Preparation and Photocatalytic Activity of Ag Modified Ti-Doped-Bi 2

Ti doped Bi2O3 (TDB) and Ag ion modified Ti doped Bi2O3 (Ag@TDB) photocatalysts were prepared by framework replacement synthesis method with different Ag loadings (0.05, 0.3, 0.75, and 1.0 mol/L AgNO3). The structural properties of the prepared catalysts were studied by scanning electron microscope (SEM), X-ray diffraction (XRD), BET surface area, and UV/Vis diffuse reflectance (DRS). The XRD spectra of the Ti doped Bi2O3 calcined at 650°C showed the diffraction peaks of a mixture of Bi12TiO20 and Bi4Ti3O12, with bits of mixed crystallite consisting of TiO2 and B2O3. A high blue shift in the range 650–550 nm was detected in the DRS band. This blue shift increased with the decreasing Ag content. The photocatalytic activities of the catalysts were evaluated for the degradation of crystal violet (CV) under UV light irradiation. The results indicated that the degradation rate of CV by using 1.0 mol/L AgNO3 doped bismuth titanate composite photocatalyst (1.0 Ag@TDB) was 1.9 times higher than that by using the bare Ti doped Bi2O3 photocatalyst. The higher activity of Ag@TDB is due to the enhancement of electron-hole pair separation by the electron trapping of silver particles

Enamel remineralization via poly(amido amine) and adhesive resin containing calcium phosphate nanoparticles

Objectives:The objective of this study was to investigate enamel remineralization using salivary statherin pro-tein-inspired poly(amidoamine) dendrimer (SN15-PAMAM) and adhesive containing nanoparticles of amor-phous calcium phosphate (NACP) in a cyclic artificial saliva/demineralizing solution for thefirst time.Methods:The enamel shear bond strengths of NACP adhesives were measured compared to commercial adhesive(Scotchbond Multi-Purpose, 3 M). Adhesive disks containing NACP were tested for calcium (Ca) and phosphorus(P) ions release. Four groups were tested: (1) enamel control, (2) enamel with NACP, (3) enamel with SN15-PAMAM, and (4) enamel with SN15-PAMAM + NACP. The specimens were treated with cyclic artificial saliva/demineralizing solution for 28 days. The remineralized enamel specimens were examined by surface and cross-sectional hardness test.Results:NACP adhesive yielded a similar shear bond strength to commercial control (Scotchbond Multi-Purpose,3 M). NACP adhesive released high levels of Ca and P ions. At 28 days, the enamel hardness of SN15-PAMAM +NACP group was 2.89 ± 0.13 GPa, significantly higher than that of control group (1.46 ± 0.10 GPa) (p< 0.05).SN15-PAMAM + NACP increased the enamel cross-sectional hardness at 28 days; at 25μm, enamel cross-sectional hardness was 90 % higher than that of control group (p< 0.05).Significance:The novel SN15-PAMAM + NACP adhesive method could achieve 90 % higher enamel reminer-alization of the artificial caries than the control under acid challenge for thefirst time. This method is promisingfor use after tooth cavity preparation, or as a coating on enamel with white spot lesions (WSLs) for prevention, toreduce secondary caries, prevent caries procession and protect tooth structures

Oncogenic state and cell identity combinatorially dictate the susceptibility of cells within glioma development hierarchy to IGF1R targeting

Glioblastoma is the most malignant cancer in the brain and currently incurable. It is urgent to identify effective targets for this lethal disease. Inhibition of such targets should suppress the growth of cancer cells and, ideally also precancerous cells for early prevention, but minimally affect their normal counterparts. Using genetic mouse models with neural stem cells (NSCs) or oligodendrocyte precursor cells (OPCs) as the cells‐of‐origin/mutation, it is shown that the susceptibility of cells within the development hierarchy of glioma to the knockout of insulin‐like growth factor I receptor (IGF1R) is determined not only by their oncogenic states, but also by their cell identities/states. Knockout of IGF1R selectively disrupts the growth of mutant and transformed, but not normal OPCs, or NSCs. The desirable outcome of IGF1R knockout on cell growth requires the mutant cells to commit to the OPC identity regardless of its development hierarchical status. At the molecular level, oncogenic mutations reprogram the cellular network of OPCs and force them to depend more on IGF1R for their growth. A new‐generation brain‐penetrable, orally available IGF1R inhibitor harnessing tumor OPCs in the brain is also developed. The findings reveal the cellular window of IGF1R targeting and establish IGF1R as an effective target for the prevention and treatment of glioblastoma

Nicotine aggravates vascular adiponectin resistance via ubiquitin-mediated adiponectin receptor degradation in diabetic Apolipoprotein E knockout mouse

There is limited and discordant evidence on the role of nicotine in diabetic vascular disease. Exacerbated endothelial cell dysregulation in smokers with diabetes is associated with the disrupted adipose function. Adipokines possess vascular protective, anti-inflammatory, and anti-diabetic properties. However, whether and how nicotine primes and aggravates diabetic vascular disorders remain uncertain. In this study, we evaluated the alteration of adiponectin (APN) level in high-fat diet (HFD) mice with nicotine (NIC) administration. The vascular pathophysiological response was evaluated with vascular ring assay. Confocal and co-immunoprecipitation analysis were applied to identify the signal interaction and transduction. These results indicated that the circulating APN level in nicotine-administrated diabetic Apolipoprotein E-deficient (ApoE−/−) mice was elevated in advance of 2 weeks of diabetic ApoE−/− mice. NIC and NIC addition in HFD groups (NIC + HFD) reduced the vascular relaxation and signaling response to APN at 6 weeks. Mechanistically, APN receptor 1 (AdipoR1) level was decreased in NIC and further significantly reduced in NIC + HFD group at 6 weeks, while elevated suppressor of cytokine signaling 3 (SOCS3) expression was induced by NIC and further augmented in NIC + HFD group. Additionally, nicotine provoked SOCS3, degraded AdipoR1, and attenuated APN-activated ERK1/2 in the presence of high glucose and high lipid (HG/HL) in human umbilical vein endothelial cells (HUVECs). MG132 (proteasome inhibitor) administration manifested that AdipoR1 was ubiquitinated, while inhibited SOCS3 rescued the reduced AdipoR1. In summary, this study demonstrated for the first time that nicotine primed vascular APN resistance via SOCS3-mediated degradation of ubiquitinated AdipoR1, accelerating diabetic endothelial dysfunction. This discovery provides a potential therapeutic target for preventing nicotine-accelerated diabetic vascular dysfunction

Metagenomic Analysis of Bacteria, Fungi, Bacteriophages, and Helminths in the Gut of Giant Pandas

To obtain full details of gut microbiota, including bacteria, fungi, bacteriophages, and helminths, in giant pandas (GPs), we created a comprehensive microbial genome database and used metagenomic sequences to align against the database. We delineated a detailed and different gut microbiota structures of GPs. A total of 680 species of bacteria, 198 fungi, 185 bacteriophages, and 45 helminths were found. Compared with 16S rRNA sequencing, the dominant bacterium phyla not only included Proteobacteria, Firmicutes, Bacteroidetes, and Actinobacteria but also Cyanobacteria and other eight phyla. Aside from Ascomycota, Basidiomycota, and Glomeromycota, Mucoromycota, and Microsporidia were the dominant fungi phyla. The bacteriophages were predominantly dsDNA Myoviridae, Siphoviridae, Podoviridae, ssDNA Inoviridae, and Microviridae. For helminths, phylum Nematoda was the dominant. In addition to previously described parasites, another 44 species of helminths were found in GPs. Also, differences in abundance of microbiota were found between the captive, semiwild, and wild GPs. A total of 1,739 genes encoding cellulase, β-glucosidase, and cellulose β-1,4-cellobiosidase were responsible for the metabolism of cellulose, and 128,707 putative glycoside hydrolase genes were found in bacteria/fungi. Taken together, the results indicated not only bacteria but also fungi, bacteriophages, and helminths were diverse in gut of giant pandas, which provided basis for the further identification of role of gut microbiota. Besides, metagenomics revealed that the bacteria/fungi in gut of GPs harbor the ability of cellulose and hemicellulose degradation

Acute benzo[a]pyrene treatment causes different antioxidant response and DNA damage in liver, lung, brain, stomach and kidney

Acute effects of oxidative damage induced by benzo[a]pyrene (B[a]P) on various organs are still not clear. In this study, we investigated oxidative stress and DNA damage in liver, lung, stomach, brain and kidney of ICR male mice induced by acute B[a]P treatment. B[a]P treatment led to a significant decrease at the different doses in body weight. For the variations of superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), glutathione (GSH) and GSH/GSSG, significant increases were observed at 24 h, then decreased till 72 h after B[a]P injection. The increase percent indicated in a dose- dependent decrease manner. However, glutathione peroxidase (GPx), GSSG and MDA were significantly increased in a time- and dose-dependent increase manner. DNA damage showed the significant and top levels at 24 h, and increased in proportion to the doses of B[a]P treatment. The total induction could be indicated by the variation of MDA at 24 h after B[a]P injection and showed the following order of predominance: lung > liver > kidney = stomach > brain. This was further certificated by histopathological changes in the examined organs. Additionally, the levels of serum glutamic-oxaloacetic transaminase (GOT), glutamic-pyruvic transaminase (GPT), and blood urea nitrogen (UN), creatinine were also significantly increased at 24 h after B[a]P injection. These findings suggested the disturbance of antioxidant responses and aggravation of DNA damages, and the different responses on various organs induced by acute B[a]P treatment in organism

Development of Improved Process with Treatment of Cellulase for Isolation of Ampelopsin from Dried Fruits of Ampelopsis grossedentata

The commercial method for isolation of ampelopsin, one of the most common flavonoids isolated from the plant species Ampelopsis grossedentata, is a simple hydrothermal extraction at high temperature. To develop an improved process to isolate ampelopsin, the effects of treatment of cellulase on hydrolysis of the dried fruit of A. grossedentata were investigated. The treatment of cellulase was found to decrease the temperature and time for hydrolysis of the dried fruit of A. grossedentata. The conditions of the filter press and continuous flow centrifuge for removal of insoluble materials from the hydrolysate of the dried fruit of A. grossedentata were optimized. The recovery yield of ampelopsin from the dried fruits of A. grossedentata was 39.4%, as determined by HPLC chromatographic analysis. A safe and economical process at low temperature with treatment of cellulase for the isolation of ampelopsin was developed in this study