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In this case, persistent HPA-axis activation, together with PD-1mediated lowering of immune tolerance and postoperative inflammation, may have created a second-hit state that further reduced the threshold for immune activation and facilitated moxifloxacin-induced T-cell cytotoxicity

Consequently, BCAAs metabolic disturbances in T1DM patients may represent a pathophysiological mechanism underlying the observed pulmonary functional alterations

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