bluuebunny/crossref_metadata_2025_split huggingface dataset:
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

AbstractAn 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

AbstractThree 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

AbstractCationic 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

AbstractRecycling 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

AbstractThe 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

AbstractThe 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

AbstractThis 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

AbstractAlthough 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

AbstractMutations 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

AbstractTelomeres, 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

AbstractAlthough 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

AbstractBRCA1 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

AbstractCrosses 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

AbstractGlycosphingolipids 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

AbstractCentral 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

AbstractActivation 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

AbstractThe 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.