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In this paper, we review the status of the multifunctional experimental platform at the National Laboratory of High Power Laser and Physics (NLHPLP). The platform, including the SG-II laser facility, SG-II 9th beam, SG-II upgrade (SG-II UP) facility, and SG-II 5 PW facility, is operational and available for interested scientists studying inertial confinement fusion (ICF) and a broad range of high-energy-density physics. These facilities can provide important experimental capabilities by combining different pulse widths of nanosecond, picosecond, and femtosecond scales. In addition, the SG-II UP facility, consisting of a single petawatt system and an eight-beam nanosecond system, is introduced including several laser technologies that have been developed to ensure the performance of the facility. Recent developments of the SG-II 5 PW facility are also presented.
Dairy cows with type II ketosis display hepatic fat accumulation and hyperinsulinemia, but the underlying mechanism is not completely clear. This study aimed to clarify the regulation of lipid metabolism by insulin in cow hepatocytes. In vitro, cow hepatocytes were treated with 0, 1, 10, or 100 nm insulin in the presence or absence of AICAR (an AMP-activated protein kinase alpha (AMPKα) activator). The results showed that insulin decreased AMPKα phosphorylation. This inactivation of AMPKα increased the gene and protein expression levels of carbohydrate responsive element-binding protein (ChREBP) and sterol regulatory element-binding protein-1c (SREBP-1c), which downregulated the expression of lipogenic genes, thereby decreasing lipid biosynthesis. Furthermore, AMPKα inactivation decreased the gene and protein expression levels of peroxisome proliferator-activated receptor-α (PPARα), which upregulated the expression of lipid oxidation genes, thereby increasing lipid oxidation. In addition, insulin decreased the very low density lipoprotein (VLDL) assembly. Consequently, triglyceride content was significantly increased in insulin treated hepatocytes. Activation of AMPKα induced by AICAR could reverse the effect of insulin on PPARα, SREBP-1c, and ChREBP, thereby decreasing triglyceride content. These results indicate that insulin inhibits the AMPKα signaling pathway to increase lipid synthesis and decrease lipid oxidation and VLDL assembly in cow hepatocytes, thereby inducing TG accumulation. This mechanism could partly explain the causal relationship between hepatic fat accumulation and hyperinsulinemia in dairy cows with type II ketosis.
Elevated levels of blood interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumour necrosis factor–α (TNF–α) increase insulin resistance and result in inflammation. It is not clear whether elevated blood level of acetoacetate (ACAC) and decreased blood level of glucose, which are the predominant characteristics of clinical biochemistry in ketotic dairy cows, increase proinflammatory cytokines and subsequent inflammation. The objective of this study was to test the hypothesis that ACAC and glucose activate the NF-κB signalling pathway to regulate cytokines expression in bovine hepatocytes. Bovine hepatocytes were cultured with ACAC (0–4·8 mm) and glucose (0–5·55 mm) with or without NF-κB inhibitor PDTC for 24 h. The secretion and mRNA levels of cytokines were determined by enzyme-linked immunosorbent assay (ELISA) and real-time fluorescence quantitative polymerase chain reaction (qRT-PCR). The NF-κB signalling pathway activation was evaluated by western blotting. Results showed that the secretion and expression of IL-1β, IL-6 and TNF-α increased in an ACAC dose-dependent manner. Additionally, there was an increase in the secretion and mRNA expression of these three cytokines in glucose treatment group, which increased significantly when the glucose concentrations exceed 3·33 mm. Furthermore, both ACAC and glucose upregulated NF-κB p65 protein expression and IκBα phosphorylation levels. However, these effects were reduced by PDTC. These results demonstrate that elevated levels of ACAC and glucose increase the synthesis and expression of proinflammatory factors by activating NF-κB signalling pathway in hepatocytes, which may contribute to inflammation injury in ketotic dairy cows.
The intensity distributions of a high-power broadband laser beam passing through a nonlinear optical medium with defects and then propagating in free space are investigated based on the general nonlinear Schrödinger equation and the split-step Fourier numerical method. The influences of the bandwidth of the laser beam, the thickness of the medium, and the defects on the light intensity distribution are revealed. We find that the nonlinear optical effect can be suppressed and that the uniformity of the beam can be improved for a high-power broadband laser beam with appropriate wide bandwidth. It is also found that, under the same incident light intensity, a thicker medium will lead to a stronger self-focusing intensity, and that the influence of defects in the optical elements on the intensity is stronger for a narrowband beam than for a broadband beam.
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