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Biomedical subjects

J A Clements

Publications and source records attributed to J A Clements.

At least 181 records · Page 10Linked to original sources
PubMed1970

Pulmonary surfactant and evolution of the lungs.

Pulmonary surfactant has been looked for and found in 11 representatives of four vertebrate classes. The amount of surfactant, estimated by quantitative spreading as a surface film, correlates well with alveolar surface area and with the amount of saturated, mainly dipalmitoyl, phosphatidylcholine in the lung parenchyma. The quantities of other phospholipids do not correlate well with alveolar surface area.

Animals↗
PubMed1970

Separation by gel chromatography of naturally occurring phosphatidylcholine mixtures according to number of ethylenic linkages.

This paper describes a procedure for the separation of lecithins according to the number of ethylenic bonds in their fatty acid residues. The procedure uses a column of alkylated dextran (Sephadex LH-20) eluted with an organic solvent system, the unsaturated lipids being separated as their mercuric acetate addition compounds. The system is capable of resolving at least four species of lecithin, and the intact lecithin molecules can be recovered for further study. The chromatographic system has been tested with lecithin derived from dog lung, rat liver, and hen's egg.

Acetates↗
PubMedDate not supplied

Androgen receptor expression in primary prostate cancers of Lobund-Wistar rats and in tumor-derived cell lines.

Prostate tumors were induced in Lobund-Wistar rats by treatment with N-methyl-N-nitrosourea (MNU) and testosterone propionate (TP). Androgen receptor (AR) expression was confirmed in 16 (100%) of the primary prostate cancers, with strong uniform staining in well-differentiated tumors and more variable AR immunoreactivity in poorly differentiated tumors. Epithelial cell lines were established from nine of the tumors. At early passages, four of the tumor cell lines tested were strongly immunoreactive for AR; however, only two of the cell lines, E2(A) and F2, have remained AR-positive. These cell lines specifically bind 5H-DHT at 40 and 19 fmol/mg protein, respectively, and express a 110 kDa AR immunoreactive protein. Proliferation in in vitro culture of both E2(A) and F2 cells was increased in the presence of 5alpha-dihydrotestosterone (DHT). The antiandrogen, hydroxyflutamide was able to prevent the DHT-induced growth of E2(A) but not F2 cells. Furthermore, hydroxyflutamide alone increased proliferation of F2 cells, suggesting that the androgen signalling pathway in this cell line may be abnormal. Tumorigenicity of the AR-expressing and nonexpressing cell lines was confirmed by xenograft formation following subcutaneous inoculation into intact male nude mice. In summary, carcinogen-induced prostate tumors of Lobund-Wistar rats express AR and two of nine cell lines derived from the tumors express AR. Further evaluation of AR structure in primary prostate tumors forming spontaneously or following MNU and TP induction will determine whether, as in human prostate cancers, disease progression in Lobund-Wistar rats is associated with mutations in the AR gene.

Androgen Antagonists↗