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[Diagnosis of cellular respiratory arrest by NADH laser fluorimetry. Applications in heart surgery and in experimental pharmacology].

The continuous measurement of intratissular NADH concentration allows early detection of cellular respiration arrest during clinical situations, i.e. allows a non-destructive, in situ, continuous measurement of ATP formation. This detection enables the physician or surgeon to intervene during a phase of cellular respiration arrest, before structural cellular alterations occur, thereby preventing potential tissular necrosis. The method has now been validated in experimental cardiac surgery for the monitoring of myocardial preservation techniques during cardiopulmonary by-pass, and in cardiac pharmacology, for analysis of drugs' effects on myocardial energetic metabolism. Its industrial development is currently under way. Preliminary investigation strongly suggests the vast potential of this diagnostic method in both clinical and experimental fields.

Adenosine Triphosphate↗

Importance of the COOH terminal of angiotensin in antigenicity and in the formation of an antigen-containing complex with cellular membrane structures.

To more carefully determine how a peptide antigen interacts with the antigen-presenting cell (APC), we have begun an analysis of the fate of APC-associated peptide antigens. These studies have shown that a stable cell-bound form of APC-associated peptide exists, which is a complex of the peptide with surface membrane structures (peak A). In the experiments described here, we have begun to examine the chemical mechanism of this peak A complex formation. By modifying either the carboxyl terminal or amino terminal group of the octapeptide antigen angiotensin II we have established that the terminal carboxyl group, but not the terminal amino group, was critical for forming the peak A complex with APC membrane structures. In addition, blocking the carboxyl but not the amino terminal dramatically reduced the antigenicity of the peptide for AII-immune T cell in vitro proliferation. These results show that the carboxyl terminal of AII is essential for both peak A formation and antigenicity, and suggest that peak A is critical for antigen presentation to T cells.

Acetylation↗