RESUMEN
To improve the thermal and combustion properties of nanothermites, a design theory of changing the state of matter and structural state of the reactants during reaction was proposed. The Al/MoO3/KClO4 (Kp) nanothermite was prepared and the Al/MoO3 nanothermite was used as a control. SEM and XRD were used to characterize the nanothermites; DSC was used to test thermal properties; and constant volume and open combustion tests were performed to examine their combustion performance. Phase and morphology characterization of the combustion products were performed to reveal the mechanism of the aluminothermic reaction. The results show that the Al/MoO3/Kp nanothermite exhibited excellent thermal properties, with a total heat release of 1976 J·g- 1, increasing by approximately 33% of 1486 J·g- 1 of the Al/MoO3 nanothermite, and activation energy of 269.66 kJ·mol- 1, which demonstrated higher stability than the Al/MoO3 nanothermite (205.64 kJ·mol- 1). During the combustion test, the peak pressure of the Al/MoO3/Kp nanothermite was 0.751 MPa, and the average pressure rise rate was 25.03 MPa·s- 1, much higher than 0.188 MPa and 6.27 MPa·s- 1 of the Al/MoO3 nanothermite. The combustion products of Al/MoO3 nanothermite were Al2O3, MoO, and Mo, indicating insufficient combustion and incomplete reaction, whereas, the combustion products of Al/MoO3/Kp nanothermite were Al2O3, MoO, and KCl, indicating complete reaction. Their "coral-like" morphology was the effect of reactants solidifying after melting during the combustion process. The characterization of reactants and pressure test during combustion reveals the three stages of aluminothermic reaction in thermites. The excellent thermal and combustion performance of Al/MoO3/Kp nanothermite is attributed to the melt and decomposition of Kp into O2 in the third stage. This study provides new ideas and guidance for the design of high-performance nanothermites.
RESUMEN
The success of a small-caliber artificial vascular graft in the host in order to obtain functional tissue regeneration and remodeling remains a great challenge in clinical application. In our previous work, a silk-based, small-caliber tubular scaffold (SFTS) showed excellent mechanical properties, long-term patency and rapid endothelialization capabilities. On this basis, the aim of the present study was to evaluate the vascular reconstruction process after implantation to replace the common carotid artery in rabbits. The new tissue on both sides of the SFTSs at 1 month was clearly observed. Inside the SFTSs, the extracellular matrix (ECM) was deposited on the pore wall at 1 month and continued to increase during the follow-up period. The self-assembled collagen fibers and elastic fibers were clearly visible in a circumferential arrangement at 6 months and were similar to autologous blood vessels. The positive expression rate of Lysyl oxidase-1 (LOXL-1) was positively correlated with the formation and maturity of collagen fibers and elastic fibers. In summary, the findings of the tissue regeneration processes indicated that the bionic SFTSs induced in situ angiogenesis in defects.
RESUMEN
Serotonin exerts important functions in several liver pathophysiological processes. In this study, we investigated the role of serotonin in concanavalin A (Con A)-induced liver fibrosis (LF) in mice and the underlying mechanisms. To establish the mouse model of LF, mice of wild-type (WT) and tryptophan hydroxylase 1 (Tph1) knockout (serotonin depletion) received Con A for 8 successive weeks. Degree of fibrosis was assessed by Sirius red staining, as well as the measurements of alpha smooth muscle actin (α- SMA), hydroxyproline (Hyp) and type I collagen in liver tissues. To elucidate the potential mechanisms, we assessed the effect of serotonin depletion on inflammatory, oxidative stress as well as TGF-ß1/Smads signaling pathway. We found that serotonin depletion significantly inhibited collagen deposition as evaluated by less collagenous fiber in Sirus Red staining and reduced contents of Hyp and type I collagen. In addition, the absence of serotonin significantly inhibited the release of several inflammatory cytokines, including interleukin-6 (IL-6), interferon-gamma (IFN-γ), tumor necrosis-alpha (TNF-α), and transforming growth factor ß1 (TGF-ß1). Oxidative stress was also largely mitigated in LF mice with serotonin deficiency as manifested by the decreases of oxidative stress markers (malonaldehyde (MDA) and myeloperoxidase (MPO)), as well as the increases of antioxidant stress indicators (glutathione (GSH), and GSH-px, catalase (CAT), superoxide dismutase (SOD)) in liver tissues. Moreover, the lack of serotonin may provide an antifibrotic role by inhibiting the intrahepatic expressions of TGF-ß1, phosphorylated-smad2 (p-smad2), and phosphorylated-smad3 (p-smad3). These results indicated that, serotonin depletion attenuates Con A-induced LF through the regulation of inflammatory response, oxidative stress injury, and TGF-ß1/Smads signaling pathway.
