11 research outputs found
Kinetics of Thermal Unimolecular Decomposition of Acetic Anhydride: An Integrated Deterministic and Stochastic Model
An
integrated deterministic and stochastic model within the master
equation/ĀRiceāRamspergerāĀKasselāMarcus
(ME/RRKM) framework was first used to characterize temperature- and
pressure-dependent behaviors of thermal decomposition of acetic anhydride
in a wide range of conditions (i.e., 300ā1500 K and 0.001ā100
atm). Particularly, using potential energy surface and molecular properties
obtained from high-level electronic structure calculations at CCSDĀ(T)/CBS,
macroscopic thermodynamic properties and rate coefficients of the
title reaction were derived with corrections for hindered internal
rotation and tunneling treatments. Being in excellent agreement with
the scattered experimental data, the results from deterministic and
stochastic frameworks confirmed and complemented each other to reveal
that the main decomposition pathway proceeds via a 6-membered-ring
transition state with the 0 K barrier of 35.2 kcalĀ·mol<sup>ā1</sup>. This observation was further understood and confirmed by the sensitivity
analysis on the time-resolved species profiles and the derived rate
coefficients with respect to the ab initio barriers. Such an agreement
suggests the integrated model can be confidently used for a wide range
of conditions as a powerful postfacto and predictive tool in detailed
chemical kinetic modeling and simulation for the title reaction and
thus can be extended to complex chemical reactions
Ultralow Absorption Coefficient and Temperature Dependence of Radiative Recombination of CH<sub>3</sub>NH<sub>3</sub>PbI<sub>3</sub> Perovskite from Photoluminescence
Spectrally resolved photoluminescence
is used to measure the band-to-band
absorption coefficient Ī±<sub>BB</sub>(āĻ) of organicāinorganic
hybrid perovskite methylammonium lead iodide (CH<sub>3</sub>NH<sub>3</sub>PbI<sub>3</sub>) films from 675 to 1400 nm. Unlike other methods
used to extract the absorption coefficient, photoluminescence is only
affected by band-to-band absorption and is capable of detecting absorption
events at very low energy levels. Absorption coefficients as low as
10<sup>ā14</sup> cm<sup>ā1</sup> are detected at room
temperature for long wavelengths, which is 14 orders of magnitude
lower than reported values at shorter wavelengths. The temperature
dependence of Ī±<sub>BB</sub>(āĻ) is calculated
from the photoluminescence spectra of CH<sub>3</sub>NH<sub>3</sub>PbI<sub>3</sub> in the temperature range 80ā360 K. Based on
the temperature-dependent Ī±<sub>BB</sub>(āĻ), the
product of the radiative recombination coefficient and square of the
intrinsic carrier density, <i>B</i>(<i>T</i>)
Ć <i>n</i><sub><i>i</i></sub><sup>2</sup>, is also obtained
Caspase-11 activation is independent of ASC and NLRC4.
<p>(<b>A</b>) Unprimed B6, <i>Casp1<sup>ā/ā</sup>Casp11<sup>ā/ā</sup></i>, or <i>Asc<sup>ā/ā</sup>Nlrc4<sup>ā/ā</sup></i> BMDMs were infected with WT <i>L. pneumophila</i> (WT Lp), Ī<i>dotA</i> Lp, Ī<i>flaA</i> Lp, or PBS (mock infection) for 20 hours, and levels of IL-1Ī± and IL-1Ī² in the supernatants were measured by ELISA. Graphs show the mean Ā± SEM of triplicate wells. (<b>B</b>) Unprimed B6, <i>Casp1<sup>ā/ā</sup>Casp11<sup>ā/ā</sup></i>, or <i>Asc<sup>ā/ā</sup>Nlrc4<sup>ā/ā</sup></i> BMDMs were infected with WT Lp, Ī<i>dotA</i> Lp, Ī<i>flaA</i> Lp, or PBS (mock infection) for 20 hours or treated with LPS+ATP for 1 hour. Levels of processed caspase-1 (casp-1 p10) and caspase-11 (casp-11 p26) in the supernatants, and pro-caspase-1, pro-caspase-11, and Ī²-actin (loading control) in the cell lysates were determined by immunoblot analysis. (<b>C</b>) 8ā12 week old B6 and <i>Asc<sup>ā/ā</sup></i> mice were infected intranasally with either 1Ć10<sup>6</sup> Ī<i>flaA</i> Lp or PBS. Bronchoalveolar lavage fluid (BALF) was collected 24 hours post-infection, and levels of IL-1Ī± and IL-1Ī² were measured by ELISA. Graphs show the mean Ā± SEM of 9 mice per group. Dashed line represents the limit of detection. Data are representative of three independent experiments (A,B) or are displayed as the pooled results of two independent experiments (C). *** is p<0.001 by two-way ANOVA with Bonferroni post-test. ** is p<0.01 by unpaired t-test. NS is not significant.</p
IL-1Ī± and IL-1Ī² control bacterial burden and neutrophil recruitment <i>in vivo</i>.
<p>(<b>A</b>) 8ā12 week old B6 or <i>Il1r1<sup>ā/ā</sup></i> mice were infected with 1Ć10<sup>6</sup> Ī<i>flaA L. pneumophila</i> intranasally (IN). Lungs were plated to quantify CFU per gram. Graph shows the mean Ā± SEM of three or four infected mice per group. Dashed line represents the limit of detection. (<b>B</b> and <b>C</b>) B6 or <i>Il1r1<sup>ā/ā</sup></i> mice were infected with 1Ć10<sup>6</sup> Ī<i>flaA</i> Lp IN. 24 hours post-infection, bronchoalveolar lavage fluid (BALF) was collected and the percentage of neutrophils in the BALF was quantified by flow cytometry. Percentages are reported as the frequency of live cells in the BALF. (B) Representative flow cytometry plots showing the percentage of Gr-1<sup>+</sup>Ly6G<sup>+</sup> neutrophils. (C) Graph showing the percentage of neutrophils. Each point represents an individual mouse and lines indicate the mean of 4 mice per group. (<b>D, E</b>, and <b>F</b>) B6 mice were injected intraperitoneally (IP) with either PBS, 100 Āµg isotype control antibody (iso), 100 Āµg anti-IL-1Ī± antibody, 100 Āµg anti-IL-1Ī² antibody, or 100 Āµg each of anti-IL-1Ī± and anti-IL-1Ī² (anti-IL-1Ī±/Ī²) 16 hours before infection. The mice were then intranasally infected with either 1Ć10<sup>6</sup> Ī<i>flaA</i> Lp or mock infected with PBS. (D and E) 24 hours post-infection, BALF was collected and flow cytometry was performed to quantify the percentage of neutrophils. (D) Representative flow cytometry plots showing the percentage of Gr-1<sup>+</sup>Ly6G<sup>+</sup> neutrophils. (E) Graph showing the percentage of neutrophils. Each point represents an individual mouse, lines indicate the mean of 8 mice per group, and error bars represent SEM. Shown are the pooled results of two independent experiments. (F) 72 hours post-infection, the lungs were plated to quantify CFU per gram. Each point represents an individual mouse. Line indicates the mean of 4 infected mice per group with error bars representing SEM. *** is p<0.001 by one-way ANOVA with Tukey post-test or unpaired t-test (C). **is p<0.01 and *is p<0.05 by unpaired t-test. NS is not significant.</p
Caspase-11 mediates inflammasome activation in response to a functional <i>Yersinia</i> type III secretion system.
<p>BMDMs from B6, <i>Casp1<sup>ā/ā</sup>Casp11<sup>ā/ā</sup></i>, <i>Casp1<sup>ā/ā</sup></i>, or <i>Casp11<sup>ā/ā</sup></i> mice were primed with 0.05 Āµg/mL LPS for 4 hours and infected with type III secretion system-deficient <i>Y. pseudotuberculosis</i> (Ī<i>yopB</i> Yp), effectorless <i>Y. pseudotuberculosis</i> ĪHOJMEK (Ī6 Yp), or PBS (mock infection) or treated with 2.5 mm ATP for 4 hours. (<b>A</b>) Levels of IL-1Ī± and IL-1Ī² in the supernatants were measured by ELISA. (<b>B</b>) Cell death (% cytotoxicity) was measured by lactate dehydrogenase (LDH) release relative to Triton X-100-lysed cells. Graphs show the mean Ā± SEM of triplicate wells. Data are representative of two independent experiments. *** is p<0.001 and ** is p<0.01 by two-way ANOVA with Bonferroni post-test. NS is not significant.</p
Caspase-11 controls multiple pathways of inflammasome activation in response to bacterial secretion systems that access the host cytosol.
<p>Three distinct inflammasome pathways are induced upon interaction of virulent bacteria with host cells. Translocation of flagellin into the host cytosol by specialized secretion systems triggers a NAIP5/NLRC4/caspase-1 inflammasome that leads to cell death, IL-1Ī±, and IL-1Ī² release. Virulent bacteria induce two separate pathways of caspase-11-dependent inflammasome activation through a two-signal model. First, TLR stimulation by PAMPs (signal one) leads to upregulation of pro-IL-1Ī±, pro-IL-1Ī², NLRP3, and pro-caspase-11. Next, cytosolic detection of virulence activity, namely type III or type IV secretion (signal two), leads to caspase-11 processing and activation. Active caspase-11 contributes to NLRP3-mediated inflammasome activation and caspase-1-dependent IL-1Ī² secretion. Caspase-11 also mediates caspase-1-independent cell death and IL-1Ī± release through a pathway that is independent of the NLRP3/ASC and NAIP5/NLRC4 inflammasomes and involves an unknown host sensor.</p
Caspase-11 mediates both NLRP3-dependent and NLRP3-independent immune responses.
<p>(<b>A</b>) B6, <i>Casp1<sup>ā/ā</sup>Casp11<sup>ā/ā</sup></i>, <i>Asc</i><sup>ā/ā</sup>, <i>Nlrc4</i><sup>ā/ā</sup>, or <i>Asc<sup>ā/ā</sup>Nlrc4<sup>ā/ā</sup></i> BMDMs were primed with 0.5 Āµg/mL LPS for 2.5 hours and infected with WT <i>L. pneumophila</i> (WT Lp), Ī<i>dotA</i> Lp, Ī<i>flaA</i> Lp, or PBS (mock infection) or treated with 2.5 mm ATP for 4 hours. Levels of IL-1Ī± and IL-1Ī² in the supernatants were measured by ELISA and cell death (% cytotoxicity) was measured by LDH release into the supernatants relative to Triton X-100-lysed cells. Graphs show the mean Ā± SEM of triplicate wells. (<b>B</b> and <b>C</b>) B6 or <i>Nlrp3<sup>ā/ā</sup></i> BMDMs were primed with 0.5 Āµg/mL LPS for 2.5 hours and infected with WT Lp, Ī<i>dotA</i> Lp, Ī<i>flaA</i> Lp, or PBS (mock infected) or treated with 2.5 mm ATP for 1 hour (C) or 4 hours (B). (B) Levels of IL-1Ī± and IL-1Ī² in the supernatants were measured by ELISA and cell death (% cytotoxicity) was measured by LDH release into the supernatants relative to Triton X-100-lysed cells. Graphs show the mean Ā± SEM of triplicate wells. (C) Levels of processed caspase-1 (casp-1 p10) in the supernatants and pro-caspase-1 in the cell lysates were determined by immunoblot analysis. Data are representative of two (A,C) or three (B) independent experiments. *** is p<0.001 by one-way ANOVA with Tukey post-test. NS is not significant.</p
Non-canonical inflammasome responses to <i>L.</i><i>pneumophila</i> occur independently of TRIF and IFNAR.
<p>(<b>A</b>) Unprimed B6, <i>Ifnar<sup>ā/ā</sup></i>, or <i>Trif<sup>ā/ā</sup></i> BMDMs were infected with WT <i>L. pneumophila</i> (WT Lp), Ī<i>dotA</i> Lp, Ī<i>flaA</i> Lp, <i>E. coli</i>, or PBS (mock infection) for 16 hours. Levels of IL-1Ī± and IL-1Ī² in the supernatants were measured by ELISA. (<b>B</b>) Unprimed B6, <i>Ifnar<sup>ā/ā</sup></i>, or <i>Trif<sup>ā/ā</sup></i> BMDMs were infected with WT Lp, Ī<i>dotA</i> Lp, Ī<i>flaA</i> Lp, or PBS (mock infection) for 16 hours. Cell death (% cytotoxicity) was measured by LDH release into the supernatants relative to Triton X-100-lysed cells. Graphs show the mean Ā± SEM of triplicate wells. (<b>C</b>) B6, <i>Ifnar<sup>ā/ā</sup></i>, or <i>Trif<sup>ā/ā</sup></i> BMDMs were primed with 0.4 Āµg/mL Pam3CSK4 for 4 hours and infected with WT Lp, Ī<i>dotA</i> Lp, Ī<i>flaA</i> Lp, or PBS for 16 hours. Levels of full-length caspase-11 (pro-casp-11) and processed caspase-11 (casp11 p26) in the supernatants and pro-casp-11 and Ī²-actin (loading control) in the cell lysates were determined by immunoblot analysis. Data are representative of two independent experiments.</p
Caspase-11 controls the release of IL-1Ī± and IL-1Ī² and pyroptosis in response to flagellin-deficient <i>L.</i><i>pneumophila</i>.
<p>B6, <i>Casp1<sup>ā/ā</sup>Casp11<sup>ā/ā</sup></i>, <i>Casp1<sup>ā/ā</sup></i>, or <i>Casp11<sup>ā/ā</sup></i> BMDMs were primed with 0.5 Āµg/mL LPS for 2.5 hours and infected with WT <i>L. pneumophila</i> (WT Lp), Ī<i>dotA</i> Lp, Ī<i>flaA</i> Lp, or PBS (mock infection) or treated with 2.5 mm ATP for 1(C) or 4(A,B) hours. (<b>A</b>) Levels of IL-1Ī± and IL-1Ī² in the supernatants were measured by ELISA. Graphs show the mean Ā± SEM of triplicate wells. (<b>B</b>) Cell death (% cytotoxicity) was measured by LDH release into the supernatants relative to Triton X-100-lysed cells. Graphs show the mean Ā± SEM of triplicate wells. (<b>C</b>) Levels of processed caspase-1 (casp-1 p10) in the supernatants and full-length caspase-1 (pro-casp-1) and Ī²-actin in the cell lysates were determined by immunoblot analysis. Data are representative of three independent experiments. *** is p<0.001 by two-way ANOVA with Bonferroni post-test, ** is p<0.01 by two-way ANOVA with Bonferroni post-test, and * is p<0.05 by unpaired t-test. NS is not significant.</p
Water-Free, Conductive Hole Transport Layer for Reproducible PerovskiteāPerovskite Tandems with Record Fill Factor
State-of-the-art perovskiteāperovskite tandem
solar cells
incorporate a water-based poly(3,4-ethylenedioxythiophene):polystyrenesulfonate
(PEDOT:PSS) hole transport layer in its low bandgap subcell. However,
there is a limitation regarding its use due to the moisture sensitivity
of perovskites and the insulating property of PSS. Here, we overcome
the limitation by using a water-free and PSS-free PEDOT-based hole
transport layer for low bandgap single-junction perovskite solar cells
and in perovskiteāperovskite tandems. The champion tandem cell
produces an efficiency of 21.5% and a fill factor of 85.8%, the highest
for any perovskite-based double-junction tandems. Results of photoelectron
spectroscopy, Fourier-transform infrared spectroscopy, and conductive
atomic force microscopy reveal evidence of enhanced conductivity of
water-free and PSS-free PEDOT compared to its conventional counterpart.
The use of water-free and PSS-free PEDOT also eliminates decomposition
of high bandgap subcell with its interfacing layer stack in a tandem
that otherwise occurs with conventional PEDOT:PSS. This leads to enhanced
reproducibility of perovskiteāperovskite tandems