Negative pressure wound therapy inhibits inflammation and upregulates activating transcription factor-3 and downregulates nuclear factor-κB in diabetic patients with foot ulcerations.

BACKGROUND: Negative pressure wound therapy (NPWT) is one of the most important treatments for diabetic foot, but the underlying mechanisms of its benefits still remain elusive. This study aims to evaluate the inflammatory signals involved in the effects of negative pressure therapy on diabetic foot ulcers. METHODS: We enrolled 22 patients with diabetic foot ulceration, 11 treated with NPWT and the other 11 treated with traditional debridement. All patients were treated and observed for 1 week. Granulation tissues were harvested and analyzed in both groups, and then were histologically and immunohistochemically analyzed. Enzyme-linked immunosorbent assay, Western blot analysis, and real-time PCR were performed to evaluate the expression of interleukin-6 (IL-6), tumor necrosis factor α (TNF-α), inducible nitric oxide synthase (iNOS), nuclear factor-κB (NF-κB) p65, Ik B-α, and activating transcription factor-3 (ATF-3). RESULTS: After 7 days of treatment, NPWT could obviously promote diabetic wound healing because of the mild inflammation and the dense cell-deposited matrix. Meanwhile, NPWT significantly decreased the expression of TNF-α, IL-6, and iNOS (all P < .05). The result of Western blotting and real-time PCR indicated that NPWT obviously decreased the level of Ik B-α and NF-κB p65, and increased the level of ATF-3 (all P < .05). CONCLUSION: NPWT exerts an anti-inflammatory effect, possibly through the suppression of proinflammatory enzymes and cytokines resulting from Ik B-α inhibition and ATF-3 activation, which may prevent the activation of the NF-κB pathway in human diabetic foot wounds.

[Urine-Cr assay with diphenylcarbazide].

Systemic investigations of chromium determination in urine with diphenylcarbazide were carried out and suitable analytic conditions for the determination established. Urine samples were first digested with nitric acid-hydrogen peroxide and then the chromium in the sample was oxidized to the hexavalent state by permanganate in acidic medium. After the excess oxidizing reagent was destroyed with sodium nitrite, chromium (VI) combined with diphenylcarbazide, forming a stable red color. The average recovery was 101.1%, ranging from 82.0% to 115.8%. Coefficients of variation were in the range from 2.0% to 8.4%. The method can be conveniently applied to the analysis of trace chromium in urine samples with satisfactory sensitivity and recovery. The method was applied to the measurement of 180 normal and 124 CHD (coronary heart disease) urine samples from Chengdu city. The mean of chromium level in normal urine was 6.1 micrograms/L and the range with 95% confidence of urine chromium was determined as 1.7-11 micrograms/L. The mean of chromium level in CHD urine samples was 4.2 micrograms/L. By statistical analysis, there was a significant difference between the means of the two groups (t' = 6.9, P less than 0.05).

[Serum lipids and apolipoproteins AI, B100, CI, CII, and CIII in 142 patients with coronary heart disease].

Serum triglycerides (TG), cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and apolipoproteins AI, B100, CI, CII and CIII were analyzed in 142 patients with coronary heart disease (CHD) and 64 age-matched healthy subjects in the Chengdu area. Significantly increased TG and decreased HDL-C were found in the CHD patients (P less than 0.001). Serum apo AI and CII were significantly decreased in the CHD patients compared with the normal subjects (P less than 0.01 or P less than 0.001). Serum apo B100 and CIII were slightly higher in the CHD group than in the normal group (P less than 0.001 or P less than 0.05). No significant differences were observed in apo CI levels in the CHD patients when compared with the normal subjects. The results were discussed.