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991.
992.
Encapsulation of electronic devices based on organic materials that are prone to degradation even under normal atmospheric conditions with hermetic barriers is crucial for increasing their lifetime. A challenge is to develop ultrabarriers that are impermeable, flexible, and preferably transparent. Another important requirement is that they must be compatible with organic electronics fabrication schemes (i.e., must be solution processable, deposited at room temperature and be chemically inert). Here, a lifetime increase of 1300 h for poly(3‐hexylthiophene) (P3HT) films encapsulated by uniform and continuous thin (≈10 nm) films of reduced graphene oxide (rGO) is reported. This level of protection against oxygen/water vapor diffusion is substantially better than conventional polymeric barriers such as Cytop, which degrades after only 350 h despite being 400 nm thick. Analysis using atomic force microscopy, X‐ray photoelectron spectroscopy, and high‐resolution transmission electron microscopy suggest that the superior oxygen gas/moisture barrier property of rGO is due to the close interlayer distance packing and absence of pinholes within the impermeable sheets. These material properties can be correlated to the enhanced lag time of 500 h. The results provide new insight for the design of high‐performance and solution‐processable transparent ultrabarriers for a wide range of encapsulation applications.  相似文献   
993.
The Src homology (SH) 3 domain has been shown recently to bind peptide sequences that lack the canonical PXXP motif. The diverse specificity in ligand recognition for a group of 15 SH3 domains has now been investigated using arrays of peptides derived from the proline-rich region of the SH2 domain-containing leukocyte protein of 76 kDa (SLP-76). A screen of the peptide arrays using individual or mixed SH3 domains has allowed the identification of a number of candidate SH3-binding peptides. Although some peptides contain the conventional PXXP motif, most are devoid of such a motif and are instead enriched in basic residues. Fluorescent polarization measurements using soluble peptides and purified SH3 domains demonstrated that several SH3 domains, including those from growth factor receptor-bound protein 2 (Grb2), NCK, and phospholipase C (PLC)-gamma1, bound with moderate affinities (10-100 microm) to a group of non-conventional peptides. Of particular interest, the PLC-gamma1 SH3 domain was found to associate with SLP-76 through at least three distinct sites, two of which bore a novel KKPP motif and the other contained the classic PXXP sequence. Intriguingly mutation of critical residues for the three sites not only affected binding of SLP-76 to the PLC-gamma1 SH3 domain but also to the Grb2 C-terminal SH3 domain, indicating that the binding sites in SLP-76 for the two SH3 domains are overlapped. Our studies suggest that the SH3 domain is an inherently promiscuous interaction module capable of binding to peptides that may or may not contain a PXXP motif. Furthermore the identification of numerous non-conventional SH3-binding peptides in SLP-76 implies that the global ligand pool for SH3 domains in a mammalian proteome may be significantly greater than previously acknowledged.  相似文献   
994.
Endothelial and smooth muscle cell-derived neuropilin-like protein (ESDN) is up-regulated in the neointima of remodeling arteries and modulates vascular smooth muscle cell (VSMC) growth. Platelet-derived growth factor (PDGF) is the prototypic growth factor for VSMCs and plays a key role in vascular remodeling. Here, we sought to further define ESDN function in primary human VSMCs. ESDN down-regulation by RNA interference significantly enhanced PDGF-induced VSMC DNA synthesis and migration. This was associated with increased ERK1/2, Src, and PDGF receptor (PDGFR)β phosphorylation, without altering total PDGFRβ expression levels. In binding assays, ESDN down-regulation significantly increased 125I-PDGF maximum binding (Bmax) to PDGF receptors on VSMCs without altering the binding constant (Kd), raising the possibility that ESDN regulates PDGFR processing. ESDN down-regulation significantly reduced ligand-induced PDGFRβ ubiquitination. This was associated with a significant reduction in the expression level of c-Cbl, an E3 ubiquitin ligase that ubiquitinylates PDGFRβ. Thus, ESDN modulates PDGF signaling in VSMCs via regulation of PDGFR surface levels. The ESDN effect is mediated, at least in part, through effects on PDGFRβ ubiquitination. ESDN may serve as a target for regulating PDGFRβ signaling in VSMCs.Vascular injury initiates a cascade of events that ultimately leads to vascular remodeling and often intimal hyperplasia. Vascular smooth muscle cell (VSMC)2 proliferation and migration are key cellular events in this process. Platelet-derived growth factor (PDGF)-BB is released by platelets, endothelial cells, VSMCs, and inflammatory cells at the sites of vascular injury and is a particularly potent regulator of VSMC proliferation and migration (1). PDGF binding to PDGF receptor (PDGFR)β in VSMCs leads to receptor dimerization, autophosphorylation, and activation of downstream signaling pathways, including MAPK. The ligand-bound receptor is internalized through the endocytotic pathway and may either recycle to the membrane or undergo ubiquitination and lysosomal degradation (2). A number of endogenous stimulatory and inhibitory regulators, including the E3 ubiquitin ligase, c-Cbl (3), tightly regulate the mitogenic stimulus by modulating the duration and intensity of the signal.We have identified endothelial and smooth muscle cell-derived neuropilin-like protein (ESDN, also called CLCP1 or DCBLD2) as a marker and regulator of cell proliferation in vascular remodeling (4). ESDN is a transmembrane protein with a domain structure similar to neuropilins (5, 6). ESDN can be induced by PDGF-BB and serum and is highly expressed in the neointima of injured rat (5), mouse (4), and human (4) arteries. ESDN expression parallels cell proliferation in the vessel wall in vivo (4). Furthermore, ESDN is up-regulated in proliferating VSMCs, and ESDN overexpression inhibits VSMC growth (4). Here, we expand the scope of our previous studies to demonstrate that ESDN regulates PDGF-induced VSMC migration and inhibits PDGF signaling in VSMCs. We further establish that this effect is mediated, at least in part, through changes in the surface expression of PDGF receptors. Finally, our study indicates that ESDN mediates PDGFRβ ubiquitination by regulating c-Cbl gene expression.  相似文献   
995.
A strain Aureobasidium pullulans AP329, was used for the production of pullulan by employing hydrolysed sweet potato as cultivation media. Hydrolysis with α-amylase alone resulted in the lowest yields of pullulan. In contrast continuous hydrolysis with pullulanase and the β-amylase in sweet potato itself gave higher yields, but prolonged hydrolysis with amyloglucosidase decreased the yield. The maximum pullulan yield (29.43 g/l) was achieved at the dextrose equivalent value of 45 and pH of 5.5 for 96 h. As a substitute of sucrose, hydrolysed sweet potato was found to be hopeful and the yield of pullulan was higher than that of glucose and sucrose. The molecular weight of pullulan obtained from hydrolysed sweet potato media was much higher than that of sucrose and glucose media. Results of this work indicated that sweet potato was a promising substrate for the economical production of pullulan.  相似文献   
996.
Background Intercellular adhesion molecule-1 (ICAM-1) was involved in the pathogenetic mechanisms responsible for ischemic stroke (IS). Population-based sample have revealed gene-gender interaction in blood pressure which is major risk for IS. We sought to evaluate whether ICAM-1 K469E polymorphism was involved in the causation of IS and whether it was different between female and male. Methods A 1:1 case-control study was conducted. The K469E polymorphism of ICAM-1 gene were analyzed by polymerase chain reaction (PCR) and restriction enzyme analysis in Chinese patients with IS (n = 309) and elderly subjects without IS (n = 309). Results ICAM-1 K469E polymorphism was significantly associated with IS. Interestingly, a further analysis stratified by sex found that there was significance between 469E genotypes and IS in female, but not in male. Multiple regression analysis revealed that ICAM-1 K469E polymorphism was still significantly associated with IS, compared with ICAM-1 KK genotype in all population (OR = 1.60, P = 0.030). Stratified by sex, EE combined EK was contributory factor to IS in female (OR = 3.03, P = 0.004), but not in male. After adjustment for confounding factors, the interaction between female and ICAM-1 EK/EE genotypes was found (OR = 3.54, P = 0.001). Conclusions It is suggested that the ICAM-1 469E allele may be important in the pathogenesis of ischemic stroke, especially in female but not in male. Xiao-Xia Li and Jian-Ping Liu have contributed equally.  相似文献   
997.
998.
Three novel cadmium(II) complexes [Cd2(tbpo)(O2CC6H4-p-NO2)2]ClO4·3CH3OH (1) [Cd2(bbap)(O2CC6H4-p-NO2)2]ClO4·4.5CH3OH·0.75H2O (2) and [Cd(ntb)(O2CC6H4-p-NO2)]ClO4·4CH3OH (3) have been synthesized and characterized by IR, elemental analysis, 1H NMR and X-ray crystallography, where tbpo and bbap are anions of N,N,N′,N′-tetrakis(2-benzimidazolylmethyl)-2-hydroxo-1,3-diaminopropane and 2,6-bis[bis(2-benzimidazolylmethyl)aminomethyl]-4-methylphenol, respectively; ntb is tris(2-benzimidazolymethyl)amine. Complexes 1 and 2 contain μ-phenolate-bridged and μ-alkoxo-bridged dicadmium(II) cores with the Cd1?Cd2 separation of 3.671 Å for complex 1 and 3.718 Å for 2. One of the 4-nitrobenzoate anions bridged the two cadmium(II) ions in syn-anti mode through its carboxylate group, the other 4-nitrobenzoate is only coordinated with Cd2 in bidentate chelating mode. The two central cadmium(II) atoms are in trigonal bipyramidal and pentagonal bipyramidal geometry. In complex 3, the cadmium(II) atom is coordinated with four nitrogen atoms of ntb and one carboxylate oxygen atom of 4-nitrobenzoate in distorted trigonal bipyramidal geometry. Experiment shows that there is a higher affinity of 4-nitrobenzoate anion as coligand with the dinuclear [Cd2(tbpo)]3+ and [Cd2(bbap)]3+ cores than that with the mononuclear [Cd(ntb)]2+ core.  相似文献   
999.
1000.
Associations of ATGL gene polymorphisms with chicken growth and fat traits   总被引:1,自引:0,他引:1  
Adipose triglyceride lipase (ATGL) catalyses the initial step in triglyceride hydrolysis, so theATGL gene is a candidate for growth and fat traits in chickens. Nine reported single-nucleotide polymorphisms (SNPs) located in 3 exons of the chickenATGL gene were chosen for genotyping an F2 population. Only 5 SNPs were confirmed for polymorphisms and used for association analyses. The results show that c.531G>A (p.E177Syn) was not associated with any growth and fat traits (P > 0.05), but c.782G>A (p.S261N) was associated with body weight (BW) on days 14, 21, 35, 63, 70, 77, cingulated fat width and abdominal fat pad weight (P< 0.05), and significantly associated with BW on days 42, 49, and 56 (P < 0.01). Significant associations of c.903C>T (p.F301Syn) with BW on days 49 and 77 days and crude protein content of breast muscle (P < 0.05), and c. 1164G>A (p.K388Syn) with BW on day 7 (P< 0.05) were also detected. Additionally, c. 1069T>C (p.L357Syn) was associated with breast muscle colour (P < 0.05), and significantly associated with crude fat (ether extract) content of breast muscle (P< 0.01). Thus the missense SNP of c.782G>A (p.S261N) was significantly associated with the largest number of chicken growth and fat traits in this study.  相似文献   
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