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The QCs (quality characteristics) of MAU (meta-action unit) determine the quality of CNC (computer numerical control) machine tools. For improving the accuracy of MAU QCs analysis, and solving the problems that the current methods either only have subjective analysis, or only have objective analysis, or the analysis process that includes both subjective and objective analysis methods is relatively complex, a comprehensive identification method of MAU QCs according to the improved MAHP (multiplicative analytic hierarchy process) method and Shannon entropy is proposed in this paper. Firstly, the QCs of the MAU are divided into quality layer and index layer. Secondly, the expert evaluation weight is introduced to improve the MAHP, then the sub quality layer of the meta-action unit was subjectively analyzed. Thirdly, the index layer of the MAU is objectively analyzed by the Shannon entropy. Finally, the results obtained by WMAHP (weighted multiplication analytic hierarchy process) method and Shannon entropy method are synthesized, and the Pareto principle is adopted to extract the key QCs of the MAU. The proposed method combines the advantages of both subjective and objective analysis, and it can reduce the fluctuation of the analysis results caused by data changes. Meanwhile, the analysis process is relatively simple. Its applicability and superiority have also been confirmed by an experiment and comparisons with various methods. The proposed method is of great significance to improve the quality of CNC machine tools.

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Taking into consideration the dynamic characteristics of motion error propagation in CNC machine tools, in order to enhance the accuracy of PRUL (precision remaining useful life) prediction analysis, this paper presents a precision degradation modeling approach based on MAU (meta-action unit) for CNC machine tools. Firstly, from the perspective of motion, the CNC machine tool is divided into the smallest unit by the decomposition of FMA (Function-Motion-Action). Secondly, the MBS (multi-body systems) theory is used to topologically describe the motion relationship between the MAU, and the spinor theory is used to model the motion error. Thirdly, considering the influence of multiple error sources on the PRUL of the CNC machine tool MAU, the motion transmission ratio is used to synthesize multiple error sources, and combined with the constructed error model, the precision degradation model of MAU is constructed, and its PRUL is accurately predicted. Finally, the CNC turntable is selected as the experimental subject to compare the proposed method with commonly used methods in terms of rationality, applicability, and simplicity, and the results verify the applicability and correctness of the method proposed in this paper.

Remifentanil is being used increasingly as one component of total intravenous anesthesia. Severe postoperative pain has occasionally been reported with discontinuation of remifentanil. This study was designed to determine the involvement of conventional protein kinase Cgamma (cPKCγ) in the inhibitory action of lidocaine on remifentanil-induced hyperalgesia of rats after propofol-remifentanil-based anesthesia. Male Sprague-Dawley rats were allocated into the following groups randomly propofol only (P), propofolremifentanil (R), propofolremifentanillidocaine (RL), and propofollidocaine (L). Cumulative pain score and withdrawal response to mechanical stimulation, immunoblotting, and immunofluorescence were applied to observe remifentanil-induced hyperalgesia and cPKCγ membrane translocation. We found that the cumulative pain score of group R increased significantly at 30, 120, and 300 minutes postanesthesia (P<0.05). After plantar incision, the withdrawal threshold on both the contralateral and the ipsilaeral side at 30, 120, and 300 minutes postanesthesia in group R was significantly lower than in groups P, RL, and L (P<0.05). Both immunoblotting and immunofluorescence showed that cPKCγ membrane translocation increased in dorsal horn neurons of propofol-remifentanil–based anesthetized rats, which could be inhibited by systemic lidocaine. These results suggested that increased cPKCγ membrane translocation was involved in remifentanil-induced hyperalgesia, which was inhibited by systemic lidocaine and may contribute to reduced postoperative pain in rats after propofol-remifentanil–based anesthesia.

Ca2calmodulin-dependent protein kinase II (CaMKII) activation through autophosphorylation at threonine 286 was involved in the modulation of neuronal excitability and neurotransmission. Both propofol and ketamine may affect the intracellular Ca2levels through N-methyl-D-aspartate receptors or voltage-dependent Ca2channels, but they have different mechanisms in general anesthesia. The purpose of this study was to investigate the effects of propofol and ketamine on CaMKII total protein and phosphorylation (p-CaMKII) levels in the brain of rats. We found that both propofol and ketamine could induce a decrease of p-CaMKII, not CaMKII total protein, in an anesthetic depth-dependent manner, whereas only ketamine caused a dose (50, 100, and 150 mgkg)-dependent depression of p-CaMKII in hippocampus and frontal cortex of rats after intraperitoneal injections for 30 minutes. The significant depressions of p-CaMKII started at 5 minutes both in hippocampus and frontal cortex of rats after 100 mgkg propofol treatment, whereas 100 mgkg ketamine-induced significant depression of p-CaMKII initiated at 30 minutes in hippocampus and 5 minutes (no reduction observed at 15 min) in frontal cortex of rats. The maximum reduction of p-CaMKII with both drugs was at 60 minutes, and then restored to control level at 240 minutes. In addition, we confirmed the depression of p-CaMKII in hippocampus and frontal cortex of rats after 100 mgkg of propofol or ketamine treatment for 60 minutes by using immunostaining. These results suggested that decreased p-CaMKII levels correlate with anesthetic depths achieved by propofol and ketamine, which may be related to the effects of propofol and ketamine on central nervous system function and their clinical effect.

A new method to importance identification and optimization of meta-action unit for electromechanical product is proposed herein. In the present method, the influence factors and optimization factors related to the importance identification and optimization of meta-action unit were given. The weight vectors of influence factors and optimization factors were obtained by the improved EAHP (extension analytical hierarchy process), and the importance matrix and optimization weight vector of meta-action unit were also built by fuzzy theory. Then, the meta-action unit importance identification and optimization model was established according to the influence factors weight vector, optimization factors weight vector, meta-action unit importance matrix, and meta-action unit comprehensive optimization weight vector. A typical domestic electromechanical product was taken as the analysis object, and the effectiveness of the new method is verified by the comparison of various methods. The proposed method is helpful to reduce the blindness of enterprises in selecting analysis objects, and also lays a foundation for improving the reliability of electromechanical products.

Accumulated reports have suggested that activation of protein kinase C (PKC) isoforms may involve the activation of extracellular signal-regulated kinases (ERKs) in the neuronal response to ischemichypoxic stimuli. We have previously demonstrated that the membrane translocation of novel PKC (nPKC) increased in the early phase of cerebral ischemichypoxic preconditioning of mice. In this study, we used Western blot analysis and propidium iodide stain to determine whether the activations of nPKC and ERKs were involved in oxygen-glucose deprivation (OGD)-induced neuroprotection via N-methyl-D-aspartate (NMDA) receptors. The hippocampal slices of mice were exposed to OGD for 10 (OGD10) or 45 minutes (OGD45) to mimic mild (causing ischemichypoxic preconditioning) and severe (causing severe OGD) ischemiahypoxia, respectively. We found that OGD10-induced nPKC membrane translocation was mediated by NMDA receptors, and both OGD10 and NMDA (1 μM, 30 min) pretreatment could protect Cornu Ammonis region 1 neurons against the subsequent severe OGD45. In addition, nPKC translocation inhibitor, V1-2 (1 μM, 30 min), and ERKs upstream mitogen-activated proteinextracellular signal regulated kinase kinase inhibitor, PD-98059 (20 μM, 30 min), could significantly inhibit OGD10 and NMDA-induced neuroprotection. These results suggest that OGD10-induced neuroprotection against severe OGD45 in the Cornu Ammonis region 1 region of the hippocampal slices was mediated by the activations of NMDA receptors, nPKC, and the downstream ERKs.

Neurogranin (Ng) is a brain-specific, postsynaptically located protein kinase C (PKC) substrate, highly expressed in the cortex, hippocampus, striatum, and amygdala. This protein is a Ca2+-sensitive calmodulin (CaM)-binding protein whose CaM-binding affinity is modulated by phosphorylation and oxidation. To investigate the role of Ng in neural function, a strain of Ng knockout mouse (KO) was generated. Previously we reported (Pak, J. H., Huang, F. L., Li, J., Balschun, D., Reymann, K. G., Chiang, C., Westphal, H., and Huang, K.-P. (2000) Proc. Natl. Acad. Sci. U. S. A.97, 11232–11237) that these KO mice displayed no obvious neuroanatomical abnormality, but exhibited deficits in learning and memory and activation of Ca2+/CaM-dependent protein kinase II. In this report, we analyzed several downstream phosphorylation targets in phorbol 12-myristate 13-acetate- and forskolin-treated hippocampal slices from wild type (WT) and KO mice. Phorbol 12-myristate 13-acetate caused phosphorylation of Ng in WT mice and promoted the translocation of PKC from the cytosolic to the particulate fractions of both the WT and KO mice, albeit to a lesser extent in the latter. Phosphorylation of downstream targets, including mitogen-activated protein kinases, 90-kDa ribosomal S6 kinase, and the cAMP response element binding protein (CREB) was significantly attenuated in KO mice. Stimulation of hippocampal slices with forskolin also caused greater stimulation of protein kinase A (PKA) in the WT as compared with those of the KO mice. Again, phosphorylation of the downstream targets of PKA was attenuated in the KO mice. These results suggest that Ng plays a pivotal role in regulating both PKC- and PKA-mediated signaling pathways, and that the deficits in learning and memory of spatial tasks detected in the KO mice may be the result of defects in the signaling pathways leading to the phosphorylation of CREB.

S-Nitrosoglutathione (GSNO) undergoes spontaneous degradation that generates several nitrogen-containing compounds and oxidized glutathione derivatives. We identified glutathione sulfonic acid, glutathione disulfideS-oxide (GS(O)SG), glutathione disulfideS-dioxide, and GSSG as the major decomposition products of GSNO. Each of these compounds and GSNO were tested for their efficacies to modify rat brain neurogranin/RC3 (Ng) and neuromodulin/GAP-43 (Nm). Among them, GS(O)SG was found to be the most potent in causing glutathiolation of both proteins; four glutathiones were incorporated into the four Cys residues of Ng, and two were incorporated into the two Cys residues of Nm. Ng and Nm are two in vivosubstrates of protein kinase C; their phosphorylations by protein kinase C attenuate the binding affinities of both proteins for calmodulin. When compared with their respective unmodified forms, the glutathiolated Ng was a poorer substrate and glutathiolated Nm a better substrate for protein kinase C. Glutathiolation of these two proteins caused no change in their binding affinities for calmodulin. Treatment of [35S]cysteine-labeled rat brain slices with xanthine/xanthine oxidase or a combination of xanthine/xanthine oxidase with sodium nitroprusside resulted in an increase in cellular level of GS(O)SG. These treatments, as well as those by other oxidants, all resulted in an increase in thiolation of proteins; among them, thiolation of Ng was positively identified by immunoprecipitation. These results show that GS(O)SG is one of the most potent glutathiolating agents generated upon oxidative stress.