Standard versus over-tensioning in the transfer of extensor indicis proprius to extensor pollicis longus for chronic rupture of the thumb extensor.

PURPOSE: The purpose of this study was to evaluate the functional outcomes of the over-tensioning technique compared with those of the standard tensioning technique in the transfer of extensor indicis proprius (EIP) to extensor pollicis longus (EPL) for the chronic rupture of the thumb extensor. METHODS: Data were collected from patients who underwent tendon transfer using EIP between March 2003 and August 2011. 23 were treated with the standard tensioning technique and 25 patients (Group B) with the over-tensioning technique. While standard tension was maintained with the thumb in full extension and the wrist in 30° of flexion, over-tension was maintained with the thumb in full extension and the wrist in the neutral position. All patients were assessed for total range of motion, elevation and flexion deficit, the thumb grip and pinch strength, and the thumb and the index extension strength compared to the unaffected side, EIP-EPL evaluation as suggested by Lemmen et al. and Disabilities of the Arm, Shoulder, and Hand questionnaire (DASH). RESULTS: Group A: total range of motion 115°, elevation deficit 2.0 cm, combined flexion deficit 1.0 cm, thumb extension strength 75%, thumb grip strength 91%, and pinch strength 87%. Functional outcomes were 13 excellent, 6 good, 3 fair, and 1 poor. Median DASH score was 21.3 points. Group B: total range of motion 125°, elevation deficit 1.0 cm, combined flexion deficit 1.5 cm, thumb extension strength 85%, thumb grip strength 88%, and pinch strength 83%. Functional outcomes were 16 excellent, 7 good, 2 fair, and 0 poor. Median DASH score was 19.8 points. There are significant differences in the range of motion, elevation deficit, and extension strength of thumb between the two groups (p=.001, p=.001, and p=.028, respectively). CONCLUSION: While the functional outcomes of both groups were favorably acceptable in a majority of the patients, there were significant differences in aspects of range of motion, elevation deficit, and strength of the thumb between both groups. LEVEL OF EVIDENCE: Case-control study, Level III.

Prevention of inflammation-mediated neurotoxicity by Rg3 and its role in microglial activation.

Considering the importance of inflammation and apoptosis in neurodegenerative conditions, the potential suppressive effects of the Rg3, a by-product obtained during the steaming of red ginseng, may indicate that Rg3 could provide a beneficial therapeutic approach to treating or preventing neurodegenerative disease. We investigated the effect of Rg3 on Abeta42-mediated microglial activation and inflammation-mediated neurotoxicity in murine BV-2 microglial and Neuro-2a neuroblastoma cells, respectively. Rg3 effectively reduced inflammatory cytokine expression in Abeta42-treated BV-2, and inhibited the binding of NF-kappaB p65 to its DNA consensus sequences, and significantly reduced the expression of TNF-alpha in activated microglia. Pretreatment with Rg3 increased the survival rate of Neuro-2a exposed to TNF-alpha. These observations suggest that Rg3 reduced neurotoxicity by inhibiting chronic inflammation through the suppression of activated microglia. In addition, the expression of pro-inflammatory cytokines in BV-2 stimulated by Abeta42 was decreased but not eliminated by Rg3 when binding to the macrophage scavenger receptor type A (MSRA) was blocked with fucoidan. This implies that the inflammatory response may not be exclusively triggered via MSRA. More interestingly, iNOS was almost completely inhibited in the presence of Rg3 when MSRA binding was blocked with fucoidan. Moreover, Rg3 increased the expression of MSRA in BV-2 transfected with siRNA targeting MSRA mRNA, and this increased MSRA expression may play a role in the phagocytosis of Abeta42 peptides. Our results indicate that inhibition of the inflammatory repertoire of microglia, neuroprotection, and increased MSRA expression induced by Rg3 may at least partly explain its therapeutic effects in chronic neurodegenerative diseases.

Artemisolide is a typical inhibitor of IkappaB kinase beta targeting cysteine-179 residue and down-regulates NF-kappaB-dependent TNF-alpha expression in LPS-activated macrophages.

Nuclear factor (NF)-kappaB regulates a central common signaling for immunity and cell survival. Artemisolide (ATM) was previously isolated as a NF-kappaB inhibitor from a plant of Artemisia asiatica. However, molecular basis of ATM on NF-kappaB activation remains to be defined. Here, we demonstrate that ATM is a typical inhibitor of IkappaB kinase beta (IKKbeta), resulting in inhibition of lipopolysaccharide (LPS)-induced NF-kappaB activation in RAW 264.7 macrophages. ATM inhibited the kinase activity of highly purified IKKbeta and also LPS-induced IKK activity in the cells. Moreover, the effect of ATM on IKKbeta activity was completely abolished by substitution of Cys-179 residue of IKKbeta to Ala residue, indicating direct targeting site of ATM. ATM could inhibit IkappaBalpha phosphorylation in LPS-activated RAW 264.7 cells and subsequently prevent NF-kappaB activation. Further, we demonstrate that ATM down-regulates NF-kappaB-dependent TNF-alpha expression. Taken together, this study provides a pharmacological potential of ATM in NF-kappaB-dependent inflammatory disorders.