{'fraction_non_alphanumeric': 0.03148854961832061, 'fraction_numerical': 0.01049618320610687, 'mean_word_length': 5.319277108433735, '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}}
Cytokines, mesangial cell activation and glomerular injury.

The mesangial cell occupies a central anatomical pos1t1on within the glomerulus [l, 2]. Historically this cell has been regarded as unifunctional, only being important in the regulation of glomerular filtration rate. However, in vitro and in vivo evidence suggests that the mesangial cell both produces and responds to biological modifiers to participate in the destructive and restorative processes that follow the initiation of glomerular injury [I, 2]. Intraglomerular expression of the cytokines, IL-1 and tumor necrosis factor-a: (TNF), has been demonstrated in both human and experimental glomerulonephritis [3, 4]. IL-I and TNF activate the mesangial cell in culture to express new structural and functional characteristics in part by inducing expression of specific genes [3, 4]. The data describing the effects of these cytokines on mesangial cells and their production by injured glomeruli have recently been summarized [3-5] and will not be discussed in detail in this review.