19 research outputs found

    Amine-Impregnated Mesoporous Silica Nanotube as an Emerging Nanocomposite for CO<sub>2</sub> Capture

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    Pristine halloysite nanotubes (HNTs) were pretreated to produce mesoporous silica nanotubes (MSiNTs), which was further impregnated with polyethenimine (PEI) to prepare an emerging nanocomposite MSiNTs/PEI (MP) for CO<sub>2</sub> capture. Thermogravimetric analysis (TGA) was employed to analyze the influences of PEI loading amount and adsorption temperature on CO<sub>2</sub> adsorption capacity of the nanocomposite. The Brunauer–Emmett–Teller (BET) surface area (<i>S</i><sub>BET</sub>) of MSiNTs was six times higher than that of HNTs, and the corresponding pore volume was more than two times higher than that of HNTs. The well dispersion of PEI within the nanotubes of MSiNTs benefits more CO<sub>2</sub> gas adsorption, and the adsorption capacity of the nanocomposite could reach 2.75 mmol/g at 85 °C for 2 h. The CO<sub>2</sub> adsorption on the nanocomposite was demonstrated to occur via a two-stage process: initially, a sharp linear weight increase at the beginning, and then a relatively slow adsorption step. The adsorption capacity could reach as high as 70% within 2 min. Also, the nanocomposite exhibited good stability on CO<sub>2</sub> adsorption/desorption performance, indicating that the as-prepared emerging nanocomposite show an interesting application potential in the field of CO<sub>2</sub> capture

    Cichoric Acid Reverses Insulin Resistance and Suppresses Inflammatory Responses in the Glucosamine-Induced HepG2 Cells

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    Cichoric acid, a caffeic acid derivative found in <i>Echinacea purpurea</i>, basil, and chicory, has been reported to have bioactive effects, such as anti-inflammatory, antioxidant, and preventing insulin resistance. In this study, to explore the effects of CA on regulating insulin resistance and chronic inflammatory responses, the insulin resistance model was constructed by glucosamine in HepG2 cells. CA stimulated glucosamine-mediated glucose uptake by stimulating translocation of the glucose transporter 2. Moreover, the production of reactive oxygen, the expression of COX-2 and iNOS, and the mRNA levels of TNF-α and IL-6 were attenuated. Furthermore, CA was verified to promote glucosamine-mediated glucose uptake and inhibited inflammation through PI3K/Akt, NF-κB, and MAPK signaling pathways in HepG2 cells. These results implied that CA could increase glucose uptake, improve insulin resistance, and attenuate glucosamine-induced inflammation, suggesting that CA is a potential natural nutraceutical with antidiabetic properties and anti-inflammatory effects

    Syntax score according to HbA1c levels in type 2 DM patients aged 60 years and older.

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    <p>Syntax score according to HbA1c levels in type 2 DM patients aged 60 years and older.</p

    Risk factors associated with MACE in a multivariable logistic regression analysis.

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    <p>COPD: chronic obstructive pulmonary disease; ACE: angiotensin converting enzyme inhibitor; ARB: angiotensin receptor blocker.</p><p>Risk factors associated with MACE in a multivariable logistic regression analysis.</p

    Kaplan-Meier event-time curve according to preoperative NT-pro-BNP levels.

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    <p>Kaplan-Meier event-time curve according to preoperative NT-pro-BNP levels.</p

    Kaplan-Meier survival curves according to preoperative NT-pro-BNP and cTnI levels

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    <p>Kaplan-Meier survival curves according to preoperative NT-pro-BNP and cTnI levels</p

    Correlation between HbA1c levels and Syntax score in type 2 DM patients aged 60 years and older.

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    <p>Correlation between HbA1c levels and Syntax score in type 2 DM patients aged 60 years and older.</p

    Chicoric Acid Induces Apoptosis in 3T3-L1 Preadipocytes through ROS-Mediated PI3K/Akt and MAPK Signaling Pathways

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    Chicoric acid has been reported to possess various bioactivities. However, the antiobesity effects of chicoric acid remain poorly understood. In this study, we investigated the effects of chicoric acid on 3T3-L1 preadipocytes and its molecular mechanisms of apoptosis. Chicoric acid inhibited cell viability and induced apoptosis in 3T3-L1 preadipocytes which was characterized by chromatin condensation and poly ADP-ribose-polymerase (PARP) cleavage. Mitochondrial membrane potential (MMP) loss, Bax/Bcl-2 dysregulation, cytochrome <i>c</i> release, and caspase-3 activation were observed, indicating mitochondria-dependent apoptosis induced by chicoric acid. Furthermore, PI3K/Akt and MAPK (p38 MAPK, JNK, and ERK1/2) signaling pathways were involved in chicoric acid-induced apoptosis. The employment of protein kinase inhibitors LY294002, SB203580, SP600125, and U0126 revealed that PI3K/Akt signaling pathway interplayed with MAPK signaling pathways. Moreover, chicoric acid induced reactive oxygen species (ROS) generation. Pretreatment with the antioxidant N-acetylcysteine (NAC) significantly blocked cell death and changes of Akt and MAPK signalings induced by chicoric acid. In addition, chicoric acid down regulated HO-1 and COX-2 via the PI3K/Akt pathway
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