5 research outputs found
Plasma-treated Ce/TiO<sub>2</sub>–SiO<sub>2</sub> catalyst for the NH<sub>3</sub>-SCR of NO<i><sub>x</sub></i>
<p>Ce/TiO<sub>2</sub>–SiO<sub>2</sub> catalysts with different Ti/Si molar ratios are prepared by the incipient impregnation method and their NH<sub>3</sub>-SCR activities are evaluated at 100–500°C on a fixed reactor. The Ce/TiO<sub>2</sub>–SiO<sub>2</sub> (3/1) catalyst, modified by non-thermal plasma (NTP) treatment and then activated by thermal treatment at 500°C for 4 h, exhibits best performance. Comprehensive deNO<i><sub>x</sub></i> performance of the catalyst is evidently improved and its efficiency reaches up to 99.21% at 350°C. NO conversion efficiency of the treated catalyst doped with K remains about 90.23% at 300°C and the catalyst also shows improved activity at lower temperatures. Various characterization methods show that the activity enhancement is correlated only with NTP treatment, as it increases the number of Ce<sup>3+</sup> species, which generates more chemisorbed oxygen, leads to improved dispersion of Brønsted and Lewis acidic sites and finally has an inherent etching effect.</p
Aged-Signal-Eliciting Nanoparticles Stimulated Macrophage-Mediated Programmed Removal of Inflammatory Neutrophils
Excessive infiltration of activated neutrophils is regarded
as
a predominant cause of tissue injury in neutrophilic inflammation.
Although programmed cell death like apoptosis maintains the homeostasis
of activated neutrophils, this process is disrupted by an abnormal
inflammatory response. Unlike endogenous calreticulin exposed during
apoptosis, exogenous calreticulin acts as an “aged”
signal and initiates premature macrophage-mediated programmed cell
removal (PrCR), which is independent of apoptosis. Here, we report
a nano-mediated strategy to stimulate the precise clearance of activated
neutrophils initiated with artificial aged signal and alleviated inflammation.
Polymeric nanoparticles PC@PLGA were fabricated by cloaking poly(lactic-co-glycolic acid) (PLGA) with a hybrid membrane derived
from platelet-derived extracellular vesicles (PEVs, denoted by P)
and the calreticulin-expressed membrane obtained from doxorubicin-treated
cells (denoted by C). P-selectin in PEVs favors PC@PLGA to anchor
activated neutrophils, while calreticulin mimics exogenous “aged”
signal secreted by macrophages to trigger PrCR. We showed that PC@PLGA
specifically targeted activated neutrophils and misled macrophages
to recognize them as “aged” neutrophils and then initiated
premature PrCR and prevented proinflammatory response and tissue damage
in a mouse model of acute lung injury and severe acute pancreatitis.
The collective findings indicate the efficiency of specific elimination
of activated neutrophils with exogenous aged signal in improving inflammation
therapy
Aged-Signal-Eliciting Nanoparticles Stimulated Macrophage-Mediated Programmed Removal of Inflammatory Neutrophils
Excessive infiltration of activated neutrophils is regarded
as
a predominant cause of tissue injury in neutrophilic inflammation.
Although programmed cell death like apoptosis maintains the homeostasis
of activated neutrophils, this process is disrupted by an abnormal
inflammatory response. Unlike endogenous calreticulin exposed during
apoptosis, exogenous calreticulin acts as an “aged”
signal and initiates premature macrophage-mediated programmed cell
removal (PrCR), which is independent of apoptosis. Here, we report
a nano-mediated strategy to stimulate the precise clearance of activated
neutrophils initiated with artificial aged signal and alleviated inflammation.
Polymeric nanoparticles PC@PLGA were fabricated by cloaking poly(lactic-co-glycolic acid) (PLGA) with a hybrid membrane derived
from platelet-derived extracellular vesicles (PEVs, denoted by P)
and the calreticulin-expressed membrane obtained from doxorubicin-treated
cells (denoted by C). P-selectin in PEVs favors PC@PLGA to anchor
activated neutrophils, while calreticulin mimics exogenous “aged”
signal secreted by macrophages to trigger PrCR. We showed that PC@PLGA
specifically targeted activated neutrophils and misled macrophages
to recognize them as “aged” neutrophils and then initiated
premature PrCR and prevented proinflammatory response and tissue damage
in a mouse model of acute lung injury and severe acute pancreatitis.
The collective findings indicate the efficiency of specific elimination
of activated neutrophils with exogenous aged signal in improving inflammation
therapy
Aged-Signal-Eliciting Nanoparticles Stimulated Macrophage-Mediated Programmed Removal of Inflammatory Neutrophils
Excessive infiltration of activated neutrophils is regarded
as
a predominant cause of tissue injury in neutrophilic inflammation.
Although programmed cell death like apoptosis maintains the homeostasis
of activated neutrophils, this process is disrupted by an abnormal
inflammatory response. Unlike endogenous calreticulin exposed during
apoptosis, exogenous calreticulin acts as an “aged”
signal and initiates premature macrophage-mediated programmed cell
removal (PrCR), which is independent of apoptosis. Here, we report
a nano-mediated strategy to stimulate the precise clearance of activated
neutrophils initiated with artificial aged signal and alleviated inflammation.
Polymeric nanoparticles PC@PLGA were fabricated by cloaking poly(lactic-co-glycolic acid) (PLGA) with a hybrid membrane derived
from platelet-derived extracellular vesicles (PEVs, denoted by P)
and the calreticulin-expressed membrane obtained from doxorubicin-treated
cells (denoted by C). P-selectin in PEVs favors PC@PLGA to anchor
activated neutrophils, while calreticulin mimics exogenous “aged”
signal secreted by macrophages to trigger PrCR. We showed that PC@PLGA
specifically targeted activated neutrophils and misled macrophages
to recognize them as “aged” neutrophils and then initiated
premature PrCR and prevented proinflammatory response and tissue damage
in a mouse model of acute lung injury and severe acute pancreatitis.
The collective findings indicate the efficiency of specific elimination
of activated neutrophils with exogenous aged signal in improving inflammation
therapy
Aged-Signal-Eliciting Nanoparticles Stimulated Macrophage-Mediated Programmed Removal of Inflammatory Neutrophils
Excessive infiltration of activated neutrophils is regarded
as
a predominant cause of tissue injury in neutrophilic inflammation.
Although programmed cell death like apoptosis maintains the homeostasis
of activated neutrophils, this process is disrupted by an abnormal
inflammatory response. Unlike endogenous calreticulin exposed during
apoptosis, exogenous calreticulin acts as an “aged”
signal and initiates premature macrophage-mediated programmed cell
removal (PrCR), which is independent of apoptosis. Here, we report
a nano-mediated strategy to stimulate the precise clearance of activated
neutrophils initiated with artificial aged signal and alleviated inflammation.
Polymeric nanoparticles PC@PLGA were fabricated by cloaking poly(lactic-co-glycolic acid) (PLGA) with a hybrid membrane derived
from platelet-derived extracellular vesicles (PEVs, denoted by P)
and the calreticulin-expressed membrane obtained from doxorubicin-treated
cells (denoted by C). P-selectin in PEVs favors PC@PLGA to anchor
activated neutrophils, while calreticulin mimics exogenous “aged”
signal secreted by macrophages to trigger PrCR. We showed that PC@PLGA
specifically targeted activated neutrophils and misled macrophages
to recognize them as “aged” neutrophils and then initiated
premature PrCR and prevented proinflammatory response and tissue damage
in a mouse model of acute lung injury and severe acute pancreatitis.
The collective findings indicate the efficiency of specific elimination
of activated neutrophils with exogenous aged signal in improving inflammation
therapy