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Employing gene editing techniques alongside both in vivo and in vitro experiments, we provide novel evidence that the dysfunction of SLC25A39-mediated mitochondrial import of GSH constitutes a pathological alteration following TBI, leading to mitochondrial dysfunction and subsequent initiation of oxidative stress and neuronal cell death

Increase of circulating Cxcl9 and Cxcl11 associated with euthyroid or subclinically hypothyroid autoimmune thyroiditis

All siRNAs were purchased from GenePharma (Shanghai, China)

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