Objective: Although nearly half of preterm survivors display persistent neurobehavioral dysfunction including memory impairment without overt gray matter injury, the underlying mechanisms of neuronal or glial dysfunction, and their relationship to commonly observed cerebral white matter injury are unclear. We developed a mouse model to test the hypothesis that mild hypoxia during preterm equivalence is sufficient to persistently disrupt hippocampal neuronal maturation related to adult cellular mechanisms of learning and memory. Methods: Neonatal (P2) mice were exposed to mild hypoxia (8%O ) for 30 min and evaluated for acute injury responses or survived until adulthood for assessment of learning and memory and hippocampal neurodevelopment.
View Article and Find Full Text PDFIntroduction: Erlotinib, a tyrosine kinase inhibitor, has improved survival and quality of life in patients with non-small cell lung cancer (NSCLC) after first- or second-line chemotherapy. Asian origin, adenocarcinoma histology, female gender, lack of tobacco use, and expression of epidermal growth factor receptor are significant independent predictors of response to Erlotinib. Although tobacco use is considered a major cause of NSCLC, other risk factors such as wood-smoke exposure (WSE) are associated.
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