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In gear skiving, early-stage cutter chipping significantly reduces tool service life, collectively resulting from the complex skiving force condition and chip flow behavior on the rake face. Thereby, chipping analysis and avoidance are of great interest in the high-performance skiving process design. In this work, we proposed a chip obstruction model in parametric space to realize the chipping prediction based on the skiving force analysis, followed by a detailed investigation on the corresponding force characterization via real-time monitoring and high-frequency force acquisition. For the first time, the chip flow obstruction was modeled with respect to the merging point of separated uncut chip cross sections, enabling the derivation on the time window to label the chipping moment for the high-frequency force monitoring. A single-tooth skiving test incorporating the phase-setover was conducted to validate the proposed model under different chip flow scenarios. Consequently, chipping is effectively avoided by modifying the infeed strategy based on the comparative study on the chipping moment. Chip obstruction was revealed as the primary underlying mechanism for cutter chipping in gear skiving. The chip-obstruction-induced skiving force shock is significant and can be well captured by the high-frequency force signal monitoring based on the proposed model, which can further advance the understanding of chip flow behavior, contributing to the gear skiving process in cutter design, infeed strategy decision-making, and process monitoring. [ABSTRACT FROM AUTHOR]

Abstract: The cryoprotective effect of intracellular free high-mannose oligosaccharides (HMOS) on mammalian cells and proteins was examined by monitoring PC-12 cell viability and assaying protein kinase C (PKC)-ε activity. 1-Deoxymannojirimycin, an inhibitor of α-mannosidase, to cause an increase in intracellular free HMOS, significantly rescued PC-12 cells with 2-h freezing insult at −15°C in a concentration (1–50mM)- and pretreatment time (48–72h)-dependent manner, as compared with unpretreated cells; full rescue from freezing injury was obtained with 1-deoxymannojirimycin at more than 25mM for 48-h pretreatment and more than 3mM for 72- and 96-h pretreatment. For PC-12 cells pretreated with 1-deoxymannojirimycin at 1mM for 72h, thawed cell viability after more than 8-w cryopreservation at −80°C in 10% (v/v) dimethyl sulfoxide was much higher than that for cells without pretreatment. PKC-ε activity was well preserved after 16-h cryopreservation at −20°C in the presence of mannose 9-N-acetylglucosamine 2 (Man9-GlcNAc2) (1 mM), an HMOS, while the activity was reduced to 15% without Man9-GlcNAc2. Collectively, the results of the present study suggest that intracellular free HMOS is a key molecule to protect mammalian cells and proteins from freezing injury; in other words, HMOS could be a new target for cryopreservation of mammalian cells and proteins. [Copyright &y& Elsevier]

Abstract: In the assay of glutamate and γ-aminobutyric acid (GABA) with a high-performance liquid chromatography, spontaneous release of glutamate and GABA from rat hippocampal slices was significantly enhanced by mecamylamine, an inhibitor of non-α7 ACh receptors, or α-bungarotoxin, an inhibitor of α7 ACh receptors in the absence of tetrodotoxin (TTX), but not in the presence of TTX. Nicotine significantly enhanced glutamate and GABA release in the absence of TTX, that is abolished by mecamylamine or α-bungarotoxin, while it had no effect on the release in the presence of TTX. In the recording of α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor-mediated excitatory postsynaptic currents (AMPA-EPSCs) and GABAA receptor-mediated inhibitory postsynaptic currents (GABAA-IPSCs) from CA1 pyramidal neurons of rat hippocampal slices, nicotine did not affect the rate and amplitude of AMPA-EPSCs and AMPA-miniature EPSCs. In contrast, nicotine significantly increased the rate of GABAA-IPSCs, without affecting the amplitude, but such effect was not obtained with GABAA-miniature IPSCs. The collective results suggest that α7 and non-α7 ACh receptors expressed in the hippocampus, activated under the basal conditions, inhibit release of glutamate and GABA controlled through multi-synaptic relays, but that otherwise, those receptors, highly activated by nicotine, stimulate both the release, with a part of GABA released from interneurons transmitting to CA1 pyramidal neurons. Furthermore, the results also suggest that α7 and non-α7 ACh receptors do not have potency sufficiently to modulate glutamate and GABA release controlled by single synapses. [Copyright &y& Elsevier]

The present study investigated the effects of amyloid-β peptides on nicotinic ACh receptors (Torpedo, α4β2, and α7 receptors) and AMPA receptors expressed in Xenopus oocytes by monitoring whole-cell membrane currents. Ten-minutes treatment with amyloid-β1–42 (1 μM) inhibited Torpedo ACh receptor currents, reaching 53% of original levels 30 min after treatment. Amyloid-β1–40 inhibited the currents in a dose-dependent manner (0.1–10 μM) during treatment, gradually reversing after treatment. Amyloid-β1–40 and amyloid-β1–42 (0.1 μM) depressed α4β2 receptor currents to each 69% and 62% of original levels at 10-min treatment and lesser depression was obtained with α7 receptors. Amyloid-β1–42 (0.1 μM) did not significantly inhibit AMPA receptor currents, but amyloid-β1–40 (0.1 μM) potentiated the currents to 145–191% of original levels. Amyloid-β peptides, thus, exert their diverse actions on nicotinic ACh receptors and AMPA receptors, and the inhibitory actions on nicotinic ACh receptors may account for the deterioration of learning and memory in Alzheimer''s disease. [Copyright &y& Elsevier]