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Postbiotics are defined as "preparation of inanimate microorganisms and/or their components that confers a health benefit on the host". Postbiotics have unique advantages over probiotics, such as stability, safety, and wide application. Although postbiotics are research hotspots, the research on them is still very limited. This review provides comprehensive information on the scope of postbiotics, the preparation methods of inanimate microorganisms, and the application and mechanisms of postbiotics in metabolic syndrome (MetS). Furthermore, the application trends of postbiotics in the food industry are reviewed. It was found that postbiotics mainly include inactivated microorganisms, microbial lysates, cell components, and metabolites. Thermal treatments are the main methods to prepare inanimate microorganisms as postbiotics, while non-thermal treatments, such as ionizing radiation, ultraviolet light, ultrasound, and supercritical CO2, show great potential in postbiotic preparation. Postbiotics could ameliorate MetS through multiple pathways including the modulation of gut microbiota, the enhancement of intestinal barrier, the regulation of inflammation and immunity, and the modulation of hormone homeostasis. Additionally, postbiotics have great potential in the food industry as functional food supplements, food quality improvers, and food preservatives. In addition, the SWOT analyses showed that the development of postbiotics in the food industry exists both opportunities and challenges. [ABSTRACT FROM AUTHOR]

Although neighborhood rough set(NRS) based attribute reduction methods have achieved excellent performance in many scenarios, the efficiency and robustness of these methods have not attracted much attention. In this study, we propose a fast fixed granular-ball model (FFGB) for attribute reduction in label noise environments. In FFGB, we propose a fast neighborhood search mechanism to improve the efficiency of NRS. This fast mechanism reduces the neighborhood search range from the universe to a neighborhood and reduces the time complexity of the neighborhood calculation to much less than O (n 2) . Based on the fast mechanism, we propose FFGB model whose definitions are relaxed to be robust to against label noise. In addition, a FFGB attribute reduction algorithm is designed. Finally, we apply the FFGB attribute reduction to medical diagnosis. The experimental results indicate that FFGB is more efficient and robust than the comparison methods. [ABSTRACT FROM AUTHOR]

The low ionic conductivity, narrow electrochemical window, poor interfacial stability with lithium metal, and non-degradability of raw materials are the main problems of solid polymer electrolytes, restricting the development of lithium solid-state batteries. In this paper, a biodegradable poly (2,3-butanediol/1,3-propanediol/succinic acid/sebacic acid/itaconic acid) ester was designed and used as a substrate to prepare biodegradable polyester solid polymer electrolytes for solid-state lithium batteries using a simple solution-casting method. A large number of ester-based polar groups in the amorphous polymer become a high-speed channel for carrying lithium ions as a weak coordination site. The biodegradable polyester solid polymer electrolyte exhibits a wide electrochemical window of 5.08 V (vs. Li/Li+), high ionic conductivity of 1.03 mS cm−1 (25 °C), and a large Li+ transference number of 0.56. The electrolyte exhibits good interfacial stability with lithium, with stable Li plating/stripping behavior at room temperature over 2100 h. This design strategy for biodegradable polyester solid polymer electrolytes offers new possibilities for the development of matrix materials for environmentally friendly lithium metal solid-state batteries. [ABSTRACT FROM AUTHOR]

Diabetic nephropathy (DN) is a worldwide health problem with increasing incidence. Diosgenin (DIO) is a natural active ingredient extracted from Chinese yams (Rhizoma dioscoreae) with potential antioxidant, anti-inflammatory, and antidiabetic effects. However, the protective effect of DIO on DN is still unclear. The present study explored the mitigating effects and underlying mechanisms of DIO on DN in vivo and in vitro. In the current study, the DN rats were induced by a high-fat diet and streptozotocin and then treated with DIO and metformin (Mef, a positive control) for 8 weeks. The high-glucose (HG)-induced HK-2 cells were treated with DIO for 24 h. The results showed that DIO decreased blood glucose, biomarkers of renal damage, and renal pathological changes with an effect comparable to that of Mef, indicating that DIO is potential active substance to relieve DN. Thus, the protective mechanism of DIO on DN was further explored. Mechanistically, DIO improved autophagy and mitophagy via the regulation of the AMPK-mTOR and PINK1-MFN2-Parkin pathways, respectively. Knockdown of CaMKK2 abolished AMPK-mTOR and PINK1-MFN2-Parkin pathways-mediated autophagy and mitophagy. Mitophagy and mitochondrial dynamics are closely linked physiological processes. DIO also improved mitochondrial dynamics through inhibiting fission-associated proteins (DRP1 and p-DRP1) and increasing fusion proteins (MFN1/2 and OPA1). The effects were abolished by CaMKK2 and PINK1 knockdown. In conclusion, DIO ameliorated DN by enhancing autophagy and mitophagy and by improving mitochondrial dynamics in a CaMKK2-dependent manner. PINK1 and MFN2 are proteins that concurrently regulated mitophagy and mitochondrial dynamics. [ABSTRACT FROM AUTHOR]

In superconductors possessing both time and inversion symmetries, the Zeeman effect of an external magnetic field can break the time-reversal symmetry, forming a conventional Fulde–Ferrell–Larkin–Ovchinnikov (FFLO) state characterized by Cooper pairings with finite momentum1,2. In superconductors lacking (local) inversion symmetry, the Zeeman effect may still act as the underlying mechanism of FFLO states by interacting with spin–orbit coupling (SOC). Specifically, the interplay between the Zeeman effect and Rashba SOC can lead to the formation of more accessible Rashba FFLO states that cover broader regions in the phase diagram3–5. However, when the Zeeman effect is suppressed because of spin locking in the presence of Ising-type SOC, the conventional FFLO scenarios are no longer effective. Instead, an unconventional FFLO state is formed by coupling the orbital effect of magnetic fields with SOC, providing an alternative mechanism in superconductors with broken inversion symmetries6–8. Here we report the discovery of such an orbital FFLO state in the multilayer Ising superconductor 2H-NbSe2. Transport measurements show that the translational and rotational symmetries are broken in the orbital FFLO state, providing the hallmark signatures of finite-momentum Cooper pairings. We establish the entire orbital FFLO phase diagram, consisting of a normal metal, a uniform Ising superconducting phase and a six-fold orbital FFLO state. This study highlights an alternative route to achieving finite-momentum superconductivity and provides a universal mechanism to preparing orbital FFLO states in similar materials with broken inversion symmetries.The discovery of an orbital Fulde–Ferrell–Larkin–Ovchinnikov state in the multilayer Ising superconductor 2H-NbSe2, in which the translational and rotational symmetries are broken, enables the preparation of such states in other materials with broken inversion symmetries. [ABSTRACT FROM AUTHOR]

Diosgenin (DIO) is a dietary steroid sapogenin possessing multiple biological functions, such as the amelioration of diabetes. However, the remission effect of DIO on diabetic nephropathy (DN) underlying oxidative stress and cell apoptosis remains unclear. Here, the effect of DIO on ROS generation and its induced cell apoptosis was studied in vitro and in vivo. Renal proximal tubular epithelial (HK-2) cells were treated with DIO (1, 2, 4 µM) under high glucose (HG, 30 mM) conditions. DN rats were induced by a high-fat diet combined with streptozotocin, followed by administration of DIO for 8 weeks. Our data suggested that DIO relieved the decline of HK-2 cell viability and renal pathological damage in DN rats. DIO also relieved ROS (O2− and H2O2) production. Mechanistically, DIO inhibited the expression of NOX4 and restored mitochondrial respiratory chain (MRC) complex I-V expressions. Further, DIO inhibited mitochondrial apoptosis by ameliorating mitochondrial membrane potential (MtMP) and down-regulating the expressions of CytC, Apaf-1, caspase 3, and caspase 9, while up-regulating Bcl2 expression. Moreover, the ER stress and its associated cell apoptosis were inhibited through decreasing PERK, p-PERK, ATF4, IRE1, p-CHOP, and caspase 12 expressions. Collectively, DIO inhibited ROS production by modulating NOX4 and MRC complexes, which then suppressed apoptosis regulated by mitochondria and ER stress, thereby attenuating DN. [ABSTRACT FROM AUTHOR]

Diosgenin (DIO) is a dietary and phytochemical steroidal saponin representing multiple activities. The present study investigated the protective effect of DIO on type II diabetes-associated nonalcoholic fatty liver disease (D-NAFLD). The rat model was established by high-fat diet and streptozotocin injection and then administered DIO for 8 weeks. The results showed that DIO reduced insulin resistance index, improved dyslipidemia, and relieved pancreatic damage. DIO decreased hepatic injury markers, including aspartate aminotransferase (AST) and alanine aminotransferase (ALT). H&E staining showed that DIO relieved hepatic lipid deposition. Mechanistically, DIO inhibited hepatic de novo lipogenesis (DNL) and increased fatty acid β-oxidation (FAO) through regulation of the AMPK-ACC/SREBP1 pathway. Endoplasmic reticulum (ER) stress was inhibited by DIO through regulation of PERK and IRE1 arms, which may then inhibit DNL. DIO also decreased reactive oxygen species (ROS) and enhanced the antioxidant capacity via an increase in Superoxide dismutase (SOD), Catalase (CAT), and Glutathione peroxidase (GPx) activities. The mitochondria are the site for FAO, and ROS can damage mitochondrial function. DIO relieved mitochondrial fission and fusion disorder by inhibiting DRP1 and increasing MFN1/MFN2 expressions. Mitochondrial apoptosis was then inhibited by DIO. In conclusion, the present study suggests that DIO protects against D-NAFLD by inhibiting DNL and improving FAO and mitochondrial function. [ABSTRACT FROM AUTHOR]

Summary: Occupational stress is associated with sleep quality among workers and the human variable number tandem repeat (VNTR) polymorphism of the period circadian regulator 3 (PER3) gene relates to sleep–wake regulation. The main aims of the present study were to examine the effects of PER3 VNTR genotypes, occupational stress, and their interactions on sleep quality. A cross‐sectional study was conducted and 729 workers were recruited in Sichuan. Sleep quality were assessed using the Pittsburgh Sleep Quality Index. Occupational stress was measured using the Generic Job Stress Questionnaire. PER3 genotypes were determined with polymerase chain reaction. High and medium occupational stress were linked to a higher risk of poor sleep quality than low levels. Unconditional logistic regression indicated that PER3 genotype was significantly associated with sleep quality, and an increased risk of poor sleep of >1.5‐times was observed in those with the allele 5 compared to allele 4. The 5/5 genotype was associated with both sleep latency and sleep duration. Crossover analysis showed an occupational stress × PER3 interaction. Compared to subjects with both low and medium occupational stress and 4/4 + 4/5 genotype, those with both high occupational stress and 5/5 genotype had a higher risk of poor sleep quality. Stratified logistic analyses found that compared with low and medium occupational stress, high occupational stress increased the risk of poor sleep by more than five‐times in 5/5 genotype carriers. Occupational stress and PER3 genotype had both separate and combined effects on poor sleep quality of workers. The results suggest that occupational stress may increase the risk of poor sleep quality through interaction with the PER3 gene polymorphism. [ABSTRACT FROM AUTHOR]

3-Chloro-1, 2-propanediol (3-MCPD) is a food-borne toxic substance well-known for more than 40 years that is mainly associated with nephrotoxicity. A better understanding of 3-MCPD nephrotoxicity is required to devise efficacious strategies to counteract its toxicity. In the present work, the role of endoplasmic reticulum (ER) stress along with its underlying regulatory mechanism in 3-MCPD-mediated renal cytotoxicity was investigated in vivo and in vitro. Our data indicated that 3-MCPD-stimulated ER stress response evidenced by sustained activation of PERK-ATF4-p-CHOP and IRE1 branches in Sprague Dawley (SD) rats and human embryonic kidney (HEK293) cells. Moreover, ER stress-associated specific apoptotic initiator, caspase 12, was over-expressed. Blocking ER stress with its antagonist, 4-phenylbutyric acid (4-PBA), improved the morphology and function of kidney effectively. 4-PBA also increased cell viability, relieved mitochondrial vacuolation, and inhibited cell apoptosis through regulating caspase-dependent intrinsic apoptosis pathways. Furthermore, the enhanced expressions of two mitochondrial fission proteins, DRP1/p-DRP1 and FIS1, and the relocation of DRP1 on mitochondria subjected to 3-MPCD were reversed by 4-PBA, while the expression of the fusion protein, MFN2, was restored. Moreover, cellular Ca2+ overload, the over-expression of CaMKK2, and the loss of mitochondria-associated membranes (MAM) were also relieved after 4-PBA co-treatment. Collectively, our data emphasized that ER stress plays critical role in 3-MCPD-mediated mitochondrial dysfunction and subsequent apoptosis as well as blockage of ER stress ameliorated kidney injury through improving mitochondrial fission/fusion and Ca2+ homeostasis. These findings provide a novel insight into the regulatory role of ER stress in 3-MCPD-associated nephropathy and a potential therapeutic strategy. [ABSTRACT FROM AUTHOR]

Transition metal dichalcogenide (TMD) monolayers, with their direct band gaps, have attracted wide attention from the fields of photonics and optoelectronics. However, monolayer semiconducting TMDs generally suffer from low excitation absorption and emission efficiency, limiting their further applications. Here a flip‐over plasmonic structure comprised of silver nano‐disk arrays supporting a WS2 monolayer sandwiched by hexagonal boron nitride (h‐BN) layers is demonstrated. The flip‐over configuration optimizes the optical process with a free excitation/emission path from the top and a strong plasmonic interaction from the bottom. As a result, the photoluminescence from the TMD monolayers can be greatly enhanced more than tenfold by optimizing the metasurface, which can be further improved nearly tenfold by optimizing the thickness of bottom h‐BN. This study shows the advantages of using the flip‐over structure, where the plasmonic interaction between the metasurface and TMDs can be tuned by introducing optimized plasmonic arrays and h‐BN layers with suitable thickness. This hybrid device configuration paves a reliable platform to study the light–matter interaction, achieving highly efficient plasmonic TMD devices. [ABSTRACT FROM AUTHOR]

Transition metal dichalcogenide (TMD) monolayers, with their direct band gaps, have attracted wide attention from the fields of photonics and optoelectronics. However, monolayer semiconducting TMDs generally suffer from low excitation absorption and emission efficiency, limiting their further applications. Here a flip‐over plasmonic structure comprised of silver nano‐disk arrays supporting a WS2 monolayer sandwiched by hexagonal boron nitride (h‐BN) layers is demonstrated. The flip‐over configuration optimizes the optical process with a free excitation/emission path from the top and a strong plasmonic interaction from the bottom. As a result, the photoluminescence from the TMD monolayers can be greatly enhanced more than tenfold by optimizing the metasurface, which can be further improved nearly tenfold by optimizing the thickness of bottom h‐BN. This study shows the advantages of using the flip‐over structure, where the plasmonic interaction between the metasurface and TMDs can be tuned by introducing optimized plasmonic arrays and h‐BN layers with suitable thickness. This hybrid device configuration paves a reliable platform to study the light–matter interaction, achieving highly efficient plasmonic TMD devices. [ABSTRACT FROM AUTHOR]

Solar-driven evaporation is highly promising for sustainable freshwater production without high energy-consumption. Till now, it has still been challenging to achieve both high performance and cost-effectiveness within one evaporator. In addition, the rarely reported strategy overcomes the obstacles of emerging microplastic-pollution in water sources and poor all-day-round evaporation. Herein, a low-cost, high-efficiency, biomass-derived three-dimensional (3D) graphene/cotton sponge with gradient vertical microchannels was readily constructed by simply stretching cotton. It served as a versatile photothermal platform with a high evaporation rate (2.49 kg m−2 h−1, normalized to both the top and side surfaces) and could withstand a large external stress of up to 8750-times its weight. Moreover, in the first attempt to efficiently evaporate water (90.6%) from a microplastic-polluted source, nearly 100% of the polyethylene (PE) microfibers were removed from evaporated water by 3D MoS2/graphene/cotton via reactive oxygen species attack and multi-level interception. New in situ FTIR microscopy technology was employed to accurately monitor the degradation mechanism of the PE microplastics. The PE degradation efficiency was as high as 19% in oxygen-enriched water, predominantly contributed by reactive O2˙−, and could be easily enhanced to 32% with the aid of additional reactive species (e.g., ˙HOO and H2O2) in 1 h. Besides, under the guidance of finite element analysis (FEA), a phase-change polyethylene glycol (PEG) layer was functionalized outside the graphene/cotton. Notably, it possessed a remarkably high all-day-round evaporation rate (1.63 kg per m2 per h per day, 1.42-times that achieved by a traditional evaporator without phase-change function) by utilizing thermal energy in the dark. This work gives promising alternative strategies for low-cost clean-water harvesting from microplastic-pollution and sustainable evaporation even under dark conditions. [ABSTRACT FROM AUTHOR]

Cu2SnS3, as a modified material for high-capacity tin-based anodes, has great potential for lithium-ion battery applications. The solvothermal method is simple, convenient, cost-effective, and easy to scale up, and has thus been widely used for the preparation of nanocrystals. In this work, Cu2SnS3 nanoparticles were prepared by the solvothermal method. The effects of high-temperature annealing on the morphology, crystal structure, and electrochemical performance of a Cu2SnS3 nano-anode were studied. The experimental results indicate that high-temperature annealing improves the electrochemical performance of Cu2SnS3, resulting in higher initial coulombic efficiency and improved cycling and rate characteristics compared with those of the as-prepared sample. [ABSTRACT FROM AUTHOR]

In this study, we designed and fabricated a poling-free piezoelectric nanogenerator using bio-based polymer and filler, a poly(l-lactic acid) (PLLA)/vitamin B2 (VB2) composite film. The addition of VB2 to PLLA led to improved crystallinity and enhanced the molecular orientation of PLLA, resulting in a significantly enhanced output performance of the PLLA/VB2 nanogenerator. The proposed nanogenerator provides a maximum power density of 75.68 mW cm−3, which is approximately 28.7 times higher than that of pure PLLA nanogenerator. Moreover, the PLLA/VB2 nanogenerator exhibits good electrical responses under both mechanical and acoustic stimulations. The collected mechanical energy from the motion of human joints can power up several LEDs. The PLLA/VB2 nanogenerator can sensitively detect sound frequency from 1 to 27 kHz. Thus, it has great application potential in ambient mechanical and acoustic energy harvesting, wearable devices, and human–machine controlling systems. [ABSTRACT FROM AUTHOR]

Layered metal monochalcogenides have attracted significant interest in the 2D family since they show different unique properties from their bulk counterparts. The comprehensive synthesis, characterization, and optoelectrical applications of 2D‐layered tin monosulfide (SnS) grown by pulsed laser deposition are reported. Few‐layer SnS‐based field‐effect transistors (FETs) and photodetectors are fabricated on Si/SiO2 substrates. The premium 2D SnS FETs yield an on/off ratio of 3.41 × 106, a subthreshold swing of 180 mV dec−1, and a field effect mobility (µFE) of 1.48 cm2 V−1 s−1 in a 14‐monolayer SnS device. The layered SnS photodetectors show a broad photoresponse from ultraviolet to near‐infrared (365–820 nm). In addition, the SnS phototransistors present an improved detectivity of 9.78 × 1010 cm2 Hz1/2 W−1 and rapid response constants of 60 ms for grow‐time constant τg and 10 ms for decay‐time constant τd under extremely weak 365 nm illumination. This study sheds light on layer‐dependent optoelectronic properties of 2D SnS that promise to be important in next‐generation 2D optoelectronic devices. [ABSTRACT FROM AUTHOR]

Delphinidin, one of the main anthocyanidins, has potent anti‐cancer properties. In this study, we investigated the effect of delphinidin on 1‐methyl‐1‐nitrosourea (MNU)‐induced breast carcinogenesis on rats and the mechanism of delphinidin via negative regulation of the HOTAIR/microRNA‐34a axis. We found administration of delphinidin could effectively suppress MNU‐induced mammal breast carcinogenesis. Delphinidin downregulated the level of HOTAIR and upregulated miR‐34a in breast carcinogenesis. Western blot analysis confirmed that delphinidin treatment can significantly decrease the expression of β‐catenin, glycogen synthase kinase‐3β (Gsk3β), c‐Myc, cyclin‐D1, and matrix metalloproteinase‐7(MMP‐7) expression in breast cancer cells, and inhibition of miR‐34a significantly reduced the effect of delphinidin on c‐Myc, cyclin‐D1, and MMP‐7. HOTAIR overexpression also blocked the effect of delphinidin on miR‐34a and the Wnt/β‐catenin signaling pathway in MDA‐MB‐231 cells. RNA immunoprecipitation (RIP) assay and chromatin immunoprecipitation (ChIP) assay results showed that delphinidin upregulated miR‐34a by inhibiting HOTAIR, coupled with enhancement of the zeste homolog 2 (EZH2) and histone H3 Lys27 trimethylation (H3K27me3). This study indicated that delphinidin may potentially suppress breast carcinogenesis and exert its anti‐cancer effect through the HOTAIR/miR‐34a axis. These findings provided new evidence for the use of delphinidin in preventing breast carcinogenesis. [ABSTRACT FROM AUTHOR]

Freshness is an important parameter for evaluating the quality of pork, which has strong correlation with the characteristic volatile organic compounds (VOCs) in meat. In this study, the pork was stored at a refrigerator, and the VOCs were determined by using headspace solid-phase microextraction-gas chromatography-mass spectrometry (HS-SPME-GC-MS). The results of HS-SPME-GC-MS measurements were compared to total viable counts, total volatile basic nitrogen, and pH value to determine possible volatile spoilage markers. The pork was stored in a refrigerator up to 5 days at 4 °C and 466 days at −18 °C. The pork became stale at 4 °C when the 2,3-butanedione, 3-methyl butyraldehyde, 3-methyl-1-butanol, and acetoin increased to 26.44, 13.72, 71.56, and 340.48 μg/L, respectively. These substances can be seen as characteristic compounds of stale pork. The VOCs such as ethyl acetate, ethyl propionate, ethyl butyrate, and ethyl hexanoate had negative correlation (P < 0.05) with the pork freshness, which can be potentially considered as characteristic compounds of fresh pork. Therefore, the selected VOCs can be used as indicators for evaluation of pork freshness, and VOCs could be potentially applied in the development of intelligent refrigerators and refrigerated storehouse. [ABSTRACT FROM AUTHOR]

To explore the feasibility of using radio frequency ( RF) heating as a method to process kiwi puree, this study compared the effects of RF heating with traditional heat pasteurisation ( TP) on various properties of kiwi puree. RF treatment completely inactivate of microbes in kiwi puree, with total aerobic bacteria counts ( TAC) decreased by 4.81 log CFU mL−1 and yeast and mould counts ( YMC) decreased by 2.62 log CFU mL−1, which are similar to TP treatment. During the 7 weeks' storage, RF-treated puree showed retarded growth of microbes. The pH, titratable acidity and °Brix values of RF-treated samples were significantly different from those of the control. The vitamin C, total phenolic compounds and antioxidant capacity of RF-treated samples were significantly higher than those of TP-treated samples during storage. RF-treated sample retained better colour than TP-treated sample throughout storage. The customer satisfaction analysis indicated that consumers prefer RF-treated kiwi puree than TP-treated samples. These findings suggest that RF heating has potential applications in processing of kiwi puree or similar products. [ABSTRACT FROM AUTHOR]

Background: Breast cancer is the common cancer in China. In previous study, we determined that 3,6-dihydroxyflavone (3,6-DHF) increases miR-34a significantly in breast carcinogenesis, but the mechanism remains unclear.Methods: We used qRT-PCR to analyze miR-34a and ten-eleven translocation (TET)1, TET2, TET3 levels in breast cancer cells. With a cellular breast carcinogenesis model and an experimental model of carcinogenesis in rats, TET1 levels were evaluated by western blot analysis and immunofluorescence. TET1 and 5hmC (5-hydroxymethylcytosine) levels were evaluated by immunofluorescence in nude mouse xenografts of MDA-MB-231 cells. Chromatin immunoprecipitation(ChIP) assayed for TET1 on the TET1 promoter, and dot blot analysis of DNA 5hmC was performed in MDA-MB-231 cells. We evaluated the mechanism of 3,6-DHF on the expression of tumor suppressor miR-34a by transfecting them with DNA methyltransferase (DNMT)1 plasmid and TET1 siRNA in breast cancer cells. Methylation-specific PCR detected methylation of the miR-34a promoter.Results: First, we found that 3,6-DHF promotes the expression of TET1 during carcinogen-induced breast carcinogenesis in MCF10A cells and in rats. 3,6-DHF also increased TET1 and 5hmC levels in MDA-MB-231 cells. Further study indicated that TET1 siRNA and pcDNA3/Myc-DNMT1 inhibited the 3,6-DHF reactivation effect on expression of miR-34a in breast cancer cells. Methylation-specific PCR assays indicated that TET1 siRNA and pcDNA3/Myc-DNMT1 inhibit the effect of 3,6-DHF on the demethylation of the miR-34a promoter.Conclusions: Our study showed that 3,6-DHF effectively increases TET1 expression by inhibiting DNMT1 and DNA hypermethylation, and consequently up-regulates miR-34a in breast carcinogenesis. [ABSTRACT FROM AUTHOR]

Hypersecretion of amylin is common in individuals with prediabetes, causes amylin deposition and proteotoxicity in pancreatic islets, and contributes to the development of type 2 diabetes. Recent studies also identified amylin deposits in failing hearts from patients with obesity or type 2 diabetes and demonstrated that hyperamylinemia accelerates the development of heart dysfunction in rats expressing human amylin in pancreatic β-cells (HIP rats). To further determine the impact of hyperamylinemia on cardiac myocytes, we investigated human myocardium, compared diabetic HIP rats with diabetic rats expressing endogenous (nonamyloidogenic) rat amylin, studied normal mice injected with aggregated human amylin, and developed in vitro cell models. We found that amylin deposition negatively affects cardiac myocytes by inducing sarcolemmal injury, generating reactive aldehydes, forming amylin-based adducts with reactive aldehydes, and increasing synthesis of the proinflammatory cytokine interleukin-1β (IL-1β) independently of hyperglycemia. These results are consistent with the pathological role of amylin deposition in the pancreas, uncover a novel contributing mechanism to cardiac myocyte injury in type 2 diabetes, and suggest a potentially treatable link of type 2 diabetes with diabetic heart disease. Although further studies are necessary, these data also suggest that IL-1β might function as a sensor of myocyte amylin uptake and a potential mediator of myocyte injury. [ABSTRACT FROM AUTHOR]

Background: The long non-coding RNA (lncRNA) HOX transcript antisense RNA (HOTAIR) plays a crucial role in cancer progression, which is regulated by the interferon regulatory factor-1 (IRF1) and up-streaming Akt activation. The present study evaluated the chemopreventive effects of delphinidin-3-glucoside (Dp), a major anthocyanin present in pigmented fruits and vegetables, on breast carcinogenesis, and investigate the role of the Akt/HOTAIR signaling pathway.Methods: Human breast epithelial cells MCF10A were treated with carcinogens (NNK and B[a]P) or co-treated with carcinogens plus Dp for 30 days. Then, the cancer-associated properties of the treated cells were evaluated to assess the carcinogenesis and the effects of Dp. HOTAIR levels were detected by qRT-PCR. The proteins expression was measured by western blots, immunofluorescence and immunohistochemistry. Xenografted tumors were made by implanting breast cancer cells MDA-MB-231-Luc-GFP in athymic mice. ChIP-qPCR analysis was used to detect the IRF1 binding to the HOTAIR promoter.Results: Carcinogens treatment induces apparent carcinogenic transformation in MCF10A cells including reduced dependence on growth factors, anchorage-independent cell growth and aberrant wound-healing ability, which is effectively suppressed by Dp co-treatment. The level of HOTAIR significantly increases in a time-dependent manner during chronic breast carcinogenesis. Dp treatment down-regulates HOTAIR expression in breast carcinogenesis and breast cancer cells. Furthermore, Dp administration inhibits the growth of xenografted breast tumors in athymic mice, and decreases HOTAIR in vivo. Further studies showed that Dp represses Akt activation, promotes IRF1 expression and increases IRF1 binding to the HOTAIR promoter. Silence of IRF1 expression via transfecting cells with IRF1 siRNAs significantly reduced the effects of Dp on HOTAIR, resulting in decreased cytotoxic effects of Dp on breast cancer cells.Conclusions: These data suggest the effective chemopreventive effect of Dp on breast carcinogenesis, in which down-regulation of HOTAIR plays a critical role. [ABSTRACT FROM AUTHOR]

Control over phase stabilities during synthesis processes is of great importance for both fundamental studies and practical applications. We describe herein a facile strategy for the synthesis of Cu2Se with phase selectivity through a simple solvothermal method. In the presence and absence of SbCl3, monoclinic α-Cu2Se and cubic β-Cu2Se can be synthesized, respectively. The formation of α-Cu2Se requires optimization of the Cu/Se molar ratio in the starting reagents, the reaction temperature, as well as the timing for the addition of SbCl3. Differential scanning calorimetry of the synthesized α-Cu2Se has shown that a part of it undergoes a phase transition to β-Cu2Se at 135 °C, and that this phase transition is irreversible on cooling to ambient temperature. Kinetic studies have revealed that in the presence of Sb species the kinetically favored β-Cu2Se transforms to the thermodynamically favored α-Cu2Se. In this β-to-α phase transition process, the distribution of Cu ions in β-Cu2Se, as determined by the Cu/Se ratio and temperature, is likely to play a crucial role. [ABSTRACT FROM AUTHOR]

Resveratrol, a natural polyphenolic compound, is abundantly found in plant foods and has been extensively studied for its anti-cancer properties. Given the important role of CSCs (Cancer Stem Cells) in breast tumorigenesis and progression, it is worth investigating the effects of resveratrol on CSCs. The article is an attempt to investigate the effects of resveratrol on breast CSCs. Resveratrol significantly inhibits the proliferation of BCSCs (breast cancer stem-like cells) isolated from MCF-7 and SUM159, and decreased the percentage of BCSCs population, consequently reduced the size and number of mammospheres in non-adherent spherical clusters. Accordingly, the injection of resveratrol (100 mg/kg/d) in NOD/SCID (nonobese diabetic/severe combined immunodeficient) mice effectively inhibited the growth of xenograft tumors and reduced BCSC population in tumor cells. After the reimplantation of primary tumor cells into the secondary mice for 30 d, all 6 control inoculations produced tumors, while tumor cells derived from resveratrol-treated mice only caused 1 tumor of 6 inoculations. Further studies by TEM (Transmission electron microscopy) analysis, GFP-LC3-II puncta formation assay and western blot for LC3-II, Beclin1 and Atg 7, showed that resveratrol induces autophagy in BCSCs. Moreover, resveratrol suppresses Wnt/β-catenin signaling pathway in BCSCs; over-expression of β-catenin by transfecting the plasmid markedly reduced resveratrol-induced cytotoxicity and autophagy in BCSCs. Our findings indicated that resveratrol inhibits BCSCs and induces autophagy via suppressing Wnt/β-catenin signaling pathway. [ABSTRACT FROM AUTHOR]

Fresh-cut lettuce has a short shelf life since it is very perishable and susceptible to enzymatic browning. The aim of this study was to examine the effectiveness of allicin treatment in prolonging the shelf life of fresh-cut lettuce ( Lactuca sativa L. var. angustana Irish). Fresh-cut lettuce slices were treated with water (control), 0.2 and 1 % of allicin solutions, respectively, and stored at 4 °C, >90 % relative humidity. Sensory parameters, microbiological indicators, and physiological indices were determined at 0, 2, 4, and 6 days of storage. The sensory analyses revealed that allicin inhibited the color change and maintained the visual quality of lettuce slice without impairing flavor. Allicin treatment delayed microbial growth at cold storage, as evidenced by the lowered total viable counts (decreased by 2.52 log cfu/g) and yeast and mold counts (decreased by 1.59 log cfu/g) after 6 days in 1 % allicin-treated samples compared to control samples. In addition, differences between lettuce treated with 1 % allicin and control slices in objective color (total color change, chrome, and hue angle), total phenolic compounds and quinones content, activities of browning-related enzymes, and antioxidative enzymes suggested that allicin had antioxidative properties. Conclusively, it was demonstrated for the first time that allicin effectively protected fresh-cut lettuce from tissue browning and microbiological spoilage. These findings indicate that allicin has great potential as a natural additive to extend the shelf life of fresh-cut lettuce. [ABSTRACT FROM AUTHOR]

Ampelopsin (AMP), a major bioactive constituent of Ampelopsis grossedentata, exerts a number of biological effects. In this study, we investigated its anti-cancer activity in human breast cancer cell lines, and explored the underlying mechanism of this action. Our results showed that treatment with AMP dose-dependently inhibited cell viability and induced apoptosis in MCF-7 and MDA-MB-231 breast cancer cells without cytotoxicity in human normal breast epithelial cells MCF-10A. Meanwhile, AMP dose- dependently triggered reactive oxygen species (ROS) generation in both breast cancer cells. The ROS scavenger N-acetyl-L-cysteine (NAC) strongly attenuated AMP-induced ROS production, along with cell growth inhibition and apoptosis. Furthermore, AMP was observed to activate endoplasmic reticulum (ER) stress, as evidenced by the up-regulation of ER stress-related proteins, including GRP78, p-PERK, p-elF2α, cleaved ATF6α and CHOP, while knockdown of ATF6α or PERK markedly down-regulated AMP-induced CHOP expression. Blocking ER stress using 4-phenylbutyric acid not only down-regulated AMP-induced GRP78 and CHOP expression, but also significantly decreased AMP-induced cell growth inhibition and apoptosis, whereas ER stress inducer thapsigargin played opposing effects. Additionally, NAC inhibited AMP-induced ER stress by down-regulating GRP78 and CHOP expression. Conversely, blocking ER stress using CHOP siRNA decreased AMP-induced ROS production and cell apoptosis. Taken together, these results demonstrate that AMP has anti-tumor effects against breast cancer cells through ROS generation and ER stress pathway, which therefore provide experimental evidences for developing AMP as a new therapeutic drug for breast cancer. [ABSTRACT FROM AUTHOR]

Background: Studies have suggested the chemopreventive effects of flavonoids on carcinogenesis. Yet numbers of epidemiologic studies assessing dietary flavonoids and breast cancer risk have yielded inconsistent results. The association between flavonoids, flavonoid subclasses (flavonols, flavan-3-ols, etc.) and the risk of breast cancer lacks systematic analysis. Objective: We aimed to examine the association between flavonoids, each flavonoid subclass (except isoflavones) and the risk of breast cancer by conducting a meta-analysis. Design:We searched for all relevant studies with a prospective cohort or case-control study design published before July 1st, 2012, using Cochrane library, MEDLINE, EMBASE and PUBMED. Summary relative risks (RR) were calculated using fixed-or random-effects models. All analyses were performed using STATA version 10.0. Results:Twelve studies were included, involving 9 513 cases and 181 906 controls, six of which were prospective cohort studies, and six were case-control studies. We calculated the summary RRs of breast cancer risk for the highest vs lowest categories of each flavonoid subclass respectively. The risk of breast cancer significantly decreased in women with high intake of flavonols (RR = 0.88, 95% CI 0.80-0.98) and flavones (RR = 0.83, 95% CI: 0.76-0.91) compared with that in those with low intake of flavonols and flavones. However, no significant association of flavan-3-ols (RR = 0.93, 95% CI: 0.84-1.02), flavanones (summary RR = 0.95, 95% CI: 0.88-1.03), anthocyanins (summary RR = 0.97, 95% CI: 0.87-1.08) or total flavonoids (summary RR = 0.98, 95% CI: 0.86-1.12) intake with breast cancer risk was observed. Furthermore, summary RRs of 3 case-control studies stratified by menopausal status suggested flavonols, flavones or flavan-3-ols intake is associated with a significant reduced risk of breast cancer in post-menopausal while not in pre-menopausal women. Conclusions: The present study suggests the intake of flavonols and flavones, but not other flavonoid subclasses or total flavonoids, is associated with a decreased risk of breast cancer, especially among post-menopausal women. [ABSTRACT FROM AUTHOR]

The WRKY transcription factors have been implicated in multiple biological processes in plants, especially in regulating defense against biotic and abiotic stresses. However, little information is available about the WRKYs in tomato ( Solanum lycopersicum). The recent release of the whole-genome sequence of tomato allowed us to perform a genome-wide investigation for tomato WRKY proteins, and to compare these positively identified proteins with their orthologs in model plants, such as Arabidopsis and rice. In the present study, based on the recently released tomato whole-genome sequences, we identified 81 SlWRKY genes that were classified into three main groups, with the second group further divided into five subgroups. Depending on WRKY domains' sequences derived from tomato, Arabidopsis and rice, construction of a phylogenetic tree demonstrated distinct clustering and unique gene expansion of WRKY genes among the three species. Genome mapping analysis revealed that tomato WRKY genes were enriched on several chromosomes, especially on chromosome 5, and 16 % of the family members were tandemly duplicated genes. The tomato WRKYs from each group were shown to share similar motif compositions. Furthermore, tomato WRKY genes showed distinct temporal and spatial expression patterns in different developmental processes and in response to various biotic and abiotic stresses. The expression of 18 selected tomato WRKY genes in response to drought and salt stresses and Pseudomonas syringae invasion, respectively, was validated by quantitative RT-PCR. Our results will provide a platform for functional identification and molecular breeding study of WRKY genes in tomato and probably other Solanaceae plants. [ABSTRACT FROM AUTHOR]

Ochratoxin A (OTA) is a toxic isocoumarin derivative produced by various species of mould which mainly grow on grain, coffee, and nuts. Recent studies have suggested that OTA induces cell death in plants. To investigate possible mechanisms of OTA phytotoxicity, both digital gene expression (DGE) transcriptomic and two-dimensional electrophoresis proteomic analyses were used, through which 3118 genes and 23 proteins were identified as being up- or down-regulated at least 2-fold in Arabidopsis leaf in response to OTA treatment. First, exposure of excised Arabidopsis thaliana leaves to OTA rapidly causes the hypersensitive reponse, significantly accelerates the increase of reactive oxygen species and malondialdehyde, and enhances antioxidant enzyme defence responses and xenobiotic detoxification. Secondly, OTA stimulation causes dynamic changes in transcription factors and activates the membrane transport system dramatically. Thirdly, a concomitant persistence of compromised photosynthesis and photorespiration is indicative of a metabolic shift from a highly active to a weak state. Finally, the data revealed that ethylene, salicylic acid, jasmonic acid, and mitogen-activated protein kinase signalling molecules mediate the process of toxicity caused by OTA. Profiling analyses on Arabidopsis in response to OTA will provide new insights into signalling transduction that modulates the OTA phytotoxicity mechanism, facilitate mapping of regulatory networks, and extend the ability to improve OTA tolerance in Arabidopsis. [ABSTRACT FROM PUBLISHER]

Foodborne Staphylococcus aureus (S. aureus) has attracted widespread attention due to its foodborne infection and food poisoning in human. Shikonin exhibits antibacterial activity against a variety of microorganisms, but there are few studies on its antibacterial activity against S. aureus. This study aims to explore the antibacterial activity and mechanism of shikonin against foodborne S. aureus. The results show that the minimum inhibitory concentrations (MICs) and the minimum bactericidal concentrations (MBCs) of shikonin were equal for all tested strains ranging from 35 μg/mL to 70 μg/mL. Shikonin inhibited the growth of S. aureus by reducing intracellular ATP concentrations, hyperpolarizing cell membrane, destroying the integrity of cell membrane, and changing cell morphology. At the non-inhibitory concentrations (NICs), shikonin significantly inhibited biofilm formation of S. aureus, which was attributed to inhibiting the expression of cidA and sarA genes. Moreover, shikonin also markedly inhibited the transcription and expression of virulence genes (sea and hla) in S. aureus. In addition, shikonin has exhibited antibacterial ability against both planktonic and biofilm forms of S. aureus. Importantly, in vivo results show that shikonin has excellent biocompatibility. Moreover, both the heat stability of shikonin and the antimicrobial activity of shikonin against S. aureus were excellent in food. Our findings suggest that shikonin are promising for use as a natural food additive, and it also has great potential in effectively controlling the contamination of S. aureus in food and reducing the number of illnesses associated with S. aureus. [ABSTRACT FROM AUTHOR]

Delphinidin is an anthocyanidin monomer, commonly found in vegetables and fruits, and has demonstrated antitumor effects in the HER-2-positive MDA-MB-453 breast cancer cell line, with low cytotoxicity on normal breast cells. However, the direct functional mechanisms underlying the effect of delphinidin on HER-2-positive breast cancer cells has not been fully characterized. In the present study, it was found that delphinidin could induce G2/M phase cell cycle arrest by inhibiting the protein expression level of cyclin B1 and Cdk1 in HER-2-positive breast cancer cell lines. In addition, delphinidin promoted the mitochondrial apoptosis pathway by inhibiting the ERK and NF-κB signaling pathway and activating the JNK signaling pathway. Therefore, delphinidin markedly suppressed the viability of the HER-2-positive breast cancer cell lines by modulating the cell cycle and inducing apoptosis. Overall, the findings from the present study demonstrated that delphinidin treatment could induce the mitochondrial apoptosis pathway in human HER-2-positive breast cancer cell lines, providing an experimental basis for the prevention and treatment of HER-2-positive breast cancer by flavonoids. [ABSTRACT FROM AUTHOR]