Salinity and alkalinity are the two main environmental factors that limit rice production. Better understanding of the mechanisms responsible for salinity and alkaline stress tolerance would allow researchers to modify rice to increase its resistance to salinity and alkaline stress. MicroRNAs (miRNAs) are ~21-nucleotide RNAs that are ubiquitous regulators of gene expression in eukaryotic organisms. Some miRNAs acts as an important endogenous regulator in plant responses to abiotic stressors. miR393 is a conservative miRNA family that occurs in a variety of different plants. The two members of the miR393 family found in rice are named osa-MIR393 and osa-MIR393b. We found that the osa-MIR393 expression level changed under salinity and alkaline stress, whereas that of osa-MIR393b did not. Target genes of osa-MIR393 were predicted, and some of these putative targets are abiotic related genes. Furthermore, we generated transgenic rice and Arabidopsis thaliana that over-expressed osa-MIR393, and the phenotype analysis showed that these transgenic plants were more sensitive to salt and alkali treatment compared to wild-type plants. These results illustrate that over-expression of osa-MIR393 can negatively regulate rice salt-alkali stress tolerance.

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Background The current standard of care for cervical myopathy is anterior discectomy and fusion (ACDF). Although well tolerated in the short term, this treatment might ultimately result in progressive degeneration of adjacent motion segments. Artificial disc arthroplasty offers the theoretical advantage of preservation of motion at the operative level with consequent stress reduction at adjacent levels. Questions/purposes We compared function, radiographic measures, and incidence of complications at 3-year followup after cervical disc arthroplasty with the Bryan

Mobi-C implant surgery is a safe alternative to ACDF surgery in cervical disc degeneration. Cite this article: Bone Joint J 2016;98-B:829-3.

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Background Osteoarthritis (OA) is a common degenerative disease, and tumor necrosis factor (TNF-α) is known to play a critical role in OA. Cortistatin (CST) is a neuropeptide discovered over 20  years ago, which plays a vital role in inflammatory reactions. However, it is unknown whether CST is involved in cartilage degeneration and OA development. Methods The interaction between CST and TNF-α receptors was investigated through Coimmunoprecipitation and Biotin-based solid-phase binding assay. Western blot, Real-time PCR, ELISA, immunofluorescence staining, nitrite production assay and DMMB assay of GAG were performed for the primary chondrocyte experiments. Surgically induced and spontaneous OA models were established and western blot, flow cytometry, Real-time PCR, ELISA, immunohistochemistry and fluorescence in vivo imaging were performed for in vivo experiments. Findings CST competitively bound to TNFR1 as well as TNFR2. CST suppressed proinflammatory function of TNF-α. Both spontaneous and surgically induced OA models indicated that deficiency of CST led to an accelerated OA-like phenotype, while exogenous CST attenuated OA development in vivo. Additionally, TNFR1- and TNFR2-knockout mice were used for analysis and indicated that TNFRs might be involved in the protective role of CST in OA. CST inhibited activation of the NF-κB signaling pathway in OA. Interpretation This study provides new insight into the pathogenesis and therapeutic strategy of cartilage degenerative diseases, including OA. Fund The , the , .

Musculoskeletal pain is a major cause of human suffering worldwide, with a prevalence between 13.7% and 47% among the global population (Bergman et al., 2001; Cimmino, Ferrone, & Cutolo, 2011). Myofascial pain syndrome (MPS) is one of the most common types of musculoskeletal pain. The presence of myofascial trigger points (MTrPs) is necessary for

Objective Boswellic acid is a plant-derived molecule with putative anti-inflammatory effects. This study was performed to determine whether oral or topical administration of boswellic acid can attenuate joint damage in a mouse model of osteoarthritis (OA). Methods Levels of boswellic acid were measured in the blood and synovium of mice treated with oral or topical boswellic acid. OA was generated by surgical destabilization of the medial meniscus (DMM). Therapy with oral or topical boswellic acid was initiated one day after surgery and continued for 12 weeks, when knees were harvested and scored histologically for degree of cartilage loss, osteophyte formation, and synovitis. Microdissected OA synovium was stimulated with IL-1β or lipopolysaccharide (LPS) in the presence or absence of boswellic acid and cytokine production by quantitative polymerase chain reaction (PCR) or multiplex enzyme linked immunoabsorbant assay (ELISA). Results Topical treatment resulted in synovial concentrations of boswellic acid 2–6-fold higher than that measured in plasma. Cartilage loss was significantly reduced in mice treated with oral or topical boswellic acid compared with vehicle control (P < 0.01 for both oral and topical therapies). Likewise, treatment with either oral boswellic acid or boswellic acid ointment reduced of synovitis (P = 0.006 and 0.025, respectively) and osteophyte formation (P = 0.009 and 0.030, respectively). In vitro, boswellic acid was able to inhibit IL-1β and TLR4 mediated induction of several inflammatory mediators from OA synovial explant tissue. Conclusions Significant synovial concentration and therapeutic efficacy can be achieved with topical boswellic acid treatment. These findings suggest that boswellic acid has potential as a disease-modifying agent in OA.