Cooperative Catalysis Mechanism of Brønsted and Lewis Acids from Al(OTf) with Methanol for β-Cellobiose-to-Fructose Conversion: An Experimental and Theoretical Study.

Al-containing catalysts, e.g., Al(OTf), show good catalytic performance toward the conversion of cellulose to fructose in methanol solution.

Coordination of sorbitol to Ga(OTf) in the liquid phase: an experimental and theoretical study.

In a solution of sorbitol (SBT) and Ga(OTf) compounds, the coordination of sorbitol (SBT) to [Ga(OTf)] ( = 0-3) has been investigated, using both ESI-MS spectra and density functional theory (DFT) calculations at the M06/6-311++g(d,p), aug-cc-pvtz level using a polarized continuum model (PCM-SMD). In sorbitol solution, the most stable conformer of sorbitol includes three intramolecular H-bonds, , O2H⋯O4, O4H⋯O6, and O5H⋯O3. Through ESI-MS spectra, in a tetrahydrofuran solution of both SBT and Ga(OTf) compounds, five main species are observed, , [Ga(SBT)], [Ga(OTf)], [Ga(SBT)], [Ga(OTf)(SBT)], and [Ga(OTf)(SBT)].

Molecular mechanism comparison of decarbonylation with deoxygenation and hydrogenation of 5-hydroxymethylfurfural catalyzed by palladium acetate.

The selective removal of oxygen from 5-hydroxymethylfurfural (HMF) is challenging for the effective utilization of biomass. The catalytic mechanisms of palladium acetate toward the conversion of HMF to furfuryl alcohol (FFA), 5-methylfurfural (5-MF) and 2,5-dihydroxymethyl furan (DHMF) have been theoretically investigated. The decarbonylation of HMF to FFA includes (i) migratory extrusion, (ii) metal-acetate-co-assisted deprotonation, (iii) decarbonylation, (iv) metal-assisted deprotonation, and (v) migratory extrusion and catalyst regeneration.

In vitro effects of reprogramming factors on the expressions of pluripotent genes and CD gene in human acute promyelocytic leukemia HL-60 cells.

Objective: Our study aims to explore the in vitro effects of reprogramming factors on the expressions of pluripotent genes and CD gene in HL-60 cells.

Methods: According to the construction of lentiviral vector LV-OSCK of reprogramming factors (Oct-4, Sox2, Klf4, c-Myc), 293T cells were transfected to detect virus titer. The endogenous pluripotent genes (Oct4, SOX2, c-Myc and Klf4) and CD mRNA and protein expressions were detected by AP staining, immunofluorescence staining, qRT-PCR and flow cytometry.

The Construction and Identification of Induced Pluripotent Stem Cells Derived from Acute Myelogenous Leukemia Cells.

Objective: The present study aimed to establish an induced pluripotent stem cell (iPSC) line from acute myelogenous leukemia (AML) cells in vitro and identify their biological characteristics.

Methods: Cells from the AML-infiltrated skin from an M6 patient were infected with a lentivirus carrying OCT4, SOX2, KLF4 and C-MYC to induce iPSCs. The characteristics of the iPSCs were confirmed by alkaline phosphatase (ALP) staining.

[Reversing effects of emodin on multidrug resistance in resistant HL-60/ADR cells].

This study was aimed to investigate the reversing effects of emodin on multidrug resistance (MDR) in resistant HL-60/ADR cells, and to explore the underlying mechanisms. The MTT assay was used to assess the chemoresistance of HL-60/ADR cells to emodin and 8 chemotherapeutic agents commonly used in clinic. The reversal effects of emodin on MDR of HL-60/ADR cells were also evaluated by MTT method.

[Expression of eIF4E in patients with leukemia and its clinical significance].

This study was aimed to compare the expression level of eIF4E in patients with leukemia and normal controls, and to explore its role in leukemogenesis. White blood cells were collected in 76 leukemia patients and 10 healthy volunteers. The mRNA and protein expressions of eIF4E were detected by QT-PCR and Western blot in 39 cases of acute myeloid leukemia (AML), 15 cases of chronic myeloid leukemia (CML), 22 cases of acute lymphocytic leukemia (ALL) and 10 healthy volunteers as normal controls.

[Effects of emodin on the proliferation inhibition and apoptosis induction in HL-60 cells and the involvement of c-myc gene].

Objective: To investigate the effects of emodin on apoptosis induction and proliferation inhibition in human apoptosis and on c-myc protein and mRNA expression in human myeloid leukemia cell line HL-60 cells.

Methods: HL-60 cells were exposed to emodin at different dosages. Growth inhibition was detected by MTT assay and colony formation assay, and cell apoptosis by flow cytometry, TUNEL labeling method, DNA fragmentation and MitoCapture apoptosis detection.