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Nerve injury can lead to defects in related motor functions. It is critical to achieve long‐term and convenient real‐time evaluation of motor function recovery status during nerve injury repair. In this study, an implantable PLLA/BTO piezoelectric sensor (PBPS) with good biodegradability and biocompatibility for real time evaluation of the motor function recovery after nerve injury is developed. PLLA fibers doped with BTO are employed as piezoelectric material in PBPS, which can convert the biomechanical signals generated by motion into electrical signals. PBPS can be implant simultaneously with commonly used tissue scaffolds for treatment in the rats with sciatic nerve injury. The linearity of the pressure and the output voltage of PBPS is ≈0.9445. For the evaluation effectiveness, as the treatment process progresses, the signals generated by PBPS exhibited good consistency with EMG signals, indicating effectively evaluation of the motor function. Moreover, the integration of PBPS and wireless module can break the limitations of time and space for sensing and realize wireless evaluation of motor function in rat. The implantable sensor based on PBPS may bring new ideas for the development of implantable bioelectronics. [ABSTRACT FROM AUTHOR]

Formaldehyde (FA) is a human leukemogen and is hematotoxic in human and mouse. The biological plausibility of FA-induced leukemia is controversial because few studies have reported FA-induced bone marrow (BM) toxicity, and none have reported BM stem/progenitor cell toxicity. We sought to comprehensively examine FA hematoxicity in vivo in mouse peripheral blood, BM, spleen and myeloid progenitors. We included the leukemogen and BM toxicant, benzene (BZ), as a positive control, separately and together with FA as co-exposure occurs frequently. We exposed BALB/c mice to 3 mg/m3 FA in air for 2 weeks, mimicking occupational exposure, then measured complete blood counts, nucleated BM cell count, and myeloid progenitor colony formation. We also investigated potential mechanisms of FA toxicity, including reactive oxygen species (ROS) generation, apoptosis, and hematopoietic growth factor and receptor levels. FA exposure significantly reduced nucleated BM cells and BM-derived colony-forming unit-granulocyte-macrophage (CFU-GM) and burst-forming unit-erythroid (BFU-E); down-regulated GM-CSFRα and EPOR expression; increased ROS in nucleated BM, spleen and CFU-GM cells; and increased apoptosis in nucleated spleen and CFU-GM cells. FA and BZ each similarly altered BM mature cells and stem/progenitor counts, BM and CFU-GM ROS, and apoptosis in spleen and CFU-GM but had differential effects on other end points. Co-exposure was more potent for several end points. Thus, FA is toxic to the mouse hematopoietic system, including BM stem/progenitor cells, and it enhances BZ-induced toxic effects. Our findings suggest that FA may induce BM toxicity by affecting myeloid progenitor growth and survival through oxidative damage and reduced expression levels of GM-CSFRα and EPOR.

Turbulence structures in flow over three types of wall roughness: sand-grain, cube roughness and a realistic, multi-scale turbine-blade roughness, are compared to structures observed in flow over a smooth wall in open channel flow at R e τ = 1000 , using direct numerical simulations. Two-point velocity correlations, length scales, inclination angles, and velocity spectra are analysed, and the applicability of Townsend's outer layer similarity hypothesis [Townsend. The structure of turbulent shear flow. Cambridge: Cambridge University Press; 1976] to these parameters was examined. Results from linear stochastic estimation suggest that, near the wall, the quasi-streamwise vortices observed in smooth-wall flow are present in the large-scale recessed regions of multi-scale roughness, whereas they are replaced by a pair of 'head-up, head-down' horseshoe structures in sandgrain and cube roughness, similar to those observed by Talapatra and Katz [Coherent structures in the inner part of a rough-wall channel flow resolved using holographic PIV. J Fluid Mech. 2012;711:161–170]. The configuration of conditional eddies near the wall suggests that the kinematical process of vortices differ for each kind of rough surface. Eddies over multiscale roughness are conjectured to obey a growth mechanism similar to those over smooth walls, while around the cube roughness the head-down horse-shoe vortices of Talapatra and Katz [Coherent structures in the inner part of a rough-wall channel flow resolved using holographic PIV. J Fluid Mech. 2012;711:161–170] may undergo solid-body rotation on top of a cube roughness on account of the strong shear layer, shortening the longitudinal extent of near-wall structure and promoting turbulence production during this process. These results illustrate the sensitivity of turbulence structure to the roughness texture, particularly within the roughness sublayer. [ABSTRACT FROM AUTHOR]

Red (Ho3+:5F5→5I8), green (Ho3+:5S2,5F4→5I8), and blue (Tm3+:1D2→3F4 and 1G4→3H6) upconversion emissions were simultaneously generated in the transparent glass ceramics containing Nd3+/Yb3+/Tm3+/Ho3+:β-YF3 nanocrystals under 796 nm excitation. It was experimentally evidenced that Yb3+ ions acted as the bridging centers to prompt energy transfer from Nd3+ to Tm3+ and Ho3+. With appropriately optimizing the contents and relative ratios of the doped rare earth species, luminescence of various colors, including bright white light, was easily tuned in the glass ceramics. The related upconversion mechanisms were proposed. [ABSTRACT FROM AUTHOR]

Haptens 2-Methyl-4-(trifluoromethyl)thiazole-5-carboxylic acid and 2,6-Dibromo-4-(trifluoromethoxy)aniline, the two moieties of thifluzamide, were conjugated with carrier proteins for the synthesis of artificial antigens. Two distinct anti-thifluzamide polyclonal antibodies (PAb-1 and PAb-2) were produced from the immunized female Balb/c mice. The indirect competitive enzyme-linked immunosorbent assay (ic-ELISA) in two formats based on the PAbs was developed for thifluzamide analysis. The concentration of 50% inhibition (IC50) of ELISA-1 was 1.39 mg L−1 and its limit of detection (LOD) was 0.082 mg L−1. Meanwhile, ELISA-2 had a similar IC50 of 1.96 mg L−1 and a LOD of 0.074 mg L−1 as ELISA-1. Both the raised PAbs exhibited high specificity to thifluzamide. The recoveries for spiked samples including water and wheat ranged from 72.0% to 128.4%, and the accuracy of ELISA was confirmed by high-performance liquid chromatography. In summary, the ic-ELISA might be a promising tool for simple, sensitive and rapid detection of thifluzamide residues in real samples. [ABSTRACT FROM AUTHOR]

Formaldehyde (FA) is an environmental pollutant and an endogenous product believed to be involved in tumorigenesis. However, the underlying mechanism of observed FA effects has not been clearly defined. Paxillin is a focal adhesion protein that may play an important role in several signaling pathways. Many paxillin-interacting proteins are involved in the regulation of actin cytoskeleton organization, which is necessary for cell motility events associated with diverse biological responses, such as embryonic development, wound repair and tumor metastasis. P53 is important in multicellular organisms, where it regulates the cell cycle and thus functions as a tumor suppressor that is involved in preventing cancer. In this study, we investigated the effects of FA on paxillin–tyrosine phosphorylation and P53 expression in Hela cells by Western blot and immunofluorescence. Western blot analysis revealed that nonlethal concentrations of FA (0.5, 1.0 and 2.0 mM, with the exposure time for 0.5, 1.0 and 2.0 h, respectively) had downregulated paxillin and wild-type p53 genes expression while upregulated paxillin–tyrosine phosphorylation significantly. At the same time, phosphotyrosine at the focal adhesion sites detected by immunofluorescence assay obviously increased in Hela cells incubated with 2.0 mM FA for 2 h. The results suggested that paxillin and p53 genes expression may be involved in FA-related adverse effects and the mechanism may be involved in paxillin–tyrosine phosphorylation. [ABSTRACT FROM AUTHOR]