Search

An improved method for the separation and purification of rubropunctatin from red yeast glutinous rice was developed. In this method, silica gel column chromatography and thin layer chromatography were used to separate the Monascus pigments. Pure methanol and a mixture of ethyl acetate and methanol (13:7, v/v) were selected as the eluent and running solvent, respectively. When compared with previously reported methods, the developed method required fewer types of solvents, and could be suitable for large-scale laboratory production. The extracted pigment was analysed by ultra-high performance liquid chromatography quadrupole time of flight mass spectrometry (UPLC-Q-TOF-MS) and nuclear magnetic resonance (NMR) (1H NMR, 13C NMR). Structural analysis revealed a molecular mass of 353.2 m/z [M-H]-, and a structure including an azaphilone body with two side chains. This structure was consistent with that reported for rubropunctatin. Therefore, the improved purification method reported herein could efficiently be used for the extraction of rubropunctatin from red yeast glutinous rice. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Some studies have confirmed that long non-coding ribonucleic acids (lncRNAs) played a vital role in the pathophysiology of various diseases, especially in oncogenesis and progression of tumors. Dysexpressed lncRNAs regulate different cellular processes, including proliferation, invasion, and apoptosis. The aim of this study was to explore the clinical significance and function of lncRNA MIR4435-2HG in colorectal cancer. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to detect the expression of lncRNA MIR4435-2HG. The Kaplan-Meier method was used to evaluate the overall survival and disease-free survival of patients with colorectal cancer. The cell proliferation was measured by Methyl thiazolyl tetrazolium (MTT) assay. The cell apoptotic rate was measured via flow cytometry method. RESULTS: LncRNA MIR4435-2HG is a novel cancer-related lncRNA that was recently found to exhibit high expression in colorectal cancer. The dysregulation of lncRNA miR4435- 2HG was significantly related to the tumor size (p<0.001), lymph node metastasis (p<0.001), and tumor node metastasis (TNM) staging (p=0.022). The patients with higher expression of lncRNA miR4435-2HG showed worse prognosis than those with low expression of lncRNA miR4435- 2HG group. Besides, the downregulated lncRNA miR4435-2HG expression could repress cell proliferation and enhance cell apoptosis. CONCLUSIONS: LncRNA MIR4435-2HG functions as an oncogene that promotes colorectal cancer progression, and likely represents a biomarker or therapeutic target of colorectal cancer. [ABSTRACT FROM AUTHOR]

Directional luminescence from coupled quantum states of individual ZnSe quantum dots (QDs) in ultrathin single quantum well structure, ZnS/(ZnSe)[sub 1]/ZnS has been observed. The cause of the formation of the states is the Coulomb interaction between holes in the ZnSe QDs. Despite the random distribution of the sizes and positions of the QDs, the coherent length of the coupled quantum states reaches about 360 nm, which can be estimated directly through the emission angle dependence of the directional luminescence. [ABSTRACT FROM AUTHOR]

The optical properties and band alignment of ZnSe/ZnMgBeSe heterostructures are investigated. Two sets of ZnSe/ZnMgBeSe multi-quantum-well structures that consist of five or three wells with different well thicknesses and 100-nm-thick ZnMgBeSe barrier layers are grown on GaAs (100) substrates by molecular beam epitaxy. Low-temperature photoluminescence spectra show dominant sharp excitonic emission whose peak position systematically shifts to the higher energy side with decreasing the well thickness. Photoluminescence excitation spectra show optical transitions between excited quantum levels in addition to the ground levels. The standard analysis based on the effective-mass approximation gives the valence band offset of ΔE[sub υ]=(0.4±0.1)ΔE[sub g]. This is consistent with calculated values based on Harrison’s linear combination of atomic orbitals theory. © 2002 American Institute of Physics. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To elucidate the influence of microRNA-125a on the biological behaviors of acute myeloid leukemia (AML) cells. MATERIALS AND METHODS: MicroRNA- 125a mimic and negative control (NC) were constructed and transfected into AML cell line HL60, respectively. Cell viability of HL60 cells transfected with microRNA-125a mimic or NC was determined by MTT (3-(4,5-dimethylthiazol- 2-yl)-2,5-diphenyl tetrazolium bromide) assay. Regulatory effects of microRNA-125a on enzyme activities of B-cell lymphoma-2 (Bcl-2), Bcl-xl, caspase-3, and caspase-9 in HL60 cells were quantified by a spectrophotometry. Changes in apoptosis and invasion of HL60 cells overexpressing microRNA-125a were detected by flow cytometry and transwell assay, respectively. Protein levels of cell cycle genes (cyclin B, cdc-2, mdm-2), pro-apoptotic gene p53 and anti- apoptotic gene Bcl-2 in HL60 cells transfected with microRNA-125a mimic or NC were assessed by Western blot. Finally, the mRNA levels of Bax, caspase-8, nuclear factor-κB (NF-κB), and c-myc in HL60 cells with microRNA-125a overexpression were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). RESULTS: MicroRNA-125a expression remarkably increased by transfection of microRNA- 125a mimic into HL60 cells, suggesting its sufficient transfection efficacy. MTT assay revealed an inhibited viability after microRNA-125a overexpression. Transfection of microRNA-125a mimic markedly enhanced enzyme activities of caspase-3 and caspase-9, but reduced activities of Bcl-2 and Bcl-xl in HL60 cells than controls (p<0.05). Moreover, microRNA-125a overexpression elevated apoptotic rate as FCM data indicated. Transwell assay demonstrated a decrease in the invasive rate of HL60 cells overexpressing microRNA-125a. Western blot analyses revealed that cell cycle genes all downregulated by transfection of microRNA-125a mimic in HL60 cells. The protein level of p53 upregulated and Bcl-2 downregulated in HL60 cells overexpressing microRNA-125a (p<0.05). Furthermore, mRNA levels of pro-apoptotic genes Bax and caspase-8 were enhanced after microRNA-125a overexpression, while mRNA levels of NF-κB and c-myc were reduced (p<0.05). CONCLUSIONS: MicroRNA-125a inhibits proliferative and invasive potentials, arrests the cell cycle in the G2/M phase of AML cells by regulating the NF-κB pathway. [ABSTRACT FROM AUTHOR]