The introduction of composite components to construct heterointerfaces is an important way to improve the electrocatalytic performance of materials. However, selecting appropriate components to ...accelerate the elementary reaction rates of the hydrogen evolution reaction (HER) in alkaline media is still in challenge. Here, a Ni‐CeF3‐VN multi‐component material is successfully constructed, which exhibits excellent HER catalytic activity (33 mV at 10 mA cm−2). The experimental and computational results show that the Ni‐VN and Ni‐CeF3 dual heterointerfaces can effectively promote the transfer of OH− adsorption site from Ni to VN and optimize the adsorption energy of intermediate H respectively, which together accelerate the rate of the multi‐step hydrogen evolution reaction in alkaline solution and thus lead to a significantly improved HER performance compared to the pure Ni. Furthermore, the solar to hydrogen (STH) efficiency can reach 10.34%. This work provides an effective guide for the design of high‐efficiency multicomponent materials in the future.
Ni‐CeF3‐VN multicomponent materials are prepared. The introduction of VN makes the OH− adsorption site transfer from Ni to VN, and then releases the blocked Ni active site; the introduction of CeF3 changes the surface charge distribution of the material, and therefore improves the adsorption of intermediate H, thus jointly promoting the multi‐step elementary reaction rate in the alkaline hydrogen evolution reaction process.
As a well-established human carcinogen, arsenic has increased the risk of lung cancer over the past decades. Wide exposure to arsenic in the environment has attracted the attention of scientists. Its ...carcinogenicity at early life stages has been observed in certain animal studies already, yet current evidence is insufficient to extrapolate this to humans. Although the mechanisms of lung cancer induced by arsenic remain unclear, most of them are related to the biotransformation of arsenic, which would further provide target sites for precaution and therapy. This review comprehensively summarizes current studies associated to arsenic exposure and lung cancer and the mechanism of its carcinogenesis in lung cancer in three sections, namely, epidemiological studies, experimental studies, and mechanistic studies. In addition, prevention and treatment strategies as well as directions for future studies are discussed.
As a well-established human carcinogen, arsenic has increased the risk of lung cancer over the past decades.
Electrocatalytic oxidation of 5‐hydroxymethylfurfural (HMF) provides an efficient way to obtain high‐value‐added biomass‐derived chemicals. Compared with other transition metal oxides, CuO exhibits ...poor oxygen evolution reaction performance, leading to high Faraday efficiency for HMF oxidation. However, the weak adsorption and activation ability of CuO to OH− species restricts its further development. Herein, the CuO–PdO heterogeneous interface is successfully constructed, resulting in an advanced onset‐potential of the HMF oxidation reaction (HMFOR), a higher current density than CuO. The results of open‐circuit potential, in situ infrared spectroscopy, and theoretical calculations indicate that the introduction of PdO enhances the adsorption capacity of the organic molecule. Meanwhile, the CuO–PdO heterogeneous interface promotes the adsorption and activation of OH− species, as demonstrated by zeta potential and electrochemical measurements. This work elucidates the adsorption enhancement mechanism of heterogeneous interfaces and provides constructive guidance for designing efficient multicomponent electrocatalysts in organic electrocatalytic reactions.
A CuO–PdO heterogeneous interface, which exhibits a low onset potential of 5‐hydroxymethylfurfural oxidation reaction and high current density, is successfully synthesized. The analytical results show that the CuO–PdO heterogeneous interface can strengthen the adsorption and activation capacity of organic molecules and OH− species, and promote the dehydrogenation and electron transfer in the process of 5‐formyl‐2‐furancarboxylic acid→2,5‐furandicarboxylic acid.
Oncogenic KRAS mutations found in 20% to 30% of all non-small cell lung cancers (NSCLC) are associated with chemoresistance and poor prognosis. Here we demonstrate that activation of the cell ...protective stress response gene NRF2 by KRAS is responsible for its ability to promote drug resistance. RNAi-mediated silencing of NRF2 was sufficient to reverse resistance to cisplatin elicited by ectopic expression of oncogenic KRAS in NSCLC cells. Mechanistically, KRAS increased NRF2 gene transcription through a TPA response element (TRE) located in a regulatory region in exon 1 of NRF2. In a mouse model of mutant KrasG12D-induced lung cancer, we found that suppressing the NRF2 pathway with the chemical inhibitor brusatol enhanced the antitumor efficacy of cisplatin. Cotreatment reduced tumor burden and improved survival. Our findings illuminate the mechanistic details of KRAS-mediated drug resistance and provide a preclinical rationale to improve the management of lung tumors harboring KRAS mutations with NRF2 pathway inhibitors.
The ternary Nowotny phase (NP), with a composition Mo3+2xSi3C0.6 (x = 0.9‐0.764), is found to be catalytically active in the field of electrochemical water splitting. The NP embedded in a porous ...SiC/C nanocomposite matrix is synthesized via a single‐source‐precursor approach which involves the reaction of allylhydridopolycarbosilane with MoO2(acac)2. Thermal treatment of the single‐source‐precursor up to 1400°C in a protective atmosphere results in the in situ formation of nanocrystalline Mo3+2xSi3C0.6 immobilized in a thermally and corrosion‐stable SiC/C matrix. The weight fractions of the observed crystalline phases Mo3+2xSi3C0.6 and SiC amount to ca. 28 (26) and 72 (74) wt%, respectively, when prepared at 1400°C (1350°C). The porosity of the formed nanocomposite is adjusted by the addition of polystyrene (PS) as a pore former to the single‐source‐precursor resulting in a specific surface area up to 206 m2/g. The electrocatalytic activity of the Mo3+2xSi3C0.6/C/SiC nanocomposite with respect to the hydrogen evolution reaction (HER) is characterized by low over potentials of 22 and 138 mV vs reversible hydrogen electrode (RHE) for applying 1 and 10 mA cm−2 of current density, respectively. The analyzed electrocatalytic performance exceeds that of most Mo‐based electrocatalysts and shows high stability (over 90%) during 35 hours.
The Nowotny phase Mo Si C (x = 0.9‐0.764) was found to be catalytically active in electrochemical water splitting. The electrocatalytic activity of the Mo Si C /C/SiC nanocomposite with respect to the hydrogen evolution reaction was characterized by low overpotentials of 22 and 138 mV vs reversible hydrogen electrode for applying 1 and 10 m A cm of current density, respectively, which exceeds that of most Mo‐based electrocatalysts and shows a high stability (over 90 %) during 35 h.
Compelling evidences have revealed the emerging role of ferroptosis in the pathophysiological process of acute lung injury (ALI), but its modulation is not clear. Here, we identified that STAT6 acted ...as a critical regulator of epithelium ferroptosis during ALI. Firstly, STAT6 expression and activity were increased in the ALI mice models caused by crystalline silica (CS), LPS and X-ray exposure. Followed by confirming the contribution of ferroptosis in the above ALI with ferrostatin-1 and deferoxamine intervention, bioinformatic analyses revealed that STAT6 expression was negatively correlated with ferroptosis. Consistently, lung epithelium-specific depletion of STAT6 in mice or STAT6 knockdown in cultured epithelial cells exacerbated ferroptosis in the above ALI. While overexpression of STAT6 in lung epithelial cells attenuated the ferroptosis. Mechanistically, SLC7A11 is a typical ferroptosis-related gene and negatively regulated by P53. CREB-binding protein (CBP) is a critical acetyltransferase of P53 acetylation, showing valuable regulation on targets' transcription. Herein, we found that STAT6 negatively regulates ferroptosis through competitively binding with CBP, which inhibits P53 acetylation and transcriptionally restores SLC7A11 expression. Finally, pulmonary-specific STAT6 overexpression decreased the ferroptosis and attenuated CS and LPS induced lung injury. Our findings revealed that STAT6 is a pivotal regulator of ferroptosis, which may be a potential therapeutic target for the treatment of acute lung injury.
Fine particulate matter (PM 2.5) is a well-known air pollutant threatening public health. Studies has confirmed that long-term exposure to the particles could reduce the pulmonary function, cause ...exacerbation of asthma and chronic obstructive pulmonary disease, and increase incidence and mortality of lung cancer. Bixin is a natural compound that is widely used as a food additive. Our previous studies demonstrated that bixin i.p. administration could protect against particles intratracheal exposure (56 days)-induced lung injury in an Nrf2-dependent manner. But the detail mechanisms are still unclarified. Our current study aimed to explore the further therapeutic potential and mechanism of bixin to slow the progression of lung injury and inflammation in vivo and in vitro. The results from the in vivo study showed that bixin treatment attenuated the accumulation of inflammatory cells, decreased the levels of tissue apoptosis, and increase the ability of cell proliferation. Besides that, bixin also could regulate the expression of MMP9, TGFβ1, and its downstream Fibronectin (FN), along with activation of Nrf2 signals. In vitro experiments in human bronchial epithelial cells demonstrated that Nrf2 activated by bixin contributes to tissue repair by alleviating oxidative stress, increasing proliferation and migration, decreasing apoptosis, which may be partially through modulating the expression of MMP9, TGFβ1, and FN. This study provides convincing experimental evidences that bixin could be used therapeutically to promote tissue repair and improve pulmonary injury induced by particles exposure.
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•Bixin attenuates the inflammation, decreases the tissue apoptosis and increases the proliferation.•Bixin contributes the tissue repair in an Nrf2-dependent manner.•Bixin modulate the expression of TGFβ1, MMP9 and FN.
Scope
Alcoholic liver disease (ALD) is a major cause of morbidity and mortality worldwide. Oxidative stress induced during the alcohol metabolism plays a crucial role in ALD, and clinical evidence ...demonstrates the prevalence and risks of vitamin D (VD) deficiency in ALD. This study aims to explore the mechanism of VD administration to ameliorate alcohol‐induced cell injury.
Methods and results
VD activates NRF2 (nuclear factor erythroid 2 (NF‐E2)‐related factor 2) signals along with upregulation of ALDH2 expression. Knockdown of NRF2 eliminates the protective effects of VD treatment. ALDH2 knockdown not only partially affects this protection, but also mildly reduces NRF2 expression. ALDH2 overexpression enhances ERK phosphorylation and upregulated NRF2 transcription via a newly identified TRE in the exon 1 of NRF2.
Conclusion
This study provides evidence that VD protects against alcohol‐induced cell injury within an NRF2‐ALDH2 feedback loop. NRF2 induced by VD could transcriptionally upregulate ALDH2 expression to help metabolize alcohol. TRE‐driven transcriptional upregulation of NRF2 through ALDH2‐ERK/MEK signals would further exert the anti‐oxidant effects. The study explores a novel potential protection of VD in alcohol‐induced liver cell injury, and contributes to alcohol‐related liver disease nutritional therapies.
A model of vitamin D (VD) shows protection against alcohol‐induced cell injury. The mechanism of VD against alcohol toxicity includes an NRF2‐ALDH2 positive feedback loop. First of all, VD directly activates NRF2 signals. Then the upregulated NRF2 signals can increase ALDH2 mRNA level, which enhance a TRE‐dependent NRF2 gene transcription by activating the MEK/ERK signaling pathway, leading to an increase in NRF2 mRNA and protein levels.
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