No abstract

MicroRNAs (miRNAs) are 21-24-nucleotide non-coding RNAs found in diverse organisms. Although hundreds of miRNAs have been cloned or predicted, only very few miRNAs have been functionally characterized. Embryo implantation is a crucial step in mammalian reproduction. Many genes have been shown to be significantly changed in mouse uterus during embryo implantation. However, miRNA expression profiles in the mouse uterus between implantation sites and inter-implantation sites are still unknown. In this study, miRNA microarray was used to examine differential expression of miRNAs in the mouse uterus between implantation sites and inter-implantation sites. Compared with inter-implantation sites, there were 8 up-regulated miRNAs at implantation sites, which were confirmed by both Northern blot and in situ hybridization. miR-21 was highly expressed in the subluminal stromal cells at implantation sites on day 5 of pregnancy. Because miR-21 was not detected in mouse uterus during pseudopregnancy and under delayed implantation, miR-21 expression at implantation sites was regulated by active blastocysts. Furthermore, we showed that Reck was the target gene of miR-21. Our data suggest that miR-21 may play a key role during embryo implantation.

We present a time-resolved spectral analysis of 51 long and 11 short bright gamma-ray bursts (GRBs) observed with the Fermi/Gamma-Ray Burst Monitor, paying special attention to E p evolution within each burst. Among eight single-pulse long GRBs, five show an evolution from hard to soft, while three show intensity tracking. The multi-pulse long GRBs have more complicated patterns. Statistically, the hard-to-soft evolution pulses tend to be more asymmetric than the intensity-tracking ones, with a steeper rising wing than the falling wing. Short GRBs have E p tracking intensity exclusively with the 16 ms time-resolution analysis. We performed a simulation analysis and suggest that for at least some bursts, the late intensity-tracking pulses could be a consequence of overlapping hard-to-soft pulses. However, the fact that the intensity-tracking pattern exists in the first pulse of the multi-pulse long GRBs and some single-pulse GRBs, suggests that intensity tracking is an independent component, which may operate in some late pulses as well. For the GRBs with measured redshifts, we present a time-resolved E p −L γ,iso correlation analysis and show that the scatter of the correlation is comparable to that of the global Amati/Yonetoku relation. We discuss the predictions of various radiation models regarding E p evolution, as well as the possibility of a precessing jet in GRBs. The data pose a great challenge to each of these models, and hold the key to unveiling the physics behind GRB prompt emission.

We describe a rapid, simple, room-temperature technique for the production of large-scale metallic thin films with tunable plasmonic properties assembled from size-selected silver nanoplates (SNPs). We outline the properties of a series of ultrathin monolayer metallic films (8-20 nm) self-assembled on glass substrates in which the localized surface plasmon resonance can be tuned over a range from 500 to 800 nm. It is found that the resonance peaks of the films are strongly dependent on the size of the nanoplates and the refractive index of the surrounding dielectric. It is also shown that the bandwidth and the resonance peak of the plasmon resonance spectrum of the metallic films can be engineered by simply controlling aggregation of the SNP. A three-dimensional finite element method was used to investigate the plasmon resonance properties for individual SNPs in different dielectrics and plasmon coupling in SNP aggregates. A 5-17 times enhancement of scattering from these SNP films has been observed experimentally. Our experimental results, together with numerical simulations, indicate that this self-assembly method shows great promise in the production of nanoscale metallic films with enormous electric-field enhancements at visible and near-infrared wavelengths. These may be utilized in biochemical sensing, solar photovoltaic, and optical processing applications.

Phase II drug-metabolizing enzymes, such as glutathione S-transferase and quinone reductase, play an important role in the detoxification of chemical carcinogens. The induction of these detoxifying enzymes by a variety of agents occurs at the transcriptional level and is regulated by a cis-acting element, called the antioxidant response element (ARE) or electrophile-response element. In this study, we identified a signaling kinase pathway that negatively regulates ARE-mediated gene expression. Treatment of human hepatoma HepG2 and murine hepatoma Hepa1c1c7 cells with tert-butylhydroquinone (tBHQ) stimulated the activity of p38, a member of mitogen-activated protein kinase family. Inhibition of p38 activation by its inhibitor, SB203580, enhanced the induction of quinone reductase activity and the activation of ARE reporter gene by tBHQ. In contrast, SB202474, a negative analog of SB203580, had little effect. Consistent with this result, interfering with the p38 kinase pathway by overexpression of a dominant-negative mutant of p38 or MKK3, an immediate upstream regulator of p38, potentiated the activation of the ARE reporter gene by tBHQ, whereas the wild types of p38 and MKK3 diminished such activation. In addition, inhibition of p38 activity augmented the induction of ARE reporter gene activity by tert-butylhydroxyanisole, sulforaphane, and ␤-naphthoflavone. Thus, p38 kinase pathway functions as a negative regulator in the AREmediated induction of phase II detoxifying enzymes.

Quantum dot (QD) light-emitting diodes (LEDs) are a promising candidate for high-efficiency, color-saturated displays. This work reports on the size effect of sol−gel synthesized ZnO nanoparticles (NPs) in which sizes of 2.9, 4.0, and 5.5 nm, were used as an electron transfer layer in QLEDs. The size of the NPs was estimated by transmission electron microscopy (TEM) and its effect on QLED performance was investigated by photoluminescence decay lifetime and electron mobility of ZnO NPs. It was found that as the size of the NP decreased from 5.5 to 2.9 nm, the conductivity increased, whereby the electron mobility was enhanced from 7.2 × 10 −4 cm 2 /V•s to 4.8 × 10 −3 cm 2 /V•s and electron decay lifetime increased from 5.11 to 6.68 ns. A comparison of NP size effects shows that the best performance is achieved with the 2.9 nm sized ZnO, which yields a turn on voltage of 3.3 V, a maximum current efficiency of 12.5 cd/A, power efficiency of 4.69 lm/W and external quantum efficiencies (EQE) of 4.2%. This is most likely due to the higher electron mobility in the smaller ZnO NPs, which facilitates electron transfer from the NPs to QDs, along with the slow exciton dissociation in the QD layer as a result of more favorable energy level alignment at the interface of smaller ZnO NPs and the adjacent emissive layer.

Background: Our study aim was to evaluate the therapeutic efficacy and mechanisms of miR-133-overexpressing mesenchymal stem cells (MSCs) on acute myocardial infarction. Methods: Rat MSCs were isolated and purified by whole bone marrow adherent culturing. After transfection with the agomir or antagomir of miR-133, MSCs were collected for assay of cell vitality, apoptosis, and cell cycle progression. At the same time, exosomes were isolated from the supernatant to analyze the paracrine miR-133. For in-vivo studies, constitutive activation of miR-133 in MSCs was achieved by lentivirus-mediated miR-133 overexpression. A rat myocardial infarction model was created by ligating the left anterior descending coronary artery, while control MSCs (vector-MSCs) or miR-133-overexpressed MSCs (miR-133-MSCs) were injected into the zone around the myocardial infarction. Subsequently, myocardial function was evaluated by echocardiography on days 7 and 28 post infarction. Finally the infarcted hearts were collected on days 7 and 28 for myocardial infarct size measurement and detection of snail 1 expression. Results: Hypoxia-induced apoptosis of MSCs obviously reduced, along with enhanced expression of total poly ADP-ribose polymerase protein, after miR-133 agomir transfection, while the apoptosis rate increased in MSCs transfected with miR-133 antagomir. However, no change in cell viability and cell-cycle distribution was observed in control, miR-133-overexpressed, and miR-133-interfered MSCs. Importantly, rats transplanted with miR-133-MSCs displayed more improved cardiac function after acute myocardial infarction, compared with those that received vector-MSC injection. Further studies indicated that cardiac expression of snail 1 was significantly repressed by adjacent miR-133-overexpressing MSCs, and both the inflammatory level and the infarct size decreased in miR-133-MSC-injected rat hearts.

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