170 research outputs found
Evaluation of genipin-crosslinked chitosan hydrogels as a potential carrier for silver sulfadiazine nanocrystals
In the present study genipin crosslinked chitosan (CHI) hydrogels, which had been
constructed and reported in our previous studies (Lei Gao, et al. Colloids Surf. B
Biointerfaces. 2014, 117: 398), were further evaluated for their advantage as a carrier
for silver sulfadiazine (AgSD) nanocrystal systems. Firstly, AgSD nanocrystals with a
mean particle size of 289 nm were prepared by wet milling method and encapsulated
into genipin crosslinked CHI hydrogels. AgSD nanocrystals displayed a uniform
distribution and very good physical stability in the hydrogel network.
Swelling-dependent release pattern was found for AgSD nanocrystals from hydrogels
and the release profile could be well fitted with Peppas equation. When AgSD
nanocrystals were encapsulated in hydrogels their fibroblast cytotoxicity decreased
markedly, and their antibacterial effects against Staphylococcus aureus, Escherichia
coli and Pseudomonas aeruginosa were still comparable to unencapsulated AgSD
nanocrystals. In vivo evaluation in excision and burn cutaneous wound models in
mice showed that AgSD nanocrystal hydrogels markedly decreased the expression of
inflammatory cytokine IL-6, but increased the levels of growth factors VEGF-A and
TGF-β1. Histopathologically, the wounds treated by hydrogels containing AgSD
nanocrystals showed the best healing state compared with commercial AgSD cream,
hydrogels containing AgSD bulk powders and blank hydrogels. The wounds treated
by AgSD nanocrystal hydrogels were dominated by marked fibroblast proliferation,
new blood vessels and thick regenerated epithelial layer. Sirius Red staining assay
indicated that AgSD nanocrystal hydrogels resulted in more collagen deposition
characterized by a large proportion of type I fibers. Our study suggested that
genipin-crosslinked CHI hydrogel was a potential carrier for local antibacterial
nanomedicines
Effect of SO<sub>2</sub> on CO<sub>2</sub> Absorption in Flue Gas by Ionic Liquid 1‑Ethyl-3-methylimidazolium Acetate
Significant efforts are being made
to develop several novel solvents
or materials for postcombustion CO<sub>2</sub> capture technology.
Traditional amine solvents suffer from mass loses due to its volatility
and poisoning by flue gas impurities. Ionic liquids (ILs) are considered
to be promising alternatives for CO<sub>2</sub> capture due to their
unique features, such as negligible vapor pressure. Despite the extensive
research on CO<sub>2</sub> capture by ILs, few studies have investigated
the effect of flue gas components on CO<sub>2</sub> absorption performance.
Because of the large differences between CO<sub>2</sub> and SO<sub>2</sub> in the absorption capacity and partial pressure in flue gas,
it is essential to study the role of SO<sub>2</sub> in CO<sub>2</sub> capture using ILs. This work focused on studying the effect of SO<sub>2</sub> with low concentration on postcombustion CO<sub>2</sub> capture
by 1-ethyl-3-methylimidazolium acetate [C<sub>2</sub>mim]Â[OAc] and
explaining the microscopic mechanism through quantum chemical calculation.
Results showed that the CO<sub>2</sub> absorption capacity was largely
decreased by 25% in the presence of SO<sub>2</sub>. After 5 cycles
of regeneration, the initial absorption capacity of CO<sub>2</sub> in [C<sub>2</sub>mim]Â[OAc] remarkably decreased by 48%. Thus, the
ionic liquid lost its excellent reversibility and regeneration property
for CO<sub>2</sub> capture under continuous exposure to SO<sub>2</sub>. The quantum chemical calculation indicated that CO<sub>2</sub> could
hardly compete with SO<sub>2</sub> for the main active sites in [C<sub>2</sub>mim]Â[OAc]. In addition, the net charge transfer amount from
acetate anion to CO<sub>2</sub> significantly decreased from −0.537
to −0.039 e in the presence of SO<sub>2</sub>, which explained
the decreased absorption capacity of CO<sub>2</sub> in [C<sub>2</sub>mim]Â[OAc]
Synthesis of Mg-Doped Ordered Mesoporous Pd–Al<sub>2</sub>O<sub>3</sub> with Different Basicity for CO, NO, and HC Elimination
Employing NH<sub>4</sub>HCO<sub>3</sub> as pore-enlarging agent
and P123 as a template agent, ordered mesoporous Mg-doped γ-Al<sub>2</sub>O<sub>3</sub> with different basicity and large surface area
have been successfully synthesized by a facile sol–gel approach
by adjusting the content of magnesium and pH value. Specifically,
the result alumina calcined at 1000 °C with large specific surface
area (234.4 m<sup>2</sup> g<sup>–1</sup>) and high pore volume
(0.72 cm<sup>3</sup> g<sup>–1</sup>) was obtained when the
Mg content was 9 wt %. These materials with ordered mesostructure
and advantageous structural properties were utilized as carriers of
Pd–Al<sub>2</sub>O<sub>3</sub> catalysts for the catalytic
reaction of simulated exhaust automobile gases including CO, NO, and
hydrocarbon (HC). The results revealed that the high catalytic performance
of Pd/9Mg-OMA originated from its more appropriate basicity, greater
PdO dispersion, and higher surface area
Inhibitors of cathepsin B reduce caspase-1 activation in macrophages infected with KIM5.
<p>BMDMs were left untreated or treated with 25 µM of E64d or CA-074 Me (CA) for 1 hr. Following infection with <i>Y. pestis</i> strains expressing YopJ<sup>KIM</sup> in the absence or presence of the inhibitors, supernatants were collected (A, B) or microscopic assay was performed (C). IL-1β ELISA (A) and LDH release assay (B) was done on supernatants collected 24 hr post-infection. Results shown are the averages from three independent experiments. Error bars represent standard deviations. (★★, <i>P</i><0.01 as determined by one way ANOVA as compared to infection in absence of inhibitor) (C) Infected BMDMs on coverslips were incubated with FAM-YVAD-FAM 9 hr post-infection stained for active caspase-1 (green) for 1 hr and PI uptake (red) immediately before observation. Representative images of phase, green and red signals were captured by digital photomicroscopy.</p
Caspase-3/7 activity is low in KIM5-infected macrophages.
<p>(A) BMDMs were left uninfected (U) or infected with <i>Y. pestis</i> strains expressing YopJ<sup>KIM</sup> or YopJ<sup>C172A</sup> in 96-white walled tissue culture plates. Caspase-3/7 activity was measured 4, 8, 12 or 24 hr post-infection with fluorometer. The results from three independent experiments were averaged and are shown as fold change compared to uninfected cells. Error bars represent standard deviations. Differences in caspase-3/7 activities between uninfected and infected cells were not significant as determined by two way ANOVA (B) BMDMs were left uninfected (U) or infected with <i>Y. pestis</i> strains expressing YopJ<sup>KIM</sup> or YopJ<sup>C172A</sup> or treated with 1 µM of staurosporine (STS) for 16 hr. Macrophage lysates were collected and analyzed by PARP immunoblotting. Sizes of molecular weight standards (kDa) are shown on the left. Positions of full length PARP and cleaved PARP (c-PARP) are showed on right.</p
HMGB1 is released from KIM5-infected macrophages.
<p>BMDMs were infected with <i>Y. pestis</i> strains expressing YopJ<sup>KIM</sup> or YopJ<sup>C172A</sup> or left uninfected (U). Medium from infected macrophages was collected at 24 hr post infection and immunoblotted for HMGB1. Total cell lysate (Lys) was used as a positive control. Position of molecular weight standard (kDa) is shown on the left.</p
Caspase-1 is not required for innate host protection against <i>Yersinia</i> endowed with enhanced cytotoxicity.
<p>(A) Six to eight-week old Casp1<i><sup>+/+</sup></i> (wild type, WT) or Casp1<i><sup>−/−</sup></i> (Casp1-) C57BL/6J mice were infected orogastrically with 1×10<sup>9</sup> CFU of <i>Y. pseudotuberculosis</i> IP26 carrying pACYC184 encoding YopP or YopJ<sup>YPTB</sup>. Mouse survival was monitored for 21 days. Results shown are pooled from two independent experiments. Total numbers of mice infected are shown in parenthesis. (B) Data from (A) are reformatted by grouping mice according to infecting strain. Significant difference between survival curves was determined by log rank test.</p
Enhanced YopP-mediated macrophage cell death is associated with elevated levels of IL-1β release.
<p><i>Y. pseudotuberculosis</i> IP26 (<i>ΔyopJ</i>) carrying the empty pACYC184 plasmid (pACYC) or pACYC184 encoding the indicated YopP or YopJ isoforms was used to infect BMDMs. Twenty four hours post-infection, medium was collected for IL-1β ELISA (A) and LDH release assay (B). Results shown are the averages from three independent experiments. Error bars represent standard deviations (★★, <i>P</i><0.01; ★★★, <i>P</i><0.001 as determined by one way ANOVA as compared to pACYC condition).</p
KIM5-infected necrotic macrophages contain active caspase-1.
<p>BMDMs were seeded on glass coverslips in a 24-well plate and left uninfected (U) or infected with <i>Y. pestis</i> strains expressing YopJ<sup>KIM</sup> or YopJ<sup>C172A</sup>. FAM-YVAD-FMK was added at 9 hr post infection to stain for active caspase-1 and PI uptake assay was performed immediately before microscopic analysis. (A) Representative images of phase, active caspase-1 (green) and PI uptake (red) signals captured by digital photomicroscopy are shown in a-c and e-g, respectively. Panels d and h show merged images of green and red signals. (B) Average percentages of BMDMs positive for active caspase-1, PI or both signals was calculated (∼100–300 cells per field) from three random fields in three independent experiments. Error bars represent standard deviations.</p
RIP1 is not required for YopJ<sup>KIM</sup>-induced cell death or IL-1β secretion.
<p>BMDMs were treated with 30 µM RIP1 inhibitor necrostatin-1 (Nec) or vehicle 1 hr prior to and during infection. BMDMs were infected with <i>Y. pestis</i> strains expressing YopJ<sup>KIM</sup> or YopJ<sup>C172A</sup> or left uninfected (U). Supernatants were collected and LDH release (A) and secreted IL-1β (B) were measured at 8 hr or 24 hr post-infection from three independent experiments. Results shown are averages and error bars represent standard deviations (★★, <i>P</i><0.01 as determined by one way ANOVA as compared to YopJ<sup>KIM</sup> no inhibitor).</p
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