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The frictional heat generated during the operation of the joint prosthesis in vivo could change the corrosion resistance of the prosthesis material. In this paper, the corrosion behavior of three medical alloys at different synovial fluid temperatures was analyzed using electrochemical measurement technology. Furthermore, the scanning electron microscope and energy‐dispersive spectrometer were used to characterize the surface morphology and composition of the alloys after long‐term immersion. The results show that increasing temperature causes the open‐circuit potential of titanium alloy to shift negatively and the corrosion tendency to increase. The increasing temperature leads to the decrease of activation energy of titanium alloy, which in turn results in the increase of corrosion current density and accelerated corrosion. The results of Nyquist curves confirmed that the radius of the capacitive arc decreased with the increase of temperature, indicating the deterioration of corrosion resistance. The CoCrMo alloy shows the same regularity as the titanium alloy in 0.9% NaCl, though no obvious regularity in 25% newborn bovine serum; this may be related to the complexity of the corrosion system. [ABSTRACT FROM AUTHOR]

Summary: Despite decades of studies meant to analyse the bacterial response to carbon limitation, we still miss a high‐resolution overview of the situation. All gene expression changes observed in such conditions cannot solely be accounted for by the global regulator Crp either free or bound to its effector, cyclic AMP. Here, for the first time, we evaluated the response of both CDS (protein‐coding sequence) and ncRNA (non‐coding RNA) genes to carbon limitation, revealed cellular functions of differentially expressed genes systematically, quantified the contribution of Crp‐cAMP and other factors to regulation and deciphered regulation strategies at a genomewide scale. Approximately one‐third of the differentially expressed genes we identified responded to Crp‐cAMP via its direct or indirect control, while the remaining genes were subject to growth rate‐dependent control or were controlled by other regulators, especially RpoS. Importantly, gene regulation mechanisms can be established by expression pattern studies. Here, we propose a comprehensive picture of how cells respond to carbon scarcity. The global regulation strategies thus exposed illustrate that the response of cell to carbon scarcity is not limited to maintaining sufficient carbon metabolism via cAMP signalling while the main response is to adjust metabolism to cope with a slow growth rate. Despite decades of studies meant to analyze the bacterial response to carbon limitation we still miss a high resolution overview of the situation. Here, for the first time, we evaluated the response of both CDS (protein‐coding sequence) and ncRNA (non‐coding RNA) genes to carbon limitation, revealed cellular functions of differentially expressed genes systematically, quantified the contribution of Crp‐cAMP and other factors to regulation and deciphered regulation strategies at a genomewide scale. The global regulation strategies thus exposed illustrate that the response of cell to carbon scarcity is not limited to maintaining sufficient carbon metabolism via cAMP signaling while the main response is to adjust metabolism to cope with a slow growth rate. [ABSTRACT FROM AUTHOR]