Transfers of the Ipsilateral C7 Plus the Spinal Accessory Nerve Versus Triple Nerve Transfers for Treatment of C5-C6 Avulsion of the Brachial Plexus.

PURPOSE: To compare the long-term results of transfers of the ipsilateral C7 (IC7) plus spinal accessory nerve (SAN) with those of triple nerve transfers (TNT) using one fascicle of the ulnar nerve to the biceps motor branch (Oberlin's procedure), SAN transferred to the suprascapular nerve, and transfer of the long head of triceps nerve branch to the anterior branch of axillary nerve to treat C5-C6 avulsion of the brachial plexus. METHODS: The IC7 group included 9 patients undergoing transfers of IC7 to the upper trunk and SAN to the suprascapular nerve. Median age at surgery was 26 years and interval between injury and surgery was 2.8 months. Patients were observed for a median of 118 months. The TNT group contained 13 patients, median age 33 years; interval between injury and surgery was 3.1 months. Patients were observed for a median of 103 months. RESULTS: In the IC7 group, median shoulder abduction was 105° and median external rotation of the shoulder was 64°, which was similar to that of the TNT group (89° abduction and 58° external rotation). Eight of nine patients recovered at least M3 (Modified Narakas scale) strength of deltoid in the IC7 group, which was similar to that in the TNT group (11 of 13 patients). Six of nine patients achieved at least Medical Research Council grade 3 (MRC3) strength of biceps in the IC7 group, which was similar to that in the TNT group (11 of 13 patients). Of 4 patients in the IC7 group with a preoperative latissimus dorsi strength of MRC3 or less, 3 gained a deltoid strength of M3 or less, and 3 a biceps strength of MRC2 or less. CONCLUSIONS: Transfers of IC7 plus SAN provide results comparable to those of TNT for treatment of C5-C6 avulsion. TYPE OF STUDY/LEVEL OF EVIDENCE: Therapeutic IV.

MicroRNA-27a alleviates IL-1ß-induced inflammatory response and articular cartilage degradation via TLR4/NF-κB signaling pathway in articular chondrocytes.

Osteoarthritis (OA) is a common disease of the articular cartilage, and inflammatory response and articular cartilage degradation have been implicated in the pathogenesis of OA. In recent years, microRNAs (miRNAs) have been potentially involved in the pathogenesis of OA. However, little is known about the role of miRNAs in the inflammatory response and articular cartilage degradation in OA and the underlying molecular mechanism. In the present study, we analyze miRNA profiles in the articular tissues from OA patients using microarray. miR-27a has attracted considerable interest for its suppressive effects on inflammation. Subsequently, the expression levels of miR-27a were validated in the articular tissues of OA patients and IL-1ß-stimulated chondrocytes. Using this IL-1ß-induced chondrocyte injury model, we found that upregulation of miR-27a suppressed articular cartilage degradation, the reactive oxygen species (ROS) production and inflammatory response as reflected by reductions in pro-inflammatory cytokines, including interleukin (IL)-6 and IL-8 and tumor necrosis factor (TNF)-α. Moreover, toll-like receptor 4 (TLR4), one upstream molecule of NF-κB signaling pathway, was identified as a direct target of miR-27a in chondrocytes. Furthermore, it was demonstrated that overexpression of TLR4 by pcDNA-TLR4 markedly abrogated the inhibitory effects of miR-27a on the inflammatory response and the degeneration of articular cartilage induced by IL-1ß. Our findings suggest that miR-27a may be considered as a potential therapeutic target in the treatment of OA.

Involvement of Notch1/Hes signaling pathway in ankylosing spondylitis.

We aimed to investigate the role of Notch1/Hes signaling pathway in the pathogenesis of abnormal ossification of hip ligament in patients with ankylosing spondylitis (AS). 22 AS patients scheduled for artificial hip arthroplasty were randomly chosen as AS group. As controls, we used 4 patients diagnosed with transcervical fracture who underwent hip replacement surgery. Notch1 and Hes mRNA expressions were detected by real-time fluorescent quantitative polymerase chain reaction (RFQ-PCR). Immunohistochemistry (IHC) was used to detect Notch1 and Hes protein expression. Correlation analyses of Notch-l and Hes with AS-related clinical factors were conducted with spearman's correlation analysis and partial correlation analysis. RFQ-PCR results showed significant differences in Notch1 and Hes mRNA expressions between AS group and the control group (all P<0.05). IHC analysis further indicated positive nuclear signals of Notch1 and Hes protein, indicating functional activation of the Notch1 and Hes pathways. Semi-quantitative IHC showed a higher Notch1 and Hes expression levels in AS group compared to the control group (all P<0.05). Correlation analysis suggested that Hes protein expression was positively associated with the clinical course of the disease in AS patients. In conclusion, Notch1 and Hes overexpression was clearly detected in hip joint ligaments of AS patients, Hes protein expression was associated with the clinical course of AS. Taken together, we suggest that signaling pathways mediated by Notch1-Hes may contribute to ligament ossification of hip joints in AS patients.