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The effect of shot peening (SP) on pre‐fatigue tested carburized steel was investigated. Plane‐bending fatigue tests were conducted on carburized CrMo steel that was pre‐fatigue tested and treated with SP. Fatigue cracks were induced by pre‐fatigue tests with a stress amplitude of σa = 1000 MPa, and the number of the pre‐fatigue test cycles was 2.0 × 104 (L5 test) and 4.0 × 104 (L15 test). We compared the fatigue lives of the fatigue‐damaged and smooth specimens without fatigue damage treated with the same SP. The fatigue life of the L5 tested specimens with SP was longer than that of the non‐fatigue damaged smooth specimens after SP. Therefore, the fatigue cracks introduced by the L5 test can be rendered harmless by SP. Furthermore, near‐surface material properties were evaluated and the mechanisms of rendering surface cracks harmless were investigated. HIGHLIGHTS: (1) Fatigue cracks were induced by pre‐fatigue tests on carburized CrMo steel. (2) The fatigue cracks could be rendered harmless by shot peening. (3) The mechanisms of rendering surface cracks harmless were investigated. (4) Shot peening is expected to be utilized in remanufacturing. [ABSTRACT FROM AUTHOR]

Ball burnishing (BB) is a surface finishing process that involves moving the tool while pressing it against the workpiece under rolling contact. We investigated the effects of BB on the fatigue strength of an aluminum alloy with a semicircular slit simulating an initial surface defect. After performing BB under a typical condition, compressive residual stress was induced to a depth of 0.4 mm, with a reduction in surface roughness by 81%. Consequently, the fatigue strength increased by 22%. BB prevented the fatigue strength reduction caused by the 0.1 mm deep slit. The result indicated that BB could render the below 0.1 mm deep surface defect harmless in terms of fatigue strength. The maximum depth of surface defect that can be rendered harmless is 0.18 mm according to fracture mechanics, which is in agreement with the experimental results. Highlights: Ball burnishing (BB) can introduce large compressive residual stress along with smoothing.BB can render a 0.1 mm deep slit harmless in terms of fatigue strength.Defect size rendered harmless can be estimated based on fracture mechanics.Compressive residual stress is the main factor rendering the surface defect harmless. [ABSTRACT FROM AUTHOR]

Growth regulation tailors development in plants to their environment. A prominent example of this is the response to gravity, in which shoots bend up and roots bend down.sup.1. This paradox is based on opposite effects of the phytohormone auxin, which promotes cell expansion in shoots while inhibiting it in roots via a yet unknown cellular mechanism.sup.2. Here, by combining microfluidics, live imaging, genetic engineering and phosphoproteomics in Arabidopsis thaliana, we advance understanding of how auxin inhibits root growth. We show that auxin activates two distinct, antagonistically acting signalling pathways that converge on rapid regulation of apoplastic pH, a causative determinant of growth. Cell surface-based TRANSMEMBRANE KINASE1 (TMK1) interacts with and mediates phosphorylation and activation of plasma membrane H.sup.+-ATPases for apoplast acidification, while intracellular canonical auxin signalling promotes net cellular H.sup.+ influx, causing apoplast alkalinization. Simultaneous activation of these two counteracting mechanisms poises roots for rapid, fine-tuned growth modulation in navigating complex soil environments. Auxin rapidly modulates root growth through simultaneous activation of two opposing mechanisms--TMK1-mediated apoplast acidification and TIR1/AFB-mediated apoplast alkalinization., Author(s): Lanxin Li [sup.1] , Inge Verstraeten [sup.1] , Mark Roosjen [sup.2] , Koji Takahashi [sup.3] [sup.4] , Lesia Rodriguez [sup.1] , Jack Merrin [sup.1] , Jian Chen [sup.5] [sup.6] [...]

The phytohormone auxin controls many processes in plants, at least in part through its regulation of cell expansion.sup.1. The acid growth hypothesis has been proposed to explain auxin-stimulated cell expansion for five decades, but the mechanism that underlies auxin-induced cell-wall acidification is poorly characterized. Auxin induces the phosphorylation and activation of the plasma membrane H.sup.+-ATPase that pumps protons into the apoplast.sup.2, yet how auxin activates its phosphorylation remains unclear. Here we show that the transmembrane kinase (TMK) auxin-signalling proteins interact with plasma membrane H.sup.+-ATPases, inducing their phosphorylation, and thereby promoting cell-wall acidification and hypocotyl cell elongation in Arabidopsis. Auxin induced interactions between TMKs and H.sup.+-ATPases in the plasma membrane within seconds, as well as TMK-dependent phosphorylation of the penultimate threonine residue on the H+-ATPases. Our genetic, biochemical and molecular evidence demonstrates that TMKs directly phosphorylate plasma membrane H.sup.+-ATPase and are required for auxin-induced H.sup.+-ATPase activation, apoplastic acidification and cell expansion. Thus, our findings reveal a crucial connection between auxin and plasma membrane H.sup.+-ATPase activation in regulating apoplastic pH changes and cell expansion through TMK-based cell surface auxin signalling. Auxin induces transmembrane-kinase-dependent activation of H.sup.+-ATPase in the plasma membrane through phosphorylation of its penultimate threonine residue, promoting apoplastic acidification and hypocotyl cell elongation in Arabidopsis., Author(s): Wenwei Lin [sup.1] [sup.2] , Xiang Zhou [sup.1] [sup.2] , Wenxin Tang [sup.1] , Koji Takahashi [sup.3] [sup.4] , Xue Pan [sup.2] , Jiawei Dai [sup.1] , Hong Ren [...]

Sound stimulation can influence electrophysiological vestibular reflexes. However, the effects of sound stimulation on space perception remain unknown.To know the effects of monaural sound stimulation on subjective visual vertical (SVV).We measured SVV with and without monaural sound stimulation (105 dB, 500 Hz short tone burst presented at 4.7 Hz) in 50 healthy volunteers (aged 20–77 [mean = 42.7] years).The mean SVV was deviated 0.139° to the left by right monaural sound stimulation and 0.123° to the right by left monaural sound stimulation. SVV changes due to right and left ear stimulations were significantly different (p = 0.019). Sound stimulation resulted in a significant change in SVV on the left side (p = 0.014) in participants aged 50 or younger (mean = 35.6 years) (n = 37).This study is the first to show the possibility that the monaural sound input deviates the SVV toward the opposite side and is more pronounced for left-ear input. The vestibular-evoked myogenic potential responses may be involved in the mechanism of the contralateral SVV deviation due to sound input. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to understand how people living with drug‐resistant focal epilepsy (DRE) navigate through lines of antiseizure medications (ASM) and experience adverse events (AEs) in the real‐world setting in the United States. Methods: A retrospective study was conducted with medical chart data from clinical practices in the United States. Eligible adults had a confirmed diagnosis of DRE and initiated a third‐line ASM therapy between January 2013 and January 2020 (i.e., the index date). Subjects must have medical history data available for ≥1 year prior to (the baseline) and ≥2 years after the index date (the follow‐up). Treatment patterns were captured from first to fourth lines. After the emergence of drug resistance, time to ASM discontinuation, reasons for discontinuation, AE experience and AE management were reported separately during third and fourth lines of treatment and beyond. Results: The study included a total of 345 individuals, with an average (standard deviation) age of 23.9 (11.9) years at first diagnosis. All individuals had at least three lines of ASMs with first and second lines during baseline, and third line during follow‐up. The first line for most individuals was monotherapy. As individuals progressed through additional lines of ASM therapy, they were more likely to receive polytherapy. The regimens were more individualized after meeting drug resistance criteria. The top reasons for discontinuing were uncontrolled seizure and/or intolerance/AEs for both third and subsequent lines. More than a third of individuals experienced at least one AE. Among those with at least one AE, many individuals had to manage these AEs with dose adjustment (39.4%), discontinuation of offending ASM (37.9%), de novo pharmacotherapy (25.8%), emergency room visit (13.6%), and hospitalization (12.1%). Significance: This study demonstrated that individuals living with DRE experience significant AEs, and many of these AEs lead to treatment disruption and significant healthcare resource utilization. Plain Language Summary: This study examined how individuals with focal epilepsy are treated across various clinics in United States and reported the adverse events these individuals experienced during treatment, along with the consequence associated with these adverse events. We found that as individuals progressed through additional treatments, they were more and more likely to receive more than one antiseizure medication, and a significant portion of individuals experienced at least one adverse event, often manifested as headache, somnolence, dizziness, and fatigue. [ABSTRACT FROM AUTHOR]