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C Su

Publications and source records attributed to C Su.

At least 19 recordsLinked to original sources

Arsenate and arsenite removal by zerovalent iron: effects of phosphate, silicate, carbonate, borate, sulfate, chromate, molybdate, and nitrate, relative to chloride.

Batch tests were performed to evaluate the effects of inorganic anion competition on the kinetics of arsenate (As(V)) and arsenite (As(III)) removal by zerovalent iron (Peerless Fe0) in aqueous solution. The oxyanions underwent either sorption-dominated reactions (phosphate, silicate, carbonate, borate, and sulfate) or reduction-dominated reactions (chromate, molybdate, and nitrate) with Peerless Fe0 in the presence of As(V) or As(III), relative to chloride. Pseudo-first-order rate equations were found to describe satisfactorily both As(V) and As(III) removal kinetics in the presence of each competing anion. Of the oxyanions tested for Peerless Fe0 in the pH range from 7 to 9, phosphate caused the greatest decrease in As removal rate (7.0 x 10(-3) to 18.5 x 10(-3) h(-1)) relative to chloride (34.9 x 10(-3) to 36.2 x 10(-3) h(-1)). Silicate, chromate, and molybdate also caused strong inhibition of As removal, followed by carbonate and nitrate, whereas borate and sulfate only caused slight inhibition to As(III) removal. Present results show that Peerless Fe0 may be an excellent permeable reactive barrier medium for a suite of mixed inorganic contaminants. The anion competing effects should be considered when designing permeable reactive barriers composed of zerovalent iron for field applications to remediate As(V) and As(III).

Adsorption↗

Arsenate and arsenite removal by zerovalent iron: kinetics, redox transformation, and implications for in situ groundwater remediation.

Batch tests were performed utilizing four zerovalent iron (Fe0) filings (Fisher, Peerless, Master Builders, and Aldrich) to remove As(V) and As(III) from water. One gram of metal was reacted headspace-free at 23 degrees C for up to 5 days in the dark with 41.5 mL of 2 mg L(-1) As(V), or As(III) or As(V) + As(III) (1:1) in 0.01 M NaCl. Arsenic removal on a mass basis followed the order: Fisher > Peerless Master Builders > Aldrich; whereas, on a surface area basis the order became: Fisher > Aldrich > Peerless Master Builders. Arsenic concentration decreased exponentially with time, and was below 0.01 mg L(-1) in 4 days with the exception of Aldrich Fe0. More As(III) was sorbed than As(V) by Peerless Fe0 in the initial As concentration range between 2 and 100 mg L(-1). No As(III) was detected by X-ray photoelectron spectroscopy (XPS) on Peerless Fe0 at 5 days when As(V) was the initial arsenic species in the solution. As(III) was detected by XPS at 30 and 60 days present on Peerless Fe0, when As(V) was the initial arsenic species in the solution. Likewise, As(V) was found on Peerless Fe0 when As(II) was added to the solution. A steady distribution of As(V) (73-76%) and As(III) (22-25%) was achieved at 30 and 60 days on the Peerless Fe0 when either As(V) or As(III) was the initial added species. The presence of both reducing species (Fe0 and Fe2+) and an oxidizing species (MnO2) in Peerless Fe0 is probably responsible for the coexistence of both As(V) and As(III) on Fe0 surfaces. The desorption of As(V) and As(III) by phosphate extraction decreased as the residence time of interaction between the sorbents and arsenic increased from 1 to 60 days. The results suggest that both As(V) and As(III) formed stronger surface complexes or migrated further inside the interior of the sorbent with increasing time.

Adsorption↗

Evolutionary dynamics of the T-cell receptor VB gene family as inferred from the human and mouse genomic sequences.

The diversity of T-cell receptors is generated primarily by the variable-region gene families, each of which is composed of a large number of member genes. The entire genomic sequence of the variable region (VB) of the T- cell receptor beta chain from humans and mice has become available. To understand the evolutionary dynamics of the VB gene family, we conducted a phylogenetic analysis of all VB genes from humans and mice, as well as a detailed analysis of internal DNA duplications in the human genomic VB region. The phylogenetic tree obtained shows that human and mouse VB genes intermingle extensively rather than forming two separate clusters and that many gene duplications occurred both before and after the divergence between primates and rodents. Analyzing the genomic maps of transposable elements (e.g., LINEs and SINEs) and relic VB genes in the VB gene region, we present evidence that a 20-kb VB region duplicated tandemly four times in the human lineage during the last 32 Myr, and 6 out of the 15 VB genes in this region have become nonfunctional during this period. Our results show that the VB gene family is subject to evolution by a birth-and-death process rather than to concerted evolution.

Amino Acid Sequence↗

Cancer preventive effect of Morinda citrifolia (Noni).

Morinda citrifolia (Noni) has been extensively used in folk medicine by Polynesians for over 2,000 years. It has been reported to have broad therapeutic effects, including anticancer activity, in both clinical practice and laboratory animal models. The mechanism for these effects remains unknown. The hypothesis that Morinda citrifolia possesses a cancer preventive effect at the initiation stage of carcinogenesis was studied. Our preliminary data indicated that 10% Tahitian Noni Liquid Dietary Supplement or Tahitian Noni Juice (TNJ), made from Morinda citrifolia fruit by Morinda Inc, in drinking water for one week was able to prevent DMBA-DNA adduct formation. The levels of DMBA-DNA adducts were reduced by 30% in the heart, 41% in the lung, 42% in the liver, and 80% in the kidney of female SD rats. Even more dramatic results were obtained in male C57 BL-6 mice: 10% TNJ was able to reduce DMBA-DNA adduct formation by 60% in the heart, 50% in the lung, 70% in the liver, and 90% in the kidney. In order to explore the mechanism of this preventive effect, the antioxidant activity of TNJ was examined in vitro by lipid hydroperoxide (LPO) and tetrazolium nitroblue (TNB) assays. In the LPO assay, LPO oxidizes leucomethylene blue to methylene blue in the presence of hemoglobin. The resultant blue color was quantified at 660 nm spectrophotometrically. In the TNB assay, superoxide anion radicals (SAR) reduce TNB into formazan blue that was also measured by absorption at 602 nm. TNJ showed a dose-dependent inhibition of both LPO and SAR in our system. The antioxidant activity of TNJ was compared to the effects of vitamin C, grape seed powder (GSP), and pycnogenol (PYC) at the daily dose per serving level recommended by U.S.RDAs or manufacturers. The results suggest that prevention of carcinogen-DNA adduct formation and the antioxidant activity of TNJ may contribute to the cancer preventive effect of Morinda citrifolia.

9,10-Dimethyl-1,2-benzanthracene↗

Staphylococcus aureus agr genotypes with enterotoxin production capabilities can resist neutrophil bactericidal activity.

Staphylococcus aureus pathogenicity is mainly due to the production of a number of secreted and cell surface-associated proteins under the regulation of the agr gene. A region of the agr gene was used to subgroup S. aureus strains according to restriction fragment length polymorphisms. Additionally, strains were subtyped according to the coagulase gene in order to strengthen discriminatory power. Virulence capabilities of agr genotype subgroups were evaluated using an in vitro neutrophil bactericidal assay, which showed that prevalent genotypes were significantly better at evading this primary host defense. Multiplex PCR was then used to detect enterotoxin genes among the genotype subgroups in order to determine possible virulence candidates that enable strains to combat neutrophil killing. The prevalent genotype strains were found to possess higher production capabilities for enterotoxin A than did low-prevalence strains. The significance of enterotoxin A production capabilities in affecting pathogenicity of S. aureus strains was evaluated and found to have a profound effect on neutrophil killing abilities. The use of a large epidemiological database as a tool for subgrouping strains with varying degrees of pathogenicity has allowed the identification of relevant and previously undefined virulence factors that affect a pathogen's capability to overcome host immune defenses.

Animals↗

High-resolution typing of Toxoplasma gondii using microsatellite loci.

High-resolution typing of Toxoplasma gondii is essential to understand the effect of genetic differences among strains on the variation in disease manifestation and transmission patterns. Current typing methods discern 3 lineages with minimal within-lineage variation. Described here are 6 new variable loci. These loci, including a minisatellite and 5 microsatellites, were more polymorphic than allozymes, restriction fragment length polymorphisms, and sequence variation in introns. Most importantly, these loci revealed, for the first time, substantial within-lineage variation that was over 6-fold higher than that detected by other markers. Genotyping at these loci facilitates classification of isolates beyond the lineage level.

Animals↗

The steroid receptor antagonists RU40555 and RU486 activate glucocorticoid receptor translocation and are not excreted by the steroid hormones transporter in L929 cells.

RU40555 is a recently available glucocorticoid receptor (GR) antagonist that differs from RU486 by a methyl radical. We have used the mouse fibroblast cell line L929 to study the in vitro effects of RU40555 on GR translocation and function and on the membrane steroid hormones transporter. The results showed that: 1) RU40555 competed for the binding of labelled dexamethasone (Dex) with a K(i) of 2.4 nM; 2) both RU40555 and RU486 were equally potent inhibitors of Dex-induced GR-mediated gene transcription; 3) maximum GR translocation induced by micromolar concentrations of Dex and the GR antagonists was approximately 30-55% loss in the cytoplasmic GR and approximately 40-90% increase in the nuclear GR (assessed by GR immunostaining in cytoplasm and nucleus and western blots of immunoprecipitated GR protein in cytosolic and nuclear fractions) and was similar for the two antagonists; 4) at nanomolar concentrations, RU40555 and RU486 induced more GR translocation than Dex (assessed by [(3)H]Dex binding and western blot of immunoreactive GR in the same cytosolic homogenates); 5) blocking the steroids membrane transporter with verapamil (100 microM) in the presence of Dex (10 nM) increased GR translocation to levels similar to those induced by RU40555 (10 nM) and RU486 (10 nM) alone; 6) verapamil did not affect GR translocation in the presence of RU40555 or RU486. These data demonstrate similar quantitative effects on GR translocation by RU486 and the new GR antagonist, RU40555. Moreover, RU40555, like RU486, is an effective GR antagonist. Finally, there is no evidence that the intracellular concentrations of RU40555 or RU486 are regulated by the steroids membrane transporter in L929 cells.

Analysis of Variance↗

Analyzing high-density oligonucleotide gene expression array data.

We have developed methods and identified problems associated with the analysis of data generated by high-density, oligonuceotide gene expression arrays. Our methods are aimed at accounting for many of the sources of variation that make it difficult, at times, to realize consistent results. We present here descriptions of some of these methods and how they impact the analysis of oligonucleotide gene expression array data. We will discuss the process of recognizing the "spots" (or features) on the Affymetrix GeneChip(R) probe arrays, correcting for background and intensity gradients in the resulting images, scaling/normalizing an array to allow array-to-array comparisons, monitoring probe performance with respect to hybridization efficiency, and assessing whether a gene is present or differentially expressed. Examples from the analyses of gene expression validation data are presented to contrast the different methods applied to these types of data.

Base Sequence↗

Potentiation of ganodermic acid S on prostaglandin E(1)-induced cyclic AMP elevation in human platelets.

Ganodermic acid S (GAS), isolated from the Chinese medicinal fungus Ganoderma lucidum (Fr.) Karst (Polyporaceae), exhibits inhibitory effects on platelet responses to various aggregating agonists. Our study demonstrated that GAS also participated in potentiating the response of human gel-filtered platelets to prostaglandin (PG) E(1). GAS at <20 microM did not show any significant change of basal cyclic AMP level in gel-filtered platelets. However, GAS potentiated the PGE(1)-evoked cyclic AMP level in a bell-shaped, concentration-dependent manner. The agent at 7.5 microM enhanced the level up to 1.8-fold of that evoked by PGE(1) alone. Collagen did not inhibit the PGE(1)-induced cyclic AMP level in platelets pretreated with GAS at 6 to 7.5 microM. In the presence of 7.5 microM GAS, the agent enhanced the inhibition of PGE(1) on platelet response to collagen in: phosphorylation of myosin light chain and pleckstrin; alpha-granule secretion; cell aggregation and protein-tyrosine phosphorylation. In addition, the agent along with PGE(1) almost abolished the dense-granule secretion and thromboxane (TX) B(2) formation. The results suggest that GAS played an additional role in potentiating the PGE(1)-induced cyclic AMP synthesis. GAS and PGE(1) inhibited additively the platelet response to collagen.

Alprostadil↗

Kinetics of manganese lipoxygenase with a catalytic mononuclear redox center.

Manganese lipoxygenase was isolated from the take-all fungus, Gaeumannomyces graminis, and the oxygenation mechanism was investigated. A kinetic isotope effect, k(H)/k(D) = 21-24, was observed with [U-(2)H]linoleic acid as a substrate. The relative biosynthesis of (11S)-hydroperoxylinoleate (11S-HPODE) and (13R)-hydroperoxylinoleate (13R-HPODE) was pH-dependent and changed by [U-(2)H]linoleic acid. Stopped-flow kinetic traces of linoleic and alpha-linolenic acids indicated catalytic lag times of approximately 45 ms, which were followed by bursts of enzyme activity for approximately 60 ms and then by steady state (k(cat) approximately 26 and approximately 47 s(-1), respectively). 11S-HPODE was isomerized by manganese lipoxygenase to 13R-HPODE and formed from linoleic acid at the same rates (k(cat) 7-9 s(-1)). Catalysis was accompanied by collisional quenching of the long wavelength fluorescence (640-685 nm) by fatty acid substrates and 13R-HPODE. Electron paramagnetic resonance (EPR) of native manganese lipoxygenase showed weak 6-fold hyperfine splitting superimposed on a broad resonance indicating two populations of Mn(II) bound to protein. The addition of linoleic acid decreased both components, and denaturation of the lipoxygenase liberated approximately 0.8 Mn(2+) atoms/lipoxygenase molecule. These observations are consistent with a mononuclear Mn(II) center in the native state, which is converted during catalysis to an EPR silent Mn(III) state. We propose that manganese lipoxygenase has kinetic and redox properties similar to iron lipoxygenases.

Ascomycota↗

Expression of human mitochondrial thymidine kinase in Escherichia coli: correlation between the enzymatic activity of pyrimidine nucleoside analogues and their inhibitory effect on bacterial growth.

Mitochondrial thymidine kinase (TK2) phosphorylates pyrimidine nucleosides to monophosphates and is expressed constitutively through the cell cycle in all cells. Because of the overlap of its substrate specificity with that of the cytosolic thymidine kinase (TK1) and deoxycytidine kinase (dCK), it has been difficult to determine the role of TK2 in activating nucleosides used in chemotherapy. In this report, we described the construction of a recombinant Escherichia coli strain which could be used to test if TK2 activity is limiting for the toxicity of nucleosides. Enzymes of bacterial origin which are involved in thymidine and deoxyuridine anabolism and catabolism were eliminated, and the cDNA for human TK2 was introduced. In the crude extract of the engineered E. coli, the level of thymidine kinase was, after induction of TK2 expression, several hundred fold higher than in the control strain. Several pharmacologically interesting nucleoside analogues, including 3'-azidothymidine, 2',3'-didehydro-2',3'-dideoxythymidine, and 2', 3'-dideoxy-beta-L-3'-thiacytidine, were tested for their effects on the growth of this recombinant strain. For a comparison, the phosphorylation of these compounds was determined with purified recombinant TK1, TK2, and dCK. A correlation was observed between the phosphorylation of several of these compounds by TK2 and their effects on bacterial growth. These results demonstrate that activation of growth-inhibiting pyrimidine nucleosides can be catalyzed by TK2, and together with recombinant E. coli strains expressing other cellular nucleoside kinases, this whole-cell bacterial system may serve as a tool to predict the efficacy and side effects of chemotherapeutic nucleosides.

Cell Division↗

Glial cell line-derived neurotrophic factor in the rat pituitary gland.

The presence of glial cell line-derived neurotrophic factor (GDNF) is described within specific regions of the adult rat pituitary gland. Immune staining methods revealed a small number of GDNF-immunopositive cells in the anterior lobe, and in areas of the neural lobe, while no immunoreactive endocrine cells were observed in the intermediate lobe. In the neural lobe, immunofluorescence methods were also used to demonstrate that GDNF and glial fibrillary acidic protein (GFAP) are co-localized in the glial cells (pituicytes) of the neural lobe. GDNF was not co-localized with neurofilament (NF) in nerve fibers of the neural lobe, suggesting that it is not present in axonal fibers. Measurements of GDNF content in separated anterior and neurointermediate lobes were also performed, using an enzyme-linked immunoassay (ELISA). Values for GDNF were slightly higher in the neurointermediate lobe than those obtained for the anterior lobe. The presence of GDNF in areas of the pituitary is discussed in the context of its possible function to support and maintain hypothalamic innervation, as well as a potential autocrine factor within endocrine cells.

Animals↗

Phylogenetic relationships of Staphylococcus aureus from bovine mastitis based on coagulase gene polymorphism.

Coagulase gene restriction fragment length polymorphism (RFLP) patterns were analyzed to determine the phylogenetic relationship among isolates of Staphylococcus aureus from the Czech Republic (n = 27), France (n = 48), Korea (n = 115) and the United States (n = 278). A total of 468 isolates of S. aureus were subtyped into 41 coagulase genotypes. Cluster analysis placed the 41 types into nine clusters. Eighteen API Staph profiles were determined for 102 S. aureus isolates representing 1 to 4 isolates of each coagulase type. The results of the study suggest that based on coagulase gene RFLP analysis, several genetic variants of S. aureus are prevalent. Comparison of coagulase and API Staph profiles indicated that the two identification system were independent of each other.

Animals↗

[Correlation of inactivation of CDKN2/p16 gene by methylation and lung cancers].

OBJECTIVE: To study the relationship between methylation state of CDKN2/p16 gene and lung cancers. METHODS: Genomic DNA was digested with methylation-sensitive enzymes and Southern blotting was used to analyses the methylation state of CDKN2/p16 gene in 89 cases of lung cancer. RESULTS: Twenty-one out of 89 lung cancers(23.6%) shown methylation of CDKN2/p16 gene, and 17 of them occurred in 42 P16 negative cases with a rate of 40.5%(17/42). CONCLUSION: Methylation of CDKN2/p16 gene 5' CpG island is probably an important mechanism of gene inactivation; it may take part in the onset and process of lung cancer.

Adult↗

[Correlation between methylation on SmaI locus of the CDKN2/p16 gene CpG island and lung cancer].

OBJECTIVE: To study the relationship between the status of methylation of the CDKN2/p16 gene 5'-CpG island and lung cancer. METHODS: Genomic DNA was digested with methylation-sensitive enzyme SmaI and Southern blotting was applied to analyze the status of methylation of the CDKN2/p16 in 89 cases of lung cancer and 10 cases of normal lung tissue. RESULTS: Of the 89 cases of lung cancer studied, the CDKN2/p16 gene was shown to be methylated in 15 cases (16.9%). It occurred in 12 of 42 p16 protein negative cases (28.6%), and in 3 of 47 p16 protein positive cases. The CDKN2/p16 gene was not shown to be methylated in 10 cases of normal lung tissue. CONCLUSION: Methylation of the CDKN2/p16 gene 5'-CpG island may be an important mechanism for gene inactivation in lung cancer progression.

Adult↗

[Relationship between tumor suppressor gene p16 and Rb and early diagnosis of lung cancers].

OBJECTIVES: To study the incidences and mechanisms of tumor suppressor gene p16 and Rb inactivation in lung cancers, and to investigate their relation to biological characters, clinical pathological diagnosis and gene classification diagnosis of lung cancers. METHODS: Immunohistochemistry, double in situ hybridization, PCR, PCR-SSCP and sequencing were applied to study the changes of p16 and Rb genes in 106 lung cancers and 23 lung tissues of benign diseases. RESULTS: Total expression rates of p16 and Rb proteins and mRNAs in lung cancers were lower than those in normal lung tissues and benign lung diseases, and they were specially related to histological type, metastasis and clinical stage of lung cancers. In stage I and II lung cancers, the obvious inactivation of tumor suppressor gene p16 or Rb was examined (32.6% or 28.3%); p16 inactivation was detected mainly in non-small cell lung cancers, and Rb inactivation mainly in small cell lung cancers. There were three mechanisms of homozygous deletions, methylations and mutations for p16 gene inactivation. The deletion rate of p16 exon1 and/or exon2 was 25.8%, mainly took place in p16 protein negative cases of non-small cell lung cancers. 15 cases (16.9%) took part in methylations on SmaI sites of CpG island of p16 gene. PCR-SSCP and sequencing showed that 9 cases had p16 gene mutations. CONCLUSIONS: p16 and Rb genes may play important roles in genesis and progression of lung cancers. Inactivation of p16 or Rb gene may be is an early link of lung canceration, that is very important for early diagnosis of lung cancers. A new gene classification model for lung cancer diagnosis would be set up based on the research of p16 and Rb genes.

Adolescent↗

[CDKN2/p16 gene cloning and its probe preparation and application in lung cancer].

OBJECTIVES: To clone CDKN2/p16(INK4a) gene, prepare its probe, and to study the change of CDKN2/p16(INK4a) gene in lung cancers. METHODS: Total RNA of normal lung tissue was extracted, CDKN2/p16(INK4a) gene cDNA synthesized, and CDKN2/p16(INK4a) gene recombinant vector, constructed. Southern blot was used to study CDKN2/p16(INK4a) gene in 46 cases of lung cancers, 3 cases of normal lung tissues, 6 cases of lung tissues near cancer, and 3 cases of lymph nodes with lung cancer metastasis. RESULTS: Cloned CDKN2/p16(INK4a) cDNA was proved by enzyme digestion and sequencing. Southern blot showed 4.3 kb band in normal lung tissues and lung tissues near cancers, and deletion of CDKN2/p16(INK4a) gene in cancer tissues and lymph nodes with lung cancer metastasis, with a deletion rate of 17.4% (8/46). CONCLUSION: CDKN2/p16(INK4a) gene may play a role to some extent in progression of lung cancers.

Blotting, Southern↗