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Compared with wild-type mice, mAChR4 GC mice had fewer small intestinal GAPs, leading to an impaired small intestinal immune response, with reduced expression of CD11b and CD11c

Instead of accurately interpreting sensory input, pain-processing circuits become hyperresponsiveturning normal movement, pressure, or minor inflammation into persistent pain

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However, inspection of the staining pattern revealed that both mutants were in fact defective for formation of biofilm at the air-liquid interface (which is not LCA-regulated), forming a thinner ring than the parent strain (Fig