{'fraction_non_alphanumeric': 0.031799163179916316, 'fraction_numerical': 0.016736401673640166, 'mean_word_length': 5.5, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 1, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Stress, alcohol metabolism and burn injury.

In the preceding letter, Professor Mezey (1998) proposes an alternative explanation of the observation published in this journal by Jones et al. (1997) that alcohol (ethanol) metabolism is accelerated in patients suffering from burns, namely that of stress-induced hormonallymediated enhancement of activity of liver alcohol dehydrogenase (ADH; EC 1.1.1.1), possibly through growth hormone elevation and dihydrotestosterone depletion, as occurs in the rat immobilization stress model (for references, see Mezey, 1998). Jones etal. (1997) earlier suggested that the accelerated ethanol metabolism observed in their patients with burns may be due to an increased mitochondrial reoxidation of NADH secondary to the increased activity of the mitochondrial respiratory chain associated with the hepatic hypermetabolic state of such patients. The response of Professor A. W. Jones is that he does not disagree with Professor Mezey's proposals, but that, because not all patients with burns are alcoholics (and certainly none of his was), NADH reoxidation must remain as a potential parallel mechanism of the accelerated ethanol metabolism in such patients.