Wound healing is a complex pathway of regulated reactions and cellular infiltrates. The mechanisms at play have been thoroughly studied but there is much still to learn. The health care system in the USA alone spends on average 9 billion dollars annually on treating of wounds. To help reduce patient morbidity and mortality related to abnormal or prolonged skin healing, an updated review and understanding of wound healing is essential. Recent works have helped shape the multistep process in wound healing and introduced various growth factors that can augment this process. The complement cascade has been shown to have a role in inflammation and has only recently been shown to augment wound healing. In this review, we have outlined the biology of wound healing and discussed the use of growth factors and the role of complements in this intricate pathway.
Background-Coronary artery disease is a significant risk factor for atrial fibrillation (AF), but the basis for this association is incompletely understood. The present study evaluated the hypothesis that atrial ischemia can create a substrate for AF maintenance. Methods and Results-Atrial ischemia was induced by occlusion of an atrial arterial branch that did not provide blood flow to the ventricles. Atrial-arterial occlusion increased the duration of AF induced by burst pacing from 57Ϯ32 seconds (control) to 803Ϯ214 seconds (PϽ0.001) after 0.5 hour of occlusion and to 887Ϯ209 seconds (PϽ0.001) after 3 hours of occlusion. Prolonged AF (Ͼ20 minutes) was induced in 0 of 16 dogs (0%) under control conditions, 7 of 16 (44%, PϽ0.01) at 0.5 to 3 hours, and 5 of 13 (38%, PϽ0.01) 3 to 5 hours after occlusion. Atrial conduction was slowed substantially within the ischemic zone: eg, conduction delay was 8Ϯ1 ms at a cycle length of 200 ms, control, versus 22Ϯ5 ms (PϽ0.01) after 0.5 hours and 27Ϯ5 ms (PϽ0.001) after 3 hours of ischemia. Refractoriness was initially unaffected but was prolonged 5 hours after occlusion. Phase-delay analysis and high-density mapping confirmed severe conduction slowing in the ischemic zone. Histological examination confirmed the location of ischemic regions and revealed extensive ischemia-induced necrosis at sites of conduction delay. Conclusions-Experimental atrial ischemia creates a substrate for AF maintenance, apparently by causing local conduction slowing that promotes reentry. These results suggest that atrial ischemia may significantly promote AF, and may be relevant to AF mechanisms in association with coronary artery disease.
A high degree of clinical suspicion must be exercised to diagnose this rare condition. Cellulitis with an atypical presentation or not responding to appropriate antibiotic treatment should trigger suspicion of Wells' syndrome. To date, the most successful treatment method is a short course of systemic corticosteroids.
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