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Although antitubulin drugs are used widely to treat human cancer, many patients display intrinsic or acquired drug resistance that imposes major obstacles to successful therapy. Mounting evidence argues that cancer cell apoptosis triggered by antitubulin drugs relies upon activation of the cell-cycle kinase Cdk1; however, mechanistic connections of this(More)
Antitubulin drugs are commonly used for the treatment of numerous cancers. However, either the intrinsic or acquired resistances of patients to these drugs result in the failure of the treatment and high mortality of cancers. Therefore, identifying genes or signalling pathways involved in antitubulin drug resistances is critical for future successful(More)
—Device-to-Device (D2D) communication underlaying cellular networks enhances system capacity through using spectrum resources of idle cellular users, which at the same time can act as relays to form cooperative D2D transmissions. On the other hand, network coding increases the efficiency of relay cooperation. In this letter, we investigate the random linear(More)
BACKGROUND The potential of secretory leukocyte protease inhibitor (SLPI) as a biomarker for colorectal cancer was studied. A prospective, randomized, controlled, clinical trial was conducted in 2013 and 2014 to confirm whether the expression of SLPI correlates with prognosis and metastasis in colorectal cancer patients. METHODS Immunohistochemistry was(More)
Crystal structure of Bacillus fastidious uricase reveals an unexpected folding of the C-terminus residues crucial for thermostability under physiological conditions " , Appl. Micriobiol. Proteasome inhibitors with pyrazole scaffolds from structure-based virtual screening " , Reaction pathway and free energy barrier for urea elimination in aqueous solution "(More)
Although antitubulin drugs are used widely to treat human cancer, many patients display intrinsic or acquired drug resistance that imposes major obstacles to successful therapy. Mounting evidence argues that cancer cell apoptosis triggered by antitubulin drugs relies upon activation of the cell-cycle kinase Cdk1; however, mechanistic connections of this(More)