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Background A ductile material, such as a polymeric material, releases energy during deformation. The dissipated energy can be evaluated as entropy generation. If the thermodynamic entropy generation can be measured, the stress state can be evaluated by the thermodynamic entropy generation. Objective In this study, the thermodynamic entropy generation of Polyamide 6 (PA6) was obtained using differential scanning calorimetry (DSC) for a material subjected to arbitrary strain. Methods Thermodynamic entropies were measured at the beginning and at each strain state of tensile tests by using DSC, and the volumetric strain was measured with Digital Image Correlation Method. Results At the 25% strain just before the necking behavior, the volumetric strain of PA6 was ~4.8%, and the entropy was ~56 kJ/K∙m 3 . Furthermore, the thermodynamic entropy generation of PA6 in carbon fiber reinforced plastics was evaluated under tensile conditions. The results showed that the thermodynamic entropy generation just before the transverse cracking (as same as necking in matrix resin) was ~69 kJ/K∙m 3 and the volumetric strain of PA6 in composite was ~ 3.56 %. As the results, the entropy generation and volumetric strain of PA6 showed almost same values in pure PA6 and PA6 in composite. Conclusions Consequently, thermodynamic entropy generation can be measured the volumetric strain of matrix resin.

Background:Many patients with RA consider improvement in pain the priority in treatment. However, pain has multiple causes, not just inflammatory. Central sensitivity syndromes (CSS) is one of the causes of pain in RA; therefore, we hypothesised that CSS may also influence satisfaction with treatment in patients with RA. To our knowledge, the effect of CSS-related pain on satisfaction with treatment has not been reported for patients with RA. We believe that improving patients’ satisfaction is important because higher satisfaction with treatment is associated with improved compliance and persistence with treatment, as well as with reduced regimen complexity and treatment burden[1].Objectives:In this cross-sectional study, we evaluated the effects of central sensitivity syndrome (CSS) in patients with rheumatoid arthritis (RA) on the assessment of clinical disease activity and satisfaction with treatment.Methods:Participants were 240 consecutive patients with RA (61 men and 179 women; mean age, 70.1 ± 11.9 years; mean disease duration, 13.3 ± 10.6 years) who were receiving long-term follow-up. All patients were evaluated for clinical disease activity and satisfaction with treatment. CSS was evaluated with the Central Sensitization Inventory (CSI) [2]. An overall score ≥40 indicates the presence of CSS and an overall score from 30 to 39 indicates the presence of mild CSS. And we asked, ‘How satisfied are you with your treatment?’; answers were (a) very satisfied, (b) satisfied, (c) not satisfied or (d) very dissatisfied. For univariable analysis, we condensed the four answers into two: ‘dissatisfied’ or ‘satisfied’ [3]. We also evaluated satisfaction with treatment by using the VAS, for which scores could range from 0 mm (very dissatisfied) to 100 mm (very satisfied).Results:Of the 240 patients, 20 (8.3%) were classified as having CSS, 22 patients (9.1%) as having mild CSS. CSI score was significantly correlated with clinical disease activity index scores (CDAI) (r=0.305, p<0.01), patient satisfaction with treatment(r=-0.278, p<0.01). With regard to patients’ satisfaction with treatment, univariable analysis showed that PtGA, pain VAS, HAQ-DI, DAS28 CRP, CDAI and CSI score of patients who were satisfied with treatment significantly differed from those of dissatisfied patients. Multivariable analysis revealed that CSI score, PtGA and HAQ-DI scores were associated with patient satisfaction (Table 1). Cut-off points determined by receiver operating characteristic analysis indicated that CSI scores of ≥30 were also associated with patient dissatisfaction, with 70.0% sensitivity and 88.2% specificity.Table 1. Independent factor of patient satisfaction determined using univariable and multivariable logistic regression analysis.Conclusion:In patients with RA, CSS may affect the disease activity index and reduce patients’ satisfaction with treatment.REFERENCES:[1] Barbosa CD, et al. A literature review to explore the link between treatment satisfaction and adherence, compliance, and persistence. Patient Prefer Adherence. 2012; 6: 39–48.[2] Mahlich J, et al. Shared Decision-Making and Patient Satisfaction in Japanese Rheumatoid Arthritis Patients: A New “Preference Fit” Framework for Treatment Assessment. Rheumatol Ther. 2019; 6(2): 269-283.[3] Mayer TG, et al. The development and psychometric validation of the central sensitization inventory. Pain Pract. 2012; 12(4): 276-285.Acknowledgements:We thank the staffs (Ms. Mayumi Tanabe and Yukari Jo) at Orthopedic Surgery, Yamaguchi University Graduate School of Medicine, for their assistance with this study.Disclosure of Interests:None declared.

Studies on mechanisms underlying the differentiation of dental pulp stem cells are critical for the understanding of the biology of odontogenesis and for dental tissue engineering. Here, we tested the hypothesis that stem cells from exfoliated deciduous teeth (SHED) differentiate into functional odontoblasts and endothelial cells. SHED were seeded in tooth slice/scaffolds and implanted subcutaneously into immunodeficient mice. SHED differentiated into functional odontoblasts that generated tubular dentin, as determined by tetracycline staining and confocal microscopy. These cells also differentiated into vascular endothelial cells, as determined by beta-galactosidase staining of LacZ-tagged SHED. In vitro, vascular endothelial growth factor (VEGF) induced SHED to express VEGFR2, CD31, and VE-Cadherin (markers of endothelium) and to organize into capillary-like sprouts. VEGF induced ERK and AKT phosphorylation (indicative of differentiation), while inhibiting phosphorylation of STAT3 (indicative of ‘stemness’). Collectively, this work demonstrates that SHED can differentiate into angiogenic endothelial cells and odontoblasts capable of generating tubular dentin.

Caloric restriction (CR) is known to retard aging and delay functional decline as well as the onset of diseases in most organisms. Ghrelin is secreted from the stomach in response to CR and regulates energy metabolism. We hypothesized that in CR ghrelin has a role in protecting aging-related diseases. We examined the physiological mechanisms underlying the ghrelin system during the aging process in three mouse strains with different genetic and biochemical backgrounds as animal models of accelerated or normal human aging. The elevated plasma ghrelin concentration was observed in both klotho-deficient and senescence-accelerated mouse prone/8 (SAMP8) mice. Ghrelin treatment failed to stimulate appetite and prolong survival in klotho-deficient mice, suggesting the existence of ghrelin resistance in the process of aging. However, ghrelin antagonist hastened death and ghrelin signaling potentiators rikkunshito and atractylodin ameliorated several age-related diseases with decreased microglial activation in the brain and prolonged survival in klotho-deficient, SAMP8 and aged ICR mice. In vitro experiments, the elevated sirtuin1 (SIRT1) activity and protein expression through the cAMP–CREB pathway was observed after ghrelin and ghrelin potentiator treatment in ghrelin receptor 1a-expressing cells and human umbilical vein endothelial cells. Furthermore, rikkunshito increased hypothalamic SIRT1 activity and SIRT1 protein expression of the heart in the all three mouse models of aging. Pericarditis, myocardial calcification and atrophy of myocardial and muscle fiber were improved by treatment with rikkunshito. Ghrelin signaling may represent one of the mechanisms activated by CR, and potentiating ghrelin signaling may be useful to extend health and lifespan.

Prosocial behavior is negatively associated with psychopathic traits and paradigms which measure prosocial behavior in the laboratory may be useful in better understanding moderators of this association. We revised a previously validated game of prosocial behavior by including a new trial type (i.e., trials where the participant will lose money and the charity will gain money). This version of the game was administered online and participants were randomized to group (exposed to a control stimulus video or a video used to elicit moral elevation, i.e. a positive response to witnessing another's act of kindness). We used repeated game administration to test whether a moral elevation stimulus affected game behavior and moderated the negative association between psychopathic traits and prosocial behavior. Prosocial behavior on the new trial types added in this revised game correlated strongly with prosocial behavior on the old trial type (i.e., trials where the participant will gain money and the charity will lose money; r = 0.71; p-value<0.001; n = 485). Graphing trial acceptance rates by trial characteristics demonstrated expected patterns of behavior. Number of prosocial choices on the game correlated with psychopathic trait score (Levenson Factor 1 score; r = -0.52; p-value<0.001). Game repetition with a control stimulus in between runs, supported high immediate test-retest reliability of overall game behavior. Exposure to the moral elevation stimulus in between runs did not affect game behavior nor moderate the association between psychopathic traits and prosocial behavior. Choices on this revised game of prosocial behavior, which can be administered online, are associated with psychopathic traits scores. The game appears to have high immediate test-retest reliability. Exposure to the moral elevation stimulus did not affect prosocial behavior or impact the relationship between psychopathic trait scores and prosocial behavior. Future research should continue to test potential moderators of this relationship. Limitations of the current study are discussed.

Microstructure evolution in Al-3 wt pct Cu alloy during equal-channel angular pressing (ECAP) at 423 K (150 °C) (~ 0.5 Tm) was studied. The processing temperature roughly corresponded to the transition point from cold to hot deformation associated with preferred formation of either cellular/deformation band structures, or more equilibrium subgrain structure, respectively. Similar to cold deformation, the main feature of warm ECAP at e = 1–2 was development of dislocation structures consisting of cell/microshear bands and larger-scale deformation bands, leading to grain fragmentation. With further straining, the cell bands gradually transformed into subgrain structure, and the microshear bands became the main sources of grain refinement. New ultrafine grains were formed due to mutual crossing of microshear bands, followed by increase in their number and misorientation. Simultaneously, coarsening of Θ(Al2Cu)-phase precipitates, the average size of which increased from 15 to 35 nm, facilitated dislocation rearrangement. As a result, an inhomogeneous structure with a fraction of high-angle boundaries of about 0.5, consisting of arrays of new grains about 1.2 μm in size and fragments of original grains, was formed at e = 8. It was concluded that grain refinement occurred mainly due to continuous dynamic recrystallization.

To investigate olfactory function in elderly subjects requiring nursing care to clarify its association with appetite and nutritional status. Facility for the elderly requiring nursing care. Participants: The subjects were 158 elderly people requiring nursing care and 37 elderly people not requiring nursing care. Experiment I: Olfactory function and factors (cognitive function, appetite, and nutritional status) that may be associated with it were compared between the elderly subjects requiring nursing care and those not requiring nursing care using covariance analysis in consideration of age. For evaluation, the OSIT-J was used for olfactory function, the HDS-R for cognitive function, the CNAQ for appetite, and BMI for nutritional status. Experiment II: The subjects were the same elderly subjects requiring nursing care in Experiment I, and food intake was surveyed in addition to the OSIT-J, HDS-R, CNAQ, and BMI. A univariate linear regression analysis was performed with OSIT-J as the response variable, and age, HDS-R, CNAQ, BMI, and food intake as the explanatory variables. Experiment I: On covariance analysis, the OSIT-J score was significantly lower for the elderly subjects requiring nursing care than for those not requiring nursing care (p<0.01). The mean score was 8 or lower in both groups, demonstrating lower olfactory function in both groups. Regarding factors that may be associated with olfactory function, a significant difference was noted in the HDS-R (p<0.01), confirming significantly lower cognitive function in the elderly subjects requiring nursing care. No significant difference was noted in the CNAQ or BMI. Experiment II: On a univariate linear regression analysis, an association with the OSIT-J was noted for age and HDS-R. Age was inversely correlated and the HDS-R was positively correlated. Factors associated with lower olfactory function in the elderly subjects requiring nursing were age and cognitive function, whereas appetite, nutritional status, and food intake were not associated. Olfactory function in elderly subjects requiring nursing care was poorer than that in those not requiring nursing care, suggesting that aging and cognitive decline are associated with lower olfactory function. In addition, no association of lower olfactory function with appetite, nutritional status, or food intake was noted in the elderly subjects requiring nursing care.

Slow-slip events frequently occur, but regular earthquakes are much less active on the H2O fluid-rich subduction interface at depths of ~ 40 km. The characteristic duration for silent earthquakes, which are categorized as the great slow-slip events, is more than five orders of magnitude longer than that for regular earthquakes. Such phenomena are often attributed to the slippage of the softer part of the subduction interface, but the impact of H2O fluid on aseismic slip is still unsolved. Here, we conduct deformation experiments on water-saturated harzburgite at pressures of 1.2 to 3.0 GPa and temperatures of 770 to 1250 K, corresponding to the conditions of the lower part of the overriding plate just above the subduction interface. We observe deformation of the harzburgite followed by silent faulting at a significantly low stress level down to 0.3 GPa under fluid-bearing conditions, even though many acoustic emissions are generated at the onset of faulting in fluid-free harzburgite. We find that the observed silent faulting is caused by the detachment of asperity contacts by high pore pressures and lubrication of the fault plane by a hydration reaction. We therefore propose that H2O fluid may prevent the occurrence of regular intraslab earthquakes, but trigger silent earthquakes.

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Stress response gene ATF3 is one of the p53 target genes and has a tumor suppressor role in cancer. However, the biological role of p53–ATF3 pathway is not well understood. Death receptor 5 (DR5) is a death domain-containing transmembrane receptor that triggers cell death upon binding to its ligand TRAIL (tumor necrosis factor-related apoptosis-inducing ligand), and a combination of TRAIL and agents that increase the expression of DR5 is expected as a novel anticancer therapy. In this report, we demonstrate that ATF3 is required for efficient DR5 induction upon DNA damage by camptothecin (CPT) in colorectal cancer cells. In the absence of ATF3, induction of DR5 messenger RNA and protein is remarkably abrogated, and this is associated with reduced cell death by TRAIL and CPT. By contrast, exogenous expression of ATF3 causes more rapid and elevated expression of DR5, resulting in enhanced sensitivity to apoptotic cell death by TRAIL/CPT. Reporter assay and DNA affinity precipitation assay demonstrate that at least three ATF/CRE motifs at the proximal promoter of the human DR5 gene are involved in the activation of DNA damage-induced DR5 gene transcription. Furthermore, ATF3 is shown to interact with p53 to form a complex on the DR5 gene by Re-chromatin immunoprecipitation assay. Taken together, our results provide a novel insight into the role of ATF3 as an essential co-transcription factor for p53 upon DNA damage, and this may represent a useful biomarker for TRAIL-based anticancer therapy.