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As Dr. Devinsky noted, seizures in turn may produce further inflammation, perpetuating the cycle.
Recurrences are common, and with each recurrence there is danger that the virus will extend deeper into the cornea and cause further inflammation and scarring, with eventual vision impairment.
Thus, adjacent spinous processes come in contact and during repetitive shearing movements there is further inflammation of an adventitious bursa present in the interspinous space [8, 11, 12].
The results indicate that HA coated carbon matrices provide a suitable environment to enhance in-growth of corneal cells without inducing further inflammation.
In fact, initial calcium deposition in response to pro-inflammatory stimuli results in the formation of spotty or granular calcification ("microcalcification"), which induces further inflammation.
Disruption of the endothelial-glycocalyx barrier exposes endothelial cell surface adhesion molecules that trigger the activation of mast cells, and the adhesion of platelets and white blood cells, thereby causing further inflammation [72] and nitric oxide production [73].
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However, the inflammatory response can also compromise healthy tissue, further exacerbating inflammation [11], [13].
Both cytokines increased the mRNA level of CCL2 and MMP3, which may further promote inflammation in WAT.
Parallel batches of H441 cells were treated simultaneously with 10 ng/ml TNFα to further stimulate inflammation.
Chemokine and cytokine activity further promote inflammation.
Th1 cells mediate cellular immunity and further regulate inflammation responses.
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