Numerical and experimental study on the relationship between pull-out force and indentation depth of aviation wire crimp terminal.

To study the numerical relationship between the pull-out force and indentation depth of aviation wire crimp terminal, the crimping process between electrical contacts and stranded conductors and the tensile process of crimping assembly were simulated by the explicit dynamic finite element method. Regarding the variation trend of the tension of the crimping assembly with the tensile displacement during the tensile process and the failure mode, the numerical results and the experimental results showed a high degree of fit, and the relative error of the pull-out force was only 2.6%, which verified the reliability of the established numerical model. This model obtained the pull-out force curve of the crimp terminal that changes with the indentation depth. The authors suggest selecting the interval where the pull-out force is not less than 95% of the peak value, and the depth is less than the corresponding value at the peak value as the best value range of the indentation depth.

Soft Polymer-Based Technique for Cellular Force Sensing.

Soft polymers have emerged as a vital type of material adopted in biomedical engineering to perform various biomechanical characterisations such as sensing cellular forces. Distinct advantages of these materials used in cellular force sensing include maintaining normal functions of cells, resembling in vivo mechanical characteristics, and adapting to the customised functionality demanded in individual applications. A wide range of techniques has been developed with various designs and fabrication processes for the desired soft polymeric structures, as well as measurement methodologies in sensing cellular forces. This review highlights the merits and demerits of these soft polymer-based techniques for measuring cellular contraction force with emphasis on their quantitativeness and cell-friendliness. Moreover, how the viscoelastic properties of soft polymers influence the force measurement is addressed. More importantly, the future trends and advancements of soft polymer-based techniques, such as new designs and fabrication processes for cellular force sensing, are also addressed in this review.

Ageing modulates human dermal fibroblast contractility: Quantification using nano-biomechanical testing.

Dermal fibroblasts play a key role in maintaining homoeostasis and functionality of the skin. Their contractility plays a role in changes observed during ageing, especially in processes such as wound healing, inflammation, wrinkling and scar tissue formation as well as structural changes on extracellular matrix. Although alternations in skin physiology and morphology have been previously described, there remains a paucity of information about the influence of chronological ageing on dermal fibroblast contractility. In this study, we applied a novel nano-biomechanical technique on cell-embedded collagen hydrogels in combination with mathematical modelling and numerical simulation to measure contraction forces of normal human dermal fibroblasts (NHDF). We achieved quantitative differentiation of the contractility of cells derived from 'young' (< 30 years old) and 'aged' (> 60 years old) donors. Transforming growth factor ß1 (TGF-ß1) was used to stimulate the fibroblasts to assess their contractile potential. NHDF from aged donors exhibited a greater basal contractile force, while in contrast, NHDF from young donors have shown a significantly larger contractile force in response to TGF-ß1 treatment. These findings validate our nano-biomechanical measurement technique and provide new insights for considering NHDF contractility in regenerative medicine and as a biomarker of dermal ageing processes.

[The expression of the inflammation-related cytokines in pneumonia mice infected with influenza virus and regulation of Shufengxuanfei and Jiebiaoqingli herbal anti-virus formulas].

OBJECTIVE: To investigate the expression of the inflammation-related cytokines in pneumonia mice infected with influenza virus and regulation of Shufengxuanfei(SFXF) and Jiebiaoqingli (JBQL) Chinese herbal anti-virus formulas. METHODS: Mice were anesthetized and then infected intranasally by dropping 0.05 mL of influenza virus suspension (4×LD50;) except normal group. Mice were divided randomly into nine groups: normal group, model group (virus only), control group [11.375 g/(kg.d)Oseltamivir], low-dose SFXF [0.94 g/(kg.d)], medium-dose SFXF [1.88 g/(kg.d)], high-dose SFXF [3.76 g/(kg.d)], low-dose JBQL [1.09 g/(kg.d)], medium-dose JBQL [2.18 g/(kg.d)] and high-dose JBQL [4.36 g/(kg.d)]. Oseltamivir group, SFXF groups and JBQL groups were administered to mice by oral gavage in equal dose of 0.2 mL daily for 4 consecutive days, while the rest of the groups received water only. Total RNA was extracted in each group. Then gene chips were used to screen these RNA samples. Select differentially expressed genes of cytokines involved in inflammation. Some candidate genes, such as IL-1ß, IL-8, IL-10, RANTES and ICAM-1 were verified by qRT-PCR. To confirm the genes expression data from the microarray involved in inflammation in response to virus infection and treatment, we used qPCR to verify mRNA relative expressions of IL-1ß, IL-8, IL-10, RANTES and ICAM-1. The expression of IL-1ß protein in lung tissues was verified by Western blotting. RESULTS: IL-1ß, CXCR2, CCL5, IL-10, IL-6, IL-18, TGF-ß1 and CCL2 were up-regulated in model group. Gene expressions of IL-1ß, CXCR2, CCL5, IL-10 and IL-6 were significantly down-regulated by all therapeutic groups. SFXF in medium-dose and low-dose down-regulated gene expressions of IL-18, TGF-ß1, CCL2 and CCL5. IL-18 and CCL5 was down-regulated by both low-dose and medium-dose JBQL. qRT-PCR and western blot experiments showed that two formulas in medium-dose can down-regulate mRNA and protein expression of IL-1ß (P<0.01). Both SFXF and JBQL in medium-dose significantly decreased the IL-8, RANTES, ICAM-1 and IL-10 mRNA expression (P<0.05 or P<0.01), compared with the model group. As expected, qRT-PCR data were in good agreement with the microarray assay. CONCLUSION: The two anti-viral formulas may inhibit inflammatory immunopathogenesis, and may have the actions of protection the lung tissue from influenza-induced injury.

Gene Expression Profiles Underlying Selective T-Cell-Mediated Immunity Activity of a Chinese Medicine Granule on Mice Infected with Influenza Virus H1N1.

A Chinese medicine granule, Shu-Feng-Xuan-Fei (SFXF), is critical for viral clearance in early phase of influenza virus infection. In this study, 72 ICR mice were randomly divided into six groups: normal control group, virus control group, Oseltamivir group, low-dose SFXF, medium-dose SFXF, and high-dose SFXF. Mice were anesthetized and inoculated with 4LD50 of influenza virus A (H1N1) except normal control group. Oseltamivir group received 11.375 mg·kg(-1) ·d(-1) Oseltamivir Phosphate. SFXF 3.76, 1.88 and 0.94 g·kg(-1) ·d(-1) were administrated to mice in all SFXF groups. Each group was in equal dose of 0.2ml daily for 4 consecutive days. Mice were sacrificed and then total RNA was extracted in lung tissue. Some genes involved in T-cell-mediated immunity were selected by DNA microarray. These candidate genes were verified by Real-Time PCR and western immunoblotting. Compared with virus control group, in Toll-like receptor signaling pathway, 12 virus-altered genes were significantly reduced following medium-dose SFXF treatment. Eighteen antigen processing presentation-associated genes were upregulated by medium-dose SFXF. In the process of T cell receptor signaling pathway, 19 genes were downregulated by medium-dose SFXF treatment. On exploration into effector T cells activation and cytokines, all of altered genes in virus control group were reversed by medium-dose SFXF. Real-time PCR and western immunoblotting showed that the regulation of medium-dose SFXF in IL-4, IFN-γ, TNF-α, IL-1ß, TLR7, MyD88, p38, and JNK was superior to Oseltamivir and high-dose SFXF group. Therefore, SFXF granules could reduce influenza infected cells and activation of T cells.