Chromosomal Location of Human Surfactant Protein Genes and a Comparative Study of Surfactant Protein Structure1

2015 ◽  
pp. 8-14
Author(s):  
James H. Fisher ◽  
Philip A. Emrie ◽  
John M. Shannon ◽  
Robert J. Mason
Keyword(s):  
Comparative Study ◽  
Chromosomal Location ◽  
Surfactant Protein ◽  
Surfactant Protein Genes

GENETIC STUDY OF RDS

PEDIATRICS ◽  
1994 ◽  
Vol 94 (1) ◽  
pp. 28-28
Author(s):  
Joanna Floros
Keyword(s):  
Genetic Study ◽  
Surfactant Protein ◽  
Multiple Births ◽  
Genetic Studies ◽  
Familial Tendency ◽  
Surfactant Protein Genes ◽  
Blood Specimens ◽  
To Receive ◽  
Prematurely Born Infants

Blood specimens are needed for genetic studies of the surfactant protein genes. We would like to receive specimens from prematurely born infants with and without RDS. We are particularly interested in specimens from families that exhibit familial tendency for RDS and specimens from twin or multiple births with and without RDS.

The effects of low-moderate dose prenatal ethanol exposure on the fetal and postnatal rat lung

2013 ◽  
Vol 4 (5) ◽  
pp. 358-367 ◽  
Author(s):  
M. E. Probyn ◽  
J. S. M. Cuffe ◽  
S. Zanini ◽  
K. M. Moritz
Keyword(s):  
Surfactant Protein ◽  
Ethanol Exposure ◽  
Mrna Levels ◽  
Prenatal Ethanol Exposure ◽  
Sprague Dawley ◽  
Aquaporin 5 ◽  
Pulmonary Tissue ◽  
Protein Levels ◽  
Gene And Protein Expression ◽  
Surfactant Protein Genes

Little is known about whether exposure of the fetus to alcohol alters pulmonary development or function. This study aimed to determine whether low-moderate ethanol (EtOH) exposure throughout gestation alters structural and non-respiratory functional aspects of the fetal and postnatal lung. Sprague–Dawley rats were fed an ad libitum liquid diet ±6% v/v EtOH daily throughout pregnancy, achieving a plasma ethanol (EtOH) concentration of 0.03%. Gene and protein expression was determined in pulmonary tissue collected from fetuses at embryonic day (E) 20 and adult offspring. The percentage of airspace and alveolar size was measured in pulmonary tissue collected at postnatal day (PN) 1. At E20, EtOH-exposed fetuses had decreased aquaporin 5 mRNA levels and a non-significant trend for decreased epithelial sodium channel type α; expression of other pulmonary fluid homeostatic and development genes and surfactant protein genes were not different between groups. At PN1, there was no difference between EtOH-exposed and control offspring in the distal airspace percentage or diameter. At 8 months, collagen type III α1 gene expression was upregulated in EtOH-exposed male offspring; this was associated with increased collagen deposition at 10 months. At 19 months, male EtOH-exposed offspring had a 25% reduction in the protein levels of surfactant protein B. The alterations observed in male EtOH-exposed offspring suggest chronic low-moderate prenatal EtOH-exposure during development may result in increased pulmonary fibrosis. Such an alteration would decrease the respiratory capacity of the lung.

SURFACTANT PROTEIN GENES AND THE RESPIRATORY DISTRESS SYNDROME IN ADULTS AND INFANTS.

Shock ◽  
1999 ◽  
Vol 12 (Supplement) ◽  
pp. 8
Author(s):  
C. Pearson ◽  
Z. Lin ◽  
V. Chinchilli ◽  
J. Floros ◽  
U. Pison
Keyword(s):  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Surfactant Protein ◽  
Surfactant Protein Genes

scholarly journals Down-Regulation of TGF-β and Expression of Surfactant Protein Genes in Type II Epithelial Cells of Human Fetal Lung

1999 ◽  
Vol 45 (4, Part 2 of 2) ◽  
pp. 52A-52A
Author(s):  
L W Gonzales ◽  
A S Kumar ◽  
S Angampalli ◽  
Y Ning ◽  
Philip L Ballard
Keyword(s):  
Epithelial Cells ◽  
Fetal Lung ◽  
Surfactant Protein ◽  
Type Ii ◽  
Down Regulation ◽  
Surfactant Protein Genes ◽  
Human Fetal Lung
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