.edu
- Lung innate host defense
Zissis C. Chroneos
University of Texas Health Center at Tyler, Assistant Professor
Lung innate host defense as mediated by surfactant proteins A and D in alveolar macrophages and
Type II epithelial cells via the receptor SP-R210/Myo18A. We study SP-R210/Myo18A-mediated mechanisms
of phagocytosis and signaling responses in mycobacterial and staphylococcal infections
Zissis.Chroneos@uthct.edu
Joanna Floros, PhD
Pennsylvania State University College of Medicine, Evan Pugh Professor of Pediatrics and Obstetrics & Gynecology, Director of The Penn State Center for Host
defense, Inflammation and Lung Disease (CHILD) Research
Innate host defense variability in response to environmental pollutants and/or infection. Humanized transgenic mice expressing different human variants of the innate
host defense molecule, surfactant protein A or SP-A, are used for study.
jfloros@psu.edu
- Oxidative stress
Alex Mitsialis
Harvard Medical School, Assistant Professor of Pediatrics
Alex Mitsialis and his colleagues are focusing on oxygen-regulated genes and on gene families that are essential in mounting lung responses to
injury, repair, tissue remodeling, and oxygen homeostasis. Dr. Mitsialis is examining gene expression associated with the activity of the enzyme
Heme Oxygenase-1 (HO-1). When oxygen levels are low, the gene for HO-1 is turned on. The induction of HO-1 stimulates the production of carbon
monoxide and biliverdin (the precursor of the antioxidant bilirubin), both of which may help prevent lung damage. If researchers can establish a
correlation between specific versions of the HO-1 gene and clinical responses to treatment, it might be possible to predict which preterm infants
would be more likely to benefit from a specific therapy.
alex.mitsialis@childrens.harvard.edu
Hellenic Bioscientific Association in the USA
HBA-USA
HBA-USA
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