{'fraction_non_alphanumeric': 0.010628875110717449, 'fraction_numerical': 0.010628875110717449, 'mean_word_length': 5.686390532544379, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
EFFECTS OF DENERVATION ON THE INCORPORATION OF 32P INTO PHOSPHATIDYL INOSITOL AND OTHER PHOSPHOLIPIDS OF RAT DIAPHRAGM

Abstract— At 24 h after denervation of the rat hemidiaphragm, incorporation of 32P into phosphatidyl inositol was depressed relative to incorporation of 32P into phosphatidyl choline (measured 75 min after injection of the isotope intraperitoneally). The ratio of the specific radioactivity of phosphatidyl choline to the specific radioactivity of Pi was unaffected by denervation which implies that denervation had depressed incorporation of isotope into phospatidyl inositol. Denervation did not cause a measurable change in the pool size of phosphatidyl inositol relative to that of phosphatidyl choline. The effect of denervation on incorporation of 32P into phosphatidyl inositol was not entirely a direct consequence of the cessation of ACh release at the motor end‐plate since the effect was clearly manifest in strips of muscle not containing motor end‐plates, but the magnitude of the denervation effect was slightly greater in the strips of denervated hemidiaphragm which contained motor end‐plates.