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A series of Sr-rich phase nitride phosphors, Eu2+ doped Ca 1-x Sr x AlSiN 3 , were synthesized by the solid state method under atmospheric pressure condition. It was found that Sr can substitute Ca in the CaAlSiN 3 lattice with the maximum solubility when x≤0.95. Under the excitation of 450 nm, the photoluminescence spectra of Ca 1-x Sr x AlSiN 3 :Eu2+ phosphors presents a blue-shift from 594 nm to 574 nm with increasing x value. The results indicate that Ca 1-x Sr x AlSiN 3 :Eu 0.001 phosphor can be a promising orange phosphor which could replace silicate orange phosphor for white light-emitting diodes.

Human respiratory syncytial virus (RSV) is a primary cause of lower respiratory tract infections and hospital visits during infancy and childhood. RSV invades host cells via a type I fusion (F) glycoprotein that has been recognized as the major viral antigen and an attractive therapeutic target against RSV infection in pediatric pneumonia. Like other type I fusion proteins such as HIV-1 gp41 and influenza hemagglutinin, the post-fusion conformation of RSV F contains a functional trimer-of-hairpins (TOH) motif that is characterized by a six-helix bundle in which three HR-C peptides antiparallelly pack against a trimeric coiled-coil core assembled by three HR-N peptides. Here, the intermolecular interaction between single HR-N and HR-C helical peptides is investigated at molecular level. An all-residue pairwise interaction potential profile is created, from which it is revealed that the packing tightness and effectiveness are not distributed evenly along the panhandling HR-N–HR-C complex interface; an intense hydrogen-bonding network is identified at one side of the complex, while the hydrophobic forces and van der Waals contacts are presented across the whole interface. A helix–helix structural module that covers the hydrogen-bonding network is stripped from the complex to define a reduced rHR-N–rHR-C interaction, which can be further truncated to derive a core region termed as minimized mHR-N–mHR-C interaction and represents the minimal requirement for the TOH helix–helix interaction of RSV F protein.

The present study was designed to evaluate the anti-inflammatory effect of fluoxetine (Flu) against cigarette smoke (CS)-induced chronic obstructive pulmonary disease (COPD) in rats. Forty male Sprague-Dawley (SD) rats were randomly assigned to five groups: control group, CS group, dexamethasone (2 mg/kg) group, and flu (2 mg/kg). H&E staining demonstrated that Flu inhibited CS-induced pathological injury. In addition, Flu could restore the levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in serum. Flu also inhibited the levels of cytokines including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β). Furthermore, flu significantly inhibited the protein levels of TLR/NF-κB and apoptosis pathway in CS-induced rats. Our findings suggested that flu might effectively ameliorate the progression of COPD via inflammation and apoptosis pathway in rats.

The aim of the present study was to assess the effects and mechanisms of Schisandrin B (SchB) on lipopolysaccharide (LPS)-induced acute lung injury (ALI). ALI was induced in mice by intratracheal instillation of LPS (1 mg/kg), and SchB (25, 50, and 75 mg/kg) was injected 1 h before LPS challenge by gavage. After 12 h, bronchoalveolar lavage fluid (BALF) samples and lung tissues were collected. Histological studies demonstrated that SchB attenuated LPS-induced interstitial edema, hemorrhage, and infiltration of neutrophils in the lung tissue. SchB pretreatment at doses of 25, 50, and 75 mg/kg was shown to reduce LPS-induced lung wet-to-dry weight ratio and lung myeloperoxidase activity. In addition, pretreatment with SchB lowered the number of inflammatory cells and pro-inflammatory cytokines including tumor necrosis factor-α, interleukin-1β, and interleukin-6 in BALF. The mRNA and protein expression levels of nuclear factor kappa B (NF-κB) signaling-related molecules activated by P2X7 were investigated to determine the molecular mechanism of SchB. The findings presented here suggest that the protective mechanism of SchB may be attributed partly to the decreased production of pro-inflammatory cytokines through the inhibition of P2X7/NF-κB activation.

The recognition and binding of viral envelope protein to pediatric receptor subverts the membrane-trafficking apparatus to mediate virion export in young children. Here, we described a successful computational design of peptide ligands to target the intermolecular interaction between the virus large envelope protein (LHB) and adaptin receptor (ADT). Based on the crystal structure of ADT in complex with an oligopeptide segment corresponding to the core binding site of LHB, a sequence-specific amino acid preference profile was determined systematically for the ADT-binding peptides using structural bioinformatics approach. With the information harvested from the profile, a genetic evolution procedure was run to improve the biological potency of a peptide population generated randomly from the LHB. A number of potential hits were obtained from the evolution, and four were measured to interact with ADT at micromolar level. A high-affinity hit peptide was then optimized according to computational structural analysis. It is revealed that a potent peptide can be divided into three regions, i.e. a negatively charged region at N-terminus, a hydrophobic core region in middle, and a small, polar region at C-terminal tail. In addition, the two termini of peptide are partially out of the active pocket of ADT, thus contributing moderately to the peptide binding.

Astragaloside IV (AS-IV) is a flavonoid from the plant Astragalus membranaceus (Fisch) Bge that has a wide range of therapeutic effects. The aim of the present study was to examine the effect of AS-IV on rats with necrotizing enterocolitis (NEC) under oxidative stress and inflammation. Newborn Sprague-Dawley rats were induced with NEC by asphyxia and hypothermia applied on 3 consecutive days. The rats were orally administered AS-IV at 25, 50 and 75 mg/kg for 4 days. The results revealed that AS-IV administration prevented NEC-induced decrease in the concentration of malondialdehyde and myeloperoxidase, and increase in the activity of glutathione (GSH) and superoxide dismutase in murine models. AS-IV also inhibited NEC-induced elevation in the levels of interleukin (IL)-6, IL-1β, tumor necrosis factor-α and nuclear factor (NF)-κB. The effects of AS-IV were achieved under inflammation and oxidative stress. Western blotting demonstrated that AS-IV substantially inhibited the phosphorylated (p)-IκBα, NF-κBp65, p-NF-κBp65 protein levels and increased vitamin D3 upregulated protein 1 (VDUP1) and IκBα protein levels. These data indicate that AS-IV may be effective in the protection of NEC-induced ileum degeneration by inhibiting the levels of inflammatory markers and oxidative stress via the regulation of the VDUP1/NF-κB signaling pathway.