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The strategy of reducing carbohydrate digestibility by controlling the activity of two hydrolyzing enzymes (α‐amylase and α‐glucosidase) to control postprandial hyperglycemia is considered as a viable prophylactic treatment of type 2 diabetes mellitus (T2DM). Thus, the consumption of foods rich in hydrolyzing enzyme inhibitors is recommended for diet therapy of diabetes. Whole cereal products have gained increasing interests for plasma glucose‐reducing effects. However, the mechanisms for whole cereal benefits in relation to T2DM are not yet fully understood, but most likely involve bioactive components. Cereal‐derived phenolic compounds, peptides, nonstarch polysaccharides, and lipids have been shown to inhibit α‐amylase and α‐glucosidase activities. These hydrolyzing enzyme inhibitors seem to make whole cereals become nutritional strategies in managing postmeal glucose for T2DM. This review presents an updated overview on the effects provided by cereal‐derived ingredients on carbohydrate digestibility. It suggests that there is some evidence for whole cereal intake to be beneficial in amelioration of T2DM through inhibiting α‐glucosidase and α‐amylase activities., The cereal‐derived α‐amylase and/or α‐glucosidase inhibitor could be targeted for developing valuable whole cereal foods in T2DM dietary managements.

Whole barley (WB) consumption is the subject of renewed interest because of its health benefits. However, there are still controversies regarding the mechanisms of the anti-obesity effects of WB. The gut microbiota has recently become a focus of research into obesity-related disorders. Therefore, the aim of this study was to investigate the contribution of the gut microbiota to the anti-obesity effects of WB. Germ-free (GF) C57BL/6J mice underwent gastric inoculation with human feces to obtain human flora-associated (HFA) mice, and then both the GF and HFA mice were fed a high fat diet (HFD) containing 46% WB or refined barley for 9 weeks. Features of obesity and dyslipidemia were compared between the GF and HFA mice and the cecal microbiota was analyzed using next-generation sequencing of microbial 16S rRNA. WB prevents obesity and hypercholesterolemia in the GF and HFA mice. The mechanism may include the inhibition of cholesterol synthesis, because sterol regulatory element-binding protein-1c (SREBP-1c) and 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA) expression was downregulated, and a reduction in cholesterol accumulation, because cholesterol 7α-hydroxylase (CYP7A1) expression was upregulated, independent of the gut microbiota. Furthermore, WB intake enriched a variety of bacterial genera that are negatively associated with obesity, including Bacteroides, Parabacteroides, and Clostridium cluster XIVa, suggesting that WB counteracted gut dysbiosis in obese mice. Thus, WB helps prevent obesity and dyslipidemia via both gut microbiota-dependent and independent mechanisms.

Gastric carcinoma is a common type of gastrointestinal tumor with high morbidity and mortality rates. IL-17 is a newly discovered cytokine that has been reported to serve an important role in the development of gastric carcinoma. The potential effect of apatinib on IL-17 expression levels in the development of gastric carcinoma has been rarely reported. The present study aimed to investigate the potential mechanism of IL-17 and apatinib in the development of gastric carcinoma. A total of 30 tumor and para-carcinoma tissues were collected from 30 patients with gastric carcinoma between January 2019 and December 2019 and the expression levels of IL-17 in the tissues were analyzed by reverse transcription-quantitative PCR and western blotting. An in vitro model of gastric carcinoma was also established using the HGC-27 cell line, in which the cells were divided into control, IL-17, IL-17-apatinib and apatinib groups. The expression levels of IL-17, Bax, Bcl-2 and caspase-3 were analyzed using reverse transcription-quantitative PCR and western blotting. An MTT assay and flow cytometry were used to analyze the proliferation and apoptosis of HGC-27 cells, respectively, and a Transwell assay was used to analyze the invasive ability of HGC-27 cells. The results revealed that the expression levels of IL-17 were significantly upregulated in the gastric carcinoma tissues compared with the para-carcinoma tissues. In vitro, IL-17 treatment promoted the proliferation and invasive ability of HGC-27 cells, but inhibited the apoptosis with the significantly downregulated expression levels of Bax and caspase-3 and the upregulated expression levels of Bcl-2 than control group. Conversely, apatinib treatment significantly inhibited the proliferative and invasive abilities of HGC-27 cells, but promoted cell apoptosis in the IL-17 and IL-17-apatinib groups.. Collectively, the present results suggested that the upregulation of IL-17 may be associated with the occurrence and development of gastric carcinoma. The findings indicated that apatinib may inhibit gastric carcinoma development by regulating IL-17 expression via the Bax/Bcl-2 signaling pathway. Therefore, the present findings may enhance the current knowledge of the effect of apatinib on gastric carcinoma cells.

Background: Pathological neovascularization in neovascular age-related macular degeneration (nAMD) is the leading cause of vision loss in the elderly. Increasing evidence shows that cells of myeloid lineage play important roles in controlling pathological endothelium formation. Suppressor of cytokine signaling 3 (SOCS3) pathway has been linked to neovascularization. Methods: We utilised a laser-induced choroidal neovascularization (CNV) mouse model to investigate the neovascular aspect of human AMD. In several cell lineage reporter mice, bone marrow chimeric mice and Socs3 loss-of-function (knockout) and gain-of-function (overexpression) mice, immunohistochemistry, confocal, and choroidal explant co-culture with bone marrow-derived macrophage medium were used to study the mechanisms underlying pathological CNV formation via myeloid SOCS3. Findings: SOCS3 was significantly induced in myeloid lineage cells, which were recruited into the CNV lesion area. Myeloid Socs3 overexpression inhibited laser-induced CNV, reduced myeloid lineage-derived macrophage/microglia recruitment onsite, and attenuated pro-inflammatory factor expression. Moreover, SOCS3 in myeloid regulated vascular sprouting ex vivo in choroid explants and SOCS3 agonist reduced in vivo CNV. Interpretation: These findings suggest that myeloid lineage cells contributed to pathological CNV formation regulated by SOCS3. Funding: This project was funded by NIH/NEI (R01EY030140, R01EY029238), BrightFocus Foundation, American Health Assistance Foundation (AHAF), and Boston Children's Hospital Ophthalmology Foundation for YS and the National Institutes of Health/National Heart, Lung and Blood Institute (U01HL098166) for PZ.

Retinal blood vessels provide the necessary energy, nutrients and oxygen in order to support visual function and remove harmful particles from blood, thus acting to protect neuronal cells. The homeostasis of the retinal vessels is important for the maintenance of retinal visual function. Neovascularization is the most common cause of blindness in patients with retinopathy. Previous studies have shown that inflammatory mediators are known key regulators in retinopathy, but their causal link has been elusive. Although inflammation is often thought to arise from inflammatory cells like macrophages, neutrophils, and resident microglia, retinal neurons have also been reported to contribute to inflammation, through inflammatory signals, which mediate blood vessel growth. Therefore, it is important to explore the detailed mechanisms of neuroinflammation's effects on retinal neovascularization. This review looks to summarize current research on the relationship between retinal angiogenesis and neuroinflammation in retinopathy, as well as the potential effects of neuroinflammation on retinal neovascularization in different animal models.

A thorough green route (which adopts common and nontoxic reactants, and generates no by-product) was developed for the synthesis of AlOOH nanoflakes. AlOOH nanoflakes were synthesized conveniently through hydrothermal treatment of Al 2 O 3 powder in deionized water at 190 °C for 12–24 h, without the use of any extra additive or template. The characterization results from X-ray diffraction, Fourier transformed infrared spectroscopy, energy dispersive X-ray spectroscopy and transmission electron microscopy confirmed the preparation of AlOOH nanoflakes, which were deficient in oxygen. Furthermore, the room temperature photoluminescence properties of the as-synthesized products were tested. It was found that all the as-synthesized products exhibited a strong emission peak centering at around 583 nm upon 291 nm excitation at room temperature, so they had potential application as a photoluminescent material.

Damage to pancreatic β‑cells is closely associated with diabetes. However, the mechanism underlying injury to pancreatic β‑cells remains unclear, although hypoxia is considered as one of the leading causes. Appoptosin is a mitochondrial protein that promotes neuronal apoptosis. Studies conducted on appoptosin thus far have primarily focused on Alzheimer's disease, and have demonstrated that the expression of appoptosin is significantly increased in ischemic‑reperfused rat brains, which indicates its close association with hypoxia. However, the role of appoptosin in pancreatic β‑cells, which are sensitive to hypoxia, remains unknown. Therefore, the current study aimed to investigate the function of appoptosin in pancreatic β‑cells in a hypoxic environment. Cobalt chloride (CoCl2) was used to mimic the hypoxic status of the cells. The results of a terminal deoxynucleotidyl transferase dUTP nick‑end labeling assay demonstrated that CoCl2 promoted apoptosis in MIN6 mouse insulinoma cells, and western blotting and reverse transcription‑quantitative polymerase chain reaction results demonstrated that the activation of appoptosin was induced, promoting mitochondrial damage and caspase 3 activation. Silencing of appoptosin using short hairpin RNA significantly reduced CoCl2‑induced apoptosis in MIN6 cells. In conclusion, CoCl2 increased the expression of appoptosin, which aggravated mitochondrial damage in MIN6 cells. Therefore, inhibiting the expression of appoptosin may benefit pancreatic β-cells survival during islet transplantation.

Type 1 diabetes is caused by destruction of the pancreatic β‑cells and, to date, no cure has been developed. Promoting the survival of pancreatic β‑cells may be beneficial for patients with type 1 diabetes. Puerarin is an estrogen analogue that been demonstrated in previous studies to be able to decreased blood glucose in patients with type 1 diabetes. Similar results were demonstrated in previous studies which additionally demonstrated that puerarin was able to decreased blood glucose in type 1 diabetic mice by protecting pancreatic β‑cells. However, the mechanism underlying the function of puerarin in pancreatic β‑cells remains unclear. Therefore, the present study sought to investigate the detailed function of puerarin in pancreatic β‑cells. In the present study, H2O2 was used to induce apoptosis. It was observed that puerarin significantly decreased H2O2‑induced apoptosis in mouse insulinoma MIN6 cells. It was additionally observed that puerarin decreased the levels of intracellular reactive oxygen species and mitochondrial superoxide in MIN6 cells. The protective effect of puerarin was markedly decreased by 6‑aminonicotinamide, an inhibitor of glucose‑6‑phosphate dehydrogenase (G6PD). In conclusion, the results of the present study suggested that puerarin may increase the activity of G6PD, decreased the level of oxidative stress in MIN6 cells, protect mitochondria and promote MIN6 cell survival. Investigating the mechanism underlying the effect of puerarin in MIN6 cells may provide a novel approach for development of a cure for type 1 diabetes.

Lipopolysaccharide/d-Galactosamine (LPS/d-Gal)-induced acute liver injury is characterized by significant inflammatory responses including TNF-α and interleukin-6 (IL-6) and is a widely applied experimental model for inflammation research. TNF-α is critical in the progression of LPS/d-Gal-induced liver injury. However, the role of IL-6 in this model is still unknown. In the present study, we aim to elucidate the involvement of IL-6 in the pathogenesis of acute liver injury induced by LPS/d-Gal in mice and its underlying mechanism. To induce acute liver injury, LPS (50μg/kg body weight) and d-Gal (400mg/kg body weight) were injected intraperitoneally in the C57BL/6 mice. The vehicle (saline) or a single dose of recombinant IL-6 (200μg/kg body weight) was administered 2h prior to LPS/d-Gal injection. Mice were sacrificed 2h and 6h after LPS/d-Gal injection. The results indicated that IL-6 treatment could protect mice from LPS/d-Gal-induced tissue damage, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) elevation, as well as hepatocyte apoptosis and inflammation. Furthermore, in vitro study showed that IL-6 treatment could significantly suppress LPS-triggered expression of proinflammatory cytokines and chemokines, TNF-α, RANTES and MCP-1 in macrophages while promoting the expression of M2 markers, such as Arg-1 and Mrc-1 in macrophages. Taken together, these findings revealed a novel and unexpected role of IL-6 in ameliorating LPS/d-Gal-induced acute liver injury via regulating inflammatory responses in hepatic macrophages.

MoS 2 nanoflake clusters were synthesized via hydrothermal treatment of an air-stable, easily obtained single-source molecular precursor (molybdenum diethyldithiocarbamate oxide, Mo((C 2 H 5 ) 2 NCS 2 ) 2 O 2 ) in deionized water at 200 °C for 24 h; and orthorhombic phase MoO 3 (α-MoO 3 ) nanoplate clusters were obtained by heating MoS 2 nanoflake clusters in air at 350 °C for 5 h. The obtained products were characterized by X-ray diffraction, X-ray photoelectron spectroscopy, Raman spectroscopy and field emission scanning electronic microscopy. Besides, the comparative synthesis experiment by direct pyrolysis of ammonium peramolybdate suggested that MoS 2 nanoflake clusters might play a template role in the formation of α-MoO 3 nanoplate clusters.

The effects of wheat bran feruloylated oligosaccharides (FOs) on the gut microbiota were studied. Furthermore, xylo-oligosaccharides (XOs) and ferulic acid (FA) as the two major moieties were used to demonstrate the structural influence of FOs on microbiota modulation effects. FOs promoted the phylum Firmicutes and Actinobacteria and decreased the relative abundance of Bacteroidetes and Proteobacteria. FA significantly increased the phylum Bacteroidetes. At the genus level, FOs promoted beneficial microorganism such as Bifidobacterium and Faecalibacterium, and inhibit the growth of disease-related bacteria such as Alistipes, Bilophila, Dorea, Enterobacteriaceae, and Oscillopira. FA significantly increased Bacteroides, Dialister and decreased Coprococcus, Enterobacteriaceae, Megamonas, Oscillospira. In terms of metabolites, FOs and XOs increased the content of short-chain fatty acids (SCFAs) but inhibited the production of branched-chain fatty acids (BCFAs). However, FA inhibited the production of both SCFAs and BCFAs. In conclusion, wheat bran FOs showed the prebiotic effects and further promoted the production of SCFAs due to the combined actions of oligosaccharides and FA moieties. Our findings highlighted that composition and structure should be taken into consideration for selecting FOs as prebiotics.

A sensitive and selective fluorescent probe for histidine has been designed by taking the advantages of the click chemistry reaction (copper(I)-catalyzed azides and alkynes cycloaddition) and the inhibition of copper(II)-induced ascorbate oxidation by histidine. The fluorescence intensity decreases with the increasing of histidine concentration, and the value of F₀/F shows a good linear relationship with the concentration of histidine over the range of 0.5-100 μM with a detection limit of 76 nM, which is lower than those of many other fluorescent sensors. Moreover, the sensor has high specificity for histidine compared to some potential interferents, such as other amino acids and metal ions. In addition, the proposed sensor has been applied to determine histidine in cellular homogenate and ovalbumin samples with satisfactory results. The preferable simplicity, sensitivity and specificity for the detection of histidine indicate that the proposed sensor have potential prospect in environmental and biomedical analysis.

A green hydrothermal method was proposed for the synthesis of nanocrystalline ZnO 2 , using Zn 5 (CO 3 ) 2 (OH) 6 powder and 6 vol% H 2 O 2 aqueous solution as the starting materials. Characterization results from X-ray diffraction, Raman, high resolution transmission electron microscopy and selected area electron diffraction revealed that the products synthesized at 80–120 °C for 6–18 h were pure cubic phase ZnO 2 nanocrystals. Room temperature photoluminescence spectra of the as-synthesized ZnO 2 nanocrystals displayed a wide and strong emission band in the visible region of about 525–570 nm upon laser excitation at 325 nm, which may have originated from their surface state and other crystal defects.

The reactions of SeO 2 with V 2 O 5 or VOSO 4 in the presence of different organic amine yield two novel vanadium selenites with layered structures, formulated as (DABCOH 2 )[(VO 2 )(SeO 3 )] 2 ·1.25H 2 O 1 (DABCO = 1,4-diazabicyclooctane) and (pipeH 2 )[(VO) 2 (C 2 O 4 )(SeO 3 ) 2 ] 2 (pipe = piperazidine). Two compounds are characterized with elemental analysis, FT-IR spectrum, TG-DTA analysis and single-crystal X-ray diffraction analysis. In compound 1 , two symmetry-related VO 6 units share an edge to form a [V 2 O 6 ] cluster. Each [V 2 O 6 ] cluster is bridged by four SeO 3 units to generate a two-dimensional grid structure. In compound 2 , VO 6 units and SeO 3 units share corners to result in a ladder motif. Adjacent chains are interlinked by the oxalate ligands, creating a 2D brick-wall structure, which is firstly observed in V/Se/O system. Diprotonated DABCO and lattice water molecules in 1 and diprotonated piperazidine molecules in 2 are located in the interlayer regions and interact with the framework oxygen atoms via hydrogen bonds, respectively.

A new kind of bismuth film modified electrode to sensitively detect trace metal ions based on incorporating highly conductive ionic liquids 1-butyl-3-methyl-imidazolium hexafluorophosphate (BMIMPF6) in solid matrices at glassy carbon (GC) was investigated. Poly(sodium 4-styrenesulfonate) (PSS), silica, and Nafion were selected as the solid matrices. The electrochemical properties of the mixed films modified GC were evaluated. The electron transfer rate of Fe(CN)(6)(4-)/Fe(CN)(6)(3-) can be effectively improved at the PSS-BMIMPF6 modified GC.

The soldering terminal solderability of component and printed circuit board (PCB) has a strong impact on the formation of solder joint interface. The good solderability of the soldering terminal will result in good interface and high reliability of solder joint. The poor solderability of the soldering terminal will result in undesirable interface of solder joint, poor wetting from macrostructure, many micro cracks at interface from Microstructure, because the solder is hindered during diffusion process. In this paper, the impact of soldering terminal solderability of component and PCB on solder joint interface were illustrated by two experiments. In experiment 1, the through-hole components that were known poor solderability were coated tin by hot dip method, then compared the solderability and the interface quality of the components before and after coating tin. In experiment two, bought new component and PCB, oxidized some components and some PCBs, then tested the solderability of new components and PCBs as well as the oxidized components and PCBs with tester Metronelec ST88, and got the solderability curve and the quantized data of the surface; soldered these new components and oxidized components with new PCBs and oxidized PCBs In combination, got the solder joints with different soldering quality, judged the crack degree and the reliability of the soldering interfaces through combining SEM analysis with quantitative solderability data, and analyzed the relationship between the solderability and the reliability in order to guide the actual production.