Failure mode and effect analysis has been applied in manufacturing and service industries but can still be improved. Failure mode and effect analysis is a common tool used to evaluate risk priority number; however, numerous scholars have doubted the effectiveness of failure mode and effect analysis and have thus proposed methods for correcting failure mode and effect analysis from its conventional formula. Because implemented actions can determine or influence resource allocation and its effects, completing one corrective action can occasionally simultaneously improve various failure modes. In this study, failure mode and effect analysis and decision-making trial and evaluation laboratory were integrated to correct failure modes and increase their effectiveness. First, failure mode and effect analysis was employed to identify the items for improvement. Second, decision-making trial and evaluation laboratory was adopted to examine the reciprocal influences and causality among these items. Finally, the priority for improving the items was proposed. By combining the advantages of failure mode and effect analysis and decision-making trial and evaluation laboratory, this research method complemented the shortcomings of the two techniques. According to the empirical research of this case study in which decision-making trial and evaluation laboratory was employed to analyze the causality among the items of the failure modes, the malfunction of production lines can be solved faster and more effectively compared with merely considering the size of risk priority number values.

Morphine is the most commonly used drug for treating physical and psychological suffering caused by advanced cancer. Although morphine is known to elicit multiple supraspinal analgesic effects, its behavioral correlates with respect to the whole-brain metabolic activity during cancer-induced bone pain have not been elucidated. We injected 4T1 mouse breast cancer cells into the left femur bone marrow cavity of BALB/c mice. All mice developed limb use deficits, mechanical allodynia, and hypersensitivity to cold, which were effectively suppressed with morphine. Serial 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) was performed for each mouse before cancer induction (0 day), after cancer-induced bone pain was established (14 days), and during effective morphine treatment (16 days). The longitudinal FDG-PET imaging analysis demonstrated that cancer-induced bone pain increased glucose uptake in the insular cortex and hypothalamus and decreased the activity of the retrosplenial cortex. Morphine reversed the activation of the insular cortex and hypothalamus. Furthermore, morphine activated the amygdala and rostral ventromedial medulla and suppressed the activity of anterior cingulate cortex. Our findings of hypothalamic and insular cortical activation support the hypothesis that cancer-induced bone pain has strong inflammatory and affective components in freely moving animals. Morphine may provide descending inhibitory and facilitatory actions in the treatment of cancer-induced bone pain in a clinical setting.

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