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However, overexpression of GM130 in HSV-1 infected Bend.3 cells by transient transfection partially attenuated the aforementioned damage caused by HSV-1 infection. When the pan-caspase inhibitor Z-VAD-fmk was used after HSV-1 infection to inhibit apoptosis, the protein levels of GM130, occludin and claudin 5 were partially restored. Taken together, these observations indicate that HSV-1 infection of Bend.3 cells triggers a GM130-mediated Golgi stress response that is involved in apoptosis, which in turn results in downregulatio

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and delayed ACL reconstruction ranged from 57% to 100%. Delaying ACL reconstruction in pediatric or adolescent patients for 12 weeks significantly increased the risk of meniscal injuries and irreparable meniscal tears; however, early and delayed operative treatment achieved satisfactory knee stability. Nonoperative management resulted in high rates of residual knee instability, increased risk of meniscal tears, and comparatively low rates of return to sports. 12 weeks significantly increased the risk of meniscal injuries and irrepar