{'fraction_non_alphanumeric': 0.016568047337278107, 'fraction_numerical': 0.009467455621301775, 'mean_word_length': 5.360902255639098, '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}}
[Clinical and subclinical lameness in young fattenin cattle].

Time dependent changes of subclinical and clinical lameness were analysed in 493 fattening bulls in three different herds with a total number of 30,621 animals. In the majority of cases subclinical lameness were observed which were caused by metabolic acidosis or deficiencies in mineral intake (P and probably Ca). The activity of alkaline phosphatase in plasma exhibited an increase and the dry matter in bone (tubera coxae) a decrease before the appearance of clinical symptoms. Changes in bone composition were accompanied by alterations of plasma Ca and P concentrations, which finally led to clinical lameness. Hence the diagnosis was verified by simple laboratory methods as the precondition for successful treatment and prophylaxis of lameness caused by metabolic disorders.