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The mechanisms by which inflammation affects tight junction structure and function and transcellular mechanisms such as endocytosis are largely unknown, although reproducible correlations have been observed between the severity of experimental and clinical disease and on the one hand and transepithelial electrical resistance, transport of paracellular markers, and systemic LPS concentrations and on the other [42, 86]
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Endogenous hydrogen sulfide and ERK1/2-STAT3 signaling pathway may participate in the association between homocysteine and hypertension
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