Heat and mass transfer simulation of the microwave-assisted toluene desorption for activated carbons regeneration.

The low cost and high efficiency of microwave-assisted regeneration render it a viable alternative to conventional regeneration methods. To enhance the regeneration performance, we developed a coupled electromagnetic, heat, and mass transfer model to investigate the heat and mass transfer mechanisms of activated carbon during microwave-assisted regeneration. Simulation results demonstrated that the toluene desorption process is governed by temperature distribution. Changing the input power and flow rate can promote the intensity of hot spots and adjust their distribution, respectively, thereby accelerating toluene desorption, inhibiting readsorption, and promoting regeneration efficiency. Ultimately, controlling the input power and flow rate can flexibly adjust toluene emissions to satisfy the processing demands of desorbed toluene. Taken together, this study provides a comprehensive understanding of the heat and mass transfer mechanisms of microwave-assisted regeneration and insights into adsorbent regeneration.

Circular RNA MKLN1 promotes epithelial-mesenchymal transition in pulmonary fibrosis by regulating the miR-26a/b-5p/CDK8 axis in human alveolar epithelial cells and mice models.

Pulmonary fibrosis involves destruction of the lung parenchyma and extracellular matrix deposition. Effective treatments for pulmonary fibrosis are lacking and its pathogenesis is still unclear. Studies have found that epithelial-mesenchymal transition (EMT) of alveolar epithelial cells (AECs) plays an important role in progression of pulmonary fibrosis. Thus, an in-depth exploration of its mechanism might identify new therapeutic targets. In this study, we revealed that a novel circular RNA, MKLN1 (circMKLN1), was significantly elevated in two pulmonary fibrosis models (intraperitoneally with PQ, 50 mg/kg for 7 days, and intratracheally with BLM, 5 mg/kg for 28 days). Additionally, circMKLN1 was positively correlated with the severity of pulmonary fibrosis. Inhibition of circMKLN1 expression significantly reduced collagen deposition and inhibited EMT in AECs. EMT was aggravated after circMKLN1 overexpression in AECs. MiR-26a-5p/miR-26b-5p (miR-26a/b), the targets of circMKLN1, were confirmed by luciferase reporter assays. CircMKLN1 inhibition elevated miR-26a/b expression. Significantly decreased expression of CDK8 (one of the miR-26a/b targets) was observed after inhibition of circMKLN1. EMT was exacerbated again, and CDK8 expression was significantly increased after circMKLN1 inhibition and cotransfection of miR-26a/b inhibitors in AECs. Our research indicated that circMKLN1 promoted CDK8 expression through sponge adsorption of miR-26a/b, which regulates EMT and pulmonary fibrosis. This study provides a theoretical basis for finding new targets or biomarkers in pulmonary fibrosis.

Bimodal Oxidation Electrochemiluminescence Mechanism of Coreactant-Embedded Covalent Organic Frameworks via Postsynthetic Modification.

Electrochemiluminescence (ECL) efficiency is determined by charge transfer between coreactants and emitters in coreactant systems, which are usually limited by their slow intermolecular charge transfer. In this study, a covalent organic framework (COF) with aldehyde residue was synthesized, and then coreactants were covalently integrated into the skeleton through the postsynthetic modification strategy, resulting in a crystalline coreactant-embedded COF nanoemitter (C-COF). Compared to the pristine COF with an equivalent external coreactant, C-COF exhibited an extraordinary 1008-fold enhancement of ECL intensity due to the rapid intrareticular charge transfer. Significantly, with the pH increase, C-COF shows protonation-induced ECL enhancement for the first ECL peaked at +1.1 V and an opposite trend for the second ECL at +1.4 V, which were attributed to the antedating oxidation of coreactant in framework and COF self-oxidation, respectively. The resulting bimodal oxidation ECL mechanism was rationalized by spectral characterization and density functional theory calculations. The postsynthetic coreactant-embedded nanoemitters present innovative and universal avenues for advancing ECL systems.

Structural insights into the substrate binding sites of O-carbamoyltransferase VtdB from Streptomyces sp. NO1W98.

The O-carbamoyltransferase VtdB catalyzes the carbamoylation of venturicidin B, which is essential for the biosynthesis of the antibiotic venturicidin A. Here, the crystal structures of VtdB and VtdB in complex with the intermediate carbamoyladenylate (VtdBCAO) were determined at resolutions of 2.99 Å and 2.90 Å, respectively. The structures resemble the conserved YrdC-like and specific Kae1-like domains. A magnesium ion and the intermediate carbamoyladenylate were also observed in the Kae1-like domain of VtdB. The structure of VtdBCAO in complex with the substrate venturicidin B was modeled by a molecular docking method to better understand the substrate binding mode, revealing a novel venturicidin B binding pocket.

m6A modification regulates lung fibroblast-to-myofibroblast transition through modulating KCNH6 mRNA translation.

Idiopathic pulmonary fibrosis (IPF) is a chronic, fatal lung disease characterized by progressive and non-reversible abnormal matrix deposition in lung parenchyma. Myofibroblasts originating mainly from resident fibroblasts via fibroblast-to-myofibroblast transition (FMT) are the dominant collagen-producing cells in pulmonary fibrosis. N6-methyladenosine (m6A) modification has been implicated in various biological processes. However, the role of m6A modification in pulmonary fibrosis remains elusive. In this study, we reveal that m6A modification is upregulated in a bleomycin (BLM)-induced pulmonary fibrosis mouse model, FMT-derived myofibroblasts, and IPF patient lung samples. Lowering m6A levels through silencing methyltransferase-like 3 (METTL3) inhibits the FMT process in vitro and in vivo. Mechanistically, KCNH6 is involved in the m6A-regulated FMT process. m6A modification regulates the expression of KCNH6 by modulating its translation in a YTH-domain family 1 (YTHDF1)-dependent manner. Together, our study highlights the critical role of m6A modification in pulmonary fibrosis. Manipulation of m6A modification through targeting METTL3 may become a promising strategy for the treatment of pulmonary fibrosis.

O-doped Graphitic Granular Biochar Enables Pollutants Removal via Simultaneous H2O2 Generation and Activation in Neutral Fe-free Electro-Fenton Process.

H2O2 generation by 2-electron oxygen electroreduction reaction (2eORR) has attracted great attention as an alternative to the industry-dominant anthraquinone process. Electro-Fenton (EF) process, which relies on the H2O2 electrogeneration, is regarded as an important environmental application of H2O2 generation by 2eORR. However, its application is hindered by the relatively expensive electrode materials. Proposing cathode materials with low cost and facile synthetic procedures are the priority to advance the EF process. In this work, a composite cathode structure that uses graphitic granular bamboo-based biochar (GB) and stainless steel (SS) mesh (GBSS) is proposed, where SS mesh functions as current distributor and GB supports synergistic H2O2 electrogeneration and activation. The graphitic carbon makes GB conductive and the oxygen-containing groups serve as active sites for H2O2 production. 11.3 mg/L H2O2 was produced from 2.0 g GB at 50 mA after 50 min under neutral pH without external O2/air supply. The O-doped biochar further increased the H2O2 yield to 18.3 mg/L under same conditions. The GBSS electrode is also effective for H2O2 activation to generate ·OH, especially under neutral pH. Ultimately, a neutral Fe-free EF process enabled by GBSS cathode is effective for removal of various model organic pollutants (reactive blue 19, orange II, 4-nitrophenol) within 120 min, and for their partial mineralization (48.4% to 63.5%). Long-term stability of the GBSS electrode for H2O2 electrogeneration, H2O2 activation, and pollutants degradation were also examined and analyzed. This work offers a promising application for biomass waste for removals of organic pollutants in neutral Fe-free EF process.

"Self-cleaning" electrochemical regeneration of dye-loaded activated carbon.

A low maintenance, "self-cleaning" electrochemical approach is evaluated for regeneration of dye-loaded granular activated carbon (GAC). To do so, batch experiments were conducted using a low-cost granular activated carbon/stainless steel mesh (GACSS) composite cathode and a stable Ti/mixed metal oxides (Ti/MMO) anode without the addition of oxidants or iron catalysts. The GACSS cathode supports simultaneous H2O2 electrogeneration via the in situ supplied O2 from Ti/MMO anode and the subsequent H2O2 activation for ·OH generation, thus enabling the cracking of dye molecules adsorbed on GAC and regenerating the GAC's sorption capacity. Results show that a prolonged electrochemical processing for 12h will achieve up to 88.7% regeneration efficiency (RE). While RE decreases with multi-cycle application, up to 52.3% could still be achieved after 10 adsorption-regeneration cycles. To identify the mechanism, experiments were conducted to measure H2O2 electrogeneration, H2O2 activation, and ·OH generation by various GAC samples. The dye-loaded GAC and GAC treated after 10 adsorption-regeneration cycles were still capable of ·OH generation, which contributes to effective "self-cleaning" and regeneration over multi-cycles.

Activated carbon as effective cathode material in iron-free Electro-Fenton process: Integrated H2O2 electrogeneration, activation, and pollutants adsorption.

Major challenges for effective implementation of the Electro-Fenton (EF) water treatment process are that conventional efficient cathodes are relatively expensive, and H2O2 activation by Fe2+ may cause secondary pollution. Herein, we propose a low-cost activated carbon/stainless steel mesh (ACSS) composite cathode, where the SS mesh distributes the current and the AC simultaneously supports H2O2 electrogeneration, H2O2 activation, and organic compounds (OCs) adsorption. The oxygen-containing groups on the AC function as oxygen reduction reaction (ORR) sites for H2O2 electrogeneration; while the porous configuration supply sufficient reactive surface area for ORR. 8.9 mg/L H2O2 was obtained with 1.5 g AC at 100 mA under neutral pH without external O2 supply. The ACSS electrode is also effective for H2O2 activation to generate ‧OH, especially under neutral pH. Adsorption shows limited influence on both H2O2 electrogeneration and activation. The iron-free EF process enabled by the ACSS cathode is effective for reactive blue 19 (RB19) degradation. 61.5% RB19 was removed after 90 min and 74.3% TOC was removed after 720 min. Moreover, long-term stability test proved its relatively stable performance. Thus, the ACSS electrode configuration is promising for practical and cost-effective EF process for transformation of OCs in water.

Efficient H2O2 electrogeneration at graphite felt modified via electrode polarity reversal: Utilization for organic pollutants degradation.

Electrochemical synthesis of H2O2 offers a great potential for water treatment. However, a significant challenge is the development of efficient cathode materials for the process. Herein, we implement a practical electrochemical cathode modification to support efficient H2O2 electrogeneration via the reduction of dissolved anodic O2. Graphite felt (GF) is in situ anodically modified by electrode polarity reversal technique in an acid-free, low-conductivity electrolyte. The modified GF exhibits a significantly higher activity towards O2 reduction. Up to 183.3% higher H2O2 yield is obtained by the anodized GF due to the increased concentrations of oxygen-containing groups and the hydrophilicity of the surface, which facilitates electron and mass transfer between GF and the electrolyte. Another significant finding is the ability to produce H2O2 at a high yield under neutral pH and low current intensity by the modified GF (35% of the charge need to produce the same amount by unmodified GF). Long-term stability testing of the modified GF showed a decay in the electrode's activity for H2O2 production after 30 consecutive applications. However, the electrode regained its optimal activity for H2O2 production after a secondary modification by electrode polarity reversal. Finally, in situ electrochemically modified GF is more effective for removal of reactive blue 19 (RB19, 20 mg/L) and ibuprofen (IBP, 10 mg/L) by the electro-Fenton process. The modified GF removed 62.7% of RB19 compared to only 28.1% by the unmodified GF in batch reactors after 50 min. Similarly, 75.3% IBP is removed by the modified GF compared to 57.6% by the unmodified GF in a flow-through reactor after 100 min.

"Floating" cathode for efficient H2O2 electrogeneration applied to degradation of ibuprofen as a model pollutant.

The performance of the Electro-Fenton (EF) process for contaminant degradation depends on the rate of H2O2 production at the cathode via 2-electron dissolved O2 reduction. However, the low solubility of O2 (≈1×10-3 mol dm-3) limits H2O2 production. Herein, a novel and practical strategy that enables the synergistic utilization of O2 from the bulk electrolyte and ambient air for efficient H2O2 production is proposed. Compared with a conventional "submerged" cathode, the H2O2 concentration obtained using the "floating" cathode is 4.3 and 1.5 times higher using porous graphite felt (GF) and reticulated vitreous carbon (RVC) foam electrodes, respectively. This surprising enhancement results from the formation of a three-phase interface inside the porous cathode, where the O2 from ambient air is also utilized for H2O2 production. The contribution of O2 from ambient air varies depending on the cathode material and is calculated to be 76.7% for the GF cathode and 35.6% for the RVC foam cathode. The effects of pH, current, and mixing on H2O2 production are evaluated. Finally, the EF process enhanced by the "floating" cathode degraded 78.3% of the anti-inflammatory drug ibuprofen after 120 min compared to only 25.4% using a conventional "submerged" electrode, without any increase in the cost.

NLRP3 participates in the regulation of EMT in bleomycin-induced pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and irreversible lung disease. Studies have shown that epithelial-mesenchymal transition (EMT) plays an important role in the development of IPF. The NLRP3 inflammasome is reported to be activated and play an important role in many respiratory diseases. However, whether the NLRP3 inflammasome is activated in alveolar epithelial cells as well as the regulatory role of NLRP3 in EMT have not been reported. In this study, we transfected NLRP3 siRNA into A549 and RLE-6TN cells and treated them with bleomycin (BLM) for 24h. Then, we detected the expression of NLRP3 inflammasome-related proteins, EMT-related proteins and transforming growth factor-ß1 (TGF-ß1) via western blotting, immunofluorescence and real-time quantitative PCR. The mRNA and protein level of NLRP3, ASC and caspase-1 increased after treatment with BLM. The IL-1ß levels were significantly decreased after inhibition of NLRP3 and caspase-1. E-cadherin expression increased and α-SMA was reduced in the BLM group when inhibited by NLRP3. The level of TGF-ß1 was reduced after NLRP3 silencing. These results indicated that the NLRP3 inflammasome was activated in alveolar epithelial cells and that NLRP3 may regulate EMT through TGF-ß1. These results may extend our understanding of the mechanism of pulmonary fibrosis and provide a new therapeutic target for pulmonary fibrosis.

Drastic Enhancement of H2O2 Electro-generation by Pulsed Current for Ibuprofen Degradation: Strategy Based on Decoupling Study on H2O2 Decomposition Pathways.

Efficient H2O2 electrogeneration from 2-electron oxygen reduction reaction (ORR) represents an important challenge for environmental remediation application. H2O2 production is determined by 2-electron ORR as well as H2O2 decomposition. In this work, a novel strategy based on the systematical investigation on H2O2 decomposition pathways was reported, presenting a drastically improved bulk H2O2 concentration. Results showed that bulk phase disproportion, cathodic reduction, and anodic oxidation all contributed to H2O2 depletion. To decrease the extent of H2O2 cathodic reduction, the pulsed current was applied and proved to be highly effective to lower the extent of H2O2 electroreduction. A systematic study of various pulsed current parameters showed that H2O2 concentration was significantly enhanced by 61.6% under pulsed current of "2s ON + 2s OFF" than constant current. A mechanism was proposed that under pulsed current, less H2O2 molecules were electroreduced when they diffused from the porous cathode to the bulk electrolyte. Further results demonstrated that a proper pulse frequency was necessary to achieve a higher H2O2 production. Finally, this strategy was applied to Electro-Fenton (EF) process with ibuprofen as model pollutant. 75.0% and 34.1% ibuprofen were removed under pulsed and constant current at 10 min, respectively. The result was in consistent with the higher H2O2 and ·OH production in EF under pulsed current. This work poses a potential approach to drastically enhance H2O2 production for improved EF performance on organic pollutants degradation without making any changes to the system except for power mode.

CARD9 gene silencing with siRNA protects rats against severe acute pancreatitis: CARD9-dependent NF-κB and P38MAPKs pathway.

We previously reported the up-regulation of caspase recruitment domain 9 (CARD9) expressions in severe acute pancreatitis (SAP) patients, but little is known about its regulation. In this study, small interfering RNA (siRNA) was used to reduce the levels of CARD9 expression in sodium taurocholate-stimulated SAP rats. CARD9 was overexpressed in SAP rats, which correlated with the severity of pancreatitis. When compared to the untreated group, the cohort that received the siRNA treatment demonstrated a significant reduction in pancreatic injury, neutrophil infiltration, myeloperoxidase activity and pro-inflammatory cytokines. Furthermore, siRNAs showed that the reduction of CARD9 in SAP rats down-regulated the expression of NF-κBp65 and P38MAPK which are involved in the transcription and release of a wide variety of inflammatory cytokines. These findings provide evidence that CARD9 is up-regulated in SAP rats and acts as a potential therapeutic target for the treatment thereof. Blocking the activation of NF-κB and P38MAPK via siRNA-mediated gene knock-down of CARD9 appears to reduce the inflammatory response in pancreatic tissue.

A positive feedback loop promotes HIF-1α stability through miR-210-mediated suppression of RUNX3 in paraquat-induced EMT.

Irreversible pulmonary fibrosis induced by paraquat (PQ) poisoning is the major cause of death in patients with PQ poisoning. The epithelial-mesenchymal transition (EMT) is postulated to be one of the main mechanisms of pulmonary fibrosis. Here, we investigated the role of miR-210 in PQ-induced EMT and its relationship with hypoxia-inducible factor-1α (HIF-1α). Western blotting, immunofluorescence, immunoprecipitation and other methods were used in this study. We found that miR-210 expression was significantly increased after PQ poisoning, and it may be regulated by HIF-1α. Overexpression of miR-210 further increased the HIF-1α protein level and promoted EMT. Moreover, miR-210 knock-down reduced the HIF-1α protein level and decreased the degree of EMT. Runt-related transcription factor-3 (RUNX3), a direct target of miR-210, was inhibited by miR-210 in response to PQ poisoning. RUNX3 increased the hydroxylation ability of prolyl hydroxylase domain-containing protein 2 (PHD2), a key enzyme that promotes HIF-1α degradation. PHD2 immunoprecipitated with RUNX3 and its level changed similarly to that of RUNX3. The expression of the HIF-1α protein was significantly reduced when RUNX3 was overexpressed. HIF-1α protein levels were markedly increased when RUNX3 was silenced. Based on these results, a positive feedback loop may exist between miR-210 and HIF-1α. The mechanism may function through miR-210-mediated repression of RUNX3, which further decreases the hydroxylation activity of PHD2, enhances the stability of HIF-1α, and promotes PQ-induced EMT, aggravating the progression of pulmonary fibrosis. This study further elucidates the mechanism of PQ-induced pulmonary fibrosis and may provide a new perspective for the future development of therapies.

Oblongifolin C and guttiferone K extracted from Garcinia yunnanensis fruit synergistically induce apoptosis in human colorectal cancer cells in vitro.

Oblongifolin C (OC) and guttiferone K (GUTK) are two anticancer compounds extracted from Garcinia yunnanensis Hu, but they act by different mechanisms. In this study we investigated whether a combination of OC and GUTK (1:1 molar ratio) could produce synergistic anticancer effects against human colorectal cancer cells in vitro. For comparison, we also examined the anticancer efficacy of ethanol extracts from G yunnanensis fruit, which contain OC and GUTK up to 5%. Compared to OC and GUTK alone, the combination of OC and GUTK as well as the ethanol extracts more potently inhibited the cancer cell growth with IC50 values of 3.4 µmol/L and 3.85 µg/mL, respectively. Furthermore, OC and GUTK displayed synergistic inhibition on HCT116 cells: co-treatment with OC and GUTK induced more prominent apoptosis than treatment with either drug alone. Moreover, the combination of OC and GUTK markedly increased cleavage of casapse-3 and PARP, and enhanced cellular ROS production and increased JNK protein phosphorylation. In addition, the combination of OC and GUTK exerted stronger effects under nutrient-deprived conditions than in complete medium, suggesting that autophagy played an essential role in regulating OC- and GUTK-mediated cell death. OC and GUTK are the main components that contribute to the anticancer activity of G yunnanensis and the compounds have apoptosis-inducing effects in HCT116 cells in vitro.

HIF-1α regulates EMT via the Snail and ß-catenin pathways in paraquat poisoning-induced early pulmonary fibrosis.

Paraquat (PQ) poisoning-induced pulmonary fibrosis is one of the primary causes of death in patients with PQ poisoning. Hypoxia-inducible factor-1α (HIF-1α) and epithelial-mesenchymal transition (EMT) are involved in the progression of pulmonary fibrosis. Snail and ß-catenin are two other factors involved in promoting EMT. However, the relationship among HIF-1α, Snail and ß-catenin in PQ poisoning-induced pulmonary fibrosis is not clear. Our research aimed to determine whether the regulation of HIF-1α in EMT occurs via the Snail and ß-catenin pathways in PQ poisoning-induced pulmonary fibrosis. Sixty-six Sprague-Dawley rats were randomly and evenly divided into a control group and a PQ group. The PQ group was treated with an intragastric infusion of a 20% PQ solution (50 mg/kg) for 2, 6, 12, 24, 48 and 72 hrs. A549 and RLE-6TN cell lines were transfected with HIF-1α siRNA for 48 hrs before being exposed to PQ. Western blotting, real-time quantitative PCR, immunofluorescence, immunohistochemistry and other assays were used in our research. In vivo, the protein levels of HIF-1α and α-SMA were increased at 2 hrs and the level of ZO-1 (Zonula Occluden-1) was reduced at 12 hrs. In vitro, the transient transfection of HIF-1α siRNA resulted in a decrease in the degree of EMT. The expression levels of Snail and ß-catenin were significantly reduced when HIF-α was silenced. These data demonstrate that EMT may be involved in PQ poisoning-induced pulmonary fibrosis and regulated by HIF-1α via the Snail and ß-catenin pathways. Hypoxia-inducible factor-1α may be a therapeutic target for the treatment of PQ poisoning-induced pulmonary fibrosis.

Nujiangexathone A, a Novel Compound Derived from Garcinia nujiangensis, Induces Caspase-Dependent Apoptosis in Cervical Cancer through the ROS/JNK Pathway.

Nujiangexathone A (NJXA), a novel compound derived from Garcinia nujiangensis, has been demonstrated to inhibit the proliferation of several human cancer cell lines. This study is the first to demonstrate the apoptosis inductive activities of NJXA and the possible underlying mechanisms. Our results demonstrated that NJXA inhibited colony formation by HeLa and SiHa cells in a dose-dependent manner. An Annexin V-FITC/PI staining assay showed that NJXA strongly triggered apoptosis in a dose-dependent manner. Western blotting analyses showed that NJXA induced the caspase-dependent apoptosis of HeLa and SiHa cells by triggering a series of events, including changes in the levels of Bcl-2 family proteins, cytochrome c release, caspase-3 activation, and chromosome fragmentation. Furthermore, we demonstrated that NJXA induced cell apoptosis by activating the reactive oxygen species (ROS)-mediated JNK signaling pathway. Consistent with this finding, a ROS scavenger, N-acetyl-l-cysteine (NAC, 10 mM), hindered NJXA-induced apoptosis and attenuated the sensitivity of HeLa and SiHa cells to NJXA. In vivo results further confirmed that the tumor inhibitory effect of NJXA was partially through the induction of apoptosis. Taken together, our results demonstrated that NJXA induced the apoptosis of HeLa and SiHa cells through the ROS/JNK signaling pathway, indicating that NJXA could be important candidate for the clinical treatment of cervical cancer.

Central role of neutrophil in the pathogenesis of severe acute pancreatitis.

Severe acute pancreatitis (SAP) is an acute abdominal disease with the strong systemic inflammatory response, and rapidly progresses from a local pancreatic damage into multiple organ dysfunction. For many decades, the contributions of neutrophils to the pathology of SAP were traditionally thought to be the chemokine and cytokine cascades that accompany inflammation. In this review, we focus mainly on those recently recognized aspects of neutrophils in SAP processes. First, emerging evidence suggests that therapeutic interventions targeting neutrophils significantly lower tissue damage and protect against the occurrence of pancreatitis. Second, trypsin activation promotes the initial neutrophils recruitment into local pancreas, and subsequently neutrophils infiltration in turn triggers trypsin production. Finally, neutrophils have the unique ability to release neutrophil extracellular traps even in the absence of pathogens.

ER stress-induced autophagy in melanoma.

The activation of RAF-MEK-extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase cascade by v-raf murine sarcoma viral oncogene homolog B1 (BRAF)(V600E) mutation is a key alteration in melanoma. Although BRAF inhibitor (BRAFi) has achieved remarkable clinical success, the positive response to BRAFi is not sustainable, and the initial clinical benefit is eventually barred by the development of resistance to BRAFi. There is growing evidence to suggest that endoplasmic reticulum (ER) stress-induced autophagy could be a potential pro-survival mechanism that contributes to genesis of melanoma and to the resistance to BRAFi. ER stress-induced autophagy is an evolutionarily conserved membrane process. By degrading and recycling proteins and organelles via the formation of autophagous vesicles and their fusion with lysosomes, the autophagy plays a key role in homeostasis as well as pathological processes. In this review, we examine the autophagy phenomenon in melanocytic nevus, primary and metastatic melanoma, and its significance in BRAFi-resistant melanoma.

Relationships between antioxidant compounds and antioxidant activities of tartary buckwheat during germination.

Relationships of changes between major non-enzymatic antioxidant compounds and antioxidant capacities of tartary buckwheat during germination were evaluated by means of correlation analysis and principal component analysis in this paper. The changes of antioxidant compounds, including vitamin C, vitamin E, flavonoids, carotenoids, and chlorophyll, and antioxidant activities were detected. A good accumulation in the content of vitamin C (0.71 mg/g), total flavonoids (19.53 mg rutin/g), and rutin (11.34 mg/g) was found after 7-day germination, but germination decreased the vitamin E activity. Germination improved the activities of buckwheat extracts to scavenge DPPH, ABTS, and superoxide free radicals by 107, 144, and 88 %, respectively. Furthermore, the correlation and principal component analysis showed that the vitamin C, total flavonoids, and rutin contents were closely related positively with free radicals scavenging properties, indicating that the compounds which play a key role in the elevated antioxidant activities during germination consisted of vitamin C, total flavonoids, and rutin, but not vitamin E and quercetin.