Objective To explore the treatment methods for brachial artery trauma associated with humeral super-middle fracture.Methods Thirty-two patients of brachial artery trauma associated with humeral super-middle fracture were treated in our department from March 2001 to April 2005 with in tramedallary expanded self-locking nail (IESN) combined with autotransplantation of great saphenous vein to repair brachial artery.Results All patients were followed up for 12 to 18 months,13.6 months on the average.No stenosis occurred at the anastomosed veins according to color Doppler ultrasound.All fractures achieyed clinical healing and the limbs survived well.Conclusion The IESN combined with autotransplantation of great saphenous vein to repair brachial artery is an effective method to treat brachial artery traumaassociated with humeral super-middle fracture,having the advantage of reasonable operation procedure.stabile immobilization and satisfactory functional recovery.

The high- and the low-molecular weight hyaluronic acids (HMW-HA and LMW-HA, respectively) showed different biological activities in inflammation. However, the role of LMW-HA in inflammatory response is controversial. In this study, we aimed to investigate the effect of bioactive hyaluronan (B-HA) on lipopolysaccharide (LPS)-induced inflammatory responses in human macrophages and mice. B-HA was produced from HA treated with glycosylated recombinant human hyaluronidase PH20. Human THP-1 cells were induced to differentiate into macrophages. THP-1-derived macrophages were treated with B-HA, LPS, or B-HA + LPS. The mRNA expression and the production of inflammatory cytokines were determined using quantitative real-time PCR and enzyme-linked immunosorbent assay. The phosphorylation levels of proteins in the nuclear factor-κB (NF-κB), mitogen-activated protein kinase (MAPK), and IRF-3 signaling pathways were measured using Western blot. The in vivo efficacy of B-HA was assessed in a mouse model of LPS-induced inflammation. Results showed that B-HA inhibited the expression of TNF-α, IL-6, IL-1, and IFN-β, and enhanced the expression of the antiinflammatory cytokine IL-10 in LPS-induced inflammatory responses in THP-1-derived macrophages and in vivo. B-HA significantly suppressed the phosphorylation of the TLR4 signaling pathway proteins p65, IKKα/β, IκBα, JNK1/2, ERK1/2, p38, and IRF-3. In conclusion, our results demonstrated that the B-HA attenuated the LPS-stimulated inflammatory response by inhibiting the activation of the TLR4 signaling pathway. B-HA could be a potential anti-inflammatory drug in the treatment of inflammatory disease.
Animals ; Cytokines ; Hyaluronic Acid ; Lipopolysaccharides ; Mice ; NF-kappa B/metabolism* ; Signal Transduction ; Toll-Like Receptor 4