60 research outputs found

    Interpretation of inverted photocurrent transients in organic lead halide perovskite solar cells: proof of the field screening by mobile ions and determination of the space charge layer widths

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    In Methyl Ammonium Lead Iodide (MAPI) perovskite solar cells, screening of the built-in field by mobile ions has been proposed as part of the cause of the large hysteresis observed in the current/voltage scans in many cells. We show that photocurrent transients measured immediately (e.g. 100 μs) after a voltage step can provide direct evidence that this field screening exists. Just after a step to forward bias, the photocurrent transients are reversed in sign (i.e. inverted), and the magnitude of the inverted transients can be used to find an upper bound on the width of the space charge layers adjacent to the electrodes. This in turn provides a lower bound on the mobile charge concentration, which we find to be ≳1 × 1017 cm−3. Using a new photocurrent transient experiment, we show that the space charge layer thickness remains approximately constant as a function of bias, as expected for mobile ions in a solid electrolyte. We also discuss additional characteristics of the inverted photocurrent transients that imply either an unusually stable deep trapping, or a photo effect on the mobile ion conductivity

    Programmable Base Editing of the Sheep Genome Revealed No Genome-Wide Off-Target Mutations

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    Since its emergence, CRISPR/Cas9-mediated base editors (BEs) with cytosine deaminase activity have been used to precisely and efficiently introduce single-base mutations in genomes, including those of human cells, mice, and crop species. Most production traits in livestock are induced by point mutations, and genome editing using BEs without homology-directed repair of double-strand breaks can directly alter single nucleotides. The p.96R > C variant of Suppressor cytokine signaling 2 (SOCS2) has profound effects on body weight, body size, and milk production in sheep. In the present study, we successfully obtained lambs with defined point mutations resulting in a p.96R > C substitution in SOCS2 by the co-injection of BE3 mRNA and a single guide RNA (sgRNA) into sheep zygotes. The observed efficiency of the single nucleotide exchange in newborn animals was as high as 25%. Observations of body size and body weight in the edited group showed that gene modification contributes to enhanced growth traits in sheep. Moreover, targeted deep sequencing and unbiased family trio-based whole genome sequencing revealed undetectable off-target mutations in the edited animals. This study demonstrates the potential for the application of BE-mediated point mutations in large animals for the improvement of production traits in livestock species

    Optoelectronic Studies of Methylammonium Lead Iodide Perovskite Solar Cells with Mesoporous TiO2: Separation of Electronic and Chemical Charge Storage, Understanding Two Recombination Lifetimes, and the Evolution of Band Offsets during J-V Hysteresis

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    Methylammonium lead iodide (MAPI) cells of the design FTO/sTiO2/ mpTiO2/MAPI/Spiro-OMeTAD/Au, where FTO is fluorine-doped tin oxide, sTiO2 indicates solid-TiO2, and mpTiO2 is mesoporous TiO2, are studied using transient photovoltage (TPV), differential capacitance, charge extraction, current interrupt, and chronophotoamperometry. We show that in mpTiO2/MAPI cells there are two kinds of extractable charge stored under operation: a capacitive electronic charge (&sim;0.2 &mu;C/ cm2) and another, larger charge (40 &mu;C/cm2), possibly related to mobile ions. Transient photovoltage decays are strongly double exponential with two time constants that differ by a factor of &sim;5, independent of bias light intensity. The fast decay (&sim;1 &mu;s at 1 sun) is assigned to the predominant charge recombination pathway in the cell. We examine and reject the possibility that the fast decay is due to ferroelectric relaxation or to the bulk photovoltaic effect. Like many MAPI solar cells, the studied cells show significant J&minus;V hysteresis. Capacitance vs open circuit voltage (Voc) data indicate that the hysteresis involves a change in internal potential gradients, likely a shift in band offset at the TiO2/MAPI interface. The TPV results show that the Voc hysteresis is not due to a change in recombination rate constant. Calculation of recombination flux at Voc suggests that the hysteresis is also not due to an increase in charge separation efficiency and that charge generation is not a function of applied bias. We also show that the J&minus;V hysteresis is not a light driven effect but is caused by exposure to electrical bias, light or dark.</div

    NF-&kappa;B&ndash;Dependent Snail Expression Promotes Epithelial&ndash;Mesenchymal Transition in Mastitis

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    Mastitis is a common and important clinical disease in ruminants. This may be associated with inflammatory fibrosis if not treated promptly. Inflammation-derived fibrosis is usually accompanied by epithelial&ndash;mesenchymal transition (EMT) in epithelial cells. However, the precise molecular mechanism underlying mastitis-induced fibrosis remains unclear. Nuclear factor kappa-B (NF-&kappa;B) and Snail are key regulators of EMT. In this study, primary goat mammary epithelial cells (GMECs) were treated with 10 &mu;g/mL lipopolysaccharide (LPS) for 14 d to mimic the in vivo mastitis environment. After LPS treatment, the GMECs underwent mesenchymal morphological transformation and expressed mesenchymal cell markers. Snail expression was induced by LPS and was inhibited by suppression of the TLR4/NF-&kappa;B signaling pathway. Snail knockdown alleviated LPS-induced EMT and altered the expression of inflammatory cytokines. Finally, we found that the expression of key molecules of the TLR4/NF-&kappa;B/Snail signaling pathway was increased in mastitis tissues. These results suggest that Snail plays a vital role in LPS-induced EMT in GMECs and that the mechanism is dependent on the activation of the TLR4/NF-&kappa;B signaling pathway

    <?A3B2 tlsb=-.005w?>G protein-coupled estrogen receptor 1 mediates proliferation and adipogenic differentiation of goat adipose-derived stem cells through ERK1/2-NF-κB signaling pathway<?A3B2 tlsb?>

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    Adipose tissue formation and moderate fat deposition are important for the production performance and eating quality of livestock meats. The self-renewal and adipogenic differentiation of adipose-derived stem cells are responsible for the formation and development of adipose tissue. In addition, estrogen targeting G protein-coupled estrogen receptor 1 (GPER1) has been reported to modulate cell proliferation and differentiation during tissue and organ development. However, the potential correlation among estrogen, GPER1, proliferation, and adipogenic differentiation in goat adipose-derived stem cells (gADSCs) is still unclear. Herein, we demonstrated that 17β-estradiol enhances the proliferative ability of gADSCs, indicated by the increased cell number and cell viability, accompanied by up-regulated expressions of cyclin D1 and PCNA. Meanwhile, the adipogenic differentiation is promoted by 17β-estradiol, supported by higher ccumulation of intracellular lipids and increased expressions of PPARγ, ACC, and FABP4. Notably, these activities are all obviously reduced by administration with GPER1 antagonist G15, but GPER1 agonist G1 enhances cell proliferation and adipogenic differentiation. Moreover, GPER1 silencing diminishes cell proliferation and adipogenic differentiation. In parallel, 17β-estradiol elevates the protein level of nuclear p-p65. Furthermore, the phosphorylation of p65 is enhanced by G1 but inhibited by G15 and GPER1 silencing. In addition, the phosphorylation of p65 is mediated by ERK1/2, suggesting that estrogen targeting GPER1 regulates cell proliferation and adipogenic differentiation of gADSCs through the ERK1/2-NF-κB signaling pathway. This study may provide a strong theoretical basis for improving meat quality, flavor, and cold resistance of livestock.<?A3B2 tlsb?

    Sulforaphane Suppresses H<sub>2</sub>O<sub>2</sub>-Induced Oxidative Stress and Apoptosis via the Activation of AMPK/NFE2L2 Signaling Pathway in Goat Mammary Epithelial Cells

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    Oxidative stress in high-yielding dairy goats adversely affects lactation length, milk quality, and the economics of dairy products. During the lactation period, goat mammary epithelial cells (GMECs) are often in a state of disordered metabolic homeostasis primarily caused by the overproduction of reactive oxygen species (ROS). Sulforaphane (SFN), an electrophilic compound that is enriched in broccoli, is a promising antioxidant agent for future potential clinical applications. The objective of the present study was to investigate the function of SFN on hydrogen peroxide (H2O2)-induced oxidative damage in primary GMECs and the underlying molecular mechanisms. Isolated GMECs in triplicate were pretreated with SFN (1.25, 2.5, and 5 μM) for 24 h in the absence or presence of H2O2 (400 μM) for 24 h. The results showed that SFN effectively enhanced superoxide dismutase (SOD) activity, elevated the ratio of glutathione (GSH)/glutathione oxidized (GSSG), and reduced H2O2-induced ROS and malondialdehyde (MDA) production and cell apoptosis. Mechanically, SFN-induced nuclear factor erythroid 2-related factor 2 (NRF2/NFE2L2) translocation to the nucleus through the activation of the adenosine monophosphate-activated protein kinase (AMPK) signaling pathway coupled with inhibition of the caspase apoptotic pathway. In addition, GMECs were transfected with NFE2L2 small interfering RNA (NFE2L2 siRNA) for 48 h and/or treated with SFN (5 μM) for 24 h before being exposed to H2O2 (400 μM) for 24 h. We found that knockdown of NFE2L2 by siRNA abrogated the preventive effect of SFN on H2O2-induced ROS overproduction and apoptosis. Taken together, sulforaphane suppressed H2O2-induced oxidative stress and apoptosis via the activation of the AMPK/NFE2L2 signaling pathway in primary GMECs
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