bluuebunny/crossref_metadata_2025_split huggingface dataset:
EQCM and Fluoroelectrochemical Studies on the Catalytic Oxidation of NADH at a Pencil 8B‐Scrawled Gold Electrode with High Detection Sensitivity
Authors: Su Yuhua , Xie Qingji , Cao Zhijun , Jia Xue'en , Yao Shouzhuo 
Published: May 2006

AbstractWe report for the first time the effective catalytic electrooxidation of nicotinamide adenine dinucleotide (NADH) on the pencil 8B‐scrawled gold electrode of an electrochemical quartz crystal microbalance (EQCM). The EQCM allowed us to quantitatively evaluate the catalytic activity of the pencil‐scrawled Au electrode. With increasing the mass of modified pencil powders, the peak potential for NADH oxidation shifted negatively, with maximum shift of −0.35 V at saturated pencil modification; the NADH‐oxidation peak current density (jp) was also notably increased, and the jp at saturated pencil modification was found to be larger than those at conventional pencil 8B and bare Au electrodes. Sensitive amperometric detection of NADH was achieved at the gold electrode with saturated pencil modification, with low detection potential (0.4 V versus SCE), low detection limit (0.08 μmol L−1) and wide linear range (0.2–710 μmol L−1). The fluoroelectrochemical measurements of NADH at bare and pencil‐modified gold electrodes were also conducted with satisfactory results. The convenient and low‐cost modification of pencil powders on the Au electrode may have presented a new functional surface of the EQCM, which is recommended for wider applications to bioelectrochemical studies, especially in view of the EQCM's capability of providing abundant in situ information in relevant processes.
CE as orthogonal technique to HPLC for alprazolam degradation product identification
Authors: Saavedra Luis , Huidobro Angel Luis , García Antonia , Cabanelas Jose Carlos , González María G. , Barbas Coral 
Published: May 2006

AbstractThe control of degradation products is currently a critical issue to the pharmaceutical industry. A degradation product that appeared in alprazolam tablets during their stability assay, 7‐chloro‐1‐methyl‐5‐phenyl‐[1,2,4]triazolo[4,3‐a]quinolin‐4‐amine, also named triazolaminoquinoline, was tested as possible candidate in the HPLC method employed for the study. The impurity showed the same retention time and spectra as the degradation product; but as all these compounds are very closely related, a confirmation with an independent technique was necessary, and CE was chosen for that purpose. Problems related to the adsorption of the analytes to the negatively charged silica surface were solved by employing a new polymeric capillary coating consisting of poly(3‐aminopropylmethylsiloxane). The polymer provided EOF towards the anode, and the two compounds were separated in less than 8 min in a 60 cm total‐length capillary, 75 µm id capillary with a BGE containing 50 mM phosphate buffer at pH 2.0 with 20% ACN. When the sample containing the degradation product was injected, the presence of triazolaminoquinoline was confirmed.
Quantification of ganciclovir in human plasma using capillary electrophoresis
Authors: Saleh Soundos , Hempel Georg 
Published: May 2006

AbstractA fast, simple, specific capillary electrophoretic method in the MEKC mode for the quantification of the antiviral drug ganciclovir is described. The separation was obtained using a 50 µm id fused‐silica capillary, 60 mM borax buffer (pH 9.25) containing 40 mM SDS using ethenoadenosine as the internal standard. Sample preparation was done by ultrafiltration with a Microcon 30 000 kDa filter. The analytes were detected with UV detector at 254 nm. A sufficient sensitivity was achieved by using a bubble cell capillary. The linear range was from 0.5 to 10 mg/L with a LOQ of 0.5 mg/L. Correlation coefficients were better than 0.999 whereas inter‐ and intraday precision and accuracy were less than 10.7%. The analysis of patients' samples after administration of ganciclovir indicates that the method is suitable for drug monitoring in the clinic.
Capillary electrophoresis and the clinical laboratory
Authors: Jabeen Rukhsana , Payne Deborah , Wiktorowicz John , Mohammad Amin , Petersen John 
Published: May 2006

AbstractOver the past 15 years, CE as an analytical tool has shown great promise in replacing many conventional clinical laboratory methods, such as electrophoresis and HPLC. CE's appeal was that it was fast, used very small amounts of sample and reagents, was extremely versatile, and was able to separate large and small analytes, whether neutral or charged. Because of this versatility, numerous methods have been developed for analytes that are of clinical interest. Other than molecular diagnostic and forensic laboratories CE has not been able to make a major impact in the United States. In contrast, in Europe and Japan an increasing number of clinical laboratories are using CE. Now that automated multicapillary instruments are commercially available along with cost‐effective test kits, CE may yet be accepted as an instrument that will be routinely used in the clinical laboratories. This review will focus on areas where CE has the potential to have the greatest impact on the clinical laboratory. These include analyses of proteins found in serum and urine, hemoglobin (A1c and variants), carbohydrate‐deficient transferrin, forensic and therapeutic drug screening, and molecular diagnostics.
Intertidal subsidence and collapse features on wave‐exposed, drift‐aligned sandy beaches subject to Amazon mud: Cayenne, French Guiana
Authors: Anthony Edward J. , Dolique Franck 
Published: May 2006

AbstractShort‐lived collapse features affecting the intertidal sandy profile were observed on mud‐rich beaches in Cayenne. They were formed in packets of beach sand accumulating over thick (several metres) fluid to under‐consolidated foreshore mud, which adjusts to this sand loading by seaward and longshore migration of fluid mud and subsequent in situ mud dewatering, thus generating subsidence and deformation of the overlying sand sheet. These sandy collapse features required active longshore sand transport and were washed out by wave processes at each rising tide. They finally disappeared permanently as adjustment of the underlying mud enabled stabilization of the beach profile. Copyright © 2006 John Wiley & Sons, Ltd.
β‐diversity fluctuations in Early–Mid Ordovician brachiopod communities of South China
Authors: Zhan R.‐B. , Jin J. , Rong J.‐Y. 
Published: May 2006

AbstractLower to Middle Ordovician transitional strata (Acrograptus filiformis Biozone to Exigraptus clavus Biozone) of the Upper Yangtze Platform contain rich and diverse brachiopods, particularly in the Daguanshan Formation of Sichuan Province, the Meitan Formation of Guizhou Province, and the Yingpan Formation of Houping, Chongqing City. On the basis of multivariate analyses of 207 samples (about 15 000 brachiopod specimens) and 61 species from these strata, 23 brachiopod‐dominated communities and associations are delineated through six graptolitic biozones (Acrograptus filiformis to Exigraptus clavus biozones). The disparity of brachiopod associations or β‐diversity, as measured by the number of contemporaneous associations across variable ecological settings, was low in the A. filiformis Biozone and increased through the overlying graptolitic biozones to reach an acme in the Azygograptus suecisus and Expansograptus hirundo biozones, where as many as nine different brachiopod associations thrived in mid‐shelf and also established in inner‐ and outer‐shelf environments. Despite a sharp increase in α‐diversity within the Didymograptellus eobifidus Biozone, β‐diversity remained relatively low, with only three distinct brachiopod communities. The diversity of brachiopod associations suffered an abrupt drop in the E. clavus Biozone, as a result of a major faunal turnover event, with only a single Metorthis Community present in an upper mid‐shelf setting. Temporally, brachiopod associations appear to be most stable in mid‐shelf settings, with the Paralenorthis, Sinorthis, Desmorthis, and Euorthisina communities having a relatively high α‐diversity and lasting through two to five graptolitic biozones. In both species composition and temporal duration, the brachiopod associations at the shallow‐ (BA1 to upper BA2) and deep‐shelf (BA4) settings are unstable, characterized by low α‐diversity and rapid vertical changes. This study implies that, during the Early and Mid Ordovician, brachiopod communities already attained a high level of organization in mid‐shelf settings, but remained poorly established in high‐stress environments of very shallow or very deep shelf settings. Copyright © 2006 John Wiley & Sons, Ltd.
MUC2 expression is regulated by histone H3 modification and DNA methylation in pancreatic cancer
Authors: Yamada Norishige , Hamada Tomofumi , Goto Masamichi , Tsutsumida Hideaki , Higashi Michiyo , Nomoto Mitsuharu , Yonezawa Suguru 
Published: May 2006

AbstractMucins are highly glycosylated proteins that play important roles in carcinogenesis. In pancreatic neoplasia, MUC2 mucin has been demonstrated as a tumor suppressor and we have reported that MUC2 is a favorable prognostic factor. Regulation of MUC2 gene expression is known to be controlled by DNA methylation, but the role of histone modification for MUC2 gene expression has yet to be clarified. Herein, we provide the first report that the histone H3 modification of the MUC2 promoter region regulates MUC2 gene expression. To investigate the histone modification and DNA methylation of the promoter region of the MUC2 gene, we treated 2 human pancreatic cancer cell lines, PANC1 (MUC2‐negative) and BxPC3 (MUC2‐positive) with the DNA methyltransferase inhibitor 5‐azacytidine (5‐aza), the histone deacetylase inhibitor trichostatin A (TSA), and a combination of these agents. The DNA methylation level of PANC1 cells was decreased by all 3 treatments, whereas histone H3‐K4/K9 methylation and H3‐K9/K27 acetylation in PANC1 cells was changed to the level in BxPC3 cells by treatment with TSA alone and with the 5‐aza/TSA combination. The expression level of MUC2 mRNA in PANC1 cells exhibited a definite increase when treated with TSA and 5‐aza/TSA, whereas 5‐aza alone induced only a slight increase. Our results suggest that histone H3 modification in the 5′ flanking region play an important role in MUC2 gene expression, possibly affecting DNA methylation. An understanding of these intimately correlated epigenetic changes may be of importance for predicting the outcome of patients with pancreatic neoplasms. © 2006 Wiley‐Liss, Inc.
H‐Ras selectively up‐regulates MMP‐9 and COX‐2 through activation of ERK1/2 and NF‐κB: An implication for invasive phenotype in rat liver epithelial cells
Authors: Lee Ki Won , Kim Mi‐Sung , Kang Nam Joo , Kim Do‐Hee , Surh Young‐Joon , Lee Hyong Joo , Moon Aree 
Published: May 2006

AbstractOne of the most frequent events in carcinogenesis is uncontrolled activation of Ras signaling pathway. A previous study demonstrated that the introduction of H‐Ras into the normal WB‐F344 rat liver epithelial (WB) cell line and adult male F344 rats resulted in tumorigenicity. The present study investigated whether H‐Ras induced the invasive and migrative phenotypes in WB cells, and subsequently aimed at characterizing the underlying mechanisms. H‐Ras induced the invasive and migrative phenotypes of WB cells with a selective up‐regulation of matrix metalloproteinase (MMP)‐9, but not MMP‐2. Cyclooxygenase (COX)‐2 and the subsequent production of prostaglandin E2(PGE2) were also induced by H‐Ras. Treatment of H‐Ras WB cells with GM6001 and NS398, the inhibitors of MMPs and COX‐2, respectively, significantly inhibited the H‐Ras‐induced invasive and migrative phenotypes. DNA binding activity of nuclear factor (NF)‐κB, but not that of activator protein (AP)‐1, was increased by H‐Ras. Caffeic acid phenethyl ester and Bay 11‐7082, specific inhibitors of NF‐κB and IKK, respectively, significantly inhibited the expression of MMP‐9 and COX‐2, invasion and migration of H‐Ras WB cells, revealing NF‐κB as a transcriptional factor responsible for H‐Ras‐induced malignant phenotypic conversion of WB cells. Activation of ERKs pathway was critical for H‐Ras‐induced invasive and migrative phenotypes, up‐regulation of MMP‐9 and COX‐2 as well as enhanced DNA binding activity of NF‐κB in WB cells. Taken together, these results demonstrate that H‐Ras up‐regulates MMP‐9 and COX‐2 through activation of ERKs and IKK‐IκBα‐NF‐κB signal pathway which may contribute to the malignant progression of WB rat liver epithelial cells. © 2006 Wiley‐Liss, Inc.
Prediction of recurrence in Ta urothelial cell carcinoma by real‐time quantitative PCR analysis: A microarray validation study
Authors: Schultz Iman J. , Wester Kenneth , Straatman Huub , Kiemeney Lambertus A. , Babjuk Marko , Mares Jaroslav , Willems Johanner L. , Swinkels Dorine W. , Witjes J. Alfred , de Kok Jacques B. , Malmström Per‐Uno 
Published: May 2006

AbstractAccurate prediction of tumor recurrence in patients with superficial urothelial cell carcinoma (UCC) might result in a significant reduction of invasive follow‐up cystoscopies. A recent study identified a panel of 26 genes from a large cDNA microarray analysis of bladder tumors that discriminated between early‐ and late‐recurring patients with superficial Ta tumors (Dyrskjøt et al., Nat Genet 2003;33:90–6). We aimed to validate this panel of genes in 44 primary Ta UCCs (23 and 21 tumors from patients with short or prolonged recurrence‐free periods, respectively), by real‐time quantitative PCR. Statistical analysis showed marginal significant different mRNA expression levels between the 2 patient groups. To evaluate a supplementary effect of genes for the identification of patients with short or prolonged recurrence‐free intervals, forward logistic regression analysis was applied. This revealed that a combination of the expression profiles of the genes HNRPK, LTB4DH and ANP32B resulted in the best performance, although the combination only marginally increased the predictive value of HNRPK alone. Comparing the receiver‐operating‐characteristic curves for HNRPK expression among patients with short or prolonged recurrence‐free periods, revealed an area under the curve of 0.696 (95% CI, 0.537–0.855). Using the median HNRPK expression level as cut‐off, a sensitivity of 69.6% and a specificity of 71.4% were obtained for the identification of patients with short or prolonged recurrence‐free periods, respectively. In conclusion, we were not able to confirm the microarray gene expression pattern of the 26 genes shown by Dyrskjøt et al. The discovery of accurate recurrence predictive markers, therefore, remains a challenge. © 2006 Wiley‐Liss, Inc.
High incidence of EMMPRIN expression in human tumors
Authors: Riethdorf Sabine , Reimers Natalie , Assmann Volker , Kornfeld Jan‐Wilhelm , Terracciano Luigi , Sauter Guido , Pantel Klaus 
Published: May 2006

AbstractExtracellular matrix metalloproteinase inducer expressed by tumor cells stimulates peritumoral fibroblasts to produce matrix metalloproteinases, thus contributing to tumor invasion and metastasis. To assess its suitability as potential therapeutic target, the overall incidence of EMMPRIN expression in normal and neoplastic tissues was analyzed. EMMPRIN expression was detected immunohistochemically using monoclonal antibodies MEM‐M6/1 and HIM6 and tissue microarrays with 2,348 and 608 tissue samples from 129 distinct tumor types and 76 different normal tissues, respectively. Expression and glycosylation state of EMMPRIN in human breast cancer cells were analyzed by Western blot analysis with monoclonal antibodies recognizing distinct carbohydrate structures and biochemical methods. EMMPRIN expression was found in 112 of 129 tumor entities analyzed with malignant tumors being EMMPRIN positive more frequently than benign tumors. A remarkable heterogeneity in EMMPRIN expression between tumor entities was observed. Among others, squamous‐cell carcinomas (60–100%), pancreatic (87%), chromophobic kidney (83%), hepatocellular (83%) or medullary breast (83%) adenocarcinomas as well as glioblastoma multiforme (79%) presented with a particular high incidence of EMMPRIN expression. There were a limited number of EMMPRIN‐positive normal cell types including proliferatively active and differentiating epithelial cells, germ cells, myocardial cells in the left heart ventricle or vascular endothelial cells of the brain. We could further demonstrate that breast cancer cells expressed EMMPRIN isoforms differing in the presence or absence of LewisX glycan structures. Our results may assist in defining the suitability of EMMPRIN as therapeutic target and predicting negative side effects. © 2006 Wiley‐Liss, Inc.
Mannose‐binding lectin‐2 genetic variation and stomach cancer risk
Authors: Baccarelli Andrea , Hou Lifang , Chen Jinbo , Lissowska Jolanta , El‐Omar Emad M. , Grillo Paolo , Giacomini Sara M. , Yaeger Meredith , Bernig Toralf , Zatonski Witold , Fraumeni Joseph F. , Chanock Stephen J. , Chow Wong‐Ho 
Published: May 2006

AbstractDeficiency of the mannose‐binding lectin (MBL) protein, an antigen‐recognition molecule involved in systemic and mucosal innate immunity, is determined by variant alleles in MBL2 gene promoter and exon‐1 regions. We conducted a population‐based study on 305 stomach cancer cases and 427 controls in Warsaw, Poland to determine whether MBL2 gene variants predispose to stomach cancer. Single nucleotide polymorphisms (SNPs) in MBL2 were determined by TaqMan™. The 5 tested MBL2 variants are in complete linkage disequilibrium and comprise 6 different haplotypes. The risk of stomach cancer was increased in subjects carrying the H/H promoter genotype (OR = 1.8, 95%CI 1.1–2.9; p = 0.020) relative to L/L carriers, after adjustment for age, gender, education and smoking. Carrying at least one D exon‐1 allele was associated with nonsignificant excess risk (OR = 1.5, 95% CI 0.9–2.4; p = 0.081). In haplotype analysis, the HYD haplotype was associated with increased risk of stomach cancer when compared with HYA, the most common haplotype (OR = 1.9, 95% CI 1.1–3.2; p = 0.021). In diplotype analysis, subjects carrying the YA/D haplotype combination showed the highest risk (OR = 3.0, 95% CI 1.2–7.1; p = 0.015), compared with YA/YA. Further analyses to examine the joint effect of MBL2 and IL‐1B polymorphisms, previously shown to predispose to stomach cancer, indicated that the combination of at‐risk IL‐1B genotypes (CT or TT at location ‐511) and HYD MBL2 haplotype was associated with a 3.5‐fold risk (OR = 3.5, 95% CI 1.6–7.6; p = 0.001). Our findings suggest that the codon 52 D MBL2 variant causing a cysteine > arginine replacement, but not B and C variants producing glycine substitutions, is specifically associated with gastric cancer risk. © 2006 Wiley‐Liss, Inc.
Prevention of oxidative degradation of polyurethane by covalent attachment of di‐tert‐butylphenol residues
Authors: Stachelek Stanley J. , Alferiev Ivan , Choi Hoon , Chan Chun Wai , Zubiate Brett , Sacks Michael , Composto Russell , Chen I‐Wei , Levy Robert J. 
Published: May 2006

AbstractPolyurethane (PU) components of cardiovascular devices are subjected to oxidation‐initiated surface degradation, which leads to cracking and ultimately device failure. In the present study, we investigated a novel bromoalkylation chemical strategy to covalently attach the antioxidant, di‐tert‐butylphenol (DBP), and/or cholesterol (Chol) to the PU urethane nitrogen groups to hypothetically prevent oxidative degradation. These experiments compared PU, PU‐DBP, PU‐Chol, and PU‐Chol‐DBP. A series of comparative oxidative degradation studies involved exposing PU samples (modified and unmodified) to H2O2–CoCl2 for 15 days at 37°C, to cause accelerated oxidative degradation. The extent and effects of degradation were assessed by attenuated total reflectance Fourier transformation infrared spectroscopy (FTIR), scanning electron microscopy (SEM), surface contact angle measurements, and mechanical testing. Both the Chol and DBP modification conferred significant resistance to oxidation related changes compared to unmodified PU per FTIR and SEM results. SEM demonstrated cavitation only in unmodified PU. However, contact angle analysis showed significant oxidation‐induced changes only in the Chol‐modified PU formulations. Most importantly, uniaxial stress–strain testing revealed that only PU‐DBP demonstrated bulk elastomeric properties that were minimally affected by oxidation; PU, PU‐Chol, PU‐Chol‐DBP showed marked deterioration of their stress–strain properties following oxidation. In conclusion, these results demonstrate that derivatizing PU with DBP confers significant resistance to oxidative degradation compared with unmodified PU. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res, 2006
Different signaling responses to anti‐proliferative agents in human aortic and venous smooth muscle cells
Authors: Lee Ray M. , Masaki Takahisa , Yang Hung‐Sheng , Liu Jihua , Chen Jun , Li Li , Blumenthal Donald K. , Cheung Alfred K. 
Published: May 2006

AbstractProliferation of smooth muscle cells (SMCs) contributes to the stenosis of coronary arteries and vascular grafts. Local delivery of anti‐proliferative drugs can prevent vascular stenosis. To understand the cellular responses to anti‐proliferative agents, we investigated the signaling events in cultured human aortic SMCs (ASMCs), saphenous venous SMCs (VSMCs), and dermal fibroblasts (DFs) in response to paclitaxel or etoposide. Cellular mitochondrial and proliferative activities were examined with the methylthiazoletetrazolium (MTT) dye reduction and the bromodeoxyuridine (BrdU) incorporation assay, respectively. Cell proliferation was almost completely suppressed by paclitaxel or etoposide, but apoptosis was achieved in only about 50% of cells at the highest drug concentrations, suggesting the presence of compensatory mechanisms to prevent apoptosis. Examination of three important signaling pathways revealed significant differences between ASMCs, VSMCs, and DFs. Treatment with either paclitaxel or etoposide caused a transient phosphorylation/activation of p42 MAPK in ASMCs and DFs, but had no effect on phospho‐p42/44 MAPK in VSMCs. High‐dose etoposide enhanced p38 MAPK activation in ASMCs, but not in VSMCs. The p38 inhibitor, PD169316, partially inhibited etoposide‐induced ASMC apoptosis, but induced apoptosis in VSMCs. The effects of etoposide and paclitaxel on Akt also differed between ASMCs and VSMCs. These observations indicate that ASMCs and VSMCs differ in the response of signaling pathways to anti‐proliferative agents. In ASMCs, p42/44 MAPK appears to serve a pro‐survival role, whereas p38 MAPK is a pro‐apoptotic regulator. In contrast, p38 MAPK is an important pro‐survival regulator in VSMCs and p42/44 MAPK appears to play a minor role in responding to anti‐proliferative drugs. J. Cell. Biochem. 99: 835–844, 2006. © 2006 Wiley‐Liss, Inc.