109 research outputs found

    Nonfullerene Ternary Organic Photovoltaics with Long-Wavelength Light-Absorption Guest Donor Materials to Improve Photovoltaic Performance

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    In order to achieve efficient organic photovoltaics (OPVs), a ternary strategy was adopted with the efficient long-wavelength light-absorption donor material of PSBTBT as the third component material (guest donor) and the D18-Cl:BTP-eC9 binary film as the host photoactive layer, which facilitates the acquisition of absorption spectra complementary to those of D18-Cl and BTP-eC9. The PL spectrum of D18-Cl was covered by the absorption spectrum of PSBTBT, which further supports the energy transfer from D18-Cl to PSBTBT. In addition, the addition of a small amount of PSBTBT to the D18-Cl:BTP-eC9 binary film slightly changed the bulk and surface morphology of the photoactive layer, while appropriate phase separation size and a smooth surface could be achieved for both the D18-Cl:BTP-eC9 binary film and the optimized ternary film. Thus, with 10% PSBTBT as the third component material (D18-Cl/PSBTBT/BTP-eC9 ratio of 0.9:0.1:1.2), the ternary OPV shows a higher power conversion efficiency (PCE) of 17.35%. The improvement of photovoltaic performance is due to the short-circuit current density (JSC) enhancement from 24.65 to 26.23 mA cm–2, even though the open-circuit voltage (VOC) weakly decreased from 0.905 to 0.900 V. This work provides an effective method to find a guest polymer that matches the host binary photoactive layer, broadens the absorption spectrum, and provides efficient energy transfer within both donor materials

    Expression of the sensory epithelium marker Parvalbumin and Sox2 in new HCs, and Sox10 in new SCs.

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    <p>(<b>A–A′</b>) Images of samples double stained with Parvalbumin and EGFP at HC layer (A) and SC layer (A′) of the ectopic sensory patches in the utricle non-sensory region of a <i>CAG<sup>CreER+</sup>; Rosa26-NICD<sup>loxp/+</sup></i> embryo treated with tamoxifen at ∼E13 and analyzed at ∼E19. The arrow points to a new Parvalbumin+ HC. (<b>B–B′</b>) Triple staining of Myosin-VI, Sox2, and EGFP. Both ectopic HCs (B) and SCs (B′) were Sox2+. The arrow points to a new Sox2+/Myosin-VI+ HC. Of note, Myosin-VI was visualized in a pseudo-green color. (<b>C–C′</b>) Triple staining of Myosin-VI, Sox10, and EGFP. The arrow points to a new Myosin-VI+/Sox10−negative HC. The SCs (either EGFP+ or EGFP−negative) were Sox10+. Note that Myosin-VI was also visualized in a pseudo-green color. Scale bars: 20 µm.</p

    Flexible Lead-Free BiFeO<sub>3</sub>/PDMS-Based Nanogenerator as Piezoelectric Energy Harvester

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    Perovskite ferroelectric BiFeO<sub>3</sub> has been extensively researched in many application fields, but has rarely been investigated for the energy conversion of tiny mechanical motions in electricity in spite of its large theoretical remnant polarization. Here we demonstrate the fabrication of a flexible piezoelectric nanogenerator based on BiFeO<sub>3</sub> nanoparticles (NPs), which were synthesized using a sol–gel process. The BiFeO<sub>3</sub> NPs–PDMS composite device exhibits an output open circuit voltage of ∼3 V and short circuit current of ∼250 nA under repeated hand pressing. The output generation mechanism from the PNG is discussed on the basis of the alignment of electric dipoles in the composite film. It is demonstrated that the output power from the PNG can directly drive the light-emitting diode (LED) and charge capacitor. These results demonstrate that BiFeO<sub>3</sub> nanomaterials have the potential for large-scale lead-free piezoelectric nanogenerator applications

    Ectopic hair cells (HCs) and supporting cells (SCs) in the utricle with overactivation of NICD at E10.5.

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    <p>(<b>A</b>) Diagram to illustrate the strategy of driving constitutive NICD expression. (<b>B–C</b>) Low-magnification image of the utricle of <i>Rosa26-NICD<sup>loxp/+</sup></i> (B) and <i>CAG<sup>CreER+</sup>; Rosa26-NICD<sup>loxp/+</sup></i> (C) embryos treated with tamoxifen at ∼E10.5 and analyzed at ∼E19. (<b>D–D″</b>) A high-magnification three-dimensional image of the white rectangular area marked in (C), which belongs to the utricle non-sensory region (NSE). (<b>E–F</b>) Triple staining of Myosin-VI, Sox10, and EGFP at the HC layer (F) and SC layer (G). (<b>G–H</b>) Whole mount (G–G′) and trans-section (H) images of the utricular endogenous sensory epithelium stained with EGFP and Myosin-VI. HCs were absent in the small white dotted line circled region in HC layer (G) and SC layer (G′). Arrow in (H) also points to the area where HCs are missing. NSE: non-sensory region; XY: Confocal XY plane; YZ: Confocal YZ plane; XZ: Confocal XZ plane. Scale bars: 200 µm in (B) and 20 µm in (D–H).</p

    Overactivation of NICD in the postnatal utricle fails to generate new HCs at P6.

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    <p>Double staining of Myosin-VI and EGFP of utricles from <i>Rosa26-NICD<sup>loxp/+</sup></i> control mice (A–A′) and <i>CAG<sup>CreER+</sup>; Rosa26-NICD<sup>loxp/+</sup></i> experimental mice (B–B′). Both groups were treated with tamoxifen at P0/P1 and analyzed at P6. Although EGFP+ cells were present, no ectopic HCs were found in the experimental group. NSE: non-sensory region. Scale bars: 200 µm.</p

    Ectopic HCs in cochlear spiral ganglion and outer sulcus region.

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    <p>(<b>A–B′</b>) Triple staining of TUJ1, Myosin-VI, and EGFP. (B) The high-magnification image of the square area in (A). (B′) The image of confocal XZ plane through the dashed line in (B). Arrows target the same ectopic HC in (B) and (B′). (<b>C</b>) Double staining image of Synaptophysin (a synaptic marker) and Myosin-VI in the cochlear spiral ganglion region. Very adjacent to the new HC (inside the dotted white circle) lies the Synaptophysin+ dot, suggesting presence of the synaptic structure. (<b>D–E</b>) Images of samples stained with Myosin-VI antibody in experimental (D) and control (E) cochlear samples. Ectopic HCs were present in outer sulcus regions in the experimental but not the control group. OC: organ of Corti; OHCs: outer hair cells; IHCs: inner hair cells; XY: Confocal XY plane; XZ: Confocal XZ plane. Scale bars: 200 µm in (A) and 20 µm in (B, D) and 10 µm (C).</p

    Ectopic HCs in the cochlea with constitutive Notch1 signaling at E10.5.

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    <p>(<b>A–B″</b>) Images of the cochlea taken from <i>Rosa26-NICD<sup>loxp/+</sup></i> embryos treated with tamoxifen at ∼E10.5 and analyzed at ∼E19. (<b>C–E″</b>) Images of the cochlea taken from <i>CAG<sup>CreER+</sup>; Rosa26-NICD<sup>loxp/+</sup></i> embryos treated with tamoxifen at ∼E10.5 and analyzed at ∼E19. White arrows in (C) point to ectopic sensory epithelia with new HCs in the spiral ganglion area. Inset in (D) shows the same EGFP+ patch (EGFP signal alone) visualized in the GER area in (D). (E–E″) High-magnification three-dimensional images of the yellow rectangular region in (<b>C</b>). OC: organ of Corti; GER: greater epithelium ridge; OHCs: outer hair cells; IHCs: inner hair cells; XY: Confocal XY plane; YZ: Confocal YZ plane; XZ: Confocal XZ plane. Scale bars: 200 µm in (A) and 20 µm in (B, D and E).</p

    Overactivation of NICD at E13 generates new HCs in the utricle but not the cochlea.

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    <p>(<b>A–C</b>) Whole-mount cochlear image of a <i>CAG<sup>CreER+</sup>; Rosa26-NICD<sup>loxp/+</sup></i> embryo treated with tamoxifen at ∼E13 and analyzed at ∼E19. Although many EGFP+ cells were present, no new HCs were observed. (<b>D–E″</b>) Whole-mount images of the utricle and 2 adjacent cristae from the same embryo. White arrows in (D″) point to the ectopic sensory epithelia region. (<b>E–E″</b>) A confocal three-dimensional, high-magnification image of the white rectangular region in (D′″). NSE: non-sensory region; XY: Confocal XY plane; YZ: Confocal YZ plane; XZ: Confocal XZ plane. Scale bars: 200 µm in (B and D′″) and 20 µm in (E).</p

    Overactivation of NICD in the postnatal utricle fails to generate new HCs at P10.

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    <p>(<b>A–C</b>) Double staining of Myosin-VI and EYFP of utricles dissected from <i>CAG<sup>CreER+</sup>; Rosa26<sup>EYFP/NICD</sup></i> mice that were treated with tamoxifen at P0/P1 and analyzed at P10. (<b>D</b>) The high-magnification image of the squared area in (C). No ectopic HCs were present in the non-sensory area. NSE: non-sensory region. Scale bars: 200 µm in (C) and 20 µm in (D).</p

    Image_1_The mode and timing of administrating nutritional treatment of critically ill elderly patients in intensive care units: a multicenter prospective study.TIF

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    IntroductionCritically ill patients are more susceptible to malnutrition due to their severe illness. Moreover, elderly patients who are critically ill lack specific nutrition recommendations, with nutritional care in the intensive care units (ICUs) deplorable for the elderly. This study aims to investigate nutrition treatment and its correlation to mortality in elderly patients who are critically ill in intensive care units.MethodA multiple-center prospective cohort study was conducted in China from 128 intensive care units (ICUs). A total of 1,238 elderly patients were included in the study from 26 April 2017. We analyzed the nutrition characteristics of elderly patients who are critically ill, including initiated timing, route, ways of enteral nutrition (EN), and feeding complications, including the adverse aspects of feeding, acute gastrointestinal injury (AGI), and feeding interruption. Multivariate logistic regression analysis was used to screen out the impact of nutrition treatment on a 28-day survival prognosis of elderly patients in the ICU.ResultA total of 1,238 patients with a median age of 76 (IQR 70–83) were enrolled in the study. The Sequential Organ Failure (SOFA) median score was 7 (interquartile range: IQR 5–10) and the median Acute Physiology and Chronic Health Evaluation (APACHE) II was 21 (IQR 16–25). The all-cause mortality score was 11.6%. The percentage of nutritional treatment initiated 24 h after ICU admission was 58%, with an EN of 34.2% and a parenteral nutrition (PN) of 16.0% in elderly patients who are critically ill. Patients who had gastrointestinal dysfunction with AGI stage from 2 to 4 were 25.2%. Compared to the survivors’ group, the non-survivors group had a lower ratio of EN delivery (57% vs. 71%; p = 0.015), a higher ratio of post-pyloric feeding (9% vs. 2%; p = 0.027), and higher frequency of feeding interrupt (24% vs. 17%, p = 0.048). Multivariable logistics regression analysis showed that patients above 76 years old with OR (odds ratio) 2.576 (95% CI, 1.127–5.889), respiratory rate > 22 beats/min, and ICU admission for 24 h were independent risk predictors of the 28-day mortality study in elderly patients who are critically ill. Similarly, other independent risk predictors of the 28-day mortality study were those with an OR of 2.385 (95%CI, 1.101–5.168), lactate >1.5 mmol/L, and ICU admission for 24 h, those with an OR of 7.004 (95%CI, 2.395–20.717) and early PN delivery within 24 h of ICU admission, and finally those with an OR of 5.401 (95%CI, 1.175–24.821) with EN delivery as reference.ConclusionThis multi-center prospective study describes clinical characteristics, the mode and timing of nutrition treatment, frequency of AGI, and adverse effects of nutrition in elderly ICU patients. According to this survey, ICU patients with early PN delivery, older age, faster respiratory rate, and higher lactate level may experience poor prognosis.</p
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