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Neonatal pneumonia is a high neonatal mortality disease. The current research was designed to elucidate the modulatory function and feasible molecular mechanism of UCA1 in LPS‐induced injury in pneumonia. Herein, LPS was applied to induce WI‐38 cell inflammatory damage. We displayed that UCA1 was elevated in LPS‐injured WI‐38 cells. In the functional aspect, intervention of UCA1 evidently aggrandized...
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