bluuebunny/crossref_metadata_2025 huggingface dataset:
Vertebrate homologues of Frodo are dynamically expressed during embryonic development in tissues undergoing extensive morphogenetic movements
Authors: Hunter Nina L. , Hikasa Hiroki , Dymecki Susan M. , Sokol Sergei Y.
Published: November 2005

Frodo has been identified as a protein interacting with Dishevelled, an essential mediator of the Wnt signaling pathway, critical for the determination of cell fate and polarity in embryonic development. In this study, we use specific gene probes to characterize stage‐ and tissue‐specific expression patterns of the mouse Frodo homologue and compare them with Frodo expression patterns in Xenopus embryos. In situ hybridization analysis of mouse Frodo transcripts demonstrates that, similar to Xenopus Frodo, mouse Frodo is expressed in primitive streak mesoderm, neuroectoderm, neural crest, presomitic mesoderm, and somites. In many cases, Frodo expression is confined to tissues undergoing extensive morphogenesis, suggesting that Frodo may be involved in the regulation of cell shape and motility. Highly conserved dynamic expression patterns of Frodo homologues indicate a similar function for these proteins in different vertebrates. Developmental Dynamics 235:279–284, 2006. © 2005 Wiley‐Liss, Inc.
Discrete pulses of molting hormone, 20‐hydroxyecdysone, during late larval development of Drosophila melanogaster: Correlations with changes in gene activity
Authors: Warren James T. , Yerushalmi Yoram , Shimell Mary Jane , O'Connor Michael B. , Restifo Linda L. , Gilbert Lawrence I.
Published: November 2005

Periodic pulses of the insect steroid molting hormone 20‐hydroxyecdysone (20E), acting via its nuclear receptor complex (EcR/USP), control gene expression at many stages throughout Drosophila development. However, during the last larval instar of some lepidopteran insects, subtle changes in titers of ecdysteroids have been documented, including the so‐called “commitment peak.” This small elevation of 20E reprograms the larva for metamorphosis to the pupa. Similar periods of ecdysteroid immunoreactivity have been observed during the last larval instar of Drosophila. However, due to low amplitude and short duration, along with small body size and staging difficulties, their timing and ecdysteroid composition have remained uncertain. Employing a rigorous regimen of Drosophila culture and a salivary gland reporter gene, Sgs3‐GFP, we used RP‐HPLC and differential ecdysteroid RIA analysis to determine whole body titers of 20E during the last larval instar. Three small peaks of 20E were observed at 8, 20, and 28 hr following ecdysis, prior to the well‐characterized large peak around the time of pupariation. The possible regulation of 20E levels by biosynthetic P450 enzymes and the roles of these early peaks in coordinating gene expression and late larval development are discussed. Developmental Dynamics 235:315–326, 2006. © 2005 Wiley‐Liss, Inc.
Inhibition of zebrafish fin regeneration using in vivo electroporation of morpholinos against fgfr1 and msxb
Authors: Thummel Ryan , Bai Shan , Sarras Michael P. , Song Peizhen , McDermott Jeffrey , Brewer Jeffrey , Perry Martin , Zhang Xiaoming , Hyde David R. , Godwin Alan R.
Published: November 2005

Increased interest in using zebrafish as a model organism has led to a resurgence of fin regeneration studies. This has allowed for the identification of a large number of gene families, including signaling molecules and transcription factors, which are expressed during regeneration. However, in cases where no specific inhibitor is available for the gene product of interest, determination of a functional role for these genes has been difficult. Here we demonstrate that in vivo electroporation of morpholino oligonucleotides is a feasible approach for protein knock‐down during fin regeneration. Morpholino oligonucleotides against fgfr1 and msxb were utilized and knock‐down of both proteins resulted in reduced fin outgrowth. Importantly, Fgfr1 knock‐down phenocopied outgrowth inhibition obtained with an Fgfr1 inhibitor. Furthermore, this method provided direct evidence for a functional role for msxb in caudal fin regeneration. Finally, knock‐down of Fgfr1, but not Msxb, affected the blastemal expression of msxc, suggesting this technique can be used to determine epistasis in genetic pathways affecting regeneration. Thus, this convenient reverse genetic approach allows researchers to quickly (1) assess the function of genes known to be expressed during fin regeneration, (2) screen genes for functional relevance during fin regeneration, and (3) assign genes to the molecular pathways underlying fin regeneration. Developmental Dynamics 235:336–346, 2006. © 2005 Wiley‐Liss, Inc.
Pea3 expression is regulated by FGF signaling in developing retina
Authors: McCabe Kathryn Leigh , McGuire Chris , Reh Thomas A.
Published: November 2005

FGF signaling has been implicated as an important regulator of retinal development. As a first step in characterizing potential downstream targets of FGF signaling in the retina, we have analyzed expression of Pea3, a member of the Pea3 class of Ets‐domain transcription factors, in the developing eye. We find that Pea3 is expressed in the developing retina, and its transcription is regulated by FGF receptor activation. In addition, FGF signaling activates Cath5, a gene necessary for retinal ganglion cell differentiation. These results suggest that FGF signaling via MAPK up‐regulates transcription factors that in turn control retinal ganglion cell differentiation. Developmental Dynamics 235:327–335, 2006. © 2005 Wiley‐Liss, Inc.
Molecular characterization of the Caenorhabditis elegans ALP/Enigma gene alp‐1
Authors: McKeown Caroline R. , Han Hsiao‐Fen , Beckerle Mary C.
Published: November 2005

Members of the ALP/Enigma family of PDZ‐LIM proteins play a role in cytoskeletal anchorage and mutations in at least one member of this family are associated with human cardiomyopathy. Here, we describe the analysis of the Caenorhabditis elegans alp‐1 gene. alp‐1 is predicted to encode the entire nematode ALP/Enigma protein family, consisting of one ALP‐related protein with a single LIM domain and three Enigma‐like proteins containing four LIM domains. We demonstrate that the ALP‐1 proteins are expressed in muscle cells, where they localize to actin anchorage and muscle attachment sites. We show that the PDZ domain of the ALP‐1 proteins is sufficient to target the protein to the dense bodies, which are important actin anchorage sites in C. elegans body wall muscle. We demonstrate that the C. elegans ALP/Enigma proteins are also localized to cell–cell junctions and to both epithelial and muscle cell nuclei. These findings suggest new roles for the ALP/Enigma protein family that may lead to the understanding of their involvement in cardiomyopathy. Developmental Dynamics 235:530–538, 2006. © 2005 Wiley‐Liss, Inc.
Identification and comparative expression analysis of a second wt1 gene in zebrafish
Authors: Bollig Frank , Mehringer Rebecca , Perner Birgit , Hartung Christina , Schäfer Matthias , Schartl Manfred , Volff Jean‐Nicolas , Winkler Christoph , Englert Christoph
Published: November 2005

The Wilms' tumor suppressor gene wt1 encodes a zinc‐finger transcription factor that plays an important role in the development of the mammalian genitourinary system. Mutations in WT1 in humans lead to anomalies of kidney and gonad development and cause Wilms' tumor, a pediatric kidney cancer. The inactivation of both wt1 alleles in mice gives rise to multiple organ defects, among them agenesis of kidney, spleen, and gonads. In zebrafish, an ortholog of wt1 has been described that is expressed in the pronephric field and is later restricted to the podocytes. Here, we report the existence of a second wt1 gene in zebrafish, which we have named wt1b (we named the initial gene wt1a). The overall sequence identity of the two Wt1 proteins is 70% and 92% between the zinc‐finger regions, respectively. In contrast to wt1a, wt1b is expressed from the earliest stages of development onward, albeit at low levels. Both wt1a and wt1b are expressed in the intermediate mesoderm, with wt1b being restricted to a smaller area lying at the caudal end of the wt1a expression domain. In adult fish, high expression levels for both genes can be found in gonads, kidney, heart, spleen, and muscle. Developmental Dynamics 235:554–561, 2006. © 2005 Wiley‐Liss, Inc.
IL‐12‐independent Th1 polarization in human mononuclear cells infected with varicella‐zoster virus
Authors: Yu Hong‐Ren , Chen Rong‐Fu , Hong Kuo‐Ching , Bong Chin‐Nam , Lee Wen‐I , Kuo Ho‐Chang , Yang Kuender D.
Published: November 2005

T helper type 1 (Th1) cells perform a critical role in fighting intracellular organisms, and interleukin‐12 (IL‐12) is known to promote a Thl response. This study was conducted to identify whether an IL‐12‐independent Th1 reaction is induced by the varicella‐zoster virus (VZV) in human beings. It was found that different intracellular microorganisms could induce IFNγ but not IL‐12 production. Induction of IFNγ production by VZV was associated with IFNα production and phosphorylation of both the signal transducer and activator of transcription‐1 (STAT‐1) and STAT‐4 in lymphocytes. In contrast, Bacillus Calmette‐Guerin (BCG) induced IL‐12 production in association with STAT‐4 but not STAT‐1 activation. Anti‐IFNα but not anti‐IL‐12 antibodies blocked the VZV‐induced Th1 polarization. A patient with an IL‐12 receptor β1 chain deficiency showed a normal VZV‐ but not a normal BCG‐induced Th1 reaction, further supporting the concept of an IFNα‐mediated, IL‐12‐independent Th1 reaction in response to certain intracellular infections. Identification of the early Th1 polarization induced by IFNα versus IL‐12 in response to specific viruses may enable the development of better therapeutic strategies tailored to different infections.
Antibody‐mediated signaling through PD‐1 costimulates T cells and enhances CD28‐dependent proliferation
Authors: del Rio María‐Luisa , Penuelas‐Rivas Giovanna , Dominguez‐Perles Raul , Ramirez Pablo , Parrilla Pascual , Rodriguez‐Barbosa Jose‐Ignacio
Published: November 2005

Programmed death‐1 (PD‐1, CD279) is a molecule expressed on activated T, B and myeloid cells. The role of the interaction of PD‐1 ligands (PD‐L1 and PD‐L2) with PD‐1 receptor and the type of signals (costimulatory or inhibitory) that are delivered is a subject of intense debate. Our study has characterized two monoclonal antibodies (mAb) against murine PD‐1, termed clone 1H10 and clone 4F10, that recognized different epitopes from that of anti‐PD‐1, clone J43. We showed that neither of them inhibited anti‐CD3‐mediated proliferation, but 1H10 mAb induced direct T cell proliferation in the absence of any other stimulus. Moreover, PD‐1 engagement with 1H10 mAb costimulated anti‐CD3‐mediated proliferation and enhanced anti‐CD3/CD28 proliferation on both CD4+ and CD8+ T cells in the low range of anti‐CD3 concentrations. Anti‐PD‐1‐mediated proliferation induced with 1H10 mAb was also observed in vivo on CD4+ and CD8+ T cells, when CFSE‐labeled splenocytes were adoptively transferred to irradiated syngeneic and allogeneic recipients. Overall, our data indicate that PD‐1 might not only deliver negative signals to T cells upon interaction through one of its ligands, PD‐L1 as reported, but also could costimulate T cells, suggesting a dual potential functional activity of the extracellular domains of this receptor.
Analysis of Lyn/CD22 double‐deficient B cells in vivo demonstrates Lyn‐ and CD22‐independent pathways affecting BCR regulation and B cell survival
Authors: Ferry Helen , Cockford Tanya L. , Silver Karlee , Rust Nigel , Goodnow Christopher C. , Cornall Richard J.
Published: November 2005

B cell fate is determined by the strength of signals from the antigen receptor and from co‐receptors that adjust the activation threshold and tune the B cell to its environment. These co‐receptors have been broadly classified into inhibitory and enhancing groups, yet some, such as CD22, may have dual effects. CD22 recruits a variety of signal enhancers at the same time as Lyn‐dependent phosphorylation leads to the binding of the inhibitory phosphatase SHP‐1. To assess the relative importance of Lyn‐ and CD22‐dependent and ‐independent pathways, we generated Lyn and CD22 single‐deficient mice and Lyn/CD22 double‐deficient mice expressing the MD4 immunoglobulin transgene against hen egg lysozyme (IgHEL). This genetic approach has enabled us to compare the contributions of Lyn and CD22 to B cell development in vivo, independent of BCR specificity and in the presence and absence of self‐antigen. Our results show that although the effects of Lyn are dominant in negative regulation of B cell hyperactivity, Lyn and CD22 have independent and additive effects on B cell survival. These findings emphasize the subtle nature of regulation at the BCR and the usefulness of genetic complementation to dissect common and parallel pathways.
Requirement of the Fc receptor common γ‐chain forγδ T cell‐mediated promotion of murine experimental autoimmune encephalomyelitis
Authors: Szalai Alexander J. , Hu Xianzhen , Raman Chander , Barnum Scott R.
Published: November 2005

Immunoglobulin Fcγ receptors (FcγR) are comprised of a ligand‐binding α‐chain that sometimes associates with a cell signaling common γ‐chain. These receptors comprise an important family of effector molecules that link humoral and cell‐mediated adaptive immunity and regulate innate immunity. Recent animal studies suggest that FcγR in general, and FcR α‐chains in particular, are required for full development of experimental autoimmune encephalomyelitis (EAE). We show here that deletion of the γ‐chain renders mice resistant to EAE, whereas deletion of the α‐chains of FcγRI, FcγRIIB and FcγRIII has no protective effect. Susceptibility to EAE is fully restored in common γ‐chain–/– mice into which wild‐type splenocytes are adoptively transferred, but EAE is not restored in common γ‐chain–/– mice given wild‐type splenocytes depleted of γδ T cells. These data indicate that although the common γ‐chain is required for full development of EAE in mice, this requirement is likely FcγR α‐chain‐independent. Expression of the common γ‐chain by γδ T cells, probably in conjunction with the T cell receptor/CD3 complex, is likely the key requirement for full development of EAE.
Glucocorticoid‐induced TNFR family‐related protein (GITR) activation exacerbates murine asthma and collagen‐induced arthritis
Authors: Patel Manish , Xu Damo , Kewin Pete , Choo‐Kang Brian , McSharry Charles , Thomson Neil C. , Liew Foo Y.
Published: November 2005

Glucocorticoid‐induced TNFR family‐related protein (GITR) is expressed at low levels on resting T cells, B cells and macrophages but at high levels on regulatory T cells (Treg). Although GITR expression is up‐regulated on CD4+effector cells upon activation, the role of GITR in Th1 and Th2 cell development is unclear. We report here that activation of GITR signalling by anti‐GITR antibody markedly enhanced the induction of both Th1 and Th2 cytokine production by naive CD4+CD25–T cells. Consistent with this observation, anti‐GITR antibody significantly enhanced the expression of the key Th1 (T‐bet) and Th2 (GATA3) transcription factorsin vitro. Administration of anti‐GITR mAb in a murine model of arthritis significantly exacerbated the severity and onset of joint inflammation with elevated production of TNF‐α, IFN‐γ, IL‐5, and collagen‐specific IgG1. Administration of anti‐GITR mAb also significantly exacerbated murine allergic airways inflammation with elevated production of OVA‐specific IFN‐γ, IL‐2, IL‐4, IL‐5, and IgE. Finally, we demonstrated that adoptive transfer of CD4+GITR+T cells effectively abolished airway inflammation induced in SCID mice reconstituted with CD4+GITR–T cells. Our results therefore provide direct evidence that GITR can modulate both Th1‐ and Th2‐mediated inflammatory diseases, and may be a potential target for therapeutic intervention.
Syntheses, Crystal Structures and Magnetic Properties of Carboxylato‐Bridged Polymeric Networks of MnII
Authors: Manna Subal Chandra , Zangrando Ennio , Drew Michael G. B. , Ribas Joan , Chaudhuri Nirmalendu Ray
Published: November 2005

Three new carboxylato‐bridged polymeric networks of MnII having molecular formula [Mn(ox)(dpyo)]n (1), {[Mn2(mal)2(bpee)(H2O)2]·0.5(bpee)·0.5(CH3OH)}n (2) and {[Mn3(btc)2(2,2′‐bipy)2(H2O)6]·4H2O}n (3) [dpyo, 4,4′‐bipyridine N,N′‐dioxide; bpee, trans‐1,2 bis(4‐pyridyl)ethylene; 2,2′‐bipy, 2,2′‐bipyridine; ox = oxalate dianion; mal = malonate dianion; btc = 1,3,5‐benzenetricarboxylate trianion] have been synthesized and characterized by single‐crystal X‐ray diffraction studies and low temperature magnetic measurements. Structure determination of complex 1 reveals a covalent bonded 2D network containing bischelating oxalate and bridging dpyo; complex 2 is a covalent bonded 3D polymeric architecture, formed by bridging malonate and bpee ligands, resulting in an open framework with channels filled by uncoordinated disordered bpee and methanol molecules. Whereas complex 3, comprising btc anions bound to three metal centers, is a 1D chain which further extends its dimensionality to 3D via ‐ and H‐bonding interactions. Low temperature magnetic measurements reveal the existence of weak antiferromagnetic interaction in all these complexes. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
Ferrocenylethynyltin Compounds – Characterization and Reactivity towards Triethylborane
Authors: Wrackmeyer Bernd , Kenner‐Hofmann Barbara H. , Milius Wolfgang , Thoma Peter , Tok Oleg L. , Herberhold Max
Published: November 2005

Ferrocenylethynyl(trimethyl)tin (1), bis(ferrocenylethynyl)dimethyltin (2), tetrakis(ferrocenylethynyl)tin (3), and chloro(ferrocenylethynyl)dimethyltin (4) have been prepared and characterized in solution by 1H, 13C, and 119Sn NMR spectroscopy. Solid‐state MAS 13C and 119Sn NMR spectra were measured for 2 and 3, and the molecular structure of one of the modifications of 2 was determined by X‐ray analysis. The reactivity of 1–4 towards triethylborane has been explored. 1,1‐Organoboration takes place in all cases, and the reactions are stereoselective for 1 and 4 to give the alkenes 5 and 6, respectively, in which the stannyl and the boryl groups are in cis‐positions at the C=C bond. In the case of 2, the final products are the 1‐stannacyclopenta‐2,4‐diene 7a and the 1‐stanna‐4‐boracyclohexa‐2,5‐diene 8a, whereas the reaction of 2 with triisopropylborane leads selectively to the six‐membered ring 8b. Zwitterionic intermediates 9a,b, in which the tin atom is coordinated side‐on to the C≡C bond of an alkynylborate, have been detected by NMR spectroscopy. Compound 3 reacts with triethylborane to give a mixture of three spirotin compounds 10–12 as the final products, where the tin atom connects five‐ and six‐membered rings. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
η2‐Iminoacyl and η2‐Acyl Monocyclopentadienyl Tantalum Complexes Bearing Oxo and Oxo‐Borane Ligands
Authors: Sánchez‐Nieves Javier , Royo Pascual , Mosquera Marta E. G.
Published: November 2005

Alkyl‐chloro ligand exchange by the reaction of [TaCp*R2{O·B(C6F5)3}] (R = CH2Ph, Me) with Ph3CCl gave the monoalkyl compounds [TaCp*RCl{O·B(C6F5)3}] (R = CH2Ph, Me). Insertion of CNAr (Ar = 2,6‐Me2C6H3) and CO into a Ta–C bond of the mono‐ and dialkyl complexes gave the iminoacyl compounds [TaCp*X{η2‐C(R)=NAr}{O·B(C6F5)3}] (X = R = CH2Ph, Me; X = Cl, R = CH2Ph) and the acyl compounds [TaCp*X{η2‐C(R)=O}{O·B(C6F5)3}] (X = R = CH2Ph, Me; X = Cl, R = CH2Ph), respectively. The related chloro compound [TaCp*Cl{η2‐C(Me)=NAr}{O·B(C6F5)3}] was isolated from the reaction of the oxo derivative [TaCp*Cl{η2‐C(Me)=NAr}(O)] with the Lewis acid B(C6F5)3. Addition of CNAr or pyridine to [TaCp*(CH2Ph){η2‐C(CH2Ph)=NAr}{O·B(C6F5)3}] afforded the borane‐free complex [TaCp*(CH2Ph){η2‐C(CH2Ph)=NAr}(O)] and the acid‐base adduct L·B(C6F5)3 (L = py, CNAr). The molecular structures of [TaCp*Cl{η2‐C(Me)=NAr}{O·B(C6F5)3}] and [TaCp*(CH2Ph){η2‐C(CH2Ph)=O}{O·B(C6F5)3}] were obtained from X‐ray diffraction studies.(© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
Ionic Liquids: Synthesis and Characterisation of Triphenylphosphonium Tosylates
Authors: Bonnet Ludovic G. , Kariuki Benson M.
Published: November 2005

Ionic liquids are currently attracting considerable interest from chemists, partly due to their potential as “green” alternatives to volatile molecular organic solvents. Phosphonium ionic liquids have received much less attention than ammonium salts in the past, but the situation is changing. The salts are applied in the liquid state but in this work, salts with higher melting points than is generally the case are investigated. They are solid at room temperature, thus enabling facile separation of liquid reaction products. Nine triphenylphosphonium tosylates have been prepared and characterised; their crystal structures have been determined and their melting points have been scrutinized, showing some sensitivity to the duration of drying. The structural information is expected to be invaluable in the understanding of the properties of the molten state.(© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
Oligo(2,5‐thienyleneethynylene)s with Terminal Donor‐Acceptor Substitution
Authors: Meier Herbert , Mühling Bastian , Oehlhof Annette , Theisinger Sonja , Kirsten Enzio
Published: November 2005

Five oligo(2,5‐thienyleneethynylene) series (OTE, n = 1–5), namely the push‐pull substituted compounds 1b‐5b and 1c‐5c, the purely donor substituted compounds 1a‐5a and two precursor series with protected and deprotected ethynyl end‐groups, respectively, were obtained by a convergent synthetic strategy. The extension of the conjugated chromophores in the donor‐acceptor OTE (DAOTE) series is superimposed by an intramolecular charge transfer (ICT), which decreases with an increasing number, n, of repeat units. The overall effect is studied by the convergence of the UV/Vis absorption maxima λmax (n) → λ∞ for n → ∞.(© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
Second‐Generation cycloSal‐d4TMP Pronucleotides Bearing Esterase‐Cleavable Sites — The “Trapping” Concept
Authors: Meier Chris , Ducho Christian , Jessen Henning , Vukadinović‐Tenter Dalibor , Balzarini Jan
Published: November 2005

An extension of the cycloSal‐pronucleotide approach is presented. Attachment of an enzyme‐cleavable ester/acylal group to the cycloSal‐d4TMP triesters should allow these compounds to be trapped intracellularly after cleavage. The ester/acylal groups were introduced in the 3‐ or 5‐position of the cycloSal ring system, and surprising differences were observed in hydrolysis studies in CEM cell extracts with respect to the ester/acylal moiety. While acetyl and levulinyl esters were readily cleaved, alkyl esters of cycloSal‐d4TMP acids proved to be resistant to enzymatic cleavage. In contrast, AM‐, POM‐ and POC‐acylals were rapidly cleaved in the extracts, leading to cycloSal‐d4TMP acids. The antiviral activity of the compounds against HIV is also presented. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
Evaluation of factors influencing membrane performance
Authors: Peng Weihua , Escobar Isabel C.
Published: November 2005

Three commercial water treatment membranes, TFC‐S (Koch membranes, San Diego, CA), ESPA1, and NTR7450 (Hydranautics, San Diego, CA), were tested under various physical and chemical conditions to investigate their fouling behaviors. It was found that TFC‐S always displayed the greatest rate of flux decline, ESPA1 displayed a mild trend in flux decline, and NTR7450 presented a nearly stable flux. Multivariable regression models showed that the flux decline rates for TFC‐S and ESPA1 were controlled by the initial permeate flux, whereas their initial (that is, instantaneous) foulings were controlled by the interaction between permeate drag and electrostatic repulsions. Feed bacteria concentration also contributed to the initial fouling of ESPA1 as a result of cell deposition on the membrane surface. NTR7450 showed an initial decline in flux followed by a steady flux, and its initial fouling was significantly affected by feed water total organic carbon (TOC) arising from the initial accumulation of colloidal organic particles on the surface. © 2005 American Institute of Chemical Engineers Environ Prog, 2005
Testing of water treatment copolymers for compatibility with polyamide reverse osmosis membranes
Authors: Gabelich Christopher J. , Ishida Kenneth P. , Bold Richard M.
Published: November 2005

Cationic polymers used in traditional water and wastewater treatment, in theory, will bind to the partially negatively charged polyamide membrane during reverse osmosis (RO) treatment. This study tested a variety of cationic, anionic, and nonionic polymers in terms of (1) aiding in turbidity removal when used in conjunction with alum coagulation [10 mg/L as Al2(SO4)3·14H2O], sedimentation, and dual‐media filtration; and (2) their binding affinity toward a polyamide membrane. Binding affinity was tested by exposing polyamide RO membranes to 50 mg/L of each polymer for 48 h and then conducting attenuated total reflectance Fourier transform infrared (FTIR) spectroscopy on the membrane samples and principal‐component analysis (PCA) of the FTIR spectra. Results from the turbidity removal tests showed that cationic polymers provided the lowest median effluent turbidity (0.03–0.11 NTU), followed by anionic polymers (0.06–0.08 NTU), and finally nonionic polymers (0.11–0.17 NTU). Although PCA of the FTIR spectra did detect differences in polymer‐exposed membranes vs. a control, no discernable difference in RO membrane performance was observed. Therefore, under the conditions studied, the issue of “membrane poisoning ” caused by organic polymer absorption onto polyamide membranes was minimal. © 2005 American Institute of Chemical Engineers Environ Prog, 2005
Industrial process water recycling: Principles and examples
Authors: Van der Bruggen Bart , Boussu Katleen , De Vreese Ilse , Van Baelen Guy , Willemse Filip , Goedemé Daan , Colen Ward
Published: November 2005

Recycling of industrial process water requires an adequate control of water quantities and qualities. A water balance has to be set up and the minimum water quality for each process has to be determined. This involves experimental determination of flows and concentrations, and a methodology to optimize the overall water consumption. This can be done either by rigorous methods or by “common sense ” methods.

The next step is the implementation of techniques for water recycling. Because quality standards differ significantly for each industrial activity, no general methods or techniques exist that can be applied in all cases. Two examples are discussed where water is regenerated and the water quality is evaluated in terms of influence on the process itself: (1) process water in the textile industry, used for dyeing, and (2) water used in car washes. Wastewater from the textile industry is treated by nanofiltration. Effluents from car washes are treated by an integrated method consisting of ultrafiltration and biological treatment of the concentrate. Results indicate that water recycling is feasible in both cases, although in‐depth studies are required to make an optimal membrane choice as a function of the proposed water quality, and to set up procedures to control membrane flux. In addition, further treatment of concentrates has to be considered in case membrane filtration is used in the regeneration step. © 2005 American Institute of Chemical Engineers Environ Prog, 2005
Recovery of copper‐contaminated sludge in a two‐stage leaching process
Authors: Hu S.H. , Tsai M.S. , Yen F.S. , Onlin T.
Published: November 2005

The purpose of this study was to develop an effective method of processing copper‐contaminated sludge, produced during the manufacture of printed circuit boards (PCBs). In the first stage, 2 N sulfuric acid was used to leach the wet sludge. A solid to liquid ratio of approximately 1:10 was used. Because hydroxide compounds in the sludge were not stable when exposed to acid, the copper extraction percentage exceeded 85% in 15 min. In the second stage, an ammonia solution was used to purify the sulfuric acid leachate by forming an ammine complex. During this process hydroxide compounds were formed by the impurities (Al3+, Fe2+, Pb2+, etc.) in the leachate at pH 10. After purification, the residual metallic hydroxide compounds were treated by the ferrite process to produce a stable oxide compound. The ammine solution was then heated to evaporate the ammonia, and copper hydroxide was formed in solution. The temperature was maintained at 80° C by aeration. In the process, copper hydroxide was transformed into copper oxide. The copper concentration reached 98.4%. © 2005 American Institute of Chemical Engineers Environ Prog, 2006
Dynamics of intraday serial correlation in the Italian futures market
Authors: Bianco Simone , Renò Roberto
Published: November 2005

The serial correlation of high‐frequency intraday returns on the Italian stock index futures (FIB30) in the period 2000–2002 is studied. It is found that intraday autocorrelation is mostly negative for time scales lower than 20 minutes, mainly due to the bid–ask bounce effect. Although this supports the efficiency of the Italian futures market, evidence that intraday serial correlation becomes positive in high‐volatility regimes is also provided. Moreover, it is found that it is mainly unexpected volatility that makes serial correlation rise, and not its predictable part. The results are supportive of the K. Chan (1993) model. © 2006 Wiley Periodicals, Inc. Jrl Fut Mark 26:61–84, 2006
The valuation of European options when asset returns are autocorrelated
Authors: Liao Szu‐Lang , Chen Chao‐Chun
Published: November 2005

This article derives the closed‐form formula for a European option on an asset with returns following a continuous‐time type of first‐order moving average process, which is called an MA(1)‐type option. The pricing formula of these options is similar to that of Black and Scholes, except for the total volatility input. Specifically, the total volatility input of MA(1)‐type options is the conditional standard deviation of continuous‐compounded returns over the option's remaining life, whereas the total volatility input of Black and Scholes is indeed the diffusion coefficient of a geometric Brownian motion times the square root of an option's time to maturity. Based on the result of numerical analyses, the impact of autocorrelation induced by the MA(1)‐type process is significant to option values even when the autocorrelation between asset returns is weak. © 2006 Wiley Periodicals, Inc. Jrl Fut Mark 26:85–102, 2006
Chromosome 18 suppresses tumorigenic properties of human prostate cancer cells
Authors: Gagnon Audrey , Ripeau Jean‐Sébastien , Zvieriev Valerii , Chevrette Mario
Published: November 2005

Although prostate cancer is still the most diagnosed cancer in men, most genes implicated in its progression are yet to be identified. Chromosome abnormalities have been detected in human prostate tumors, many of them associated with prostate cancer progression. Indeed, alterations (including deletions or amplifications) of more than 15 human chromosomes have been reported in prostate cancer. We hypothesized that transferring normal human chromosomes into human prostate cancer cells would interfere with their tumorigenic and/or metastatic properties. We used microcell‐mediated chromosome transfer to introduce human chromosomes 10, 12, 17, and 18 into highly tumorigenic (PC‐3M‐Pro4) and highly metastatic (PC‐3M‐LN4) PC‐3‐derived cell lines. We tested the in vitro and in vivo properties of these hybrids. Introducing chromosome 18 into the PC‐3M‐LN4 prostate cancer cell line greatly reduced its tumorigenic phenotype. We observed retarded growth in soft agar, decreased invasiveness through Matrigel, and delayed tumor growth into nude mice, both subcutaneously and orthotopically. This phenotype is associated with a marker in the 18q21 region. Combined with the loss of human chromosome 18 regions often seen in patients with advanced prostate cancer, our results show that chromosome 18 encodes one or more tumor‐suppressor genes whose inactivation contributes to prostate cancer progression. © 2005 Wiley‐Liss, Inc.
The glycine 90 to aspartate alteration in the Aβ subunit of PP2A (PPP2R1B) associates with breast cancer and causes a deficit in protein function
Authors: Esplin Edward D. , Ramos Purita , Martinez Bobbie , Tomlinson Gail E. , Mumby Marc C. , Evans Glen A.
Published: November 2005

Mutations of the PPP2R1B gene, which encodes the Aβ scaffolding subunit of serine/threonine protein phosphatase 2A (PP2A), have been identified in several types of cancer including lung and breast carcinoma. One of these mutations results in an alteration of glycine 90 to aspartic acid (G90D), which has been found in both tumor and genomic DNA, raising the possibility that it is associated with an increased risk for cancer. A novel microarray‐based technology was used to screen for this single‐nucleotide polymorphism in 387 cancer patients and 329 control individuals. These data were used for case–control and family‐based comparisons in order to study the association of this polymorphism with susceptibility to lung carcinoma, breast carcinoma, and acute lymphoblastic leukemia. The frequency of the G90D polymorphism in breast cancer patients was significantly higher in cases (3%) than in controls (0.3%). The wild‐type Aβ subunit interacted with the B56γ (PPP2R5C), PR72 (PPP2R3A), and PR48 subunits of PP2A but did not interact with the B55α (PPP2R2A), B56α (PPP2R5A), or B56β (PPP2R5B) regulatory subunits in an in vitro binding assay. The G90D alteration inhibited the interaction of Aβ with the B56γ subunit but had no effect on binding to the PR72 subunit. These results provide evidence that the G90D alteration of the Aβ subunit of PP2A is associated with a low frequency of breast carcinoma and that the role of this alteration in transformation is likely to involve decreased interaction with the B56γ regulatory subunit. © 2005 Wiley‐Liss, Inc.
Critically short telomeres in acute myeloid leukemia with loss or gain of parts of chromosomes
Authors: Swiggers Susan J. J. , Kuijpers Marianne A. , de Cort Maartje J. M. , Beverloo H. Berna , Zijlmans J. Mark J. M.
Published: November 2005

Telomeres, nucleoprotein complexes at chromosome ends, protect chromosomes against end‐to‐end fusion. Previous in vitro studies in human fibroblast models indicated that telomere dysfunction results in chromosome instability. Loss of telomere function can result either from critical shortening of telomeric DNA or from loss of distinct telomere‐capping proteins. It is less clear whether telomere dysfunction has an important role in human cancer development in vivo. Acute myeloid leukemia (AML) is a good model to study mechanisms that generate chromosome instability in human cancer development because distinct groups of AML are characterized either by aberrations that theoretically could result from telomere dysfunction (terminal deletions, gains/losses of chromosome parts, nonreciprocal translocations), or aberrations that are unlikely to result from telomere dysfunction (e.g., reciprocal translocations or inversions). Here we demonstrate that AML with multiple chromosome aberrations that theoretically could result from telomere dysfunction is invariably characterized by critically short telomeres. Short telomeres in this group are not associated with low telomerase activity or decreased expression of essential telomeric capping proteins TRF2 and POT1. In contrast, telomerase activity levels are significantly higher in AML with short telomeres. Notably, short telomeres in the presence of high telomerase may relate to significantly higher expression of TRF1, a negative regulator of telomere length. Our observations suggest that, consistent with previous in vitro fibroblast models, age‐related critical telomere shortening may have a role in generating chromosome instability in human AML development. © 2005 Wiley‐Liss, Inc.
Post‐transplant lymphoproliferative disorder subtypes correlate with different recurring chromosomal abnormalities
Authors: Djokic Miroslav , Le Beau Michelle M. , Swinnen Lode J. , Smith Sonali M. , Rubin Charles M. , Anastasi John , Carlson Katrin M.
Published: November 2005

Although cytogenetic analysis advanced the understanding of the pathogenesis of primary non‐Hodgkin lymphoma and led to improved clinical management, there have been no large cytogenetic studies of post‐transplant lymphoproliferative disorder (PTLD). We examined the karyotypes of 36 PTLD cases and correlated them with clinical, laboratory, and pathologic findings. The cases included 2 early lesions, 13 polymorphic PTLDs, and 21 monomorphic PTLDs (18 B‐cell and 3 T‐cell proliferations). Cytogenetic abnormalities were identified in 72% of monomorphic B‐cell PTLDs and in all T‐cell PTLDs, but in only 15% of polymorphic PTLDs and in no early lesions. The most frequent clonal abnormalities in monomorphic PTLD were trisomies 9 and/or 11 (5 cases), followed by rearrangements of 8q24.1 (4 cases), 3q27 (2 cases), and 14q32 (2 cases). MYC rearrangement (8q24.1) and T‐cell‐associated chromosomal abnormalities correlated with poor outcome and short survival. PTLD with trisomy 9 and/or 11 developed early after transplant, presenting as Epstein–Barr virus–positive large B‐cell lymphoma with prolonged survival. © 2005 Wiley‐Liss, Inc.
Disruption of BRCA1 function results in telomere lengthening and increased anaphase bridge formation in immortalized cell lines
Authors: French Juliet D. , Dunn Jasmyn , Smart Chanel E. , Manning Nathan , Brown Melissa A.
Published: November 2005

BRCA1 is a tumor suppressor that functions in controlling cell growth and maintaining genomic stability. BRCA1 has also been implicated in telomere maintenance through its ability to regulate the transcription of hTERT, the catalytic subunit of telomerase, resulting in telomere shortening, and to colocalize with the telomere‐binding protein TRF1. The high incidence of nonreciprocal translocations in tumors arising from BRCA1 mutation carriers and Brca1‐null mice also raises the possibility that BRCA1 plays a role in telomere protection. To date, however, the consequences for telomere status of disrupting BRCA1 have not been reported. To examine the role of BRCA1 in telomere regulation, we have expressed a dominant‐negative mutant of BRCA1 (trBRCA1), known to disrupt multiple functions of BRCA1, in telomerase‐positive mammary epithelial cells (SVCT) and telomerase‐negative ALT cells (GM847). In SVCT cells, expression of trBRCA1 resulted in an increased incidence of anaphase bridges and in an increase in telomere length, but no change in telomerase activity. In GM847 cells, trBRCA1 also increased anaphase bridge formation but did not induce any change in telomere length. BRCA1 colocalized with TRF2 in telomerase‐positive cells and with a small subset of ALT‐associated PML bodies (APBs) in ALT cells. Together, these results raise the possibility that BRCA1 could play a role in telomere protection and suggest a potential mechanism for one of the phenotypes of BRCA1‐deficient cells. © 2005 Wiley‐Liss, Inc.
Genetic evidence for a maternal effect locus controlling genomic imprinting and growth
Authors: Duselis Amanda R. , Wiley Christopher D. , O'Neill Michael J. , Vrana Paul B.
Published: November 2005

Crosses between two species of deer mouse (Peromyscus) yield dramatic parent‐of‐origin effects. Female P. maniculatus (BW) crossed with male P. polionotus (PO) produce animals smaller than either parent. PO females crossed with BW males yield lethal overgrowth that has been associated with loss‐of‐imprinting (LOI). Previously, we mapped two loci influencing fetal growth. These two loci, however, do not account for the LOI, nor for the dysmorphic phenotypes. Here we report that maternal genetic background strongly influences the LOI. Analyses of crosses wherein maternal genetic background is varied suggest that this effect is likely due to the action of a small number of loci. We have termed these putative loci Meil. Estimation of Meil loci number was confounded by skewed allelic ratios in the intercross line employed. We show that the Meil loci are not identical to any of the DNA methyltransferases shown to be involved in regulation of genomic imprinting. genesis 43:155–165, 2005. © 2005 Wiley‐Liss, Inc.
Conditional LoxP‐flanked glucosylceramide synthase allele controlling glycosphingolipid synthesis
Authors: Yamashita Tadashi , Allende Maria Laura , Kalkofen Danielle N. , Werth Norbert , Sandhoff Konrad , Proia Richard L.
Published: November 2005

Glycosphingolipids are organizational building blocks of plasma membranes that participate in key cellular functions, such as signaling and cell‐to‐cell interactions. Glucosylceramide synthase—encoded by the Ugcg gene—controls the first committed step in the major pathway of glycosphingolipid synthesis. Global disruption of the Ugcg gene in mice is lethal during gastrulation. We have now established a Ugcg allele flanked by loxP sites (floxed). When cre recombinase was expressed in the nervous system under control of the nestin promoter, the floxed gene underwent recombination, resulting in a substantial reduction of Ugcg expression and of glycosphingolipid ganglio‐series levels. The mice deficient in Ugcg expression in the nervous system show a striking loss of Purkinje cells and abnormal neurologic behavior. The floxed Ugcg allele will facilitate analysis of the function of glycosphingolipids in development, physiology, and in diseases such as diabetes and cancer. genesis 43:175–180, 2005. Published 2005 Wiley‐Liss, Inc.
Generation of conditional alleles of the murine iron regulatory protein (IRP)‐1 and ‐2 genes
Authors: Galy Bruno , Ferring Dunja , Hentze Matthias W.
Published: November 2005

Central aspects of cellular iron metabolism are controlled by IRP1 and IRP2, which are ubiquitously expressed in mouse organs and cells. Total and constitutive deficiency of both IRPs causes embryonic lethality in the mouse. To bypass the early lethality and to study organ‐specific and/or temporal functions of IRP1 and/or IRP2 we generated Irp1 and Irp2 conditional alleles. We used mouse lines where a βGeo gene trap construct was inserted into the second intron of the Irp1 and the Irp2 gene, generating hypomorphic alleles by interrupting the corresponding open reading frame near the amino‐termini. The gene trap cassettes are flanked by Frt sites and were co‐inserted with LoxP sites flanking exon 3. Flp‐mediated removal of the gene trap construct generates floxed alleles with wildtype functions. For both Irp genes, Cre‐assisted deletion of exon 3 generates complete null alleles that, in the case of IRP2, are associated with altered body iron distribution and compromised hematopoiesis. If not removed, the gene trap construct causes partially penetrant embryonic lethality unrelated to IRP deficiency when inserted within the Irp1 but not the Irp2 locus. We discuss the implications for functional genomics in the mouse. genesis 43:181–188, 2005. © 2005 Wiley‐Liss, Inc.
Mouse model for ablation of proliferating microgliain acute CNS injuries
Authors: Gowing Geneviève , Vallières Luc , Julien Jean‐Pierre
Published: November 2005

Activation of microglia, the primary immune effectors of the CNS and proinflammatory signaling, is a hallmark of brain damage. However, it remains controversial whether microglial cells have beneficial or detrimental functions in various neuropathological conditions. We report the generation of transgenic mice that express a mutant form of herpes simplex virus type 1 thymidine kinase (HSV‐1 TKmt‐30) driven by the myeloid‐specific CD11b promoter. Using two paradigms of nervous system damage, hypoglossal nerve axotomy, and cortical stab injury, we show that specific ablation of proliferating microglia in CD11b‐TKmt‐30 mice can be achieved by administration of ganciclovir. For example, after hypoglossal nerve injury, a 75% reduction in proliferating microglial cells was observed at the site of injury. The CD11b‐TKmt‐30 transgenic mouse should provide a valuable tool for studying the role of microglia in CNS damage and repair. © 2005 Wiley‐Liss, Inc.
Identifying human parieto‐insular vestibular cortex using fMRI and cytoarchitectonic mapping
Authors: Eickhoff Simon B. , Weiss Peter H. , Amunts Katrin , Fink Gereon R. , Zilles Karl
Published: November 2005

The parieto‐insular vestibular cortex (PIVC) plays a central role in the cortical vestibular network. Although this region was first defined and subsequently extensively studied in nonhuman primates, there is also ample evidence for a human analogue in the posterior parietal operculum. In this study, we functionally and anatomically characterize the putative human equivalent to macaque area PIVC by combining functional magnetic resonance imaging (fMRI) of the cortical response to galvanic vestibular stimulation (GVS) with probabilistic cytoarchitectonic maps of the human parietal operculum. Our fMRI data revealed a bilateral cortical response to GVS in posterior parieto‐insular cortex. Based on the topographic similarity of these activations to primate area PIVC, we suggest that they constitute the functionally defined human equivalent to macaque area PIVC. The locations of these activations were then compared to the probabilistic cytoarchitectonic maps of the parietal operculum (Eickhoff et al. [2005a]: Cereb Cortex, in press; Eickhoff et al. [2005c]: Cereb Cortex, in press), whereby the functionally defined PIVC matched most closely the cytoarchitectonically defined area OP 2. This activation of OP 2 by vestibular stimulation and its cytoarchitectonic features, which are similar to other primary sensory areas, suggest that area OP 2 constitutes the human equivalent of macaque area PIVC. Hum Brain Mapp, 2005. © 2005 Wiley‐Liss, Inc.
Dealing with the shortcomings of spatial normalization: Multi‐subject parcellation of fMRI datasets
Authors: Thirion Bertrand , Flandin Guillaume , Pinel Philippe , Roche Alexis , Ciuciu Philippe , Poline Jean‐Baptiste
Published: November 2005

The analysis of functional magnetic resonance imaging (fMRI) data recorded on several subjects resorts to the so‐called spatial normalization in a common reference space. This normalization is usually carried out on a voxel‐by‐voxel basis, assuming that after coregistration of the functional images with an anatomical template image in the Talairach reference system, a correct voxel‐based inference can be carried out across subjects. Shortcomings of such approaches are often dealt with by spatially smoothing the data to increase the overlap between subject‐specific activated regions. This procedure, however, cannot adapt to each anatomo‐functional subject configuration. We introduce a novel technique for intra‐subject parcellation based on spectral clustering that delineates homogeneous and connected regions. We also propose a hierarchical method to derive group parcels that are spatially coherent across subjects and functionally homogeneous. We show that we can obtain groups (or cliques) of parcels that well summarize inter‐subject activations. We also show that the spatial relaxation embedded in our procedure improves the sensitivity of random‐effect analysis. Hum Brain Mapp, 2005. © 2005 Wiley‐Liss, Inc.