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1.
J Cell Physiol ; 235(1): 454-464, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31264215

RESUMO

Lung adenocarcinomas injured greatly on the people worldwide. Although clinic experiments and gene profiling analyses had been well performed, to our knowledge, systemic coexpression analysis of human genes for this cancer is still limited to date. Here, using the published data GSE75037, we built the coexpression modules of genes by Weighted Gene Co-Expression Network Analysis (WGCNA), and investigated function and protein-protein interaction network of coexpression genes by Database for Annotation, visualization, and Integrated Discovery (DAVID) and String database, respectively. First, 11 coexpression modules were conducted for 5,000 genes in the 83 samples recently. Number of genes for each module ranged from 90 to 1,260, with the mean of 454. Second, interaction relationships of hub-genes between pairwise modules showed great differences, suggesting relatively high scale independence of the modules. Third, functional enrichment of the coexpression modules showed great differences. We found that genes in modules 8 significantly enriched in the biological process and/or pathways of cell adhesion, extracellular matrix (ECM)-receptor interaction, focal adhesion, and PI3K-Akt signaling pathway, and so forth. It was inferred as the key module underlying lung adenocarcinomas. Furthermore, PPI analysis revealed that the genes COL1A1, COL1A2, COL3A1, CTGF, and BGN owned the largest number of adjacency genes, unveiling that they may functioned importantly during the occurrence of lung adenocarcinomas. To summary, genes involved in cell adhesion, ECM-receptor interaction, focal adhesion, and PI3K-Akt signaling pathway play crucial roles in human lung adenocarcinomas.

2.
Chem Commun (Camb) ; 55(86): 12996-12999, 2019 Oct 24.
Artigo em Inglês | MEDLINE | ID: mdl-31608348

RESUMO

No methodology has been built to distinguish intracellular SERS nanosensors from cell outer membrane bound-ones. Here we propose a "turning off" strategy by combining etchable SERS nanosensors with a non-permeable etchant. The SERS signals outside the living cells can be rapidly removed, leaving only the internalized nanosensors for imaging and thereby allowing accurate intracellular pH and H2O2 sensing.

3.
Clin Pharmacol Ther ; 2019 Oct 25.
Artigo em Inglês | MEDLINE | ID: mdl-31654399

RESUMO

Overexpression of AKR1C3, an aldo-keto reductase, was recently discovered in liver cancers. In this study, an inverse correlation between AKR1C3 expression and liver cancer patient survival was observed. AKR1C3 inhibitors, however, failed to suppress liver cancer cell growth. The prodrug TH3424, which releases a DNA alkylating reagent upon reduction by AKR1C3, was developed to target tumors with overexpression of AKR1C3. TH3424 showed specific killing of liver cancer cells with AKR1C3 overexpression both in vitro and in vivo. In patient-derived mouse xenograft models, TH3424 at doses as low as 1.5 mg/kg eliminated liver tumors with no apparent toxicity. Conclusion: TH3424 is a promising drug candidate for liver cancer and other types of cancers overexpressing AKR1C3.

4.
Hemoglobin ; : 1-3, 2019 Oct 25.
Artigo em Inglês | MEDLINE | ID: mdl-31650882

RESUMO

Here we report a 67-year-old Chinese male carrying an unstable novel hemoglobin (Hb) variant in compound heterozygosity with the - -SEA (Southeast Asian) α-thalassemia (α-thal) deletion. Hemoglobin analysis by capillary electrophoresis (CE) revealed a rapid degradation feature of the variant. Sanger sequencing of the Hb gene revealed a novel homozygous mutation in exon 2 of the α1-globin gene [α52(E1)Ser→Cys (TCT>TGT); HBA1: c.158C>G]. We named this novel variant Hb Dongguan for the place of origin of the proband. Additionally, gap-polymerase chain reaction (gap-PCR) indicated the presence of the heterozygous - -SEA α-thal deletion.

5.
J Cell Physiol ; 2019 Oct 14.
Artigo em Inglês | MEDLINE | ID: mdl-31608989

RESUMO

This review aims to summarize and discuss the most recent advances in our understanding of the underlying mechanisms of the paradoxical effects of sortilin on lipid metabolism. The vacuolar protein sorting 10 protein (Vps10p) domain in the sortilin protein is responsible for substrate binding. Its cytoplasmic tail interacts with adaptor molecules, and modifications can determine whether sortilin trafficking occurs via the anterograde or retrograde pathway. The complicated trafficking behaviors likely contribute to the paradoxical roles of sortilin in lipid metabolism. The anterograde pathway of sortilin trafficking in hepatocytes, enterocytes, and peripheral cells likely causes an increase in plasma lipid levels, while the retrograde pathway leads to the opposite effect. Hepatocyte sortilin functions via the anterograde or retrograde pathway in a complicated and paradoxical manner to regulate apoB-containing lipoprotein metabolism. Clarifying the regulatory mechanisms underlying the trafficking behaviors of sortilin is necessary and may lead to artificial sortilin intervention as a potential therapeutic strategy for lipid disorder diseases. Conclusively, the paradoxical regulation of sortilin in lipid metabolism is likely due to its complicated trafficking behaviors.

6.
EMBO Mol Med ; : e10469, 2019 Oct 14.
Artigo em Inglês | MEDLINE | ID: mdl-31609086

RESUMO

Caloric restriction mimetics (CRMs) are natural or synthetic compounds that mimic the health-promoting and longevity-extending effects of caloric restriction. CRMs provoke the deacetylation of cellular proteins coupled to an increase in autophagic flux in the absence of toxicity. Here, we report the identification of a novel candidate CRM, namely 3,4-dimethoxychalcone (3,4-DC), among a library of polyphenols. When added to several different human cell lines, 3,4-DC induced the deacetylation of cytoplasmic proteins and stimulated autophagic flux. At difference with other well-characterized CRMs, 3,4-DC, however, required transcription factor EB (TFEB)- and E3 (TFE3)-dependent gene transcription and mRNA translation to trigger autophagy. 3,4-DC stimulated the translocation of TFEB and TFE3 into nuclei both in vitro and in vivo, in hepatocytes and cardiomyocytes. 3,4-DC induced autophagy in vitro and in mouse organs, mediated autophagy-dependent cardioprotective effects, and improved the efficacy of anticancer chemotherapy in vivo. Altogether, our results suggest that 3,4-DC is a novel CRM with a previously unrecognized mode of action.

7.
J Hypertens ; 2019 Oct 03.
Artigo em Inglês | MEDLINE | ID: mdl-31584510

RESUMO

OBJECTIVES: The current study aimed to investigate the value of the computed tomography-based left-versus-right adrenal gland volume ratio (L/Rv) in screening patients with unilateral primary aldosteronism. METHODS: The current study recruited 114 patients who underwent successful adrenal venous sampling (AVS) and adrenal computed tomography at West China Hospital of Sichuan University. The patients were divided into three groups according to the AVS results: AVS-left, AVS-bilateral, and AVS-right primary aldosteronism. The volumes of the left and right adrenal glands were semiautomatically calculated. The L/Rv of each patient was computed, and its value in identifying unilateral primary aldosteronism was analyzed. RESULTS: The mean value of the L/Rv was larger in AVS-left patients and smaller in AVS-right patients than that in AVS-bilateral patients. In AVS-left primary aldosteronism patients, the cutoff value of the L/Rv with the highest Youden index was 1.344 [area under the curve (AUC) 0.851, sensitivity 80.0%, specificity 78.1%]. The optimal cutoff value was 1.908, of which 46.0% (23/50) of AVS-left primary aldosteronism patients could be identified (specificity 100.0%). In AVS-right primary aldosteronism patients, the cutoff value of the L/Rv with the highest Youden index was 1.267 (AUC 0.868, specificity 72.8%, sensitivity 87.9%). The optimal cutoff value was 0.765, of which 27.3% (9/33) of AVS-right primary aldosteronism patients could be identified (specificity 100.0%). Patients with L/Rv more than 1.908 or less than 0.765 had higher complete success rate postsurgery. CONCLUSION: Although not perfect, the L/Rv is an applicable index to screen unilateral primary aldosteronism patients for surgery. Primary aldosteronism patients, even those aged more than 35 years, with an L/Rv more than 1.908 or less than 0.765 can be spared AVS before surgery.

8.
Stem Cell Reports ; 13(4): 642-656, 2019 Oct 08.
Artigo em Inglês | MEDLINE | ID: mdl-31564646

RESUMO

Cellular responses to transforming growth factor ß (TGF-ß) depend on cell context. Here, we explored how TGF-ß/nodal signaling crosstalks with the epigenome to promote mesendodermal differentiation. We find that expression of a group of mesendodermal genes depends on both TRIM33 and nodal signaling in embryoid bodies (EBs) but not in embryonic stem cells (ESCs). Only in EBs, TRIM33 binds these genes in the presence of expanded H3K18ac marks. Furthermore, the H3K18ac landscape at mesendodermal genes promotes TRIM33 recruitment. We reveal that HDAC1 binds to active gene promoters and interferes with TRIM33 recruitment to mesendodermal gene promoters. However, the TRIM33-interacting protein p300 deposits H3K18ac and further enhances TRIM33 recruitment. ATAC-seq data demonstrate that TRIM33 primes mesendodermal genes for activation by maintaining chromatin accessibility at their regulatory regions. Altogether, our study suggests that HDAC1 and p300 are key factors linking the epigenome through TRIM33 to the cell context-dependent nodal response during mesendodermal differentiation.

9.
Mar Drugs ; 17(10)2019 Oct 09.
Artigo em Inglês | MEDLINE | ID: mdl-31601054

RESUMO

Actinomycin V, extracted and separated from marine-derived actinomycete Streptomyces sp., as the superior potential replacement of actinomycin D (which showed defect for its hepatotoxicity) has revealed an ideal effect in the suppression of migration and invasion in human breast cancer cells as referred to in our previous study. In this study, the involvement of p53 in the cell cycle arrest and pro-apoptotic action of actinomycin V was investigated in human non-small-cell lung carcinoma A549 cells. Results from the 3-(4,5-dimethylthiazol)-2,5-diphenyltetrazolium bromide assay showed that cytotoxic activity of actinomycin V on A549 cells (with wild-type p53) was stronger than the NCI-H1299 cells (p53-deficient). Actinomycin V upregulated both of the protein and mRNA expression levels of p53, p21Waf1/Cip1 and Bax in A549 cells. For this situation, actinomycin V decreased the M-phase related proteins (Cdc2, Cdc25A and Cyclin B1) expression, arrested cells in G2/M phase and subsequently triggered apoptosis by mediating the Bcl-2 family proteins' expression (Bax and Bcl-2). Furthermore, the effects of cell cycle arrest and apoptosis in A549 cells which were induced by actinomycin V could be reversed by the pifithrin-α, a specific inhibitor of p53 transcriptional activity. Collectively, our results suggest that actinomycin V causes up-regulation of p53 by which the growth of A549 cells is suppressed for cell cycle arrest and apoptosis.

10.
Cell Death Dis ; 10(10): 771, 2019 Oct 10.
Artigo em Inglês | MEDLINE | ID: mdl-31601788

RESUMO

The retention using selective hooks (RUSH) system allows to retain a target protein fused to green fluorescent protein (GFP) and a streptavidin-binding peptide (SBP) due to the interaction with a molar excess of streptavidin molecules ("hooks") targeted to selected subcellular compartments. Supplementation of biotin competitively disrupts the interaction between the SBP moiety and streptavidin, liberating the chimeric target protein from its hooks, while addition of avidin causes the removal of biotin from the system and reestablishes the interaction. Based on this principle, we engineered two chimeric proteins involved in autophagy, namely microtubule-associated proteins 1A/1B light chain 3B (MAP1LC3B, best known as LC3) and sequestosome-1 (SQSTM1, best known as p62) to move them as SBP-GFP-LC3 and p62-SBP-GFP at will between the cytosol and two different organelles, the endoplasmic reticulum (ER) and the Golgi apparatus. Although both proteins were functional in thus far that SBP-GFP-LC3 and p62-SBP-GFP could recruit their endogenous binding partners, p62 and LC3, respectively, their enforced relocation to the ER or Golgi failed to induce organelle-specific autophagy. Hence, artificial tethering of LC3 or p62 to the surface of the ER and the Golgi is not sufficient to trigger autophagy.

11.
Molecules ; 24(20)2019 Oct 22.
Artigo em Inglês | MEDLINE | ID: mdl-31652659

RESUMO

Ivalin, a natural compound isolated from Carpesium divaricatum, showed excellent microtubule depolymerization activities among human hepatocellular carcinoma in our previous work. Here, we investigated its functions on mitochondria-mediated apoptosis in hepatocellular carcinoma SMMC-7721 cells. DAPI (4',6-diamidino-2-phenylindole) staining, annexin V-fluorexcein isothiocyanate (FITC) apoptosis detection, and western blotting were applied to explore the apoptotic effect of Ivalin. Next, the induction effect of Ivalin on the mitochondrial pathway was also confirmed via a series of phenomena including the damage of mitochondria membrane potential, mitochondria cytochrome c escape, cleaved caspase-3 induction, and the reactive oxygen species generation. In this connection, we understood that Ivalin induced apoptosis through the mitochondrial pathway and the overload of reactive oxygen species. Furthermore, we found that the activation of nuclear factor-κB (NF-κB) and subsequent p53 induction were associated with the apoptotic effect of Ivalin. These data confirmed that Ivalin might be a promising pro-apoptotic compound that can be utilized as a potential drug for clinical treatment.

12.
Oncol Rep ; 2019 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-31578585

RESUMO

Platinum­containing doublet chemotherapy is the cornerstone of lung cancer treatment; however, cisplatin resistance is a major obstacle in the treatment of lung cancer. However, the mechanism underlying this resistance has not been fully elucidated. Previous studies have shown that serum apurinic/apyrimidinic endonuclease 1 (APE1) levels in patients with NSCLC are inversely associated with progression­free survival after platinum­containing doublet chemotherapy, and can serve as a biomarker for predicting disease prognosis and treatment efficacy. The present study was designed to investigate the role played by APE1 in the resistance of lung cancer to cisplatin. The levels of mitochondrial apurinic endonuclease 1 (m­APE1) and total APE1 (t­APE1) protein in a cisplatin­resistant A549 cell line (A549/DDP) and cisplatin­sensitive A549 cells were analyzed by western blotting. Mitochondrial membrane potential was detected by using the JC­1 staining method. The cisplatin­resistance of APE1­overexpressing A549 cells and APE1­silenced A549/DDP cells was assessed by cell apoptosis and colony formation assays. The results revealed that cisplatin­resistant A549 cells contained high levels of APE1, and exhibited elevated levels of autophagy. The levels of m­APE1 and t­APE1 protein were increased in the A549/DDP cells when compared with these levels in the A549 cells. Overexpression of APE1 and Mia40 enhanced the cisplatin resistance and autophagy of the A549 cells. APE1 knockdown restored the cisplatin sensitivity and reduced the levels of LC3II and Parkin in the A549/DDP cells, but promoted the release of cytochrome c. Furthermore, Parkin silencing or treatment with 3­methyladenine (3­MA, an autophagy inhibitor) promoted the apoptosis of APE1­overexpressing A549 cells, indicating that Parkin­mediated mitophagy plays an important role in the APE1­induced cisplatin resistance of A549 cells. In conclusion, APE1 promotes the cisplatin resistance of lung cancer cells by inducing Parkin­mediated mitophagy.

13.
Turk J Gastroenterol ; 30(10): 883-891, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31633484

RESUMO

BACKGROUND/AIMS: Metabolic acidosis is a common complication in patients with cirrhosis at the intensive care units (ICUs) and associated with increased mortality. The aim of our research was to explore the epidemiology and risk factors of metabolic acidosis in critically ill patients with cirrhosis. MATERIALS AND METHODS: A total of 975 patients with cirrhosis were selected into our study, and all participants were followed up for at least 28 days. Cox regression model and machine-learning algorithm were used to identify the importance of different risk factors, respectively. Finally, an improved prognostic model as Model for End-stage Liver Disease and metabolic acidosis (MELD-MA) was developed. RESULTS: Among the 975 patients with liver cirrhosis, 506 had metabolic acidosis, including 257 patients who had decompensated metabolic acidosis at ICU admission. The 28-day mortality was 41% (206/506) in patients with metabolic acidosis. Bilirubin (hazard ratio (HR): 1.023, 95% confidence interval (CI): 1.011-1.036), international normalized ratio (HR: 1.527, 95% CI: 1.332-1.750), pH (HR: 0.173, 95% CI: 0.047-0.640), BE-Lac (HR: 0.907, 95% CI: 0.868-0.948), and BE-Na (HR: 0.923, 95% CI: 0.859-0.991) were considered as independent prognostic parameters for 28-day mortality. MELD-NA had significantly higher discrimination (area under the receiver operating characteristic curve 0.79) than MELD and Child-Pugh score. CONCLUSION: Critically ill patients with cirrhosis have a high mortality rate and poor prognosis because of the high prevalence of metabolic acidosis. Lactic acidosis is the worst prognosis of all types of metabolic acidosis. MELD-MA performs well on the short-term mortality assessment in critically ill patients with cirrhosis and metabolic acidosis.

14.
Small ; 15(44): e1903831, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31513340

RESUMO

In this study, a highly sensitive and self-driven near-infrared (NIR) light photodetector based on PdSe2 /pyramid Si heterojunction arrays, which are fabricated through simple selenization of predeposited Pd nanofilm on black Si, is demonstrated. The as-fabricated hybrid device exhibits excellent photoresponse performance in terms of a large on/off ratio of 1.6 × 105 , a responsivity of 456 mA W-1 , and a high specific detectivity of up to 9.97 × 1013 Jones under 980 nm illumination at zero bias. Such a relatively high sensitivity can be ascribed to the light trapping effect of the pyramid microstructure, which is confirmed by numerical modeling based on finite-difference time domain. On the other hand, thanks to the broad optical absorption properties of PdSe2 , the as-fabricated device also exhibits obvious sensitivity to other NIR illuminations with wavelengths of 1300, 1550, and 1650 nm, which is beyond the photoresponse range of Si-based devices. It is also found that the PdSe2 /pyramid Si heterojunction device can also function as an NIR light sensor, which can readily record both "tree" and "house" images produced by 980 and 1300 nm illumination, respectively.

15.
Atherosclerosis ; 289: 143-161, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31518965

RESUMO

BACKGROUND AND AIMS: Krüppel-like factor 14 (KLF14) is known to play a role in atherosclerosis, but the underlying mechanisms are still largely unknown. The aim of our study was to explore the effects of KLF14 on lipid metabolism and inflammatory response, providing a potential target for lowering the risk of atherosclerosis-causing disease. METHODS AND RESULTS: mRNA and protein levels of KLF14 were significantly decreased in oxidized low-density lipoprotein (oxLDL)-treated macrophages and in the atherosclerotic lesion area. Chromatin immunoprecipitation (ChIP) and luciferase reporter gene assays were used to confirm that KLF14 positively regulated miR-27a expression by binding to its promoter. We also found that KLF14 could restored appropriate cellular lipid homeostasis and inflammatory responses via negatively regulating lipoprotein lipase (LPL) expression in THP1-derived macrophages through miR-27a. In addition, gypenosides (GP), a KLF14 activator, delayed the development of atherosclerosis in apolipoprotein E deficient (apoE-/-) mice. CONCLUSIONS: KLF14 plays an antiatherogenic role via the miR-27a-dependent down-regulation of LPL and subsequent inhibition of proinflammatory cytokine secretion and lipid accumulation.

16.
Exp Cell Res ; 384(1): 111618, 2019 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-31505167

RESUMO

End binding protein 1 (EB1) is a key regulator of microtubule dynamics that orchestrates hierarchical interaction networks at microtubule plus ends to control proper cell division. EB1 activity is known to be regulated by serine/threonine phosphorylation; however, how tyrosine phosphorylation affects EB1 activity remains poorly understood. In this study, we mapped the tyrosine phosphorylation pattern of EB1 in synchronized cells and identified two tyrosine phosphorylation sites (Y217 and Y247) in mitotic cells. Using phospho-deficient (Y/F) and phospho-mimic (Y/D) mutants, we revealed that Y247, but not Y217, is critical for astral microtubule stability. The Y247D mutant contributed to increased spindle angle, indicative of defects in spindle orientation. Time-lapse microscopy revealed that the Y247D mutant significantly delayed mitotic progression by increasing the duration times of prometaphase and metaphase. Structural analysis suggests that Y247 mutants lead to instability of the hydrophobic cavity in the EB homology (EBH) domain, thereby affecting its interactions with p150glued, a protein essential for Gαi/LGN/NuMA complex capture. These findings uncover a crucial role for EB1 phosphorylation in the regulation of mitotic spindle orientation and cell division.

17.
J Matern Fetal Neonatal Med ; : 1-6, 2019 Sep 16.
Artigo em Inglês | MEDLINE | ID: mdl-31522571

RESUMO

Objective: To assess the value and accuracy of gestational age at diagnosis in predicting postnatal outcomes of prenatally diagnosed congenital diaphragmatic hernia (CDH). Study design: The medical records of 158 prenatally diagnosed neonates with CDH from 2008 to 2018 were retrospectively reviewed. Data were analyzed using parametric and nonparametric tests, appropriately. Results: Gestational age at diagnosis predicted postnatal survival independently. Survival rate at discharge increased when gestational age at diagnosis increased (p < .001). Area under the receiver operator curve for survival for gestational age at diagnosis was 0.74, observed-to-expected lung to head ratio 0.74, and liver herniation 0.76. Patients diagnosed with CDH before 25 gestational weeks had a larger size of the diaphragmatic defect, more need for patch repair, longer duration of mechanical ventilation and hospital stay than those after 25 gestational weeks. Conclusions: Gestational age at diagnosis is an independent predictor of CDH prognosis. It has a similar ability to predict survival compared to observed-to-expected lung to head ratio and liver herniation.

18.
Chem Res Toxicol ; 2019 Sep 30.
Artigo em Inglês | MEDLINE | ID: mdl-31524377

RESUMO

Endoplasmic reticulum (ER) stress has been shown to be involved in the hepatotoxicity of acetaminophen (APAP). Guanabenz (GA), a widely known antihypertensive drug, is reported to exhibit an anti-ER stress effect. In this study, we investigated the potential of GA as an antidote against APAP-induced hepatotoxicity. The underlying biochemical mechanisms for the hepatoprotective effect of GA were explored. Here we found that treatment of mice with GA (10 mg/kg) before APAP overdose dramatically prevented APAP-induced liver enzyme elevation and resultant toxicity in mice, as indicated by suppression of elevated serum alanine aminotransferase (ALT) levels and liver histological analysis. Importantly, delayed administration of GA within 6 h after APAP overdose also showed an almost equivalent protective effect against APAP liver toxicity. Mechanistically, several pathways are involved in the protective effect of GA against APAP-induced live toxicity, including attenuation of ER stress and oxidative stress, increased levels of nontoxic phase I and II metabolites of APAP, decrease in the formation of toxic N-acetyl-p-benzoquinone imine (NAPQI), and its subsequent protein binding. Importantly, combination of GA with APAP exhibited synergistic interaction in the latter's analgesic activity, while sparing its antipyretic action. These findings provide the preclinical evidence of GA as a promising antidote for treatment of APAP-induced liver toxicity and raise a possibility of its combination with APAP in clinical settings.

19.
ACS Nano ; 13(9): 10754-10760, 2019 Sep 24.
Artigo em Inglês | MEDLINE | ID: mdl-31487455

RESUMO

Deuteration has found important applications in synthetic chemistry especially for pharmaceutical developments. However, conventional deuteration methods using transition-metal catalysts or strong bases generally involve harsh reaction conditions, expensive deuterium source, insufficient efficiency, and poor selectivity. Herein, we report an efficient visible-light-driven dehalogenative deuteration of organic halides using plasmonic Au/CdS as photocatalyst and D2O as deuterium donor. Electron transfer from Au to CdS, which has been confirmed by surface-enhanced Raman spectroscopy, plays a decisive role for the plasmon-mediated dehalogenation. The deuteration is revealed to proceed via a radical pathway in which substrates are first activated by the photoinduced electron transfer to generate aryl radicals, and the radicals are further trapped by D2O to give deuterated products. Under visible-light irradiation, excellent deuteration efficiency is achieved with high functional group tolerance and a wide range of substrates at room temperature. Compared with bare CdS, the photocatalytic activity increases ∼18 times after the loading of plasmonic Au nanoparticles. This work sheds light on the interfacial charge transfer between plasmonic metals and semiconductors as an important criterion for rational design of visible-light photocatalysts.

20.
J Agric Food Chem ; 67(41): 11489-11497, 2019 Oct 16.
Artigo em Inglês | MEDLINE | ID: mdl-31560530

RESUMO

The design of gelatin-based hydrogels with high mechanical strength, high gelation temperature, and a rapid self-healing property still presents a challenge to researchers. In the present study, single cross-linked gelatin-oxidized tannic acid (SC-GT/OTA) hydrogels were fabricated through covalent cross-linking between gelatin and tannic acid (TA) oxidized by using sodium periodate (NaIO4). Double cross-linked gelatin-OTA-FeCl3·6H2O (DC-GT/OTA/FeIII) hydrogels were also created using metal coordination bonds formed between the catechol groups present in OTA and FeIII in ferric chloride. As a result, the maximum gelling temperature of the SC-GT/OTA hydrogel (37 °C) was considerably higher than that of the pure gelatin hydrogel (15.4 °C). Moreover, the maximum values of compressive stress of SC-GT/OTA hydrogels increased significantly by almost seven times the original value as the molar ratio of NaIO4 to TA increased from 3:1 to 5:1. When the molar ratio of NaIO4 to TA was maintained at the constant of 4:1, the storage modulus values of DC-GT/OTA/FeIII hydrogels with the FeIII-to-TA molar ratio of 1.5:1 were three to 4 orders of magnitude higher than those of SC-GT/OTA hydrogels in the whole angular frequency range. The double cross-linked gelatin hydrogels developed in this research can be used widely in agriculture and material science fields.

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