NIH-funded Predoctoral Training Program in "Cell Signaling and Lung Pathobiology"

The T32 Training Program in "Cell Signaling and Lung Pathobiology" is in its second 5-year cycle of funding (2009-2014) from the National Heart, Lung and Blood Institute (HL076125).  The Program supports predoctoral trainees enrolled in the interdisciplinary Basic Medical Sciences PhD program at the University of South Alabama College of Medicine.  Program faculty, affiliated with the Basic Science Departments and the Center for Lung Biology, provide a breadth of expertise with respect to lung biology and pathobiology, with extramurally funded research focusing on regulation of lung endothelial barrier function, acute lung injury and repair, etiology and treatment of pulmonary hypertension, epithelial solute transport and cystic fibrosis, smooth muscle function in normal and diseased lung, and regulation of gene expression and DNA repair.  We have the expertise to train students in diverse state-of-the art research approaches ranging from those used to explore molecular mechanisms to those applicable to evaluating integrative function.  The effectiveness of this program is evidenced by the success of trainees in publication, accrual of individual extramural fellowships, and progression to biomedical research jobs in academia, industry and the government.  

Typical Timeline for Training

YR 1

YR 2

YR 3

YR 4

YR 5

Interdisciplinary Core Curriculum - Basic Medical Sciences PhD Program

Advanced Coursework

Appointment of Dissertation Advisory Committee

Development of Research Prospectus

Qualifying Exam

Dissertation Research

Dissertation Research

COM Stipend Support

T32 Training Program Support -
Cell Signaling and Lung Pathobiology

Stipend support from individual extramural fellowships, Major Advisor, or Department

Students selected will be initially appointed to the Training Program for one year.  Renewal of appointment for a second year of support is contingent upon maintenance of good academic standing and progress in training.  Reappointment for a third year of support may be considered in some cases.  Trainees will receive the current NIH predoctoral stipend, health insurance, and funds for trainee travel to professional meetings.  Stipends are supplemented by the Center and/or Departments to bring the total stipend to $23,000 per year.  All trainees receive tuition waivers.

Advanced Coursework in Lung Biology

Recommended Electives

IDL 636  Advanced Signal Transduction
IDL 640  Biostatistics and Experimental Design
IDL 630  Lung Biology
IDL 631  Lung Pathobiology
IDL 676  Journal Club: Research-in-Progress

IDL 590   Special Topics:  Presentation Skills. Abstracts
IDL 641   Effective Scientific Writing
IDL 650  Special Topics in Lung Biology
IDL 656  Translational Research Conference (joint with
the Pulmonary Div., Department of Medicine)

Other facets of the research training experience (committee meetings, qualifying examinations, participation in journal clubs and seminars, etc.) adhere to the requirements set by the Basic Medical Sciences Ph.D. Program.  Trainees will be required to complete the Qualifying Examination early in the second year of Training Grant support and to subsequently submit a proposal for an individual predoctoral fellowship to an extramural funding agency. 

Dr. Mary Townsley, Program Director
Center for Lung Biology
5851 USA Drive N., Rm 3340
University of South Alabama, Mobile, AL 36688
Phone: 251-460-6815

Training Program Faculty

Mary Townsley, Ph.D., Professor, Departments of Physiology/Medicine, Program Director
Regional heterogeneity and transient receptor potential cation channels in regulation of lung endothelial permeability, adaptations to chronic pulmonary hypertension

Stephen Ballard, Ph.D., Professor, Department of Physiology
Biophysical transport processes which control lung airway liquid secretion, defects in chloride ion transport and impact on mucocilliary clearance in cystic fibrosis

Karen Fagan, M.D., Associate Professor, Chief of Pulmonary Division, Department of Medicine
Role of intermittent hypoxia, inflammation, sustained abnormal vasoconstriction and proximal vascular stiffening in pulmonary hypertension, therapeutic clinical trials in PAH

Brian Fouty, M.D., Associate Professor, Department of Medicine
Vascular remodeling in pulmonary hypertension

William Gerthoffer, Ph.D., Professor and Chair, Department of Biochemistry
Smooth muscle contractility, actin cytoskeleton, myosin motor proteins and small heat shock proteins by protein kinases

Mark Gillespie, Ph.D., Professor and Chair, Department of Pharmacology
Inter- and intracellular signaling which contribute to hypertensive pulmonary vascular remodeling, impact of reactive oxygen species on gene regulation

Richard Honkanen, Ph.D., Professor, Department of Biochemistry
Role of phosphatases in the cross-talk between glucocorticoid and hypoxia-induced signaling networks, regulation of cell growth and apoptosis

Susan LeDoux, Ph.D., Professor and Vice Chair, Department of Cell Biology/Neuroscience
Mechanisms of cellular protection against genotoxic insult, including nuclear and mitochondiral DNA repair

Thomas Lincoln, Ph.D., Professor and Chair, Department of Physiology
Nitric oxide-dependent regulation of protein kinase G and  vascular smooth muscle cell gene expression

Ivan McMurtry, Ph.D., Professor, Department of Pharmacology
Pulmonary vasoregulation and endothelial control of tone in pulmonary hypertension, RhoA/Rho kinase signaling

Thomas Rich, Ph.D., Assistant Professor, Department of Pharmacology
Biophysics, modeling of β adrenergic receptor- and cyclic nucleotide-mediated signaling

Troy Stevens, Ph.D., Professor, Department of Pharmacology, Director Center for Lung Biology
Cellular mechanisms promoting lung endothelial barrier disruption in inflammation; ion channels and endothelial phenotypic heterogeneity

David Weber, Ph.D., Assistant Professor, Department of Physiology
Role of reactive oxygen species in vascular smooth muscle migration

Glenn Wilson, Ph.D., Professor and Chair, Department of Cell Biology/Neuroscience
Environmental factors leading to nuclear and mitochondrial DNA damage, mechanisms of aging

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