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Objective To explore the anti corrosion ability of laser welded composite wire in artificial saliva con⁃ taining salivary amylase and pancreatic amylase, and to compare the effect of two kinds of amylase on corrosion resis⁃ tance of wire and its mechanism. Methods The corrosion resistance of composite wire was evaluated by electrochemi⁃ cal polarization and immersion test. The soluble corrosion products after 28 d immersion in artificial saliva were detect⁃ ed by plasma spectrometer. The surface morphology was analyzed by scanning electron microscope, energy spectrometer and atomic force microscope. Results Salivary amylase and pancreatic amylase could improve the corrosion resistance of the composite arch wire; the same isomerase would have different effects on the same alloy corrosion resistance. Con⁃ clusion When the new metal biological material is applied to the oral cavity, the amylase may have influence on its corrosion resistance.

To mimic the function of metallohydrolase, [M(bqad)Cl2] (M = Zn(II) (1), Co(II) (2), where bqad = N,N′-bis(2-quinolinylmethyl)amantadine), have been synthesized and characterized by elemental analysis, electronic absorption, IR, and single crystal X-ray diffraction. The structural analysis indicated that metal ions in1and2were coordinated by three nitrogens from bqad and two chlorides, resulting in a distorted trigonal bipyramidal geometry. Kinetic experiments for hydrolytic cleavage ofp-nitrophenyl acetate (pNA) catalyzed by1and2were performed at pH 7.50–10.00 and 298 K. The second-order rate constants (kobs) increased exponentially with variation of pH values. The Co(II) complex exhibited potent catalytic activity. [ABSTRACT FROM AUTHOR]

Cancer-induced bone pain can severely compromise the life quality of patients, while tolerance limits the use of opioids in the treatment of cancer pain. Monocyte chemoattractant protein-1 (MCP-1) is known to contribute to neuropathic pain. However, the role of spinal MCP-1 in the development of morphine tolerance in patients with cancer-induced bone pain remains unclear. The aim of the present study was to investigate the role of spinal MCP-1 in morphine tolerance in bone cancer pain rats (MTBP rats). Bone cancer pain was induced by intramedullary injection of Walker 256 cells into the tibia of the rats, while morphine tolerance was induced by continuous intrathecal injection of morphine over a period of 9 days. In addition, anti-MCP-1 antibodies were intrathecally injected to rats in various groups in order to investigate the association of MCP-1 with mechanical and heat hyperalgesia using the paw withdrawal threshold (PWT) and thermal withdrawal latency (TWL) tests, respectively. Furthermore, MCP-1 and CCR2 expression levels were measured using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analysis, and CCR2 expression levels were measured using RT-qPCR. The results indicated that MCP-1 and CCR2 expression levels were significantly increased in the spinal cord of MTBP rats. Intrathecal administration of anti-MCP-1 neutralizing antibodies was observed to attenuate the mechanical and thermal allodynia in MTBP rats. Therefore, the upregulation of spinal MCP-1 and CCR2 expression levels may contribute to the development of mechanical allodynia in MTBP rats. In conclusion, MCP-1/CCR2 signaling may serve a crucial role in morphine tolerance development in rats suffering from cancer-induced bone pain.