Search

A three dimensional porous carbon nanomembrane (CNM), silica-supported CNM (SS-CNM), is developed by formation of a self-assembled monolayer of an enediyne compound on the surface of mesoporous silica (SBA-15) followed by Bergman cyclization and carbonization. The SS-CNM is applied as a conductive support for the electroactive material Co3O4 to fabricate advanced supercapacitors. A large fraction of Co3O4 clusters (66% of total weight) are impregnated in the SS-CNM host to form regularly packed nanorods with diameters of 7 nm. The specific capacitance of the supercapacitor electrode material reaches 1086 F g−1 (1645 F g−1 based on Co3O4) with aqueous electrolyte. This extraordinary high performance of the electrode material is attributed to the unique pore structure of the SS-CNM support that enhances the use of active material and shortens the transport path of ions and electrons.

Group-selective molecularly imprinted polymers (MIPs) were synthesized from three kinds of sulfonamides (SAs) and three different functional monomers, with those employing sulfamerazine (SMR) and 2-vinylpyridine (2-Vpy) found to be optimal. The BET test, static adsorption and solid-phase extraction (SPE) recovery indicate that the MIPs exhibit strong affinity toward SAs in aqueous solution. Therefore they were used for the quantitative analysis of five SAs in wastewater from treatment plants by off-line SPE coupled to reversed-phase HPLC/DAD. The recoveries and relative standard deviation (RSD) of the molecularly imprinted solid-phase extraction (MISPE) method are 84.1–98.6% and 1.5 to 7.4% in wastewater. The limit of detection (LOD) and the enrichment factor (EF) for SAs were 4.09–19.29 ng L−1 and 411–506 respectively. Five SAs analytes were detected in influents, with residues still remaining in effluents in the range of 29.30–1389.80 ng L−1.

Case-based reasoning is one of the most preferred method for problem solving and decision making in complex and dynamically changing situations. Case-based reasoning solves problems by relating some previously solved problems or experiences to a current, unsolved problem in a way that facilitates the search for an acceptable solution. In this paper we propose a computational case-based reasoning model, and investigate its feasibility to decision support. A performance comparison among two computational models, including ours, and a symbolic model is also conducted. We view our model not as a replacement technology, but rather as a complementary technology to the symbolic approaches for the purpose of supporting unstructured-oriented decisions. >

Background: Type II diabetes and obesity are important risk factors for post-menopausal luminal A (LA) and triple negative (TN) pre-menopausal breast cancers, particularly in African American (AA) and Hispanic women. Breast cancer patients with these chronic metabolic diseases also have a worse prognosis, independent of other factors. We have published that metformin inhibits cell growth (S phase arrest) and induces apoptosis, only in TN cell lines in vivo and in vitro. It is less active, growth inhibitory (G1 arrest) and does not induce apoptosis in other breast cancer cell subtypes (Cell Cycle, 2009).Methods: We investigated the effects of glucose as a mitogen at physiologic (5mM), metabolic syndrome (7mM) or diabetic levels (10mM), with or without insulin (100 ng/ml) or leptin (100 ng/ml) using cell lines representing all molecular subtypes of breast cancer. Metformin was then used in combination with the above, to determine whether it would block the mitogenic or signaling effects of supraphysiological glucose, insulin or leptin.Results: The LA (MCF-7) and 2 of 5 TN cell lines (derived from AA patients; HCC 1806 and MDA 468) showed the most cell growth in response to glucose >5mM (75% for MCF-7, 30-50% for AA TN lines). Three TN cell lines from Caucasians (MDA231, HCC1937, BT20), the HER2 (SKBR3) and luminal B (BT-474) cells showed less growth induction with glucose >5mM. In TN lines only, glucose associated mitogenesis was associated with increased EGFR, pEGFR, IGF1R, pIGF1R, AKT and pAKT and decreases in AMPK, pAMPK, p38, IRS2, and the cyclins D1, E and A in a dose dependent manner. Metformin abrogated glucose induced cell growth and the aforementioned protein expression/phosphorylation changes involving EGFR, IGF1R, and AKT, increased AMPK and pAMPK and induced a profound reduction in Cyclin D1 across all glucose concentrations in TN cell lines from AA women. It reduced but did not eliminate glucose associated mitogenesis in the TN cell lines from Caucasian patients. Metformin had a more variable effect on cell lines of other molecular subtypes grown under high glucose conditions. The 5 TN breast cancer cell lines were uniformly resistant to both leptin and insulin associated mitogenesis, across a wide range of glucose concentrations. In contrast, both leptin and insulin significantly promoted LA breast cancer cell growth. These effects were resistant to metformin treatment. Leptin and insulin had the least growth promoting effects on HER2 breast cancer cell lines, whereas they induced modest growth induction in LB cell lines.Conclusions: All TN cell lines showed significant mitogenesis in response to glucose >5mM, whereas they were uniformly resistant to both leptin and insulin. The glucose associated mitogenesis was more pronounced in lines derived from AA patients, as were the anti-mitgenic effects of metformin. LA cells showed marked growth induction by glucose, leptin and insulin, whereas HER2 cell lines showed general resistance to all of these factors. These data suggest that metabolic and hormonal shifts with obesity and diabetes, as well as metformin response vary by the molecular subtype of breast cancer cells and ethnicity. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 5154.

In the title compound, C(14)H(12)N(2)O(6), the half mol-ecule in the asymmetric unit of the cell is completed by a crystallographic twofold rotation axis, and the two benzene rings of the complete mol-ecule make a dihedral angle of 60.5 (3)°. Furthermore, inter-molecular weak C-H⋯O hydrogen bonds link adjacent mol-ecules, forming a two-dimensional sheet. These sheets are stablized by face-to-face weak π-π contacts [centroid-centroid distance = 3.682 (1) Å] between the nearly parallel [dihedral angle = 0.12 (7)°] benzene rings of the neighboring mol-ecules, resulting in a three-dimensional network.

α-Phenylthio acylmethylene triphenylarsoranes, the first stable α-thiyl arsonium ylides, are prepared by phenylsulfenylation–transylidation reaction of the corresponding acylmethylene triphenylarsoranes with phenylsulfenyl chloride; Wittig reactions are carried out under mild reaction conditions on the arsonium ylides to provide α-phenylthio-α,β-unsaturated ketones.

In the axially chiral title compound, C(14)H(9)N(5)O(12), the dihedral angle between the two benzene rings is 86.0 (8)°. In the crystal structure, the mol-ecules display a two-dimensional framework formed by weak inter-molecular C-H⋯O hydrogen bonds.

The title compound, [Ag(C3H4N2)2]2(C10H6O6S2), exists in the form of isolated cations and anions with electrostatic inter­action between them. The Ag atom is two-coordinated by the N atoms of two crystallographically independent imidazole mol­ecules. The naphthalene-1,5-disulfonate anion is located on a crystallographic center of symmetry. The cations and anions are connected through inter­molecular N—H⋯O hydrogen bonds.

In the molecule of the title compound, C14H16N2O3, the dihedral angle between the pyridyl rings is 87.74 (3)°. In the crystal structure, intermolecular C—H...O hydrogen bonds link the molecules into infinite zigzag chains.

AIM: To explore the antitumor bioactivity of adenovirus-mediated mutant type p27kip1 gene in a colorectal cancer cell line SW480. METHODS: We constructed recombinant adenovirus vector expressing a mutant type p27kip1 gene (ad-p27mt), with mutation of Thr-187/Pro-188 (ACGCCC) to Met-187/Ile-188 (ATGATC), and transduced into SW480 cells. Then we detected expression of p27, Bcl-2 and Bax protein in the transductants by Western blotting, cell cycle of transductants by a digital flow cytometric system, migrating potential with Boyden Chamber and SW480 tumor cell growth inhibition in vitro and in vivo. RESULTS: We found that a recombinant adenovirus vector of expressing ad-p27mt, with mutation of Thr-187/Pro-188 (ACGCCC) to Met-187/Ile-188 (ATGATC) has potent inhibition of SW480 tumor cell growth in vitro and in vivo. Furthermore, ad-p27mt induced cell apoptosis via regulating bax and bcl-2 expressions, and G1/S arrest in SW480 cells and inhibited cell migration. CONCLUSION: ad-p27mt has a strong anti-tumor bioactivity and has the potential to develop into new therapeutic agents for colorectal cancer.

To examine the expression of nuclear factor kappaB (NF-kappaB) and its target genes in intestinal metaplasia (IM), dysplasia (DYS) and gastric carcinoma (GC) infected with Helicobacter pylori (H pylori) and to investigate the mechanism underlying H pylori cytotoxin associated gene A (cag A) infection leading to gastric adenocarcinoma.Expressions of NF-kappaB/p65 and its target genes: c-myc, cyclinD1 and bcl-xl were immunohistochemically examined in 289 cases of gastric biopsy and resection specimens from patients with IM, DYS and GC infected with H pylori. H pylori in the above mentioned tissues was detected by Warthin-Starry stain and rapid urease tests. IgG antibody to cagA in sera of the patients was measured by ELISA.The positive rates of NF-kappaB/p65 were significantly higher in groups with cagA of IMI-II(28/33), IM III(48/52), DYSI(27/31), DYS II-III(28/32), GC(35/40) than in groups without cagA of IMI-II(4/17), IMIII(3/20), DYSI(3/20), DYSII-III(6/21), GC(10/23). The expressions of c-myc, cyclinD1, and bcl-xl were significantly higher in groups with cagA of IM III(47/52, 49/52, 46/52), DYSII-III(29/32, 26/32, 25/32) than in groups without cagA of IM III(8/20, 7/20, 5/20), DYSII-III(10/21, 8/21, 3/21), which were in conformity with the expression of NF-kappaB in IM III, and DYSII-III. A significantly higher expression level of NF-kappaB/p65, c-myc, cyclinD1 and bcl-xl was detected in intestinal type GC(27/28, 18/28, 22/28, 24/28) than in diffuse type GC(8/12, 3/12, 3/12, 6/12), respectively.There may be two different molecular mechanisms in the occurrence of intestinal and diffuse type gastric carcinomas. Intestinal type gastric carcinoma is strongly associated with high expression of c-myc, cyclinD1 and bcl-xl through NF-kappaB/p65 activated by H pylori cagA. Inhibiting the activity of NF-kappaB is an effective and promising way to prevent intestinal type gastric carcinoma.

AIM: TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) has been reported to specifically induce apoptosis of cancer cells although only a small percentage of cell lines were sensitive to it. Cell lines not responding to TRAIL in vitro were said to be more prone to apoptosis when TRAIL was combined with another anticancer agent. Generally, factors affecting drug-sensitivity involve many apoptosis-related proteins, including p53. The expression of wild-type p53 gene was proposed as an important premise for tumor cells responding to chemotherapy. The present study was to investigate the cell killing action of TRAIL on colon cancer cell line SW480, its synergistic effect with doxorubicin, and the possible mechanisms. METHODS: SW480 cells were cultured in the regular condition and incubated with different levels of agents. Morphologic changes in these cells after treatment were observed under phase-contrast microscope and cytotoxicity by TRAIL alone and in combination with doxorubicin was quantified by a 1-day microculture tetrazolium dye (MTT) assay. In addition, flow cytometry assay (FCM) and transmission electron microscopy were used to detect apoptosis among these cells. Variation of p53 protein level among different groups according to concentrations of agents was measured by Western blot assay. RESULTS: (1) SW480 cells were not sensitive to TRAIL, with IC50 > 1 mg•l-1 and dose-independent cytotoxicity. (2) SW480 cells were sensitive to doxorubicin at a certain degree, with dose-dependent cytotoxicity and IC50 = 65.25 ± 3.48 μmol•l-1. (3) TRAIL could synergize with doxorubicin to kill SW480 cells effectively, which was represented by the boosted killing effect of doxorubicin on theses cells. IC50 of doxorubicin against SW480 cells sharply reduced when it was combined with TRAIL. (4) Subtoxic TRAIL (100 μg•l-1), combined with subtoxic doxorubicin (0.86 μmol•l-1), could kill SW480 cells sufficiently. Cytotoxicity by MTT assay arrived at 80.12% ± 2.67%, which was significantly higher than that by TRAIL or doxorubicin alone, with P = 0.006 and 0.003 respectively. This killing effect was partly due to apoptosis. It was proved by large amounts of apoptotic cells under phase-contrast microscopy, cell apoptosis rate of 76.82% ± 1.93% by FCM assay and typical apoptotic morphology observed through transmission electron microscopy. Increase of apoptosis after combined treatment had no relation with protein level of p53 (P > 0.05). CONCLUSION: SW480 cells are not sensitive to TRAIL, but TRAIL can synergize with lower concentration of doxorubicin to induce apoptosis effectively. The status of p53 protein is not involved in the mechanism of synergistic apoptosis. It suggests the potential therapeutic applicability of the combination of TRAIL with doxorubicin against colon cancers.

AIM:To investigate the expression of inducible NOS (iNOS) in human gastric cancer and its relationship with the angiogenesis in gastric cancer and lymphocyte metastasis. METHODS:The expression of iNOS in 50 patients with gastric cancer was studied by immunohistochemical SP method with anti-iNOS. Microvessel density (MVD) of human gastric cancer was also determined with anti-CD34 as the labels. RESULTS:The expression rate of iNOS in 50 cases was 70 %, and the rates of node negative and node positive in gastric cancer were 54.2 % and 84.6 %,respectively, with significant difference (P

AIM: To probe into the genetic susceptibility of HLA-DRB1 alleles to esophageal carcinoma in Han Chinese in Hubei Province. METHODS: HLA-DRB1 allele polymorphisms were typed by polymerase chain reaction with sequence-specific primers (PCR-SSP) in 42 unrelated patients with esophageal cancer and 136 unrelated normal control subjects and the associated HLA-DRB1 allele was measured by nucleotide sequence analysis with PCR.SAS software was used in statistics. RESULTS: Allele frequency (AF) of HLA-DRB1*0901 was significantly higher in esophageal carcinoma patients than that in the normal controls (0.2500 vs0.1397, P=0.028, the odds ratio 2.053, etiologic fraction 0.1282). After analyzed the allele nucleotide sequence of HLA-DRB1*0901 which approachs to the corresponded exon 2 sequence of the allele in genebank. There was no association between patients and controls in the rested HLA-DRB1 alleles. CONCLUSION: HLA-DRB1*0901 allele is more common in the patients with esophageal carcinoma than in the healthy controls, which is positively associated with the patients of Hubei Han Chinese. Individuals carrying HLA-DRB1*0901 may be susceptible to esophageal carcinoma.

We developed a gas chromatography/mass spectrometry method for detection and quantitation of anabolic steroids in head hair. Following alkaline digestion and solid-phase extraction, the MO-TMS derivatives gave a specific fragmentation pattern with EI ionization. For stanozolol, the TMS-HFBA derivative showed several diagnostic ions. For androstanolone, mestanolone (methylandrostanolone), and oxymetholone two chromatographic peaks for cis and trans isomers of derivatives were seen. Recoveries were 35 to 45% for androstanolone, oxymetholone, chlorotestosterone-acetate, dehydromethyltestosterone, dehydrotestosterone, fluoxymesterone, mestanolone, methyltestosterone, and nandrolone; 52% for mesterolone, trenbolone; 65% for bolasterone; 24% for methenolone and 17% for stanozolol. Limits of detection were 0.002 to 0.05 ng/mg and of quantitation were 0.02 to 0.1 ng/mg. Seven white male steroid abusers provided head hair samples (10 to 63 mg) and urine. In the hair samples, methyltestosterone was detected in two (confirmed in urine); nandrolone in two (also confirmed in urine); dehydromethyltestosterone in four (but not found in urine); and clenbuterol in one (but not in urine). Oxymethalone was found in urine in one, but not in the hair. One abuser had high levels of testosterone: 0.15 ng/mg hair, and 1190 ng/mL urine. We conclude that head hair analysis has considerable potential for the detection and monitoring of steroid abuse.