{'fraction_non_alphanumeric': 0.018077239112571898, 'fraction_numerical': 0.0008216926869350862, 'mean_word_length': 5.4787234042553195, '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}}
In vitro fixation of guinea pig complement by renal biopsies.

The in vitro fixation of heterologous complement by cryostat sections of human renal biopsy material was studied to determine the mechanism of complement activation. Various types of guinea pig sera with different parts of the complement system inhibited were used, the fixation of complement being detected by direct immunofluorescence. Cases of idiopathic focal nephritis with mesangial IgA (mesangial IgA disease), Henoch-Schönlein purpura (HSP) and mesangio-capillary glomerulonephritis (MCGN) fixed complement by the alternative pathway alone and in systemic lupus erythematosus (SLE) both the classical and alternative pathways were involved. Only one of the seven cases of membranous glomerulonephritis fixed complement and this was by the classical pathway. After prior treatment with C3b inactivator, the in vitro complement fixation in mesangial IgA disease, HSP and MCGN was greatly reduced. In SLE it was slightly reduced and in membranous glomerulonephritis there was no change. This is a convenient method of studying the biological properties of complexes which is believed to reflect the in vivo behaviour of the tissue deposited complex.