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TNF-aTumor Necrosis Factor alpha
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Meso scale discovery (MSD) system (MSD, Rockville, MD, USA)[sup][12] was used to measure the concentrations of proinflammatory cytokines and chemokines for IL-1[sz], IL-6, IL-17, IL-18, TNF-a, CXCL8, CXCL10, CCL2, CCL4, CCL11, CCL13, CCL17, CCL22, and CCL26 using a commercial kit (K15054G-2).
Results: The results showed highly significant decrease in urinary TNF-a and caspase 3 enzyme (P values < 0.
Considering the cold chain process, all samples were then taken to the Bio-chemistry Lab at ZaUMS to measure the serum levels of leptin, ghrelin and TNF-a.
They further said that factors that stimulate osteoclast formation were regulated by both TNF-a and a downstream mediator, FOXO1.
Interestingly, TNF-a effects have been suggested to be partly mediated by oxidative stress and cardiac mitochondrial dysfunction.
Although TNF-a inhibitors have become a mainstay of AS treatment, they are not often the first-line treatment.
sup][7] Matrix metalloproteinase-9 (MMP-9), one of effector molecules of TNF-a signaling, plays an important role in the pathogenesis of elastin breakdown.
That is good news for the PsA patients who fail to respond to TNF-a inhibitors; treatment options are limited for these patients.
In the United Kingdom, TNF-a inhibitors are prescribed in hospitals, and physicians must apply to local PCT directorates to prescribe these drugs to new patients.
The overproduction of TNF-a has the effect of promoting greater viral replication in AIDS patients and therefore we expect that its removal would decrease viral load and lead to clinical improvement.