bluuebunny/crossref_metadata_2025_split huggingface dataset:
Plasmacytoid Dendritic Cells Regulate Autoreactive B Cell Activation via Soluble Factors and in a Cell-to-Cell Contact Manner
Authors: Ding Chuanlin , Cai Yihua , Marroquin Jose , Ildstad Suzanne T. , Yan Jun 
Published: November 2009

Abstract
Plasmacytoid dendritic cells (pDCs) are specialized type I IFN producers, which play an important role in pathogenesis of autoimmune disorders. Dysregulated autoreactive B cell activation is a hallmark in most autoimmune diseases. This study was undertaken to investigate interactions between pDCs and autoreactive B cells. After coculture of autoreactive B cells that recognize self-Ag small nuclear ribonucleoprotein particles with activated pDCs, we found that pDCs significantly enhance autoreactive B cell proliferation, autoantibody production, and survival in response to TLR and BCR stimulation. Neutralization of IFN-α/β and IL-6 abrogated partially pDC-mediated enhancement of autoreactive B cell activation. Transwell studies demonstrated that pDCs could provide activation signals to autoreactive B cells via a cell-to-cell contact manner. The involvement of the ICAM-1-LFA-1 pathway was revealed as contributing to this effect. This in vitro enhancement effect was further demonstrated by an in vivo B cell adoptive transfer experiment, which showed that autoreactive B cell proliferation and activation were significantly decreased in MyD88-deficient mice compared with wild-type mice. These data suggest the dynamic interplay between pDCs and B cells is required for full activation of autoreactive B cells upon TLR or BCR stimulation.
Limited Role of CD4+Foxp3+ Regulatory T Cells in the Control of Experimental Cerebral Malaria
Authors: Steeg Christiane , Adler Guido , Sparwasser Tim , Fleischer Bernhard , Jacobs Thomas 
Published: November 2009

Abstract
Cerebral malaria (CM) associated with Plasmodium berghei ANKA (PbA) infection is an accepted model of human CM. CM during PbA infection critically depends on sequestration of T cells into the brain. Several studies aimed to address the role of regulatory T cells (Treg) in modulating this pathogenic T cell response. However, these studies are principally hampered due to the fact that until recently no reagents were available to deplete Foxp3+ Treg specifically. To study the function of Treg in the genesis of CM, we used depletion of Treg mice that are transgenic for a bacterial artificial chromosome expressing a diphtheria toxin receptor-enhanced GFP fusion protein under the control of the foxp3 gene locus. These mice allow for a selective depletion of Foxp3+ Treg by diphtheria toxin injection, and also their specific detection and purification during an ongoing infection. Using depletion of Treg mice, we found only a small increase in the absolute numbers of Foxp3+ Treg during PbA infection and, consequently, the ratio of Treg to T effector cells (Teff) decreased due to the rapid expansion of Teff. Although the latter sequester in the brains of infected mice, almost no Treg were found in the brains of infected mice. Furthermore, we demonstrate that depletion of Treg has no influence on sequestration of Teff and on the clinical outcome, and only minor influence on T cell activation. Using ex vivo analysis of purified Treg from either naive mice or PbA-infected mice, we found that both exhibit similar inhibitory capacity on Teff.
Estrogen Regulates Transcription Factors STAT-1 and NF-κB to Promote Inducible Nitric Oxide Synthase and Inflammatory Responses
Authors: Dai Rujuan , Phillips Rebecca A. , Karpuzoglu Ebru , Khan Deena , Ahmed S. Ansar 
Published: November 2009

Abstract
Estrogen regulation of inflammatory responses has broad physiological and pathological consequences. However, the molecular mechanism of estrogen regulation of inflammation is still poorly understood. In this study, we report that activation of both STAT-1 and NF-κB signaling is essential for Con A-induced inducible NO synthase (iNOS) and NO in murine splenocytes. Estrogen enhances STAT-1 DNA-binding activity without increasing the expression of phosphorylated and total STAT-1 protein. We have recently reported that estrogen blocks the nuclear expression of NF-κB p65 and modifies nuclear NF-κBp50. Here, we demonstrated that both nuclear STAT-1 and NF-κB are modified by serine protease-mediated proteolysis, which resulted in altered STAT-1 and NF-κB activity/signaling in splenocytes from estrogen-treated mice. Inhibition of serine protease activity with 4-(2-aminoethyl)benzenesulfonyl fluoride hydrochloride (AEBSF) restores the nuclear expression of full-length STAT-1 and NF-κB proteins, and resulted in decreased STAT-1 DNA-binding activity and formation of NF-κB p65/p50 binding complexes in nuclei of splenocytes from estrogen-treated mice. Consequently, there is significantly decreased iNOS and IFN-γ production in AEBSF-treated splenocytes from estrogen-treated mice, which suggests a positive regulatory role of truncated STAT-1 and/or NF-κB. Interestingly, there is increased production of MCP-1 in STAT-1 or NF-κB small interfering RNA-transfected cells, as well as in AEBSF-treated splenocytes from estrogen-treated mice. These data suggest a differential role of truncated STAT-1 and NF-κB in regulation of various inflammatory molecules in splenocytes from estrogen-treated mice. Together, our data reveal a novel molecular mechanism of estrogen-mediated promotion of inflammatory responses, which involves posttranslational modification of STAT-1 and NF-κB proteins.
Dynamic Regulation of CXCR1 and CXCR2 Homo- and Heterodimers
Authors: Martínez Muñoz Laura , Lucas Pilar , Navarro Gemma , Checa Ana I. , Franco Rafael , Martínez-A. Carlos , Rodríguez-Frade José Miguel , Mellado Mario 
Published: November 2009

Abstract
Although homo- and heterodimerization are reported for some chemokine receptors, it remains unclear whether these functional states are in dynamic equilibrium and how receptor/ligand levels influence oligomerization. In human neutrophils and in cell lines that coexpress the chemokine receptors CXCR1 and CXCR2, we used fluorescence resonance energy transfer techniques to show that these two receptors form homo- and heterodimers. Receptor expression and ligand activation were found to regulate the balance between these complexes, adapting the response to changes in the milieu. CXCL8, a ligand for both receptors, alters heterodimeric complexes, whereas it stabilizes homodimers and promotes receptor internalization. Oligomerization of receptors, together with the regulation of their expression and desensitization, could thus contribute to the fine control of chemokine functions.
Th1, Th17, and Th9 Effector Cells Induce Experimental Autoimmune Encephalomyelitis with Different Pathological Phenotypes
Authors: Jäger Anneli , Dardalhon Valérie , Sobel Raymond A. , Bettelli Estelle , Kuchroo Vijay K. 
Published: November 2009

Abstract
Experimental autoimmune encephalomyelitis (EAE) is a model of human multiple sclerosis induced by autoreactive Th cells that mediate tissue inflammation and demyelination in the CNS. Initially, IFN-γ-producing Th1 cells and, more recently, IL-17-producing Th17 cells with specificity for myelin Ags have been implicated in EAE induction, but whether Th17 cells are encephalitogenic has been controversial. Moreover, a new effector T cell subset, Th9 cells, has been identified; however, the ability of this T cell subset to induce EAE has not been investigated. Here, we have developed protocols to generate myelin oligodendrocyte glycoprotein-specific Th17, Th1, Th2, and Th9 cells in vitro, so that we could directly compare and characterize the encephalitogenic activity of each of these subsets upon adoptive transfer. We show that myelin oligodendrocyte glycoprotein-specific Th1, Th17, and Th9 cells but not Th2 cells induce EAE upon adoptive transfer. Importantly, each T cell subset induced disease with a different pathological phenotype. These data demonstrate that different effector T cell subsets with specificity for myelin Ags can induce CNS autoimmunity and that the pathological heterogeneity in multiple sclerosis lesions might in part be due to multiple distinct myelin-reactive effector T cells.
RREB-1 Is a Transcriptional Repressor of HLA-G
Authors: Flajollet Sébastien , Poras Isabelle , Carosella Edgardo D. , Moreau Philippe 
Published: November 2009

Abstract
The nonclassical HLA-G is a molecule specifically involved in immune tolerance with highly restricted tissue distribution in healthy conditions. Yet it is overexpressed in numerous tumors and in allografts with better acceptance. Major mechanisms involved in regulation of HLA-G transcription are still poorly described. Thus, to characterize these mechanisms we have developed a specific proteomic approach to identify proteins that bind differentially to the HLA-G gene promoter by promoter pull-down assay followed by spectrometry mass analysis. Among specific binding factors, we focused on RREB-1, a ras-responsive element binding protein 1. We demonstrated that RREB-1 represses HLA-G transcriptional activity and binds three ras response elements within the HLA-G promoter. RREB-1 protein, specifically in HLA-G-negative cells, interacts with subunits of CtBP complex implicated in chromatin remodeling. This demonstration is the first of a repressor factor of HLA-G transcriptional activity taking part in HLA-G repression by epigenetic mechanisms.
Innate Immune CD11b+Gr-1+ Cells, Suppressor Cells, Affect the Immune Response during Theiler’s Virus-Induced Demyelinating Disease
Authors: Bowen Jenna L. , Olson Julie K. 
Published: November 2009

Abstract
Multiple sclerosis is a demyelinating disease associated with an inflammatory immune response in the CNS. Theiler’s murine encephalomyelitis virus (TMEV)-induced demyelinating disease is a relevant mouse model for the study of multiple sclerosis. TMEV infection of susceptible mice leads to a persistent virus infection of the CNS which contributes to development of demyelinating disease. We have previously shown that the innate immune response can affect the development and progression of demyelinating disease. In the current studies, we determined that the predominant infiltrating cells during the innate immune response are CD11b+Ly6C+ cells. CD11b+Ly6C+ cells are immature myeloid cells that have exited the bone marrow without maturing and have been shown to suppress CD4+ and CD8+ T cell responses. Therefore, we wanted to determine what role these cells play in development and progression of demyelinating disease. TMEV-infected mice depleted of CD11b+Ly6C+ cells during the innate immune response developed a reduced demyelinating disease which was associated with a decreased myelin-specific CD4+ T cell response and a decreased inflammatory immune response in the CNS. TMEV-infected mice depleted of CD11b+Ly6C+ cells had increased virus-specific CD4+ and CD8+ T cell responses during early virus infection associated with increased expression of IFN-γ and IL-17 and decreased expression of IL-10 in the CNS. These results suggest that CD11b+Ly6C+ cells which infiltrate into the CNS during the innate immune response are myeloid-derived suppressor cells that suppress virus-specific T cell responses and contribute to the development of demyelinating disease.
In Vitro Assays of Inorganic Arsenic Methylation
Authors: Drobna Zuzana , Styblo Miroslav , Thomas David J. 
Published: November 2009

AbstractInorganic arsenic is extensively metabolized to produce mono‐, di‐, and trimethylated products. The formation of these metabolites produces a variety of intermediates that differ from inorganic arsenic in terms of patterns of distribution and retention and in toxic effects. In order to elucidate the pathway for arsenic methylation, it was necessary to develop a reliable in vitro assay system in which the formation of methylated metabolites could be monitored. Here, we describe an in vitro assay system that uses the postmicrosomal supernatant from rat liver as the source of the enzymatic activity that catalyzes methylation reactions. This system can be used to study the requirements for methylation reactions (e.g., identifying the donor of methyl groups) and for screening of compounds as potential activators or inhibitors of arsenic methylation. Curr. Protoc. Toxicol. 42:4.32.1‐4.32.10. © 2009 by John Wiley & Sons, Inc.
Analysis of Arsenical Metabolites in Biological Samples
Authors: Hernandez‐Zavala Araceli , Drobna Zuzana , Styblo Miroslav , Thomas David J. 
Published: November 2009

AbstractQuantitation of iAs and its methylated metabolites in biological samples provides dosimetric information needed to understand dose‐response relations. Here, methods are described for separation of inorganic and mono‐, di‐, and trimethylated arsenicals by thin‐layer chromatography. This method has been extensively used to track the metabolism of the radionuclide [73As] in a variety of in vitro assay systems. In addition, a hydride generation‐cryotrapping‐gas chromatography‐atomic absorption spectrometric method is described for the quantitation of arsenicals in biological samples. This method uses pH‐selective hydride generation to differentiate among arsenicals containing trivalent or pentavalent arsenic. Curr. Protoc. Toxicol. 42:4.33.1‐4.33.17. © 2009 by John Wiley & Sons, Inc.
Purification of Arsenic (+3 Oxidation State) Methyltransferase from Rat Liver Cytosol
Authors: Drobna Zuzana , Styblo Miroslav , Thomas David J. 
Published: November 2009

AbstractDemonstrating the enzymatic basis of arsenic methylation is critical to further studies of the pathway for the conversion of inorganic arsenic into a variety of methylated metabolites. This protocol describes a procedure for the purification of an arsenic methyltransferase from rat liver cytosol. Purification of this enzyme and subsequent cloning of its gene has permitted studies of enzyme structure and function, and has lead to the identification of orthologous genes in genomes of organisms ranging in complexity from sea urchins to humans. These proteins are referred to as arsenic (+3 oxidation state) methyltransferases. Curr. Protoc. Toxicol. 42:4.34.1‐4.34.13. © 2009 by John Wiley & Sons, Inc.
Olefin Polymers
Authors: Kissin Yury V. , Pebsworth Lloyd W. , Kissin Yury V. , Kissin Yury V. , Lieberman Richard B. , Kissin Yury V. , Lappin G. R. , Nemec L. H. , Sauer J. D. , Wagner J. D. 
Published: November 2009

Abstract

POLYETHYLENE

LOW DENSITY POLYETHYLENE

HIGH DENSITY POLYETHYLENE

LINEAR LOW DENSITY POLYETHYLENE

POLYPROPYLENE

POLYMERS OF HIGHER OLEFINS

OLEFINS, HIGHER
Differential Staining of Bacteria: Acid Fast Stain
Authors: Reynolds Jackie , Moyes Rita B. , Breakwell Donald P. 
Published: November 2009

AbstractAcid‐fastness is an uncommon characteristic shared by the genera Mycobacterium (Section 10A) and Nocardia. Because of this feature, this stain is extremely helpful in identification of these bacteria. Although Gram positive, acid‐fast bacteria do not take the crystal violet into the wall well, appearing very light purple rather than the deep purple of normal Gram‐positive bacteria. Curr. Protoc. Microbiol. 15:A.3H.1‐A.3H.5. © 2009 by John Wiley & Sons, Inc.
Absorber intercooling in CO2 absorption by piperazine‐promoted potassium carbonate
Authors: Plaza Jorge M. , Chen Eric , Rochelle Gary T. 
Published: November 2009

AbstractIntercooling was evaluated as a process option in CO2 absorption by piperazine (PZ) promoted potassium carbonate. The system performance with 4.5 m K+/4.5 m PZ was simulated by a model in Aspen Plus® RateSep™. The absorber was evaluated for use with a double matrix stripper by optimizing the position of the semilean feed and intercooling stages to maximize CO2 removal. Additionally, a simple absorber system was modeled to observe the effect of intercooling on systems with variable CO2 lean loading. Intercooling increases CO2 removal by as much as 10% with the double matrix configuration. With a simple absorber, the effectiveness of intercooling depends on solvent rate. Near a critical liquid/gas ratio (L/G) there is a large improvement with intercooling. This is related to the position of the temperature bulge. An approximation is proposed to estimate the critical L/G where intercooling may maximize removal. © 2009 American Institute of Chemical Engineers AIChE J, 2010
Prediction of the enantioselectivity of lipases and esterases by molecular docking method with modified force field parameters
Authors: Ji Liu , Xiaoling Tang , Hongwei Yu 
Published: November 2009

AbstractIn the work, molecular docking method was applied to extensively predict the enantioselectivity of lipases and esterases. A ligand library consisted of 69 chiral substrates was docked to four lipases and two esterases to set up the prediction model. During the docking process, necessary modification was carried out on van de Waals and hydrogen bond parameters of enzyme/substrate pair so that the ligands were able to adopt productive geometry in the enzymes. The docking results correctly indicated the enantiopreference for 91% (63/69) of docking pairs and the docking energy difference between substrate enantiomers (ΔΔGdocking) was significantly (correlation coefficient = 0.72, P < 0.05) correlated with the activation free energy difference (ΔΔG≠) that was quantitatively correlated with enantioselectivity of the enzymes. The prediction method was further validated by docking with another 12 enzyme/substrate pairs. Moreover, the prediction error was susceptible to the size of groups bonded to substrate's chiral center and expected ΔΔG≠ values but was not related to the substrate type and reaction medium. The possible reasons of observed error were discussed. It is demonstrated that the docking method has great application potential in high performance prediction of enzyme enantioselectivity. Biotechnol. Bioeng. 2010. 105: 687–696. © 2009 Wiley Periodicals, Inc.
Solvent‐Dependent Dihydrogen/Dihydride Stability for [Mo(CO)(Cp*)H2(PMe3)2]+[BF4]− Determined by Multiple Solvent⋅⋅⋅Anion⋅⋅⋅Cation Non‐Covalent Interactions
Authors: Dub Pavel A. , Belkova Natalia V. , Filippov Oleg A. , Daran Jean‐Claude , Epstein Lina M. , Lledós Agustí , Shubina Elena S. , Poli Rinaldo 
Published: November 2009

AbstractLow‐temperature (200 K) protonation of [Mo(CO)(Cp*)H(PMe3)2] (1) by Et2O⋅HBF4 gives a different result depending on a subtle solvent change: The dihydrogen complex [Mo(CO)(Cp*)(η2‐H2)(PMe3)2]+ (2) is obtained in THF, whereas the tautomeric classical dihydride [Mo(CO)(Cp*)(H)2(PMe3)2]+ (3) is the only observable product in dichloromethane. Both products were fully characterised (νCO IR; 1H, 31P, 13C NMR spectroscopies) at low temperature; they lose H2 upon warming to 230 K at approximately the same rate (ca. 10−3 s−1), with no detection of the non‐classical form in CD2Cl2, to generate [Mo(CO)(Cp*)(FBF3)(PMe3)2] (4). The latter also slowly decomposes at ambient temperature. One of the decomposition products was crystallised and identified by X‐ray crystallography as [Mo(CO)(Cp*)(FH⋅⋅⋅FBF3)(PMe3)2] (5), which features a neutral HF ligand coordinated to the transition metal through the F atom and to the BF4− anion through a hydrogen bond. The reason for the switch in relative stability between 2 and 3 was probed by DFT calculations based on the B3LYP and M05‐2X functionals, with inclusion of anion and solvent effects by the conductor‐like polarisable continuum model and by explicit consideration of the solvent molecules. Calculations at the MP4(SDQ) and CCSD(T) levels were also carried out for calibration. The calculations reveal the key role of non‐covalent anion–solvent interactions, which modulate the anion–cation interaction ultimately altering the energetic balance between the two isomeric forms.
Hydrophilic Interaction Chromatography Based Enrichment of Glycopeptides by Using Click Maltose: A Matrix with High Selectivity and Glycosylation Heterogeneity Coverage
Authors: Yu Long , Li Xiuling , Guo Zhimou , Zhang Xiuli , Liang Xinmiao 
Published: November 2009

AbstractGlycosylation analysis based on mass spectrometry (MS) of glycopeptides requires the isolation of glycopeptides from complex glycoprotein digests to facilitate structural determination of the glycopeptides. To this end, hydrophilic interaction chromatography (HILIC)‐based methods have been developed to selectively enrich glycopeptides by utilizing the hydrophilicity of the glycans. However, the application of these methods is limited by the medium selectivity of HILIC matrices. To improve the effectiveness of HILIC‐based methods, we introduced a customized hydrophilic matrix named “click maltose” and characterized its selectivity and glycosylation heterogeneity coverage. In the selectivity assessment, the non‐glycopeptides causing ion suppression to the glycopeptides were effectively removed by click maltose, leading to the identification of 27 glycopeptides in the fractions enriched from human serum immunoglobulin G digest, compared to 13 glycopeptides enriched using Sepharose CL‐6B, a commercially available matrix. For the assessment of glycosylation heterogeneity coverage, more than 140 glycopeptides covering all the five glycosites of human serum α1‐acid glycoprotein were captured using click maltose. Click maltose was synthesized by linking alkynyl‐derivatized maltose to azide‐derivatized silica through click chemistry. The resulting flexible saccharide chain structure remarkably enhances the hydrogen‐bonding interactions between the glycans of the glycopeptides and the matrix, which are responsible for the increased selectivity and glycosylation heterogeneity coverage of click maltose.
A Nucleic Acid Dependent Chemical Photocatalysis in Live Human Cells
Authors: Arian Dumitru , Cló Emiliano , Gothelf Kurt V. , Mokhir Andriy 
Published: November 2009

AbstractOnly two nucleic acid directed chemical reactions that are compatible with live cells have been reported to date. Neither of these processes generate toxic species from nontoxic starting materials. Reactions of the latter type could be applied as gene‐specific drugs, for example, in the treatment of cancer. We report here the first example of a chemical reaction that generates a cytotoxic drug from a nontoxic prodrug in the presence of a specific endogeneous ribonucleic acid in live mammalian cells. In this case, the prodrug is triplet oxygen and the drug is singlet oxygen. The key component of this reaction is an inert molecule (InP–2′‐OMe‐RNA/Q–2′‐OMe‐RNA; P: photosensitizer; Q: quencher), which becomes an active photosensitizer (InP–2′‐OMe‐RNA) in the presence of single‐stranded nucleic acid targets. Upon irradiation with red light, the photosensitizer produces over 6000 equivalents of toxic singlet oxygen per nucleic acid target. This reaction is highly sequence specific. To detect the generation of singlet oxygen in live cells, we prepared a membrane‐permeable and water‐soluble fluorescent scavenger, a derivative of 2,5‐diphenylisobenzofurane. The scavenger decomposes upon reaction with singlet oxygen and this is manifested in a decrease in the fluorescence intensity. This effect can be conveniently monitored by flow cytometry.
Cytomorphological diagnosis of tendinous xanthomatosis: A case report
Authors: Aggarwal Seema , Gandhi Akansha , Arora Vinod Kumar 
Published: November 2009

AbstractXanthoma is a reactive histiocytic proliferation in response to altered lipid levels. These develop usually in skin and subcutis but may also develop in deep soft tissue as tendon sheath or synovium. We report a rare case of tendinous xanthomatosis in a 23‐year‐old female, diagnosed on aspiration cytology. Diagn. Cytopathol. 2010. © 2009 Wiley‐Liss, Inc.