Silicon nanowires have been synthesized in high yield and high purity by using a high-temperature laser-ablation method with growth rates ranging from 10 to 80 μm/h. Transmission electron microscopic investigation shows that the nanowires are crystalline Si, and have diameters ranging from 3 to 43 nm and length up to a few hundreds microns. Twins and stacking faults have been observed in the Si core of the nanowires. The lattice structure and constant of the nanowires as determined from x-ray diffraction (XRD) are nearly identical to those of bulk Si, although the relative XRD peak intensities are different from those of randomly oriented Si crystallites. Raman scattering from the nanowires shows an asymmetric peak at the same position as that of bulk crystalline silicon.

Silicon nanowires have been synthesized by laser ablation of Si powder targets at 1200 °C. Transmission electron microscopy study showed that most Si nanowires had smooth surfaces and nearly the same diameter of about 16 nm. Beside the most abundant smooth-surface nanowires, four other forms of nanowires, named spring-shaped, fishbone-shaped, frog-egg-shaped, and necklace-shaped nanowires, were observed. The formation of nanowires into different shapes was explained by the two-step growth model based on the vapor–liquid–solid mechanism.

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Background: Immunoglobulin E (IgE) belongs to a class of immunoglobulins involved in immune response to specific allergens. However, the roles of IgE and IgE receptor (FcεR1) in pathological cardiac remodeling and heart failure (HF) are unknown. Methods: Serum IgE levels and cardiac IgE receptor (FcεR1) expression were assessed in diseased hearts from human and mouse. The role of FcεR1 signaling in pathological cardiac remodeling was explored in vivo by FcεR1 genetic depletion, anti-IgE antibodies, and bone-marrow (BM) transplantation. The roles of IgE-FcεR1 pathway were further evaluated in vitro in primary cultured rat cardiomyocytes (CMs) and cardiac fibroblasts (CFs). RNA-seq and bioinformatic analyses were used to identify biochemical changes and signaling pathways that are regulated by IgE/FcεR1. Results: Serum IgE levels were significantly elevated in patients with HF as well as in two mouse cardiac disease models induced by chronic pressure overload via transverse aortic contraction (TAC) and chronic angiotensin II (Ang II) infusion. Interestingly, FcεR1 expression levels were also significantly up-regulated in failing hearts from human and mouse. Blockade of the IgE-FcεR1 pathway by FcεR1 knockout alleviated TAC- or Ang II-induced pathological cardiac remodeling and/or dysfunction. Anti-IgE antibodies (including the clinical drug, omalizumab) also significantly alleviated Ang II-induced cardiac remodeling. BM transplantation experiments indicated that IgE-induced cardiac remodeling was mediated through non-BM-derived cells. FcεR1 was found to be expressed in both CMs and CFs. In cultured rat CMs, IgE-induced CM hypertrophy and hypertrophic marker expression were abolished by depleting FcεR1. In cultured rat CFs, IgE-induced CF activation and matrix protein production were also blocked by FcεR1 deficiency. RNA-seq and signaling pathway analyses revealed that transforming growth factor-β (TGF-β) may be a critical mediator and blocking TGF-β indeed alleviated IgE-induced cardiomyocyte hypertrophy and cardiac fibroblast activation in vitro . Conclusions: Our findings suggest that IgE induction plays a causative role in pathological cardiac remodeling, at least partially via the activation of IgE-FcεR1 signaling in CMs and CFs. Therapeutic strategies targeting the IgE-FcεR1 axis may be effective for managing IgE-mediated cardiac remodeling.

Introduction: Quercetin was recently reported to help protect against osteoarthritis (OA) progression, but the molecular mechanism for that protective affect remains unclear. Methods: Here, OA model rats were intraperitoneally injected with quercetin, and the severity of cartilage damage in the rats was evaluated by H&E, Safranin O, and Toluidine blue, as well as by using the Osteoarthritis Research Society International (OARSI) Scoring System. Additionally, rat chondrocytes were treated with quercetin and then stimulated with IL-1β. The levels of pro-inflammatory cytokines (IL-1β, IL-18, and TNF-α) were detected by ELISA.Cell apoptosis was evaluated by flow cytometry and Hoechst staining. ROS levels were measured using a DCFH-DA probe. Protein expression was evaluated by Western blotting, immunohistochemical staining, and immunofluorescence. Results: Our data showed that quercetin attenuated the degeneration and erosion of articular cartilage, suppressed inflammation and apoptosis, and downregulated the levels of IRAK1, NLRP3, and caspase-3 expression. In vitro data showed that overexpression of NLRP3 could reverse the suppressive effect of quercetin on IL-1β-induced rat chondrocyte injuries. Importantly, rescue experiments confirmed that quercetin inhibited IL-1β-induced rat chondrocyte injuries in vitro by suppressing the IRAK1/NLRP3 signaling pathway. Conclusion:Our study indicated that quercetin inhibits IL-1β-induced inflammation and cartilage degradation by suppressing the IRAK1/NLRP3 signaling pathway.

The structure and bonding of amorphous carbon nanowires and amorphous carbon nanowires-converted multiwalled carbon nanotubes have been investigated with carbon K-edge near-edge x-ray absorption fine structure using surface-sensitive total electron yield, and bulk-sensitive fluorescence yield. The results strongly support that amorphous carbon nanowire is a precursor to multiwalled carbon nanotubes.

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