Application of radio frequency energy in processing of fruit and vegetable products.

Thermal processing is commonly employed to ensure the quality and extend the shelf-life of fruits and vegetables. Radio frequency (RF) heating has been used as a promising alternative treatment to replace conventional thermal processing methods with advantages of rapid, volumetric, and deep penetration heating characteristics. This article provides comprehensive information regarding RF heating uniformity and applications in processing of fruit and vegetable products, including disinfestation, blanching, drying, and pasteurization. The dielectric properties of fruits and vegetables and their products have also been summarized. In addition, recommendations for future research on RF heating are proposed to enhance practical applications for fruits and vegetables processing in future.

Investigation of the potential direct and cross protection effects of sublethal injured Salmonella Typhimurium induced by radio frequency heating stress.

Many studies demonstrated that radio frequency (RF) was an effective pasteurization method for low-moisture foods (LMFs), and our previous study confirmed RF heating stress generated sublethal injured cells (SICs) of Salmonella enterica serovar Typhimurium (S. Typhimurium) in red pepper powder with initial aw ≥ 0.53. So this study investigated the potential direct protection and cross protection effects of the SICs of S. Typhimurium to multiple stresses, and analyzed fatty acid composition and cell morphology. Results showed that the SICs were repaired after incubating for 5 h, and there were no obvious direct and cross protection effects by exposing to different external stresses (heat, 15% ethanol, pH 3.0 acid buffer solution, 10% salt). According to the fatty acid composition analysis, no significant difference (p > 0.05) between the ratio of unsaturated to saturated fatty acids (UFA/SFA) was observed for SICs of S. Typhimurium and control cells, indicating the same membrane fluidity which can support the experimental results. This study investigated and confirmed there are no direct and cross protection effects for the SICs of S. Typhimurium induced by RF heating stress, and it would be helpful for deeply understand the response of pathogens under RF heating stress.

Molecular interaction between pectin and catechin/procyanidin in simulative juice model: Insights from spectroscopic, morphology, and antioxidant activity.

The interactions between polysaccharides and phenolics in foods affect their physicochemical properties and bioactivity. Pectin and catechin/procyanidin present in plants ubiquitously and attracting more attentions for the potential health benefits. This work investigates the interactions between high methoxyl pectin and catechin/procyanidin in a simulative juice model using multiple microscopic and spectroscopic approaches and their influences on the antioxidant activity of phenolics were evaluated in the Caco-2 cells model. The results showed that pectin with either of phenolic compunds exhibited lower transmittance, zeta potential, viscosity, and larger particle size than it alone. The morphology of pectin complexes with either of phenolics under experimental conditions (pH = 3.5) was observed. The ΔH° (-6.821 kJ mol-1 ) and ΔS° (6.357×10-2  kJ mol-1 ) indicated that pectin interacts with procyanidin via electrostatic interaction, whereas hydrophobic interaction was the dominant drive force between pectin and catechin (ΔH° = 1.422 kJ mol-1 ; ΔS° = 13.048 × 10-2  kJ mol-1 ). The antioxidant activities of catechin/procyanidin decreased while binding with pectin based on indexes of glutathione peroxidase, total superoxide dismutase, total antioxidant capacity, and malondialdehyde. PRACTICAL APPLICATION: The findings of this work indicated that the physicochemical property of pectin and the antioxidant activity of catechin/procyanidin were influenced by the interactions between pectin and catechin/procyanidin in a simulative food system. This study provides insights into the molecular interactions between pectin and phenolics in a simulative food system.

Polyphenol binding disassembles glycation-modified bovine serum albumin amyloid fibrils.

Glycation of protein results in the formation of advanced glycation end-products (AGEs) and leads to deposition as amyloid fibrils. Adhesive structural properties of polyphenols to aromatic amino acids draw significance in promoting, accelerating and/or stabilizing on-pathway and off-pathway folding intermediates, although the mechanistic action remains unclear. In this study, polyphenols remodeling mature AGEs modified amyloid fibrils were investigated through UV-visible spectroscopy, fluorescence spectroscopy, transmission electron microscopy, atomic force microscopy, circular dichroism spectroscopy, MALDI-MS/MS analysis and molecular docking studies. Our findings confirmed the glycation-mediated transformation of native protein into ß-sheet rich amyloid fibrils. SDS-PAGE results suggested the presence of shorter peptide fragments ranging from ~10 kDa to ~40 kDa. MALDI-MS/MS results identified the plausible sequences to be His105-His181, Arg193-Lys242, Leu325-Tyr410, and Ala451-Tyr529. TEM and AFM results suggested that polyphenols binding mature amyloid fibrils remodel/disassemble them into distinct aggregate structures or non-amyloid fibrils. Circular dichroism studies suggested that polyphenols upon binding amyloid fibrils stabilizes and transforms the secondary structure towards helical or random coil-like conformation. Molecular modeling studies suggested high binding affinity and hydrophobic interaction to be the main driving force in remodeling perspective. Together, our findings suggest that polyphenols could differentially remodel mature AGEs-modified amyloid fibrils into distinct aggregate structures through non-covalent interactions and can alleviate AGEs-mediated amyloidosis.

Self-assembly of N-terminal Alzheimer's ß-amyloid and its inhibition.

Peptide sequence modulates amyloid fibril formation and triggers Alzheimer's disease. The N-terminal region of amyloid peptide is disordered and lack any specific secondary structure. An ionic interaction of Aß1-11 with factor XII is critical for the activation of the contact system in Alzheimer's disease. In this study, we report the self-assembly of fluctuating N-terminal Aß1-11 into nanotubes using atomic force micrography, transmission electron microscopy, circular dichroism studies and molecular modeling studies. The effect of four polyphenols: baicalein, rutin, vanillin and cyanidin-3-O-glucoside (C3G) was also explored on the amyloid fibril inhibitor perspective using amyloid specific dye Thioflavin T (ThT). AFM micrographs suggested the self-assembly of Aß1-11 into nanotubes after three weeks of incubation. Microwave treatment results in the conformational variation of disordered structure to ß-sheet rich amyloid fibrils. The presence of salts (sodium and potassium chloride) induces the structural transformation of Aß1-11 to super-helix. Fluorescence spectroscopy studies using ThT suggested differential inhibition of amyloid fibrils formation in the presence of polyphenols. Molecular modeling studies suggested that binding of polyphenols to Aß1-11 through hydrophobic interaction (Phe4 and Tyr 10) and hydrogen bonding (Glu3 and Arg5) play a substantial role in stabilizing Aß1-11-polyphenols complex. In the presence of polyphenols, Aß1-11 transforms to hybrid nanostructures thus hindering amyloid fibril formation. These results provide structural insights and importance of the N-terminal residues in the Aß1-42 self-assembly mechanism.

Clinical Significance of Down-Regulated CD70 and CD27 Expression in Poor Prognosis of Esophageal Squamous Cell Carcinoma.

INTRODUCTION: CD27 is a co-stimulatory immune checkpoint molecule in the tumor necrosis factor receptor superfamily. CD27 regulates the generation and maintenance of T cell immunity by binding to CD70 and regulating B-cell activation and immunoglobulin synthesis. MATERIALS AND METHODS: CD27 and CD70 expression were assessed in esophageal squamous cell carcinoma (ESCC) compared to normal tissue samples in the GSE53625 dataset of 179 paired cases and in 153 Chinese cases using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and immunohistochemistry. The correlation was also investigated between CD27 and CD70 expression and immune-related pathways, including CD8+ T cell recruitment, function, and other inhibitory immune checkpoints. RESULTS: Levels of both CD27 and CD70 expression were down-regulated in ESCC compared to the paired normal tissues. CD27 and CD70 expression was mainly present in lymphocytes surrounding and infiltrating the tumor lesions but rarely expressed in tumor cells. Lost expression of CD27 and CD70 was associated with clinicopathological features, including depth of tumor invasion and better patient survival. Furthermore, CD27 expression was significantly associated with levels of CD8A, GZMB, IFNG, the CD8+ T cell recruitment-associated chemokines (CXCL9, CXCL10, and CXCL11), and CD8 receptors (CCR5, CXCR6, and CXCR3), while CD70 expression was inversely associated with levels of immunosuppressive checkpoints (PD-L1, PD-L2, and HHLA2). CONCLUSION: Detection of CD70/CD27 expression could be further verified as a biomarker for ESCC early detection and prognosis prediction.

Polyphenols redirects the self-assembly of serum albumin into hybrid nanostructures.

Chronic hyperglycemia results in the formation of advanced glycation end-products (AGEs) and triggers amyloid fibril formation. Molecules designed to inhibit amyloid fibrils function by eliminating toxic oligomers or reducing fibril formation. Here, the bioactivity of polyphenols in redirecting the self-assembly of amyloid fibrils was reported through microscopic, spectroscopic and molecular docking studies. Our findings illustrate that glycation causes BSA to self-assemble into amyloid fibrils. 17 Lys residues had modified to carboxy methyl lysine (CML) but only Lys523 was probable of modifying into carboxy ethyl lysine (CEL). In contrast, only 6 Arg residues are identified to be modified to Argpyrimidine (Arg-p). A simple polyphenol baicalein (BLN) redirect the self-assembly of amyloid fibrils into off-pathway hybrid nanostructures. Circular dichroism spectroscopic studies suggested that in the presence of BLN helical conformation was favored. Molecular modeling studies suggested that hydrogen bonding and hydrophobic interaction of polyphenols preferentially at crucial amyloidogenic regions can hinder amyloid fibrillation (Phe133, Lys136, Tyr137, Ile141, Tyr160 and Arg185). Mass spectrometric results illustrated that the presence of a simple polyphenol BLN several residues are unmodified to CML, CEL or Arg-p. Together, our findings suggest that polyphenols could have a protective effect and the redirection can help alleviate the amyloid fibril formation.

Liver toxicity of macrolide antibiotics in zebrafish.

Macrolide antibiotics (macrolides) are among the most commonly prescribed antibiotics worldwide and are used for a wide range of infections, but macrolides also expose people to the risk of adverse events include hepatotoxicity. Here, we report the liver toxicity of macrolides with different structures in zebrafish. The absorption, distribution, metabolism, excretion and toxicology (ADMET) parameters of macrolide compounds were predicted and contrasted by utilizing in silico analysis. Fluorescence imaging and Oil Red O stain assays showed all the tested macrolide drugs induced liver degeneration, changed liver size and liver steatosis in larval zebrafish. Through RNA-seq analysis, we found seven co-regulated differentially expressed genes (co-DEGs) associated with metabolism, apoptosis and immune system biological processes, and two co-regulated significant pathways including amino sugar and nucleotide sugar metabolism and apoptosis signaling pathway. We found that only fosab of seven co-DEGs was in the two co-regulated significant pathways. fosab encoded proto-oncogene c-Fos, which was closely associated with liver diseases. The whole-mount in situ hybridization showed high transcription of c-Fos induced by macrolide compounds mainly in the liver region of zebrafish larvae. Cell Counting Kit-8 (CCK-8) and lactate dehydrogenase (LDH) leakage assays revealed that macrolides exerts significant cytotoxic effects on L02 cells. qRT-PCR and western blot analysis demonstrated macrolides also promoted human c-Fos expression in L02 cells. The c-Fos overexpression significantly reduced cell viability by using CCK-8 assay. These data indicate that hepatotoxicity induced by macrolides may be correlated with c-Fos expression activated by these compounds. This study may provide a biomarker for the further investigations on the mechanism of hepatotoxicity induced by macrolide drugs with different structures, and extend our understanding for improving rational clinical application of macrolides.

Spectroscopic and molecular docking studies on the interaction of phycocyanobilin with peptide moieties of C-phycocyanin.

The binding of C-phycocyanin (CPC), a light harvesting pigment with phycocyanobilin (PCB), a chromophore is instrumental for the coloration and bioactivity. In this study, structure-mediated color changes of CPC from Spirulina platensis during various enzymatic hydrolysis was investigated based on UV-visible, circular dichroism, infra-red, fluorescence, mass spectrometry, and molecular docking. CPC was hydrolyzed using 7.09 U/mg protein of each enzyme at their optimal hydrolytic conditions for 3 h as follows: papain (pH 6.6, 60 °C), dispase (pH 6.6, 50 °C), and trypsin (pH 7.8, 37 °C). The degree of hydrolysis was in the order of papain (28.4%) > dispase (20.8%) > trypsin (7.3%). The sequence of color degradation rate and total color difference (ΔE) are dispase (82.9% and 40.37), papain (72.4% and 24.70), and trypsin (58.7% and 25.43). The hydrolyzed peptides were of diverse sequence length ranging from 8 to 9 residues (papain), 7-12 residues (dispase), and 9-63 residues (trypsin). Molecular docking studies showed that key amino acid residues in the peptides interacting with chromophore. Amino acid residues such as Arg86, Asp87, Tyr97, Asp152, Phe164, Ala167, and Val171 are crucial in hydrogen bonding interaction. These results indicate that the color properties of CPC might associate with chromopeptide sequences and their non-covalent interactions.

IL28A protein homotetramer structure is required for autolysosomal degradation of HCV-NS5A in vitro.

Interferon lambda-2 (IL28A) has a wide antiviral effect with fewer side-effects. Autophagy is a host mechanism to maintain intracellular homeostasis and defends invasion of pathogenic microorganisms. HCV NS5A can disable host defense systems to support HCV replication. Thus, molecular mechanism of interaction among interferon lambda, autophagy, and HCV was concerned and explored in this study. We report that HCV NS5A activated an incomplete autophagy by promoting the autophagic ubiquitylation-like enzymes ATG3, ATG5, ATG7, ATG10, and autophagosome maker LC3B, but blocked autophagy flux; IL28A bound to NS5A at NS5A-ISDR region, and degraded HCV-NS5A by promoting autolysosome formations in HepG2 cells. A software prediction of IL28A protein conformation indicated a potential structure of IL28A homotetramer; the first α-helix of IL28A locates in the interfaces among the four IL28A chains to maintain IL28A homotetrameric conformation. Co-IP and cell immunofluorescence experiments with sequential deletion mutants demonstrate that IL28A preferred a homotetramer conformation to a monomer in the cells; the IL28A homotetramer is positively correlated with autolysosomal degradation of HCV NS5A and the other HCV proteins. Summarily, the first α-helix of IL28A protein is the key domain for maintaining IL28A homotetramer which is required for promoting formation of autolysosomes and degradation of HCV proteins in vitro.

A new transcription factor ATG10S activates IFNL2 transcription by binding at an IRF1 site in HepG2 cells.

IFNL2 is a potent antiviral interferon, but the regulation of its gene expression is not fully clear. Here, we report the regulation of ATG10S for IFNL2 transcription. Through sequential deletion of the IFNL2 promoter sequence, we found LP1-1, a fragment of the promoter responding to ATG10S activity. Subcellular localization and DNA immunoprecipitation assays showed ATG10S translocating into the nucleus and binding to LP1-1. Online prediction for transcription factor binding sites showed an IRF1 targeting locus in LP1-1. Luciferase assays, RT-PCR, and western blot analysis revealed a core motif (CAAGAC) existing in LP1-1, which determined ATG10S and IRF1 activity; individual nucleotide substitution showed that the functional nucleotides of ATG10S targeting were C1, A3, and C6, and the ones associated with IRF1 were A3 and G4 within the core motif. Co-immunoprecipitation assays revealed ATG10S combination with KPNA1/importin α, KPNB1/importin ß, and IRF1. The knockdown of endogenous IRF1 increased ATG10S activity on IFNL2 transcription. These results indicate that ATG10S as a transcription factor competes with IRF1 for the same binding site to promote IFNL2 gene transcription. Abbreviations: ATG10: autophagy related 10; ATG10S: the shorter isoform of autophagy related 10; BD: binding domain; CM: core motif; co-IP: co-immunoprecipitation; GFP: green fluorescent protein; HCV: hepatitis C virus; IF: immunofluorescence; IFN: interferon; IRF: interferon regulatory factor; LP: lambda promoter; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; RLU: relative light unit; SQSTM1: sequestosome 1.

Black rice anthocyanins embedded in self-assembled chitosan/chondroitin sulfate nanoparticles enhance apoptosis in HCT-116 cells.

Self-assembled nanoparticles using the biopolymers chitosan (CH) and chondroitin sulfate (CS) were developed to improve the biological activity of anthocyanin (ACN). The 86.32 ±â€¯0.15% (w/w) of ACN was incorporated into ACN/CH/CS nanoparticles, with the particle size of 350.1 ±â€¯0.99 nm in diameter (i.d.) and 42.55 ±â€¯0.54 in zeta potential (mV). Morphological study and thermogravimetric analysis suggested that the ACN/CH/CS nanoparticles exhibited heterogeneous morphology and high thermal stability. Significant increases in apoptosis by 12.1% and 35.1% were observed with 0.05 mg/ml ACN and ACN/CH/CS nanoparticles in the HCT-116 cell line, indicating that the nanoparticle system led to significant increase in apoptosis (p < 0.05). Structural changes in mitochondria caused by ACN/CH/CS nanoparticles indicated that the nanoparticles had negative impacts on mitochondria. These results showed that nanoparticles could potentially be used as a carrier system to improve the efficacy of ACN.

Insights into the importance of dietary chrysanthemum flower (Chrysanthemum morifolium cv. Hangju)-wolfberry (Lycium barbarum fruit) combination in antioxidant and anti-inflammatory properties.

Dietary chrysanthemum flower and wolfberry alone or together are widely consumed as a health beverage on a daily basis for centuries. The study aims to evaluate combinative effects of flower heads of Chrysanthemum morifolium cv. Hangju (C) and Lycium barbarum fruit (wolfberry, W) served as tea on chemical compounds, antioxidant and anti-inflammatory activities in RAW 264.7 macrophages. Eight phenolics were mainly detected in chrysanthemum flowers, whereas polysaccharides were dominant in wolfberry. The infusion of five combinations showed significantly antioxidant activities positively associated with the chrysanthemum flower content in chemical methods (ORAC and FRAP). However, the cellular-based CAA assay exhibited the highest antioxidant activities of the infusion at C:W = 1:1, indicating a synergistic interaction (CI = 0.11, P < .01). Additionally, the anti-inflammatory effect of infusion, specifically at a combination of C:W = 1:1, was observed by reducing the LPS-induced nitric oxide production, and inhibiting the expression of iNOS, TNF-α, IL-1ß, and IL-6 mRNA (P < .05). The infusion prepared at a C:W = 1:1 was found to inactivate MAPKs (ERK and JNK) and NF-κB. The antioxidant and anti-inflammatory mechanisms might be attributed to acacetin-7-O-rutinoside, luteolin-7-O-glucoside and chlorogenic acid from chrysanthemum flower, and wolfberry polysaccharide via multiple inflammatory pathways.

Differential Effects of Autophagy-Related 10 Protein on HCV Replication and Autophagy Flux Are Mediated by Its Cysteine44 and Cysteine135.

Autophagy-related 10 (ATG10) is essential for autophagy since it promotes ATG5-ATG12 complex formation. Our previous study found that there are two isoforms of the ATG10 protein, ATG10 (a longer one) and ATG10S, which have identical sequences except an absence of a 36-amino acid fragment (peptide B) in ATG10S, yet exhibit distinct effects on HCV genome replication. Here, we report the existence of two amino acids, cysteine at residue 44 and 135 (Cys44 and Cys135, respectively), in ATG10 being related to differential effects of ATG10 on HCV replication and autophagy flux. Through a series of ATG10 mutation experiments and protein modeling prediction, we found that Cys44 was involved in the dual role of the two isoforms of ATG10 protein on HCV replication and autophagy flux, and that Cys135 plays similar roles as Cys44, but the disulfide bond of Cys44-Cys135 was not verified in the ATG10 protein. Further analyses by full HCV virion infection confirmed the roles of -SH of Cys44 and Cys135 on HCV replication. ATG10 with deleted or mutated Cys44 and/or Cys135 could activate expression of innate immunity-related genes, including il28a, irf-3, irf-7, and promote complete autophagy by driving autophagosomes to interact with lysosomes via IL28A-mediation. Subcellular localization assay and chromatin immunoprecipitation assay showed that ATG10 with the sulfydryl deletion or substitution of Cys44 and Cys135 could translocate into the nucleus and bind to promoter of IL28A gene; the results indicated that ATG10 with Cys44 and/or Cys135 absence might act as transcriptional factors to trigger the expression of anti-HCV immunological genes, too. In conclusion, our findings provide important information for understanding the differential roles on HCV replication and autophagy flux between ATG10 and ATG10S, and how the structure-function relationship of ATG10 transformed by a single -SH group loss on Cys44 and Cys135 in ATG10 protein, which may be a new target against HCV replication.

Discovery and evolution of aloperine derivatives as a new family of HCV inhibitors with novel mechanism.

Aloperine (1), a Chinese natural product with a unique endocyclic scaffold, was first identified to be a potent hepatitis C virus (HCV) inhibitor in our laboratory. Thirty-four new aloperine derivatives were designed, synthesized and evaluated for their anti-HCV activities taking 1 as the lead. Among them, compound 7f exhibited the potential potency with EC50 values in a micromolar range against both wild-type and direct-acting antiviral agents (DAAs)-resistant variants, and synergistically inhibited HCV replication with approved DAAs. Furthermore, it also owned a good oral pharmacokinetic and safety profile, suggesting a highly druglike nature. The primary mechanism showed that 7f might target host components, distinctly different from the DAAs currently used in clinic. Therefore, we consider aloperine derivatives to be a novel class of anti-HCV agents, and compound 7f has been selected as a promising antiviral candidate for further investigation.

Intracellular Insulin and Impaired Autophagy in a Zebrafish model and a Cell Model of Type 2 diabetes.

Type 2 diabetes mellitus is characterized by insulin resistance. However, the complete molecular mechanism remains unclear. In this study, zebrafish were fed a long-term high-fat diet to induce type 2 diabetes, which resulted in a higher body weight, body mass index, more lipid vacuoles in liver, increased insulin transcription level in liver, brain and muscle, and high fasting blood glucose in the high-fat diet zebrafish. Oppositely, the transcription levels of insulin substrate-2 and glucose transporter 2 were significantly decreased, indicating insulin signaling pathway and glucose transport impaired in the insulin-targeting tissues. Transcription of the autophagy-related genes, ATG3, ATG4B, ATG5, ATG7, ATG12, and FOXO3, were decreased but autophagy inhibitor gene m-TOR increased, and autophagy-flux was inhibited in liver of the high-fat diet zebrafish. Main of these changes were confirmed in palmitic acid-treated HepG2 cells. Further, in co-immunoprecipitation and subcellular co-localization experiments, the conjunction of preproinsulin with cargo-recognition protein p62 increased, but conjuncts of autophagosome with p62-cargo, lysosomes with p62-cargo, and autolysosomes decreased apparently. Interestingly, lysosomes, autolysosomes and conjuncts of p62-insulin localized at the periphery of palmitic acid-treated cells, the margination of lysosomes may mediate deactivation of proteases activity. These findings suggest that intracellular high-lipid may trigger defective autophagy, defective downstream signaling of insulin and accumulated intracellular preproinsulin, leading to dysregulation of cell homeostasis mechanism, which may be one of reasons involved in insulin-resistance in type 2 diabetes.

Up-regulation of autophagy-related gene 5 (ATG5) protects dopaminergic neurons in a zebrafish model of Parkinson's disease.

Parkinson's disease (PD) is one of the most epidemic neurodegenerative diseases and is characterized by movement disorders arising from loss of midbrain dopaminergic (DA) neurons. Recently, the relationship between PD and autophagy has received considerable attention, but information about the mechanisms involved is lacking. Here, we report that autophagy-related gene 5 (ATG5) is potentially important in protecting dopaminergic neurons in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD model in zebrafish. Using analyses of zebrafish swimming behavior, in situ hybridization, immunofluorescence, and expressions of genes and proteins related to PD and autophagy, we found that the ATG5 expression level was decreased and autophagy flux was blocked in this model. The ATG5 down-regulation led to the upgrade of PD-associated proteins, such as ß-synuclein, Parkin, and PINK1, aggravation of MPTP-induced PD-mimicking pathological locomotor behavior, DA neuron loss labeled by tyrosine hydroxylase (TH) or dopamine transporter (DAT), and blocked autophagy flux in the zebrafish model. ATG5 overexpression alleviated or reversed these PD pathological features, rescued DA neuron cells as indicated by elevated TH/DAT levels, and restored autophagy flux. The role of ATG5 in protecting DA neurons was confirmed by expression of the human atg5 gene in the zebrafish model. Our findings reveal that ATG5 has a role in neuroprotection, and up-regulation of ATG5 may serve as a goal in the development of drugs for PD prevention and management.

Effect of complexes of cyanidin-3-diglucoside-5-glucoside with rutin and metal ions on their antioxidant activities.

Studies have enabled a molecular understanding of the anthocyanin copigmentation phenomenon over several decades. However, the effect of combinations of, or even supramolecular assemblies of, anthocyanins with other phenols and/or metal ions on their antioxidative activity was unclear. In this study, anthocyanin complexes of cyanidin-3-diglucoside-5-glucoside (CY3D5G), rutin and Mg(II)/Fe(III) were constructed, analyzed, and evaluated for their antioxidant effects. The CY3D5G-rutin-Fe(III) exhibited supramolecular properties via visible, CD and FTIR spectra among complexes. The interaction of CY3D5G-rutin, CY3D5G-rutin-Mg(II), or CY3D5G-rutin-Fe(III) was synergistic (P<0.05) in the ORAC assay. On cellular ROS levels, the median effective concentration of the CY3D5G-rutin-Mg(II) was 7.76µmol QE/L and exhibited a synergistic interaction (CI=0.67, P<0.05), whereas the CY3D5G-rutin-Fe(III) (CI=0.79, P=0.074) was additive. The results indicate that the antioxidant properties were affected by the molecular combination. Additionally, Fe(III) might exhibit a negative effect, since the CY3D5G-Fe(III) required a greater concentration than CY3D5G to achieve the same effect on cells.

Effects of Vitamin B6 Deficiency on the Composition and Functional Potential of T Cell Populations.

The immune system is critical in preventing infection and cancer, and malnutrition can weaken different aspects of the immune system to undermine immunity. Previous studies suggested that vitamin B6 deficiency could decrease serum antibody production with concomitant increase in IL4 expression. However, evidence on whether vitamin B6 deficiency would impair immune cell differentiation, cytokines secretion, and signal molecule expression involved in JAK/STAT signaling pathway to regulate immune response remains largely unknown. The aim of this study is to investigate the effects of vitamin B6 deficiency on the immune system through analysis of T lymphocyte differentiation, IL-2, IL-4, and INF-γ secretion, and SOCS-1 and T-bet gene transcription. We generated a vitamin B6-deficient mouse model via vitamin B6-depletion diet. The results showed that vitamin B6 deficiency retards growth, inhibits lymphocyte proliferation, and interferes with its differentiation. After ConA stimulation, vitamin B6 deficiency led to decrease in IL-2 and increase in IL-4 but had no influence on IFN-γ. Real-time PCR analysis showed that vitamin B6 deficiency downregulated T-bet and upregulated SOCS-1 transcription. This study suggested that vitamin B6 deficiency influenced the immunity in organisms. Meanwhile, the appropriate supplement of vitamin B6 could benefit immunity of the organism.

A comparison of mandible preservation method and mandibulotomy approach in oral and oropharyngeal cancer: A meta-analysis.

OBJECTIVE: This study aims to compare the prognoses outcomes of mandibular preservation method (MPM) and the mandibulotomy approach (MLA) in oral and oropharyngeal cancer (OOPC) patients. METHOD: We searched PubMed, Web of Science, EMBASE, Chinese BioMedical Literature Database (CBM), Cochrane Library, and clinicaltrials.gov up to September 2016 to identify the studies that compared the prognoses of the MPM versus the MLA in OOPC patients. Two authors individually extracted the data and performed quality assessment. The surgical margins, overall survival rate, total and local recurrence rates, fistula formation, and other functional outcomes were evaluated. RESULT: Six studies with 309 patients were included in our analysis. No significant difference was found regarding the surgical margins, overall survival rate, total and local recurrence rates, and speech and tongue movement between the MPM and MLA groups. However, the MPM group showed a significantly lower fistula formation rate than the MLA group after the operation. CONCLUSION: These findings suggest that the MPM may provide a similar clinical outcome to the MLA, but that the MPM has a lower complication rate in the treatment of OOPC patients.