{'fraction_non_alphanumeric': 0.02664796633941094, 'fraction_numerical': 0.002805049088359046, 'mean_word_length': 6.0, '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}}
Glucose control with insulin results in reduction of NF‐κB‐binding activity in mononuclear blood cells of patients with recently manifested type 1 diabetes

Aim:  Chronic elevated blood glucose levels are associated with the formation of advanced glycation endproducts (AGEs). Hyperglycaemia and AGEs have been shown to induce activation of the redox‐sensitive transcription factor nuclear factor‐κB (NF‐κB). To validate the hypothesis that the maintenance of normal glucose levels results in the reduction of NF‐κB‐binding activity in vivo, the redox‐sensitive transcription factor NF‐κB was used as marker of hyperglycaemia‐induced mononuclear cell activation in patients who recently developed type 1 diabetes.