[Progress on tendon-to-bone healing after rotator cuff repair].

Rotator cuff tear is a common disease that causes shoulder pain and limitation of activity. Rotator cuff repair with arthroscope has become the mainstream method with advance in surgical techniques. In spite of this, the highly rate of retear after surgery mainly because the tendon to bone interface form scar tissue rather than native tissue. Biomechanical of the interface is so poor to retear because of the change of Histological. In recent years, more and more researchers are devoted to the study of biology and biomechanical for improving the process of tendon to bone healing and restoring the original structure at the interface, This article reviews the research progress with four factors(inflammation, slow or limited bone ingrowth into the tendon graft, Mechanical stimulation, scant stem cell) and physiotherapy that affect tendon to bone healing.

Effects of paclitaxel on proliferation and apoptosis in human acute myeloid leukemia HL-60 cells.

AIM: To investigate the regulatory effect of paclitaxel on proliferation and apoptosis in human acute leukemia HL-60 cells. METHODS: HL-60 cell growth was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tertrazolium bromide (MTT) colorimetric assay. Cell cycle kinetics and apoptosis were analyzed by flow cytometry and microscopic examination. In addition, DNA microarrays containing 14,400 EST elements were used to investigate the gene expression pattern of HL-60 cells exposed to paclitaxel 1 micromol/L. RESULTS: Paclitaxel inhibited HL-60 cell growth significantly in a dose-dependent and time-dependent manner (P<0.01). Marked cell accumulation in G2/M phase and multinucleated cells were also observed after treatment with paclitaxel 0.1 and 1 micromol/L. Among 14400 EST elements, 277 genes were found to be markedly up- or down-expressed in the HL-60 cells treated with paclitaxel 1 micromol/L for 0.5 h, comprising 210 known genes and 67 unknown genes. CONCLUSION: Paclitaxel suppresses the growth of HL-60 cells in vitro by causing cell-cycle arrest and apoptosis. The results of microarray suggest that paclitaxel initiates apoptosis through multiple mechanisms.