Coproduction of Furfural, Phenolated Lignin and Fermentable Sugars from Bamboo with One-Pot Fractionation Using Phenol-Acidic 1,4-Dioxane

A one-pot fractionation method of Moso bamboo into hemicellulose, lignin, and cellulose streams was used to produce furfural, phenolated lignin, and fermentable sugars in the acidic 1,4-dioxane system. Xylan was depolymerized to furfural at a yield of 93.81% of the theoretical value; however, the prolonged processing time (5 h) led to a high removal ratio of glucan (37.21%) in the absence of phenol. The optimum moderate condition (80 °C for 2 h with 2.5% phenol) was determined through the high fractionation efficiency. Consequently, 77.28% of xylan and 84.83% of lignin were removed and presented in the hydrolysate, while 91.08% of glucan was reserved in the solid portion. The formation of furfural from xylan remained high, with a yield of 92.92%. The extracted lignin was phenolated with an increasing content of phenolic hydroxyl. The fractionated lignin yield was 51.88%, which suggested this could be a low-cost raw material to product the activated carbon fiber precursor. The delignified pulp was subjected to enzymatic hydrolysis and the glucose yield reached up to 99.03% of the theoretical

The facet selectivity of inorganic ions on silver nanocrystals in etching reactions

The facet selectivity of the halide ions and chlorauric acid for several shaped silver nanocrystals is presented in this paper. Two inorganic ions show different representations when they are used for etching silver nanocrystals in the self-sacrificial template reaction. The morphological changes of the silver nanocrystals indicate that the halide ions prefer to etch the (110) facets of silver nanocrystals, while in the chlorauric acid etching reaction, gold first modifies the (110) facets and then lets chlorauric acid etch the (111) facets instead. The selective facet etching on individual nanoparticles in the solution phase has crucial significance in the control-synthesis of nanocrystals and the facet asymmetric reaction.<br /

Tumor necrosis factor-α sensitizes breast cancer cells to natural products with proteasome-inhibitory activity leading to apoptosis.

The inflammatory microenvironment plays an important role in the process of tumor development. Tumor necrosis factor-α (TNF-α), a key pro-inflammatory cytokine, has a significant role in this process. Natural medicinal products such as Withaferin A (WA) and Celastrol (Cel) have shown anti-cancer and anti-inflammatory properties that can be attributed to multiple mechanisms including, but not limited to, apoptosis induction due to the inhibition of proteasomal activities. This study aimed to investigate the effects of TNF-α in combination with WA or Cel in vitro in MDA-MB-231 breast cancer cells. TNF-α, when combined with WA or Cel, activated caspase-3 and -9 and downregulated XIAP in a dose-dependent manner, leading to induction of apoptosis in MDA-MB-231 breast cancer cells. The combination also caused accumulation of the proteasomal target protein IκBα, resulting in inhibition of the nuclear translocation of nuclear factor-κB (NF-κB). Taken together, these results suggest that TNF-α could sensitize breast cancer cells MDA-MB-231 to WA and Cel, at least in part, through inhibiting the activation of NF-κB signaling, leading to XIAP inhibition with subsequent upregulation of caspase-3 and -9 activities. Thus, the anti-cancer activities of TNF-α are enhanced when combined with the natural proteasome inhibitors, WA or Cel

One-Pot Synthesized Aptamer-Functionalized CdTe:Zn²⁺ Quantum Dots for Tumor-Targeted Fluorescence Imaging in Vitro and in Vivo

High quality and facile DNA functionalized quantum dots (QDs) as efficient fluorescence nanomaterials are of great significance for bioimaging both in vitro and in vivo applications. Herein, we offer a strategy to synthesize DNA-functionalized Zn²⁺ doped CdTe QDs (DNA-QDs) through a facile one-pot hydrothermal route. DNA is directly attached to the surface of QDs. The as-prepared QDs exhibit small size (3.85 ± 0.53 nm), high quantum yield (up to 80.5%), and excellent photostability. In addition, the toxicity of QDs has dropped considerably because of the Zn-doping and the existence of DNA. Furthermore, DNA has been designed as an aptamer specific for mucin 1 overexpressed in many cancer cells including lung adenocarcinoma. The aptamer-functionalized Zn²⁺ doped CdTe QDs (aptamer-QDs) have been successfully applied in active tumor-targeted imaging in vitro and in vivo. A universal design of DNA for synthesis of Zn²⁺ doped CdTe QDs could be extended to other target sequences. Owing to the abilities of specific recognition and the simple synthesis route, the applications of QDs will potentially be extended to biosensing and bioimaging

WA and Cel sensitize MDA-MB-231 cells to TNF-α resulting in inhibition of cell proliferation.

<p>(A) Concentration dependent effect of WA or Cel with or without TNF-α on cell viability. MDA-MB-231 cells were treated with different concentrations of WA (upper) or Cel (lower) with or without TNF-α (10 ng/ml) for 48 hours, followed by measurement of cell viability by MTT assay. IC₅₀ was calculated by Origin. (B) Colony formation assays of cells treated with WA or Cel with or without TNF-α. WA (left) or Cel (right) at shown concentrations with or without TNF-α (10 ng/ml) were added to the cells for 24 hours. The medium was subsequently removed and the cells were maintained in culture for a further 10 days. (C) Scratch wound-healing assay for cells treated with WA or Cel with or without TNF-α at shown concentrations. Photographs were taken at 24 hours after treatment and scratching of the well. (D) Colony forming efficiency was calculated. (E) Actual migration speed was calculated by Image-Pro plus. Data are shown as mean ± SD of three experiments. (*P<0.05, versus the untreated group. #P<0.05, WA/Cel treated versus WA/Cel+TNF-α).</p

Kinetic and dose effects of TNF plus WA/Cel on cellular proteasome activity in MDA-MB-231 cells.

<p>Cells were treated with TNF-α (10 ng/ml) or TNF-α (10 ng/ml) plus WA or Cel for the indicated times and doses, followed by measurement of the proteasomal CT-like activity using Z-GGL-AMC or Western blotting for ubiquitinated proteins and IκBα. (A) Kinetic effects of TNF-α plus WA on CT-like activity, ubiquitinated proteins and IκBα. Cells were treated with WA (2.5 µM) with or without TNF-α for the indicated times. (B) Kinetic effects of TNF-α plus Cel on CT-like activity, ubiquitinated proteins and IκBα. Cells were treated with Cel (1 µM) with or without TNF-α for the indicated times. (C) Dose effects of TNF-α plus WA on proteasomal activity, ubiquitinated proteins and IκBα. Cells were treated with the indicated doses of WA with or without TNF-α for 24 hours. (D) Dose effects of TNF-α plus Cel on proteasomal activity, ubiquitinated proteins and IκBα. Cells were treated with the indicated doses Cel with or without TNF-α for 24 hours. Data are shown as mean ± SD of three experiments. (*<i>P</i><0.05, as compared with the untreated control. #<i>P</i><0.05, WA/Cel treated versus WA/Cel+TNF-α).</p

WA or Cel sensitize MDA-MB-231 cells to TNF-α-induced apoptosis.

<p>(A, B) Cells were treated with different concentrations of WA or Cel with (right) or without (left) TNF-α (10 ng/ml) for 48 hours, followed by measurement of cell viability by flow cytometry. (C) Cell death inducing abilities of WA and TNF-α or Cel and TNF-α combination in a dose responsive manner. Cells were treated with different concentrations of WA (upper) or Cel (lower) as shown with or without TNF-α (10 ng/ml) for 24 hours, followed by detection of PARP by Western blotting. Data are shown as mean ±SD of three experiments. (*<i>P</i><0.05, as compared with the untreated control. #<i>P</i><0.05, WA/Cel treated versus WA/Cel+TNF-α).</p

Inhibition of NF-κB target gene expression by WA/Cel and small interfering RNA.

<p>(A) MDA-MB-231 cells were transfected with <i>si</i>RNA against NF-κBp65 for 6 hours. As a negative control, cells were transfected with the same amount of non targeting control -<i>si</i>RNA. Following transfection, cells were treated with TNF-α (10 ng/ml) for 24 hours. Cells that were not transfected were treated with TNF-α (10 ng/ml) plus WA (5 µM) or Cel (2.5 µM) for 24 hours. The mRNA levels of NF-κB-p65, XIAP and cIAP1/2 were detected by RT-qPCR. (B) MDA-MB-231 cells were transfected with <i>si</i>RNA against NF-κBp65 for 6 hours. The negative control was treated with the same amount of vector-<i>si</i>RNA. Following transfection, cells were treated by TNF-α (10 ng/ml) for 48 hours. Cells that were not transfected were treated with TNF-α (10 ng/ml) plus WA (5 µM) or Cel (2.5 µM) for 48 hours. The levels of NF-κBp65, XIAP and cIAP1/2 proteins were detected by Western blotting. Data are shown as mean ± SD of three experiments.</p