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Based on our current findings, we suggest that ROS/RNS initiate and sustain the arthrofibrotic response driving aggressive fibroblast proliferation and subsequent HO.
Established risk factors include male gender, diffuse idiopathic skeletal hyperostosis (DISH), ankylosing spondylitis, previous THA and subsequent HO formation, rheumatoid arthritis, osteonecrosis and previous trauma to the hip [ 8, 9].
Systemic blast exposure and contamination of the open wounds with both local and hospital-acquired micro-organisms is ubiquitous in combat-wounded patients, and likely play a vital role in inflammation and subsequent HO formation in these patients.
Recent research investigating the effect of inflammation and local ischaemia on stem cell manipulation and subsequent HO formation has proposed the possibility that HO formation is likely to be stimulated by local and systemic factors contributing to the pathological picture [ 1, 11– 16].
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These data together indicate that Src is the critical protein kinase that is responsible for mediating the induced activation of STAT3 and the subsequent HO-1-dependent autophagy in the DOX-treated MDA-MB-231 cells.
"Fast Eddie!" Ho ho ho.
Ho, ho, ho.
Ho ho ho, readers.
"Ho, ho, ho!" Gingrich exclaimed.
"Ho, ho, ho," went Santa.
Ho ho ho! Happy Holidays!
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