The amount of elongation factor 2 (EF2) in the cytoplasm and ribosome of breast muscle cell from normal and dystrophic strains of chicken was measured. Concentration in the cytoplasm of 20-day-old embryonic dystrophic muscle was higher than that in normal muscle, but no difference in content was found in muscles of 15-day-old embryos. The amount of EF2 bound to ribosomes was identical in normal and dystrophic muscles during all stages of development. Peptide mapping patterns of partial proteolytic fragments of EF2 from normal and dystrophic chicken breast muscles were similar. The increase in cytoplasmic protein synthetic activity of dystrophic breast muscles reported previously seems to be due to the corresponding increase in the number of EF2 molecules rather than to their modification in dystrophic muscle.

Animals↗

PubMedDate not supplied

Ca overload and the action of calcium sensitive proteases, phospholipases and prostaglandin E2 in myocardial cell degradation.

The mechanism of Ca overload-induced myocardial cell injury under hypoxia was examined for the involvement of calcium-activated neutral proteases (CANP), calcium-dependent phospholipases (CDP) or prostaglandins with measuring 45Ca entry, intake of biologically inert dye, nigrosin, into the cultured myocytes, as was useful for the quantification of sarcolemma permeability, and the release of creatine phosphokinase (CPK) to the culture medium. A Ca channel blocker, verapamil (1 and 10 micrograms/ml) or a Ca ionophore, A23187 (0.5 to 4 micrograms/ml) dose-dependently decreased or increased both the Ca entry and nigrosin intake in accordance with the CPK release. Furthermore, the inhibitors against CANP, NCO-700 (2 and 20 micrograms/ml) that was demonstrated to permeate sarcolemma using 14C-labelled reagent, against CDP, mepacrine (1 and 10 micrograms/ml) or against cyclooxygenase, indomethacin (1 and 10 micrograms/ml) caused no effect on the Ca entry, nigrosin intake nor CPK release under hypoxia. These results suggest that the Ca overdose into the myocardial cells potentiates their injury and it is not primarily related to the activation of CANP, CDP nor cyclooxygenase.

Aniline Compounds↗

PubMedDate not supplied

Anomalous pancreaticobiliary junction demonstrated by extraductal ultrasonography using transduodenoscopic miniprobe.

We present a case of an anomalous pancreaticobiliary junction (a long common channel) that was clearly demonstrated by extraductal ultrasonography with a transduodenoscopic miniprobe placed in the duodenal lumen. The present case suggests a potential indication for the ultrasound miniprobe, in extraductal ultrasonography, in the pancreatobiliary region. In this method, the position of a miniprobe can readily be adjusted under endoscopic guidance, unlike ordinary endoscopic ultrasonography.

Aged↗

PubMedDate not supplied

Plasma endothelin-1 concentrations in the coronary sinus in dogs with artificially induced myocardial infarction.

We have previously reported the marked increase in plasma levels of endothelin-1 in patients with acute myocardial infarction (AMI). To investigate the effects of severe myocardial ischemia on the production of endothelin-1, plasma concentrations of endothelin-1 were measured by a sandwich-type enzyme immunoassay that we developed recently in both the coronary sinus and the aorta of dogs with artificially induced AMI. Dogs were anesthetized and chests were opened. The proximal left anterior descending coronary artery was completely occluded by ligation for 1 h and then was reperfused for 1 h. Throughout the experiment (at the end of occlusion for 1 h, at the beginning of reperfusion, at the end of reperfusion for 1 h), plasma endothelin-1 levels were not significantly altered either in the coronary sinus or in the aorta. The present findings indicate that severe myocardial ischemia itself does not affect the production of endothelin-1 in the coronary circulation of dogs.

Animals↗