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Metal magnetic memory (MMM) method is a novel and potential nondestructive evaluation (NDE) technique to assess residual fatigue life of the ferromagnetic structure, such as hydraulic cylinder. In this paper, an evaluation framework was proposed. Firstly, the MMM signals under different fatigue cycles were recorded in the tensile-tensile experiment. A representative signal characteristic Hpp was defined as an evaluation index. The monotonic change trend and abrupt change point was investigated. Statistical results show that Hpp can be used to predict residual fatigue life. Except for a few specimens, almost all specimens produced an abrupt change at the normalized fatigue life coefficient k = 0.91. This can be used to distinguish different stages of fatigue life. The sensitivity, specificity, and diagnostic performance were analyzed using Receiver Operating Characteristic (ROC) curves. The statistical results show that when the coefficient k = 0.91, the diagnostic performance is relatively best with an area under the curve (AUC) is about 0.85, and Jorden's index is about 0.75.

During the start-stop process of high-precision instruments in service, the critical materials of instruments undergo thermal cycling, resulting in changes in microstructure and dimension. In this paper, the evolution and coupling effects of dislocations and precipitates within 2024 Al alloy during 500 cycles were investigated, and their influence on the dimensional change was quantitatively characterized and decoupling analyzed. Transmission Electron Microscopy (TEM)/aberration-corrected scanning TEM (CS-TEM), X-ray diffraction (XRD), and Three-Dimensional Atom Probe Tomography (3D-APT) were used for microstructural evolution analysis and quantitative statistics. The dislocation density increased from 3.32 × 1014 m−2 to 5.75 × 1014 m−2 after 500 cycles, which accelerated elemental diffusion and provided nucleation sites of precipitates, contributing to an increase in the number density of the S'/S phase from 1.04 × 1024 m−3 to 1.41 × 1024 m−3. Based on the quantitative statistics of precipitate types and corresponding volume fractions, the dimensional change induced by precipitate evolution was −1.25 × 10−4. The dimensional change caused by the free volume introduced by dislocation density was 3.32 × 10−6. Comparing these values with the experimental value of −1.94 × 10−4, it is clear that the precipitate evolution is the main factor that triggers the dimensional change.

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Background: Fear extinction alone does not erase the original fear memory. Interventions that enhance extinction can be beneficial for the treatment of fear-related disorders. Repetitive transcranial magnetic stimulation has been shown to improve memory performance. The present study examined the effects of intermittent theta-burst stimulation (iTBS) on fear extinction and the return of fear memory in humans., Methods: Ninety-one young healthy volunteers underwent 3 experiments using a randomized controlled experimental design. Participants first acquired fear conditioning, after which they received 30 Hz iTBS before and after extinction training. The iTBS was applied to 1 of 2 targets: the left dorsolateral prefrontal cortex (dlPFC) and the vertex (control). Fear responses were measured 24 hours later and 1 month later., Results: During the spontaneous recovery and reinstatement tests, iTBS of the left dlPFC before and after extinction significantly reduced fear response, whereas iTBS of the vertex had no effect on fear memory performance. This combined approach had a relatively long-lasting effect (i.e., at least 1 month)., Limitations: We did not explore the effect of iTBS of the dlPFC on the expression of fear without extinction training. The neural mechanisms of iTBS with fear extinction to inhibit the fear response are unclear. Our results are preliminary and should be interpreted with caution., Conclusion: `The present results showed that 30 Hz iTBS of the left dlPFC enhanced retention of fear extinction. Our study introduces a new intervention for fear memory and suggests that the left dlPFC may be a treatment target for fear-related disorders., Competing Interests: None declared., (© 2021 Joule Inc. or its licensors.)

Objective: To explore the role of cell-surface nucleolin in lipopolysaccharide (LPS)-stimulated expression and secretion of TNF-alpha and IL-1beta in human THP-1 monocytes., Methods: Immuno-fluorescence assay and Western blot were used to identify the expression of nucleolin on the surface of THP-1 monocytes. Inactivation of nucleolin was induced by anti-nucleolin monoclonal antibody blockage, and the expression and secretion of TNF-alpha and IL-1beta were observed by using reverse transcription polymerase chain reaction (RT-PCR) and enzyme linked immuno-sorbent assay (ELISA)respectively in LPS-mediated human THP-1 monocyte inflammatory model., Results: Immuno-fluorescence showed that nucleolin was localized on the cell surface of THP-1 monocytes as indicated by dotted red fluorescence. Western blot assay indicated that nucleolin existed in the cell membrane fractions. RT-PCR assay showed that the expressions of TNF-alpha and IL-1beta mRNA significantly increased at 2 h and 3 h after the treatment with 1000 microg/L LPS. After 1 h pretreatment with anti-nucleolin antibody, the levels of TNF-alpha and IL-1beta mRNA decreased compared with an anti-nucleolin antibody untreated group and an irrelevant IgG+LPS group (P<0.05). ELISA assay showed that the pretreatment with anti-nucleolin antibody inhibited significantly the secretion of LPS-induced levels of TNF-alpha and IL-1beta after 4, 12 and 24 h treatment with 1000 microg/L LPS., Conclusion: Nucleolin expresses on the cell surface of THP-1 monocytes and involves in the LPS-mediated expression and secretion of TNF-alpha and IL-1beta.

Objective: To explore the protective effect of HSP72 on the acute injury of cardiomyocyte induced by oxidative stress., Methods: Cardiomyocytes of neonatal rats treated with heat shock (42 degrees C, 30 min, recovery for 6 h) to induce the expression of HSP72 and HSP72 antisense oligonucleotide was transformed to block the expression of HSP72. 0.5 mmol/L (final concentration) H2O2 was added into the culture medium to mimic oxidative stress, and to induce the acute injury of neonatal cardiomyocytes. The release of LDH and the total protein synthesis were applied to evaluate the injury of cardiomyocyte of neonatal rats., Results: Oxidative stress could significantly increase the release of LDH, and inhibit the total protein synthesis. By inducing the expression of HSPs, heat shock pretreatment significantly reduced the release of LDH and relieved the oxidative stress-mediated inhibition of total protein synthesis. Moreover, HSP7-2 anti-sense oligonucleotide could remarkably block the protective effect of heat shock pretreatment on the cellular injuries induced by H2O2., Conclusion: HSP72 plays a most important role in the acute injury of cardiomyocyte mediated by oxidative stress.

Objective: To investigate the effect of oxidative stress on the accumulation of heat shock protein 70 (HSP70) within C2C12 myogenic cells., Methods: Heat shock response (42 degrees C for 1 h and recovery for 12 h at 37 degrees C) was used to induce the expression of heat shock protein 70. We constructed a recombinant plasmid of HSP70 with enhanced green fluorescent protein (EGFP). After being transfected transiently into C2C12 cells, immunoblotting was used to detect the expression of HSP70 induced by heat shock response and transfection. Immunocytochemistry, fluorescent microscopy and immunoblotting were used to detect the translocation of HSP70., Results: Immunoblotting showed that the overexpression of HSP70 was induced by heat shock response and transient transfenction. HSP70 localized within the cytoplasm of the normal cells, but HSP70 translocated from the cytoplasm to the nucleus and the nucleolus at 1 h after the treatment of oxidative stress (0.5 mmol/L H2O2) by using immunocytochemistry, fluorescent microscopy and immunoblotting for cellular partial proteins., Conclusion: Oxidative stress may induce the accumulation of heat shock protein 70 within the nucleolus.