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Faculty Detail    
Name SADIS MATALON
 
Campus Address BMR2 224 Zip 2172
Phone 205-934-4231
E-mail sadis@uab.edu
Other websites
     


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Anesthesiology   Anesthesiology Chair Office Professor
Secondary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Professor
Secondary  Environmental Health Sciences  Environmental Health Sciences Professor
Center  Arthritis & Musculoskeletal Diseases Center  Arthritis & Musculoskeletal Diseases Center Professor
Center  Cystic Fibrosis Research Center  Cystic Fibrosis Research Center Professor
Center  Medicine  Gene Therapy Center Professor

Graduate Biomedical Sciences Affiliations
Hughes Med-Grad Fellowship Program 
Integrative Biomedical Sciences 
Medical Scientist Training Program 

Biographical Sketch 
Sadis Matalon (b.1948), came to this country from Greece in 1966 as a Fulbright Scholar. He received his B.A. with Special Departmental Honors in Physics at Macalester College (1970), and his M.S. in Physics and Ph.D. in Physiology from the University of Minnesota, Minneapolis (1975). He spent six months as an Associate in Children's Hospital at Northwestern University and then moved to the State University of New York at Buffalo as Research Assistant Professor of Physiology where he worked with Dr. Leon Farhi on gas exchange. He was promoted to Assistant Professor in 1977 and Associate Professor of Physiology with tenure in1982. He joined the UAB faculty as Professor of Anesthesiology in July of 1987 after a six month sabbatical with Dr. Bruce Freeman. He was named the Alice McNeal Professor of Anesthesiology in 1999. Currently, Dr. Matalon has secondary appointments as Professor of Physiology and Biophysics, Pediatrics, Genomics and Pathobiology, and Environmental Health Sciences. He is also a member of the Centers for Free Radical Research, Cystic Fibrobis and Gene Therapy. He was appointed Associate Dean for Postdoctoral Education of the University of Alabama at Birmingham in March 2001.

Society Memberships
Organization Name Position Held Org Link
American Physiological Society     

Research/Clinical Interest
Title
Free Radical Protection from and Exacerbation of Lung Injury
Description
Dr. Matalonís research interests also focus on the role of free radicals as protective agents and as mediators of tissue injury, specifically in the context of the alveolar epithelium. Currently, two approaches are being pursued. The first is an investigation of the role of reactive oxygen-nitrogen intermediates in the killing of Mycoplasma pneumoniae. These mycoplasmas account for 20 to 30 percent of all pneumonias in humans, and exacerbate the pathophysiology of asthma, chronic obstructive disease and other pulmonary diseases. Man is the only host of M. pneumoniae, but M. pulmonis infection in mice provides an excellent animal model that reproduces the essential features of human disease. Moreover, C3H/He mice are susceptible but C57BL/6 mice are resistant. Presently, the basic mechanisms by which some hosts, but not others, kill mycoplasmas in vivo have not been elucidated. Dr. Matalon and colleagues have hypothesizes that in the early stages of infection, mycoplasmas are killed by reactive oxygen-nitrogen intermediates (ROS) produced by activated alveolar macrophages (AM). Surfactant protein A (SP-A) is essential and necessary or this killing to occur by (i) upregulating production of nitric oxide by activated AM, and (ii) stimulating phagocytosis of mycoplasmas by AM. Furthermore, injury to SP-A by reactive oxygen-nitrogen species abrogates its host-defense functions. This hypothesis is being tested in vitro, using AM isolated from the lungs of these mice, and in vivo using congenic germ-free knock-out mice. The second series of studies involves analysis of hyeroxic injury. Active sodium (Na+) transport across the adult alveolar epithelium plays an important role in the maintenance of lung fluid balance, especially after sublethal hyperoxic injury to the blood-gas barrier, when the effectiveness of the passive Starling forces is diminished. Presently, the mechanisms by which Na+ ions enter the apical membranes of normal and oxygen-injured alveolar epithelial cells, have not been elucidated. Based on preliminary data, Dr. Matalon and colleagues hypothesize that alveolar type II cells (ATII) contain Na+ channels with low affinity to amiloride and that the properties and spatial distribution of these channels may be altered by exposure to sublethal hyperoxia. Since sodium channels conduct at rates far exceeding that of any other transporter, and their activities may be upregulated by a number of agents, they may form a major pathway for the entry of Na+ ions into alveolar epithelial cells.

Selected Publications 
Publication PUBMEDID
Hickman-Davis JM, Lindsey JR, Zhu S, Matalon S: Surfactant protein A mediates mycoplasmacidal activity of alveolar macrophages. Am J Physiol 274:L270-7, 1998   
Guo Y, DuVall MD, Crow JP, Matalon S: Nitric oxide inhibits Na+ absorption across cultured alveolar type II monolayers. Am J Physiol 274:L369-77, 1998.   
Hickman-Davis J, Gibbs-Erwin J, Lindsey JR, Matalon S: Surfactant protein A mediates mycoplasmacidal activity of alveolar macrophages by production of peroxynitrite. Proc Natl Acad Sci USA 96:4953-8, 1999.   
Zhu S, Basiouny KF, Crow JP, Matalon S: Carbon dioxide enhances nitration of surfactant protein A by activated alveolar macrophages. Am J Physiol 278:L1025-31, 2000.   
Lazrak A, Samanta A, Venetsanou K, Barbry P, Matalon S: Modification of biophysical properties of lung epithelial Na(+) channels by dexamethasone. Am J Physiol 279:C762-70, 2000.   

Keywords
Acute Lung Injury, pulmonary edema, pulmonary surfactant, alveolar epithelium, free radicals, nitric oxide, sodium channels