@article {2698,
	title = {Barrier Capacity of Hydrophilic Polymer Brushes To Prevent Hydrophobic Interactions: Effect of Graft Density and Hydrophilicity},
	journal = {Macromolecules},
	volume = {42},
	number = {13},
	year = {2009},
	note = {ISI Document Delivery No.: 472NJTimes Cited: 7Cited Reference Count: 57Zou, Yuquan Rossi, Nicholas A. A. Kizhakkedathu, Jayachandran N. Brooks, Donald E.},
	month = {Jul},
	pages = {4817-4828},
	type = {Article},
	abstract = {The performance of biomaterials in contact with biological systems can be greatly affected by hydrophobic interactions at the interface between the biomaterial surface and surrounding biomolecules. Polymer brushes can function as a protective layer, preventing such interfacial hydrophobic interactions. In this paper, a systematic study of the barrier properties of a hydrophilic polymer brush is made by investigating the influence of graft density and its chemical nature (hydrophilicity/hydrophobicity) on hydrophobic interactions with the surface. To achieve this, it series of novel thermoresponsive poly-N-[(2,2-dimethyl-1,3-dioxolane)methyl]acrylamide (PDMDOMA) polymer brushes were grown from silicon wafers via surface-initiated atom transfer radical polymerization. Without changing graft density or degree of polymerization, the hydrophilicity of the PDMDOMA brushes was manipulated by partial or complete hydrolysis or the pendent dioxolane moieties. A lower critical solution temperature (LCST) was observed at 22-24 degrees C, below which the PDMDOMA brush was Found to be in a hydrated state (amphiphilic), while at temperatures above the LCST, the PDMDOMA brush formed a collapsed. more hydrophobic structure. A physical method was developed to analyze the ability of these brushes to act as a barrier against hydrophobic interactions based on AFM force-distance measurements. The adhesive forces between the Si3N4 tip and the silicon wafer surface upon (a) modification with ATRP initiator, (b) grafting of PDMDOMA brushes, and (c) partial and complete hydrolysis of PDMDOMA were investigated. Hydrophobic interactions decreased after each modification, while graft density and the degree of hydrolysis increased the barrier function of the surface layer. In particular, when graft density was above 0.22 chains/nm(2), the barrier capacity completely counteracted the hydrophobic interactions, as evidenced from the disappearance of the adhesive force in AFM measurements. Further Studies revealed that the barrier property its assessed by AFM correlated well with the wettability of the surfaces.},
	keywords = {ATOMIC-FORCE MICROSCOPY, BLOOD-PLASMA, CELL-ADHESION, CHAIN-LENGTH, HUMAN, MOLECULAR-WEIGHT, protein adsorption, SERUM-ALBUMIN, SINGLE-MOLECULE, SURFACE, TRANSFER RADICAL POLYMERIZATION},
	isbn = {0024-9297},
	url = {<Go to ISI>://000268138500067},
	author = {Zou, Y. Q. and Rossi, N. A. A. and Kizhakkedathu, J. N. and Brooks, D. E.}
}
@article {2450,
	title = {Quantitative analysis of propofol in whole blood using capillary electrophoresis},
	journal = {Journal of Chromatography B-Analytical Technologies in the Biomedical and Life Sciences},
	volume = {877},
	number = {8-9},
	year = {2009},
	note = {ISI Document Delivery No.: 424NVTimes Cited: 2Cited Reference Count: 19Hui, Yu Raedschelders, Koen Zhang, Hong Ansley, David M. Chen, David D. Y.},
	month = {Mar},
	pages = {703-709},
	type = {Article},
	abstract = {We have developed a straightforward capillary electrophoresis method capable of quantifying clinically relevant propofol concentrations in whole blood from patients undergoing aortocoronary bypass grafting with cardiopulmonary bypass. The method utilizes 400 mu L of whole blood and is capable of detecting propofol in the ng/mL range. Factors affecting reproducibility and reliability of analytical results for clinically relevant samples are discussed. The method was used to evaluate propofol concentrations in blood samples from 30 patients. The distribution in the whole blood concentration achieved in patients advocates the need for target-achieved monitoring techniques. (C) 2009 Elsevier B.V. All rights reserved.},
	keywords = {Aortocoronary bypass, BIOPHARMACEUTICAL INDUSTRY, BREATH, capillary electrophoresis, Cardiopulmonary bypass, CHROMATOGRAPHY-MASS-SPECTROMETRY, grafting, HUMAN, Method development, PLASMA, POPULATION, Propofol, Whole blood},
	isbn = {1570-0232},
	url = {<Go to ISI>://000264574300006},
	author = {Hui, Y. and Raedschelders, K. and Zhang, H. and Ansley, D. M. and Chen, D. D. Y.}
}
@article {648,
	title = {Revealing system dynamics through decomposition of the perturbation domain in two-dimensional correlation spectroscopy},
	journal = {Applied Spectroscopy},
	volume = {57},
	number = {12},
	year = {2003},
	note = {ISI Document Delivery No.: 753MHTimes Cited: 5Cited Reference Count: 36},
	month = {Dec},
	pages = {1551-1560},
	type = {Article},
	abstract = {A technique is presented to simply and effectively decompose the perturbation domain in two-dimensional (2D) correlation maps calculated on a given set of vibrational spectra. Decomposition of the perturbation domain exposes a wealth of kinetic information complementary to the information extracted from conventional 2D correlation spectroscopy. It is shown that the technique produces "perturbation profile maps" that can be utilized in both the interpretation of the conventional 2D correlation maps and the independent kinetic analysis of the given system. Discrimination between spectral features exhibiting similar, but not identical, dynamics is facilitated by the decomposition, and spectral features exhibiting identical dynamics over the perturbation interval are quickly identified. Spectral features exhibiting similar dynamics over only a sub-range of the full perturbation are also identifiable. Interpretation of phase information illuminated in synchronous and asynchronous maps is simplified. Comparison between similar spectral features present in different samples is facilitated with the technique. The simplicity and ease of implementation of the technique make decomposition of the perturbation domain a valuable addition to the tools available in 2D correlation analysis.},
	keywords = {cross-correlation, FT-RAMAN, HUMAN, INFRARED CORRELATION SPECTROSCOPY, multivariate data, POLYACRYLAMIDE GELS, POLYMER GEL DOSIMETERS, RADIATION-DOSIMETRY, Raman spectroscopy, SAMPLE-SAMPLE, SECONDARY STRUCTURE, SERUM-ALBUMIN, SPECTRA, STRUCTURAL-CHANGES, two-dimensional correlation spectroscopy},
	isbn = {0003-7028},
	url = {<Go to ISI>://000187234800013},
	author = {Jirasek, A. and Schulze, G. and Blades, M. W. and Turner, R. F. B.}
}
@article {648,
	title = {Revealing system dynamics through decomposition of the perturbation domain in two-dimensional correlation spectroscopy},
	journal = {Applied Spectroscopy},
	volume = {57},
	number = {12},
	year = {2003},
	note = {ISI Document Delivery No.: 753MHTimes Cited: 5Cited Reference Count: 36},
	month = {Dec},
	pages = {1551-1560},
	type = {Article},
	abstract = {A technique is presented to simply and effectively decompose the perturbation domain in two-dimensional (2D) correlation maps calculated on a given set of vibrational spectra. Decomposition of the perturbation domain exposes a wealth of kinetic information complementary to the information extracted from conventional 2D correlation spectroscopy. It is shown that the technique produces "perturbation profile maps" that can be utilized in both the interpretation of the conventional 2D correlation maps and the independent kinetic analysis of the given system. Discrimination between spectral features exhibiting similar, but not identical, dynamics is facilitated by the decomposition, and spectral features exhibiting identical dynamics over the perturbation interval are quickly identified. Spectral features exhibiting similar dynamics over only a sub-range of the full perturbation are also identifiable. Interpretation of phase information illuminated in synchronous and asynchronous maps is simplified. Comparison between similar spectral features present in different samples is facilitated with the technique. The simplicity and ease of implementation of the technique make decomposition of the perturbation domain a valuable addition to the tools available in 2D correlation analysis.},
	keywords = {cross-correlation, FT-RAMAN, HUMAN, INFRARED CORRELATION SPECTROSCOPY, multivariate data, POLYACRYLAMIDE GELS, POLYMER GEL DOSIMETERS, RADIATION-DOSIMETRY, Raman spectroscopy, SAMPLE-SAMPLE, SECONDARY STRUCTURE, SERUM-ALBUMIN, SPECTRA, STRUCTURAL-CHANGES, two-dimensional correlation spectroscopy},
	isbn = {0003-7028},
	url = {<Go to ISI>://000187234800013},
	author = {Jirasek, A. and Schulze, G. and Blades, M. W. and Turner, R. F. B.}
}
@article {465,
	title = {DNA damage induced by methylated trivalent arsenicals is mediated by reactive oxygen species},
	journal = {Chemical Research in Toxicology},
	volume = {15},
	number = {12},
	year = {2002},
	note = {ISI Document Delivery No.: 627VUTimes Cited: 104Cited Reference Count: 48},
	month = {Dec},
	pages = {1627-1634},
	type = {Article},
	abstract = {Arsenic is a human carcinogen; however, the mechanisms of arsenic{\textquoteright}s induction of carcinogenic effects have not been identified clearly. We have shown previously that monomethylarsonous acid (MMA(III)) and dimethylarsinous acid (DMA(III)) are genotoxic and can damage supercoiled phiX174 DNA and the DNA in peripheral human lymphocytes in culture. These trivalent arsenicals are biomethylated forms of inorganic arsenic and have been detected in the urine of subjects exposed to arsenite and arsenate. We show here by molecular, chemical, and physical methods that reactive oxygen species (ROS) are intermediates in the DNA-damaging activities of MMA(III) and DMA(III). Using the phiX174 DNA nicking assay we found that the ROS inhibitors Tiron, melatonin, and the vitamin E analogue Trolox inhibited the DNA-nicking activities of both MMA(III) and DMA(III) at low micromolar concentrations. The spin trap agent 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) also was effective at preventing the DNA nicking induced by MMA(III) and DMA(III.) ESR spectroscopy studies using DMPO identified a radical as a ROS intermediate in the DNA incubations with DMA(III). This radical adduct was assigned to the DMPO-hydroxyl free radical adduct on the basis of comparison of the observed hyperfine splitting constants and line widths with those reported in the literature. The formation of the DMPO-hydroxyl free radical adduct was dependent on time and the presence of DMA(III) and was completely inhibited by Tiron and Trolox and partially inhibited by DMSO. Using electrospray mass spectrometry, micromolar concentrations of DMA(v) were detected in the DNA incubation mixtures with DMA(III). These data are consistent with the conclusions that the DNA-damaging activity of DMA(III) is an indirect genotoxic effect mediated by ROS-formed concomitantly with the oxidation of DMA(III) to DMA(v).},
	keywords = {DIMETHYLARSINIC ACID, DRINKING-WATER, ENZYMATIC METHYLATION, FREE-RADICALS, HEPATOCYTES, HUMAN, HUMAN URINE, MALE F344 RATS, MONOMETHYLARSONOUS ACID MMA(III), ORAL-EXPOSURE, RAT-LIVER CYTOSOL},
	isbn = {0893-228X},
	url = {<Go to ISI>://000179957500017},
	author = {Nesnow, S. and Roop, B. C. and Lambert, G. and Kadiiska, M. and Mason, R. P. and Cullen, W. R. and Mass, M. J.}
}
@article {5144,
	title = {Methylated trivalent arsenic species are genotoxic},
	journal = {Chemical Research in Toxicology},
	volume = {14},
	number = {4},
	year = {2001},
	note = {ISI Document Delivery No.: 424XZTimes Cited: 253Cited Reference Count: 55},
	month = {Apr},
	pages = {355-361},
	type = {Article},
	abstract = {The reactivities of methyloxoarsine (MAsIII) and iododimethylarsine (DMAsIII), two methylated trivalent arsenicals, toward supercoiled phi X174 RFI DNA were assessed using a DNA nicking assay. The induction of DNA damage by these compounds in vitro in human peripheral lymphocytes was assessed using a single-cell gel (SCG, "comet") assay. Both methylated trivalent arsenicals were able to nick and/or completely degrade phi X174 DNA in vitro in 2 h incubations at 37 degreesC (pH 7.4) depending on concentration. MAsIII was effective at nicking phi X174 DNA at 30 mM; however, at 150 muM DMAsIII, nicking could be observed. Exposure of (phi X174 DNA to sodium arsenite (iAs(III); from 1 nM up to 300 mM), sodium arsenate (from 1 muM to 1 M), and the pentavalent arsenicals, monomethylarsonic acid (from 1 muM to 3 M) and dimethylarsinic acid (from 0.1 to 300 mM), did not nick or degrade phi X174 DNA under these conditions. In the SCG assay in human lymphocytes, methylated trivalent arsenicals were much more potent than any other arsenicals that were tested. On the basis of the slopes of the concentration-response curve for the tail moment in the SCG assay, MAsIII and DMAsIII were 77 and 386 times more potent than iAs(III), respectively. Because methylated trivalent arsenicals were the only arsenic compounds that were observed to damage naked DNA and required no exogenously added enzymatic or chemical activation systems, they are considered here to be direct-acting forms of arsenic that are genotoxic, though they are not, necessarily, the only genotoxic species of arsenic that could exist.},
	keywords = {CELLS, DIMETHYLARSINIC ACID, DRINKING-WATER, ENZYMATIC METHYLATION, FIBROBLASTS, GLUTATHIONE-REDUCTASE, HUMAN, HUMAN URINE, INHIBITION, MONOMETHYLARSONOUS ACID, SODIUM ARSENITE},
	isbn = {0893-228X},
	url = {<Go to ISI>://000168260400005},
	author = {Mass, M. J. and Tennant, A. and Roop, B. C. and Cullen, W. R. and Styblo, M. and Thomas, D. J. and Kligerman, A. D.}
}
@article {4942,
	title = {Comparative toxicity of trivalent and pentavalent inorganic and methylated arsenicals in rat and human cells},
	journal = {Archives of Toxicology},
	volume = {74},
	number = {6},
	year = {2000},
	note = {ISI Document Delivery No.: 349ZATimes Cited: 358Cited Reference Count: 37},
	month = {Aug},
	pages = {289-299},
	type = {Article},
	abstract = {Biomethylation is considered a major detoxification pathway for inorganic arsenicals (iAs). According to the postulated metabolic scheme, the methylation of iAs yields methylated metabolites in which arsenic is present in both pentavalent and trivalent forms. Pentavalent mono- and dimethylated arsenicals are less acutely toxic than iAs. However, little is known about the toxicity of trivalent methylated species. In the work reported here the toxicities of iAs and trivalent and pentavalent methylated arsenicals were examined in cultured human cells derived from tissues that are considered a major site for iAs methylation (liver) or targets for carcinogenic effects associated with exposure to iAs (skin, urinary bladder, and lung). To characterize the role of methylation in the protection against toxicity of arsenicals, the capacities of cells to produce methylated metabolites were also examined. In addition to human cells, primary rat hepatocytes were used as methylating controls. Among the arsenicals examined, trivalent monomethylated species were the most cytotoxic in all cell types. Trivalent dimethylated arsenicals were at least as cytotoxic as trivalent iAs (arsenite) for most cell types. Pentavalent arsenicals were significantly less cytotoxic than their trivalent analogs. Among the cell types examined, primary rat hepatocytes exhibited the greatest methylation capacity for iAs followed by primary human hepatocytes, epidermal keratinocytes, and bronchial epithelial cells. Cells derived from human bladder did not methylate iAs. There was no apparent correlation between susceptibility of cells to arsenic toxicity and their capacity to methylate iAs. These results suggest that (1) trivalent methylated arsenicals, intermediary products of arsenic methylation, may significantly contribute to the adverse effects associated with exposure to iAs, and (2) high methylation capacity does not protect cells from the acute toxicity of trivalent arsenicals.},
	keywords = {ARSENATE, arsenic, ARSENITE, BINDING, bladder, cell culture, CELLULAR UPTAKE, DIMETHYLARSINIC ACID, dimethylarsinous acid, DRINKING-WATER, ENZYMATIC METHYLATION, GLUTATHIONE, HEPATOCYTES, HUMAN, IN-VITRO METHYLATION, LIVER, lung, METABOLISM, methylarsonic acid, methylarsonous acid, METHYLATION, RABBIT LIVER, SKIN, TOXICITY},
	isbn = {0340-5761},
	url = {<Go to ISI>://000089074500001},
	author = {Styblo, M. and Del Razo, L. M. and Vega, L. and Germolec, D. R. and LeCluyse, E. L. and Hamilton, G. A. and Reed, W. and Wang, C. and Cullen, W. R. and Thomas, D. J.}
}
