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The micro-cracks in a material lead to a reduction in its overall strength and service life. The emerging capsule-based self-healing system provides a new strategy for repairing the cracks, effectively delaying the potential damage of the matrix, and prolonging the service life of composite materials. Determining the optimal size and dosage of microcapsules required to repair cracks in the matrix is essential for the development and design of capsule-based self-healing materials. This paper presents a novel two-dimensional capsule-based self-healing model composite material whose surface is paved by reproducible and random cells and some microcapsules are randomly dispersed in those cells to investigate the rupture behavior of microcapsules forced by growing cracks. An analytical model is proposed from the viewpoint of geometrical probability to express the probability characteristics of the embedded microcapsules stimulated by linear cracks in a two-dimensional capsule-based self-healing model composite. Additionally, the effect of the size and dosage of the embedded microcapsules on the intersection probability is analyzed, and the maximal probability is also found to improve the self-healing efficiency. Finally, the accuracies of these probability values and theoretical solutions are verified via computer simulation, and the results show that the developed model of the geometrical probability of the crack intersection with microcapsules randomly distributed in the cells of the matrix will help to provide a theoretical basis for the quantitative design of capsule-based self-healing materials.

In controlling the angle error of laser profilometer contact measurement, the control model used in the past is subject to more external interference, which affects the measurement of other parameters, resulting in poor error control effect. Therefore, the angle error control model of laser profilometer contact measurement is designed by determining the initial zero position of the profilometer measuring sensor, compensating the non-linear error, designing the interference signal processing circuit, and avoiding the error measurement influenced by external factors. From the main error sources such as the perpendicularity, standard error, sensor error and other errors of the coordinate axis of the profilometer, the accuracy is distributed. According to the equal action principle, the measurement uncertainty of the profilometer is calculated, and the measurement is obtained. According to the interference signal processing circuit and measurement index, the serial communication control circuit is designed, and the angle error control model of laser profilometer contact measurement is constructed. The experimental results show that the designed laser profilometer contact measurement angle error control model has high precision and does not affect other parameters in the control process, which shows that the control model has good effect in practical application.

BackgroundThe occurrence of liver cancer is higher in males than in females, and the incidence increases during aging. Signaling pathways regulated by retinoid x receptor alpha (RXRalpha) are involved in hepatocellular carcinogenesis. The phenotype of hepatocyte RXRalpha deficient mice is different between genders. To explore the impact of hepatocyte RXRalpha deficiency on gender-dependent hepatic gene expression, we compared the expression profiles of cancer-related genes in 6 and 24 month old male and female mice.ResultsIn 6 month old mice, male mutant mice showed more cancer-related genes with alteration in mRNA levels than females did (195 vs. 60). In aged mice (24 month), female mutant mice showed greater deviation in mRNA expression levels of cancer-related genes than their male counterparts (149 vs. 82). The genes were classified into five categories according to their role in carcinogenesis: apoptosis, metastasis, cell growth, stress, and immune respnse. In each category, dependent upon age and gender, the genes as well as the number of genes with altered mRNA levels due to RXRalpha deficiency varies.ConclusionThe change in hepatic cancer-related gene expression profiles due to RXRalpha deficiency was gender- and age-dependent. The alteration of mRNA levels of cancer-related genes implied that aberrant RXRalpha signaling could potentially increase the risk of liver cancer and that retinoid signaling might contribute to gender- and age-associated liver cancer incidence.

Abstract Background The occurrence of liver cancer is higher in males than in females, and the incidence increases during aging. Signaling pathways regulated by retinoid × receptor α (RXRα) are involved in hepatocellular carcinogenesis. The phenotype of hepatocyte RXRα deficient mice is different between genders. To explore the impact of hepatocyte RXRα deficiency on gender-dependent hepatic gene expression, we compared the expression profiles of cancer-related genes in 6 and 24 month old male and female mice. Results In 6 month old mice, male mutant mice showed more cancer-related genes with alteration in mRNA levels than females did (195 vs. 60). In aged mice (24 month), female mutant mice showed greater deviation in mRNA expression levels of cancer-related genes than their male counterparts (149 vs. 82). The genes were classified into five categories according to their role in carcinogenesis: apoptosis, metastasis, cell growth, stress, and immune respnse. In each category, dependent upon age and gender, the genes as well as the number of genes with altered mRNA levels due to RXRα deficiency varies. Conclusion The change in hepatic cancer-related gene expression profiles due to RXRα deficiency was gender- and age-dependent. The alteration of mRNA levels of cancer-related genes implied that aberrant RXRα signaling could potentially increase the risk of liver cancer and that retinoid signaling might contribute to gender- and age-associated liver cancer incidence.

Abstract Background Our previous cDNA array results indicated KIAA0101 as one of the differentially expressed genes in human hepatocellular carcinoma (HCC) as compared with non-cancerous liver. However, it is necessary to study its expression at protein level in HCC and its biological function for HCC cell growth. Method Western blot and tissue array were performed to compare KIAA0101 protein expression level in paired human HCC and non-cancerous liver tissues from the same patients. Investigation of its subcellular localization was done by using dual fluorescence image examination and enriched mitochondrial protein Western blot analysis. The in vitro cell growth curve was used for examing the effect of over-expression of KIAA0101 in HCC cells. FACS was used to analyze the cell cycle pattern in KIAA0101 expression positive (+) and negative (-) cell populations isolated by the pMACSKKII system after KIAA0101 cDNA transfection. Results Western blot showed KIAA0101 protein expression was down-regulated in HCC tissues as compared with their counterpart non-cancerous liver tissues in 25 out of 30 cases. Tissue array also demonstrated the same pattern in 161 paired samples. KIAA0101 was predominantly localized in mitochondria and partially in nuclei. KIAA0101 cDNA transfection could inhibit the HCC cell growth in vitro. In cell cycle analysis, it could arrest cells at the G1 to S phase transition. Conclusion KIAA0101 protein expression was down-regulated in HCC. This gene could inhibit the HCC cell growth in vitro and presumably by its blocking effect on cell cycle.

Perovskite light‐emitting diodes (PeLEDs) are emerging candidates for the applications of solution‐processed full‐color displays. However, the device performance of deep‐blue PeLED still lags far behind that of their red and green counterparts, which is largely limited by low external quantum efficiency (EQE) and poor operational stability. Here, a facile and reliable crystallization strategy for perovskite grains is proposed, with improved deep‐blue emission through rational interfacial engineering. By modifying the substrate with potassium cation (K+) as the supplier of heterogeneous nucleation seeds, the interfacial K+‐guided grain growth is realized for well‐packed perovskite assemblies with high surface coverage and the controlled crystal orientation, leading to the enhanced radiative recombination and hole‐transport capabilities. Synergistical boost in device performance is achieved for deep‐blue PeLEDs emitting at 469 nm with a peak EQE of 4.14%, a maximum luminance of 451 cd m–2, and spectrally stable color coordinates of (0.125, 0.076) that matches well with the National Television System Committee (NTSC) standard blue. [ABSTRACT FROM AUTHOR]

Background: Neuroinflammation associated with advanced human immunodeficiency virus (HIV)-1 infection is often exacerbated by chronic cocaine abuse. Cocaine exposure has been demonstrated to mediate up-regulation of inflammatory mediators in in vitro cultures of microglia. The molecular mechanisms involved in this process, however, remain poorly understood. In this study, we sought to explore the underlying signaling pathways involved in cocaine-mediated activation of microglial cells.Methods: BV2 microglial cells were exposed to cocaine and assessed for toll-like receptor (TLR2) expression by quantitative polymerase chain reaction (qPCR), western blot, flow cytometry, and immunofluorescence staining. The mRNA and protein levels of cytokines (TNFα, IL-6, MCP-1) were detected by qPCR and ELISA, respectively; level of reactive oxygen species (ROS) production was examined by the Image-iT LIVE Green ROS detection kit; activation of endoplasmic reticulum (ER)-stress pathways were detected by western blot. Chromatin immunoprecipitation (ChIP) assay was employed to discern the binding of activating transcription factor 4 (ATF4) with the TLR2 promoter. Immunoprecipitation followed by western blotting with tyrosine antibody was used to determine phosphorylation of TLR2. Cocaine-mediated up-regulation of TLR2 expression and microglial activation was validated in cocaine-injected mice.Results: Exposure of microglial cells to cocaine resulted in increased expression of TLR2 with a concomitant induction of microglial activation. Furthermore, this effect was mediated by NADPH oxidase-mediated rapid accumulation of ROS with downstream activation of the ER-stress pathways as evidenced by the fact that cocaine exposure led to up-regulation of pPERK/peIF2α/ATF4 and TLR2. The novel role of ATF4 in the regulation of TLR2 expression was confirmed using genetic and pharmacological approaches.Conclusions: xThe current study demonstrates that cocaine-mediated activation of microglia involves up-regulation of TLR2 through the ROS-ER stress-ATF4-TLR2 axis. Understanding the mechanism(s) involved in cocaine-mediated up-regulation of ROS-ER stress/TLR2 expression and microglial activation could have implications for the development of potential therapeutic targets aimed at resolving neuroinflammation in cocaine abusers. [ABSTRACT FROM AUTHOR]