【Abstract】 Objective To study the outcome of wound-heal ing hydrogel in treating chronic venous ulcer of lowerextremities so as to find a new therapy. Methods From April 2007 to September 2007, 60 patients with chronic venous ulcer of lower extremities were randomly assigned to wound-heal ing hydrogel group (group A, 30 cases) and control group (normal sal ine, group B, 30 cases). In group A, there were 24 males and 6 females, aging (57.3 ± 6.8) years; the disease course was (2.9 ± 0.7) years; and the ulcer area was (3.4 ± 0.6) cm2. In group B, there were 20 males and 10 females, aging (60.1 ± 7.4) years; the disease course was (3.3 ± 0.9) years; and the ulcer area was (3.1 ± 0.4) cm2. There were no differences in age, area of ulcer and course of disease between two groups (P gt; 0.05). The area of ulcer was measured every week after the treatment, and the effect of treatmentwas evaluated after 15 days. Results The ulcer area of 7 days and 14 days after treatment was (2.6 ± 0.7) and (1.1 ± 0.2) cm2 in group A, and (2.8 ± 0.6) and (2.3 ± 0.7) cm2 in group B, respectively; showing no statistically significant differences 7 days after treatment (P gt; 0.05), and showing statistically significant difference 14 days after treatment between two groups (P lt; 0.05).The average heal ing time was (12.0 ± 1.7) days in group A, and (31.0 ± 2.9) days in group B, respectively, showing statisticallysignificant difference (P lt; 0.01). The results were excellent, good, fair and poor in 16, 9, 4 and 1 of group A , and were in 3, 9, 14 and 4 of group B, respectively; showing statistically significant difference (P lt; 0.01). Conclusion Wound-heal ing hydrogel is effective in treating chronic venous ulcer of lower extremities.
Ischemic stroke (IS) is one of the important diseases threatening human health. The occurrence and development of IS can trigger a series of complex pathophysiological changes, including damage to the blood-brain barrier, ion imbalance, oxidative stress, mitochondrial damage, which ultimately lead to the apoptosis and necrosis of nerve cells in the ischemic area. Impaired blood-brain barrier is a key factor for cerebral edema, hemorrhagic transformation and poor prognosis in patients with IS, and neuroinflammatory response plays an important role in the damage and repair of the blood-brain barrier. This article mainly focuses on the neuroinflammatory response mediated by glial cells, pro-inflammatory cytokines and matrix metalloproteinases and the related mechanisms of IS blood-brain barrier damage and repair, in order to provide new directions for the treatment of IS.