{'fraction_non_alphanumeric': 0.023059185242121444, 'fraction_numerical': 0.009223674096848577, 'mean_word_length': 5.259615384615385, '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}}
Inhibition of Epidermal Growth Factor Receptor by Erlotinib: Wound Healing of Experimental Tympanic Membrane Perforations

Hypothesis: Inhibition of epidermal growth factor receptor (EGFR) may arrest wound healing of experimental tympanic membrane perforation in rats. Background: An animal model of chronic tympanic membrane perforation is needed for experiments on supporting wound healing of tympanic membrane perforations. The EGFR has been implicated in the regulation of wound healing. Methods: Thirty animals were administered 80 or 40 mg/kg/d EGFR tyrosine kinase inhibitor, or vehicle only for 5 days. The right-sided tympanic membrane of each animal was perforated at Day 2. Rat ears were inspected repeatedly to analyze the status of perforation. Tympanic membranes were examined histologically. Results: Unfortunately, five animals in the 80-mg/kg group and four in the 40-mg/kg group died before they reached their scheduled endpoint. Taking into account the small sample sizes, we observed a delayed closure of perforations in the 80-mg/kg group and differences in the histologic parameters between treated groups and control group. Conclusion: The inhibition of EGFR by systemic application of erlotinib seems not to be suitable to create a chronic tympanic membrane perforation in rat.