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Objective By observing the needle-knife of KOA rabbit morphology, knee joint cartilage p-FAK, p-PI3K, Aggrecan gene, and protein expression, to study the effect of needle-knife to promote cartilage cell synthesis metabolism mechanism. Method 49 male New Zealand rabbits, randomly divided into normal group (Z), model group (M), model-inhibitors (MP), needle-knife group (D), needle-knife inhibitors group (DP), electroacupuncture group (E), and electroacupuncture inhibitors (EP). RT-PCR and Western Blot were used to test each animal cartilage p-FAK, p-PI3K, and Aggrecan gene and protein expression level. Results Compared with N group, p-FAK and p-PI3K protein and mRNA expression of M group, D group, and E group increased (P < 0.05), while the protein and mRNA expression of Aggrecan reduced (P < 0.05). Compared with M group, p-FAK, p-PI3K, Aggrecan protein, and mRNA of E and D group increased (P < 0.05). Compared with E group, p-FAK, p-PI3K, Aggrecan protein, and mRNA expression of D group increased (P < 0.05); after adding inhibitors, p-FAK, p-PI3K, Aggrecan protein, and mRNA expression reduced (P < 0.05). Conclusion Needle-knife therapy can promote the repairment of cartilage cells by activating FAK-PI3K signaling pathways, promoting the synthesis of cartilage cell metabolism.

The transcription factors TBX2 and TBX3 are overexpressed in various human cancers. Here, we investigated the effect of overexpressing the orthologous Tbx genes Drosophila optomotor-blind (omb) and human TBX2 in the epithelium of the Drosophila wing imaginal disc and observed two types of cell motility. Omb/TBX2 overexpressing cells could move within the plane of the epithelium. Invasive cells migrated long-distance as single cells retaining or regaining normal cell shape and apico-basal polarity in spite of attenuated apical DE-cadherin concentration. Inappropriate levels of DE-cadherin were sufficient to drive cell migration in the wing disc epithelium. Omb/TBX2 overexpression and reduced DE-cadherin-dependent adhesion caused the formation of actin-rich lateral cell protrusions. Omb/TBX2 overexpressing cells could also delaminate basally, penetratingthe basal lamina, however, without degradation of extracellular matrix. Expression of Timp, an inhibitor of matrix metalloproteases, blocked neither intraepithelial motility nor basal extrusion. Our results reveal an MMP-independent mechanism of cell invasion and suggest a conserved role of Tbx2-related proteins in cell invasion and metastasis-related processes.

Animal morphogenesis requires folds or clefts to separate populations of cells which are often associated with different cell affinities. In the Drosophila wing imaginal disc, the regional expression of the Iroquois complex (Iro-C) in the notum leads to the formation of the hinge/notum (H/N) fold that separates the wing hinge and notum territories. Although Decapentaplegic (Dpp) signaling has been revealed as essential for the hinge/notum subdivision through the restriction of Iro-C toward the notum region, the mechanism by which the H/N border develops into a fold is unknown. Here, we report that a Dpp target gene, optomotor-blind (omb), mediates the role of Dpp signaling in Iro-C inhibition. omb is complementarily expressed on the dorsal hinge side, abutting the Iro-C domain along the H/N border. Ectopic omb expression inhibits Iro-C in the notum territory, independent of known Iro-C regulators Msh and Stat92E. Uniform manipulation of either omb or Iro-C genes spanning the presumptive H/N border significantly suppresses H/N fold formation via inhibition of the apical microtubule enrichment. Ectopically sharp border or discontinuity in level of Iro-C or Omb is enough to generate ectopic fold formation. These results reveal that omb and Iro-C not only are complementarily expressed but also cooperate to promote H/N fold formation. Our data help to understand how Dpp signaling is interpreted region-specifically during tissue subdivision.

Actinidia kolomikta (Rupr. et Maxim.) Planch. The chemical structures of the isolated compounds were established by application of chemical and spectroscopic analysis. The new acetylated flavonoid was screened for its protective effect on human erythrocytes against AAPH-induced hemolysis, and it can slow the hemolysis induced by AAPH.