{'fraction_non_alphanumeric': 0.02541544477028348, 'fraction_numerical': 0.017595307917888565, 'mean_word_length': 5.2439024390243905, 'pattern_counts': {'":': 0, '<': 1, '<?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}}
ACTUAL INSPIRED OXYGEN CONCENTRATION AND OXYGEN SATURATION DURING PRETERM RESUSCITATION

300 ng, 600 ng, 1.2 ug intravenously) over 3 days. The duration of FBMs was assessed using LabChart. PGE2 expression in brainstem respiratory centres and cerebrospinal fluid (CSF) was assessed by immunohistochemistry and ELISA. Inflammation and cell death in the brainstem were assessed by qRT-PCR. OneWay/Two-Way ANOVA was used for statistical analysis. Results: LPS caused a significant reduction in FBMs, decreased oxygen saturation, increased blood lactate levels and caused mild acidosis (all P<0.05) on days 1 and 2 compared to the control group, however lambs became tolerant to the LPS on day 3. LPS increased PGE2 expression in brainstem neurons and CSF and increased inflammation and cell death. Conclusion: Acute exposure to LPS suppresses FBMs which coincides with increased PGE2 in brainstem neurons and CSF suggesting that brainstem inflammation may have a significant role in respiratory depression in preterm newborns.