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"Guo Chen"
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Solar hydrogen generation : transition metal oxides in water photoelectrolysis
\"Expert techniques for extracting hydrogen from water using transition metal oxides as catalysts Solar Hydrogen Generation details the complex process of separating hydrogen from oxygen--photoelectrolysis. This book comprehensively covers the chemical characteristics of transition metal oxides, explaining how to covert solar energy to electron energy through transition metal oxides. Past experimentations and future directions are discussed. Solar Hydrogen Generation Comprehensively reviews physical characteristics of transition metal oxides both in electrochemical and photocatalytic applications Includes history and future prospects for water photoelectrolysis Reviews state-of-the-art achievements in the fields of condensed matter physics, nanostructured material science, electrochemistry, and photocatalysis Addresses potential problems and solutions In-depth coverage: Hydrogen Production; Electrochemistry and Photoelectrolysis; Transition Metal Oxides; Molecular Structure, Crystal Structure, and Electronic Structure; Optical Properties and Light Absorption; Bandgap, Band Edge, and Engineering; Impurity, Dopants, and Defects; Photocatalytic Reactions, Oxidation and Reduction; Organic and Inorganic Systems; Surface and Interface Chemistry; Nanostructured and Morphology; Synchrotron Radiation and Soft X-Ray Spectroscopy\"--Provided by publisher.
Book
Curcumin overcome primary gefitinib resistance in non-small-cell lung cancer cells through inducing autophagy-related cell death
Background
Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) are being wildly used as target therapy in non-small-cell lung cancer (NSCLC). However, NSCLC patients with wild-type EGFR and KRAS mutation are primary resistant to EGFR-TKIs such as gefitinib. Curcumin has been known as a potential therapeutic agent for several major human cancers. In this study, we investigated the effect of curcumin on the reversal of gefitinib resistance in NSCLC cells as well as their molecular bases.
Methods
H157 (wild-type EGFR and KARS mutation) and H1299 (wild-type EGFR and HRAS mutation) cells were treated with gefitinib or curcumin alone, or the two combination, and then cell viability, EGFR activity, expressions of Sp1 and Sp1-dependent proteins and receptor tyrosine kinases, markers of autophagy and apoptosis were examined by using CCK-8, colony formation, immunoblot, quantitative PCR, immunofluoscence, and flow cytometry assays. Also xenograft experiments were conduced to test the synergism of curcumin to gefitinib.
Results
Our results showed that curcumin significantly enhanced inhibitory effect of gefitinib on primary gefitinib-resistant NSCLC cell lines H157 and H1299. Combination treatment with curcumin and gefitinib markedly downregulated EGFR activity through suppressing Sp1 and blocking interaction of Sp1 and HADC1, and markedly suppressed receptor tyrosine kinases as well as ERK/MEK and AKT/S6K pathways in the resistant NSCLC cells. Meanwhile, combination treatment of curcumin and gefitinib caused dramatic autophagy induction, autophagic cell death and autophagy-mediated apoptosis, compared to curcumin or gefitinib treatment alone, as evidenced by the findings that curcumin and gefitinib combination treatment-produced synergistic growth inhibition and apoptosis activation can be reversed by pharmacological autophagy inhibitors (Baf A1 or 3-MA) or knockdown of Beclin-1 or ATG7, also can be partially returned by pan-caspase inhibitor (Z-VAD-FMK) in H157 and H1299 cells. Xenograft experiments in vivo yielded similar results.
Conclusions
These data indicate that the synergism of curcumin on gefitinib was autophagy dependent. Curcumin can be used as a sensitizer to enhance the efficacy of EGFR-TKIs and overcome the EGFR-TKI resistance in NSCLC patients with wild-type EGFR and/or KRAS mutation.
Journal Article
Crosstalk between mitochondrial biogenesis and mitophagy to maintain mitochondrial homeostasis
Mitochondrial mass and quality are tightly regulated by two essential and opposing mechanisms, mitochondrial biogenesis (mitobiogenesis) and mitophagy, in response to cellular energy needs and other cellular and environmental cues. Great strides have been made to uncover key regulators of these complex processes. Emerging evidence has shown that there exists a tight coordination between mitophagy and mitobiogenesis, and their defects may cause many human diseases. In this review, we will first summarize the recent advances made in the discovery of molecular regulations of mitobiogenesis and mitophagy and then focus on the mechanism and signaling pathways involved in the simultaneous regulation of mitobiogenesis and mitophagy in the response of tissue or cultured cells to energy needs, stress, or pathophysiological conditions. Further studies of the crosstalk of these two opposing processes at the molecular level will provide a better understanding of how the cell maintains optimal cellular fitness and function under physiological and pathophysiological conditions, which holds promise for fighting aging and aging-related diseases.
Journal Article
Synthetic Biology and Genome-Editing Tools for Improving PHA Metabolic Engineering
Polyhydroxyalkanoates (PHAs) are a diverse family of biopolyesters synthesized by many natural or engineered bacteria. Synthetic biology and DNA-editing approaches have been adopted to engineer cells for more efficient PHA production. Recent advances in synthetic biology applied to improve PHA biosynthesis include ribosome-binding site (RBS) optimization, promoter engineering, chromosomal integration, cell morphology engineering, cell growth behavior reprograming, and downstream processing. More importantly, the genome-editing tool clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9) has been applied to optimize the PHA synthetic pathway, regulate PHA synthesis-related metabolic flux, and control cell shapes in model organisms, such as Escherichia coli, and non-model organisms, such as Halomonas. These synthetic biology methods and genome-editing tools contribute to controllable PHA molecular weights and compositions, enhanced PHA accumulation, and easy downstream processing.
The bioplastic PHA, which features biodegradability, biocompatibility, and thermoprocessibility, is moving toward low-cost microbial production to replace nondegradable petrochemical plastics.Wild-type or weakly engineered bacteria are insufficient to meet demands for improved PHA structures and low production cost.Synthetic biology and genome-editing approaches can promote PHA synthesis, enlarge cells for more PHA storage, control shape changes, accelerate growth, aid the co-production of multiple products, direct flux toward final products, and make product recovery more convenient.Optimized promoters and RBSs increase the expression of PHA synthesis genes.CRISPR interference and CRISPR/Cas9 are useful for downregulating the expression of multiple genes simultaneously, allowing more flux to be directed to PHA synthesis in an optimized strain.
Journal Article
Acceptor Copolymerized Axially Chiral Conjugated Polymers with TADF Properties for Efficient Circularly Polarized Electroluminescence
Chiral conjugated polymer has promoted the development of the efficient circularly polarized electroluminescence (CPEL) device, nevertheless, it remains a challenge to develop chiral polymers with high electroluminescence performance. Herein, by the acceptor copolymerization of axially chiral biphenyl emitting skeleton and benzophenone, a pair of axially chiral conjugated polymers namely R‐PAC and S‐PAC are synthesized. The target polymers exhibit obvious thermally activated delayed fluorescence (TADF) activities with high photoluminescence quantum yields of 81%. Moreover, the chiral polymers display significant circularly polarized luminescence features, with luminescence dissymmetry factor (|glum|) of nearly 3 × 10−3. By using the chiral polymers as emitters, the corresponding circularly polarized organic light‐emitting diodes (CP‐OLEDs) exhibit efficient CPEL signals with electroluminescence dissymmetry factor |gEL| of 3.4 × 10−3 and high maximum external quantum efficiency (EQEmax) of 17.8%. Notably, considering both EQEmax and |gEL| comprehensively, the device performance of R‐PAC and S‐PAC is the best among all the reported CP‐OLEDs with chiral conjugated polymers as emitters. This work provides a facile approach to constructing chiral conjugated TADF polymers and discloses the potential of axially chiral conjugated luminescent skeletons in architecting high‐performance CP‐OLEDs. Axially chiral conjugated polymers with thermally activated delayed fluorescence features are synthesized by copolymerizing chiral unit and benzophenone acceptor. By using the obtained polymers as emitters, high‐performance solution‐processed circularly polarized organic light‐emitting diodes are fabricated featuring efficient circularly polarized electroluminescence properties with the maximum external quantum efficiency and dissymmetry factor of up to 17.8% and 3.4 × 10‐3, respectively.
Journal Article
Artemisinin compounds sensitize cancer cells to ferroptosis by regulating iron homeostasis
The antimalarial drug artemisinin and its derivatives have been explored as potential anticancer agents, but their underlying mechanisms are controversial. In this study, we found that artemisinin compounds can sensitize cancer cells to ferroptosis, a new form of programmed cell death driven by iron-dependent lipid peroxidation. Mechanistically, dihydroartemisinin (DAT) can induce lysosomal degradation of ferritin in an autophagy-independent manner, increasing the cellular free iron level and causing cells to become more sensitive to ferroptosis. Further, by associating with cellular free iron and thus stimulating the binding of iron-regulatory proteins (IRPs) with mRNA molecules containing iron-responsive element (IRE) sequences, DAT impinges on IRP/IRE-controlled iron homeostasis to further increase cellular free iron. Importantly, in both in vitro and a mouse xenograft model in which ferroptosis was triggered in cancer cells by the inducible knockout of GPX4, we found that DAT can augment GPX4 inhibition-induced ferroptosis in a cohort of cancer cells that are otherwise highly resistant to ferroptosis. Collectively, artemisinin compounds can sensitize cells to ferroptosis by regulating cellular iron homeostasis. Our findings can be exploited clinically to enhance the effect of future ferroptosis-inducing cancer therapies.
Journal Article