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Martensitic phase analysis in hardened gear hobbing (hard-hobbing) is crucial to function-oriented gear manufacturing process. A "weighted deviation factor" has been proposed to integrate machining-induced martensitic alterations into ferritic-martensitic grain analysis. It aimed to assess the martensitic phase using the orientation deviation angle of martensite lattice to the parent austenite to replace the traditional fraction-based assessment. Therefore, the martensitic phase integrity was evaluated with strain-phase hardening to correlate the gear surface function performance. The proposed factor incorporated the martensitic phase integrity as a function of the grain area, local misorientation, and crystallographic deviation, advancing phase-based hardened steel surface modification analysis. [ABSTRACT FROM AUTHOR]

Abstract: Long-term potentiation (LTP) was monitored from the CA1 region of the intact rat hippocampus by delivering high frequency stimulation (HFS) to the Schaffer collateral commissural pathway. Intraventricular injection with mutant amyloid β1–42 peptide lacking glutamate-22 (Aβ1–42E22Δ), favoring oligomerization, 10min prior to HFS, inhibited expression of LTP, with the potency more than wild-type amyloid β1–42 peptide. Intraperitoneal injection with the linoleic acid derivative 8-[2-(2-pentyl-cyclopropylmethyl)-cyclopropyl]-octanoic acid (DCP-LA) 70min prior to HFS neutralized mutant Aβ1–42E22Δ peptide-induced LTP inhibition. In the water maze test, continuous intraventricular injection with mutant Aβ1–42E22Δ peptide for 14 days prolonged the acquisition latency as compared with that for control, with the potency similar to wild-type Aβ1–42 peptide, and intraperitoneal injection with DCP-LA shortened the prolonged latency to control levels. The results of the present study indicate that DCP-LA neutralizes mutant Aβ1–42E22Δ peptide-induced impairment of LTP and spatial learning. [Copyright &y& Elsevier]

Abstract: Expression of Schaffer collateral-CA1 long-term potentiation (LTP) and long-term depression (LTD) was not affected in hippocampal slices from wild-type mice pretreated with lipopolysaccharide (0.25mg/kg, i.p.), to increase interleukin-18 (IL-18) concentrations in the brain. For IL-18 knock-out (IL-18 KO) mice, the LTP was still expressed, the extent being similar to that for wild-type mice. In the open-field test to assess motor activity, rearing activity for IL-18 KO mice was significantly suppressed as compared with that for wild-type mice, without significant difference in the locomotion activity between two groups. In the passive avoidance test to assess fear memory, the retention latency for IL-18 KO mice was much shorter than for wild-type mice, without significant difference in the acquisition latency between two groups. In the water maze test, the acquisition latency for IL-18 KO mice significantly prolonged as compared with that for wild-type mice, without significant difference in the retention latency between two groups. For IL-18 KO mice, intraventricular injection with IL-18 for 4 days (total, 240fg) prior to water maze task shortened the prolonged acquisition latency, reaching a level similar to that for wild-type mice. The results of the present study, thus, suggest that IL-18 is a critical regulator for exploratory activity, fear memory, and spatial learning. [Copyright &y& Elsevier]

Abstract: 1-Palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPhtCho) (1μM) enhanced long-term depression (LTD), a synaptic plasticity relevant to learning and memory, in the CA1 region of rat hippocampal slices, where expression of the α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor subunit GluR1 on the plasma membrane was decreased. In the water maze test, oral administration with POPhtCho (5mg/kg) significantly shortened the prolonged retention latency for rats intraperitoneally injected with scopolamine (1mg/kg), while the acquisition latency was not affected. For humans with mild cognitive impairment and dementia (average of Mini Mental State Examination score, 18), oral intake with POPhtCho (300mg/day, once after breakfast) everyday raised the score to over 20, corresponding to normal cognitive functions, throughout 6 months after intake. The results of the present study, thus, indicate that POPhtCho could ameliorate cognitive disorders, possibly by enhancing LTD. [Copyright &y& Elsevier]

Abstract: Aims: The present study was conducted to understand the role of 1,2-dilynoleoyl-sn-glycero-3-phosphocholine (DLPhtCho) in cognitive functions. Main methods: Two-electrode voltage-clamp was made to Xenopus oocytes expressing rat α7 acetylcholine (ACh) receptors. Field excitatory postsynaptic potentials (fEPSPs) were monitored from the CA1 region of rat hippocampal slices. Water maze test was carried out to assess spatial learning and memory for rats. Key findings: In the oocyte expression system, DLPhtCho at a concentration of 10 µM potentiated ACh-evoked currents to approximately 190% of basal amplitudes 70 min after 10-min treatment. In contrast, 1-stearoyl-2-lynoleoyl-sn-glycero-3-phosphocholine (SLPhtCho), 1-palmitoyl-2-linoleoyl-sn-glycero-3-phosphocholine (PLPhtCho), and 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPhtCho) had no effect on the currents. DLPhtCho (10 µM) enhanced slope of fEPSPs to about 150% of basal levels at 70-min treatment, that is inhibited by α-bungarotoxin, an inhibitor of α7 ACh receptors, while no enhancement was obtained with SLPhtCho, PLPhtCho, or POPhtCho. In the water maze test, oral administration with DLPhtCho (5 mg/kg) significantly shortened the prolonged acquisition latency for rats intraperitoneally injected with scopolamine (1 mg/kg). Significance: The results of the present study show that DLPhtCho improves scopolamine-induced learning and memory deficits, possibly by facilitating hippocampal synaptic transmission under the control of α7 ACh receptors. DLPhtCho, therefore, could be developed as a beneficial anti-dementia drug. [Copyright &y& Elsevier]

The present study examined the effects of the proinflammatory cytokine interleukin-18 (IL-18) on mouse hippocampal synaptic transmission. IL-18 (100 ng/ml) significantly increased amplitude and frequency of α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor-mediated miniature excitatory postsynaptic currents (AMPA–mEPSCs), that are monitored from CA1 pyramidal neurons of mouse hippocampal slices. IL-18 (100 ng/ml) enhanced slope of basal field excitatory postsynaptic potentials (fEPSPs) that are recorded from the CA1 region of mouse hippocampal slices. There was no significant difference in the expression of Schaffer collateral/CA1 long-term potentiation (LTP) between in the presence and absence of IL-18, although IL-18 tended to inhibit saturation levels of the potentiation induced by tetanic stimulation in a dose-dependent manner at concentrations ranged from 10 ng/ml to 1 μg/ml. Paired-pulse facilitation in the presence of IL-18 (100 ng/ml) was not influenced after tetanic stimulation, while that in the absence of IL-18 was depressed. The results of the present study, thus, suggest that IL-18 stimulates synaptically released glutamate and enhances postsynaptic AMPA receptor responses in CA1 pyramidal neurons of mouse hippocampal slices, thereby facilitating basal hippocampal synaptic transmission without affecting the LTP. [Copyright &y& Elsevier]

In a whole-cell patch-clamp configuration, currents through N-methyl-d-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor channels were monitored in cultured rat hippocampal neurons, and those currents were depressed to 25 and 28% of basal levels, respectively, by 3-min treatment with tunicamycin (10 μM), an inhibitor of protein N-glycosylation. Tunicamycin (10 μM) reduced amplitude of population spikes elicited in the dentate gyrus of rat hippocampal slices, reaching 78% of basal levels 60 min after the beginning of treatment, and long-term potentiation (LTP) of the perforant path was never induced in the presence of tunicamycin. Tunicamycin, thus, appears to serve as a modulator for NMDA and AMPA receptors, regardless of N-glycosylation, thereby inhibiting neurotransmission and LTP in the dentate gyrus. [Copyright &y& Elsevier]

Abstract: Olprinone, an inhibitor of cyclic nucleotide phosphodiesterase III, inhibited an increase in intracellular Ca2+ concentrations for acutely dissociated rat hippocampal pyramidal neurons induced by extracellular high K+ (35mM) depolarization. Olprinone (100μM) significantly reduced spontaneous glutamate release from rat hippocampal slices. Furthermore, olprinone significantly decreased the rate of α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor-mediated miniature excitatory postsynaptic currents (AMPA-mEPSCs) monitored from CA1 pyramidal neurons of rat hippocampal slices, and the effect was blocked by KT5823, an inhibitor of protein kinase G (PKG), but not by H-89, an inhibitor of protein kinase A (PKA). In the PKA assay using PC-12 cells, olprinone did not activate PKA. Taken together, the results of the present study show that olprinone attenuates intracellular Ca2+ rise through voltage-sensitive Ca2+ channels and inhibits presynaptic glutamate release via a cGMP/PKG pathway. [Copyright &y& Elsevier]

Abstract: Linoleic acid (C18:2ω6) (10 μM) depressed ACh-evoked whole-cell membrane currents followed by potentiation of the currents in Xenopus oocytes expressing Torpedo ACh receptors. The potentiation was never obtained with linoleoylamide (10 μM), which contains CONH2 instead of COOH on linoleic acid. In the assay of protein kinase C (PKC) using a reversed phase high-performance liquid chromatography, linoleic acid activated PKC-ε but linoleoylamide otherwise had no effect on it. Of a variety of cis-unsaturated free fatty acids with 20 hydrocarbon chains (C20), 8-eicosenoic acid (C20:1ω12) potentiated ACh receptor channel currents without depression. 11,14-Eicosadienoic acid (C20:2ω6), 5,8,11-eicosatrienoic acid (C20:3ω9), 5,8,11,14-eicosatetraenoic acid (arachidonic acid) (C20:4ω6), and 5,8,11,14,17-eicosapentaenoic acid (C20:5ω3) depressed and potentiated the currents. In contrast, only a depression was obtained with 5-eicosenoic acid (C20:1ω15), 11-eicosenoic acid (C20:1ω9), and 8,11,14-eicosatrienoic acid (C20:3ω6). All the free fatty acids (C20) involved PKC-ε activation, with no significant difference in the potency among them. Taken together, it appears that carboxyl on cis-unsaturated free fatty acids plays a significant role in PKC-ε activation and potentiation of nicotinic ACh receptor responses. The role of the number and position of the cis-double bonds in the receptor responses, however, remains an open question. [Copyright &y& Elsevier]

[Display omitted] • Approach and recess fillets produced by the gear skiving were studied. • Metallurgical and mechanical properties were revealed. • Deformation mode was classified and assessed by the grain long axis. • Geometrically necessary dislocation was derived for showing the strain hardenability. The subsurface integrity of the fillet affects the gear service life during high-power-density transmission. To clarify the fillet formation in the gear skiving process, the internal subsurface integrity of gear fillets at the approach and recess sides were investigated by considering the surface texture. Metallurgical and mechanical investigations were conducted to advance the understanding of the fillet formation mechanism. The long-axis angle of the deformed grains and geometrically necessary dislocations (GNDs) of the subsurface revealed the dominant deformation mode and strain hardenability. As a result, the surface texture must be analyzed to elucidate the local cutting feature-induced plastic deformation owing to the high velocity gradient near the skived surface. The long-axis angle difference at the fillet of recess side increased approximately 5 to 10 times compared to that of the approach side, indicating that the refinement and slip-dominated deformation mode prevails at the formation of the leading and trailing fillets, respectively. Greater strain hardenability at the subsurface of the leading fillet was elucidated by the nanoindentation test and grain dislocation density. This work advances the understanding of microstructural alteration at the subsurface of the leading and trailing fillets, contributing to the gear functionality-based assessment of the gear skiving process. [ABSTRACT FROM AUTHOR]

In gear skiving, large variations in cutting features significantly affect the cutting condition and surface integrity of a newly formed gear flank (NGF). This study aimed to improve the understanding of the effects of local cutting features on the surface integrity of approach and recess NGFs from the resulting microstructure produced by the multiple radial-infeed (MRI) strategy. For the first time, the boundary of the NGF regime and associated local cutting features were calculated from the uncut chip geometry (UCG) using a novel boundary-based level contour method. The theoretical and experimental results revealed that the local rake angle and uncut chip thickness are the most influential factors altering the plastic deformation conditions of the approach and recess NGFs. For the finishing pass, the uncut chip thickness developments within approach and recess NGFs were elucidated, showing the burnishing regime dominated the recess NGF formation. The strain–stress characteristics of the recess NGF show the strain-hardening effect due to the severe plastic deformation. Kernel average misorientation mapping showed a partial reduction in the misorientation angle under the recess NGF. This points to the accumulated deformation in the interaction between successive skiving passes further facilitating the localized recrystallization. Proposed local cutting feature calculations can be applied for further kinematic parameter optimization and MRI infeed rate design. [Display omitted] • Boundary of the newly formed gear flank is derived from the uncut chip geometry. • Calculation method for local cutting features is proposed to clarify the skiving process. • An adequate analysis on gear flank formation is achieved by the clarification of local cutting feature. • Mechanism on the surface integrity alteration between approach and recess flanks is clarified. [ABSTRACT FROM AUTHOR]

2-Pyrrolidinone, a metabolite of aniracetam, potentiated currents through α7 receptors expressed in Xenopus oocytes, in a bell-shaped dose-dependent manner at concentrations ranged from 1 nM to 10 μM, with a maximum at 100 nM (189% of original levels 60 min after 20-min treatment). The potentiation was inhibited by GF109203X, a selective inhibitor of protein kinase C (PKC), but not by KN-93, a selective inhibitor of CaMKII, or H-89, a selective inhibitor of protein kinase A (PKA). In the PKC assay using reversed-phase high-performance liquid chromatography, 2-pyrrolidinone enhanced activity of PKC-ϵ activated by linoleic acid to about 1.8-times greater than that in the absence of 2-pyrrolidinone, although it did not directly activate PKC-ϵ. In the Western immunoblot analysis, rat hippocampal slices treated with 2-pyrrolidinone (100 nM) was more reactive to an antibody against phosphorylated myristoylated alanine-rich C kinase substrate (MARCKS) than untreated slices. 2-Pyrrolidinone (100 nM) induced a long-lasting facilitation of hippocampal synaptic transmission in the CA1 region of rat hippocampal slices, and the facilitation was inhibited by GF109203X or α-bungarotoxin, an inhibitor of α7 receptors. The results of the present study suggest that 2-pyrrolidinone enhances activity of activated PKC, thereby potentiating α7 receptor responses, and then leading to a facilitation of hippocampal synaptic transmission. [Copyright &y& Elsevier]

The present study investigated the effects of (−)-epigallocatechin gallate (EGCG), which is the major component of polyphenol in green tea, on nitric oxide (NO) stress-induced neuronal damage, by monitoring NO mobilizations in the intact rat hippocampus and assaying the viability of cultured rat hippocampal neurons. A 10-min ischemia increased NO (NO3−/NO2−) concentrations in the intact rat hippocampus, while EGCG (50 mg/kg i.p.) inhibited the increase by 77% without affecting hippocampal blood flow. The NO donor, sodium nitroprusside (SNP; 50 μM), produced NO (NO3−/NO2−), while EGCG inhibited it in a dose-dependent manner at concentrations ranging from 50 to 200 μM. Treatment with SNP (100 μM) reduced the viability of cultured rat hippocampal neurons to 22% of control levels, while EGCG caused it to recover to 51% for 10 μM, 73% for 20 μM, and 70% for 50 μM. Taken together, it appears that EGCG could protect against ischemic neuronal damage by deoxidizing peroxynitrate/peroxynitrite, which is converted to NO radical or hydroxy radical. [Copyright &y& Elsevier]