Laser‐driven solid‐state lighting with super‐brightness and compactness is recognized as a promising alternative to white light‐emitting diodes. However, it is quite difficult to achieve laser‐driven warm white light with long‐term stability due to the shortage of robust orange‐ or red‐emitting laser phosphors. In this work, an efficient and thermally robust orange‐red (La,Y)3Si6N11:Ce3+ (LYSN)‐BN phosphor‐in‐glass (PiG) film is proposed to realize warm white light, where h‐BN acts as an optical medium to enhance light scattering, a heat sink to reduce the temperature, and a protective layer to prevent LYSN from oxidation. The “LYSN+15 wt.% BN” PiG film shows an internal quantum efficiency of 70% and a luminance saturation threshold of 12.82 W mm−2, much higher than those without h‐BN (i.e., 57.5% and 7.63 W mm−2). A warm white light lamp fabricated by combining “LYSN+15 wt.% BN” PiG film with blue laser diodes, showing tunable correlated color temperatures (2800–5000 K), has a maximal luminous flux of 740 lm and a luminous efficacy of 133.5 lm W−1, which promises high collimation and penetration lighting in the rainy or foggy weather. By designing a composite orange‐red‐emitting phosphor converter, this work lays a foundation for realizing high quality laser‐driven warm white lighting source.
The objectives of the current study were to explore the effects of mannan oligosaccharide (MOS) supplementation in the diets of sow and (or) their offspring on intestinal bacteria, intestinal and systemic inflammation in the piglet. A total of 60 multiparous sows (4 ± 1 parity; Landrace × Yorkshire) were fed either control diet (sCON, n = 30) or a diet containing 400 mg kg−1 MOS (sMOS, n = 30) from day 86 of gestation until weaning (day 20 of postpartum). On day 7 of age, offspring (Duroc × Landrace Yorkshire) were assigned within sow treatments and fed control diet (pCON) or diet containing 800 mg kg−1 MOS (pMOS) for 28 d (end at 35 d of age), resulting in four piglet diet groups (n = 15 litters per diet group): sCON-pCON, sCON-pMOS, sMOS-pCON, and sMOS-pMOS. Results found that piglet diet MOS increased or tend to increase Lactobacillus amount in the ileum digesta (P < 0.01) and jejunum digesta (P = 0.07), respectively; while tend to decrease Escherichia coli amount in jejunum digesta (P =0.06) and cecum digesta (P = 0.08). Both sow and piglet diets add MOS (sMOS-pMOS) increased Lactobacillus amount but decreased E. coli amount in jejunum digesta (P < 0.05) compared with the sCON-pCON diet group. In addition, sow diet MOS (rather than piglet diet MOS) increased sIgA content in piglet jejunum mucosa compared with control (P = 0.04). Sow diet MOS decreased toll-like receptor 2 (TLR2), toll-like receptor 4 (TLR4), and interleukin 8 (IL-8) mRNA levels (P < 0.05) and tended to decrease nuclear factor-κB p65 (NF-κB p65) mRNA level (P = 0.07) in piglet intestinal lymphatic. The interaction effects between sow and piglet diets were found on the mRNA levels of NF- κB p65 (P = 0.03) and IL-8 (P = 0.02) in piglet jejunum. Finally, the sow diet MOS decreased proinflammatory cytokines IL-2 (P < 0.01) and IL-4 (P < 0.01) concentrations in piglet serum. Piglets diet MOS decreased the contents of IL-2 (P = 0.03), IL-4 (P = 0.01) and interferon (IFN)-γ (P < 0.01) while increased anti-inflammatory cytokine IL-10 (P < 0.01) content in serum. The interaction effects between sows and piglet diets on IL-4 (P = 0.02), IL-10 (P < 0.01), and IFN-γ (P = 0.08) were observed. In conclusion, sow and/or piglet diet MOS could improve intestinal microbiota, enhance intestinal mucosal immune competence, and suppress intestinal and systemic inflammation in the piglet.
Bronchial asthma poses a serious threat to human health. Previous studies have documented the role of long non-coding rnas (lncrnas) in asthma. However, the molecular mechanism underlying bronchial asthma remains unclear. The aim of the present study was to evaluate the role of the lncrna opa-interacting protein 5 antisense rna1 (oiP5-aS1) in the house dust mite-induced inflammatory response in human bronchial epithelial cells. BeaS-2B cells were treated with Dermatophagoides pteronyssinus peptidase 1 (der p1) to establish an in vitro model of asthma. oiP5-aS1 expression levels increased in BeaS-2B cells following der p1 treatment, while microrna (mir)-143-3p was downregulated. additionally, the levels of the pro-inflammatory factors tumor necrosis factor-α, interleukin (il)-6 and il-8 were measured, and apoptosis was evaluated following oiP5 silencing. oiP5-aS1 knockdown reduced the inflammatory response and apoptosis in BeaS-2B cells. Furthermore, using dual luciferase reporter assays and co-transfection experiments, it was demonstrated that the function of oiP5-aS1 was mediated by mir-143-3p. mir-143-3p overexpression attenuated the Der p1-induced inflammatory response and apoptosis of BeaS-2B cells by targeting high mobility group box 1 (HMGB1). in summary, oiP5-aS1 exacerbated Der p1-induced inflammation and apoptosis in BeaS-2B cells by targeting mir-143-3p via HMGB1.
Many studies have shown that resistant maltodextrin (RMD) possesses blood cholesterol lowering and anti-obesity effects. In order to investigate the effect of RMD on lipid metabolism in the liver, rats were fed with a high-fat (HF) diet for 7 weeks to induce hyperlipidemia and fatty liver. Normal control rats were fed with a normal diet. HF-diet-fed rats were treated with 5% RMD for 8 weeks. The results showed that the increased plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities, the increased hepatic triglyceride and total cholesterol levels, and fatty liver in HF-diet-fed rats were significantly decreased after supplementation with RMD. Supplementation with RMD significantly (1) induced AMP-activated protein kinase (AMPK) phosphorylation; (2) inhibited the activities of acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), and HMG-CoA reductase (HMGCR); (3) suppressed the protein expression of peroxisome proliferator activated receptor (PPAR)-γ; (4) increased β-oxidation of fatty acids by increasing the protein expression carnitine palmitoyl transferase 1α (CPT-1α) in the livers of HF-diet-fed rats. Taken together, supplementation of RMD was capable of inhibiting lipogenic enzyme activities and inducing fatty acid β-oxidation through increasing AMPK activation, thereby reducing lipid accumulation in the liver.
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