bluuebunny/crossref_metadata_2025_split huggingface dataset:
Density‐Dependent Effects in Jehlius cirratus (Darwin, 1854) (Cirripedia: Chthamalidae) under Different Growth Conditions
Authors: López Daniel A. , González María L. 
Published: December 2003

Abstract.  We analyse the effects of crowding (‘hummocking’) on the growth, reproduction and mortality of the chthamaloid barnacle Jehlius cirratus (Darwin, 1854) on the coast of Chile. Recruitment intensity, ranging from solitary individuals to dense groups, generates different growth conditions. Density‐dependent effects are reflected in the shape, growth parameters, fecundity, sexual maturity and mortality of solitary and crowded specimens. The skewing of size distribution during growth was not significant at the beginning of the growth period, irrespective of initial density. Nevertheless, skewness in size increased with time, both at high and low densities, indicating that the dominance and suppression exerted by larger specimens over smaller ones generate a density‐dependent effect on size during growth. Mortality was greatest when high‐density recruitment occurred immediately before the period when water temperature and food quantity are highest (spring), when it is assumed that growth is greatest; this seasonal effect was not detected at lower levels of recruitment density. Similarly, no differences in mortality were detected between recruitment densities during the period when temperatures are lowest (autumn) and growth is probably slower. In the middle‐high intertidal zone, where J. cirratus co‐exists with Notochthamalus scabrosus (Darwin, 1854), the proportion of dead J. cirratus specimens was directly related both to the relative abundance of N. scabrosus and the total barnacle density. Although the mortality of J. cirratus was density dependent, the increase in the number of N. scabrosus towards the lower section of the middle intertidal zone could have a greater effect on J. cirratus mortality than intra‐specific competition.
FROM EXPERIENCE: Creating Synergy between Marketing and Research and Development*
Authors: Rein Gail L. 
Published: December 2003

The tensions between marketing and research and development (R&D) are so common that we have come to accept them as the way organizations are. If we remain resigned like this, how will we ever reap some of the benefits that can accrue from these groups working better together? If we can improve the working relationships between marketing and R&D, researchers promise a variety of desirable organizational outcomes, such as cycle‐time reduction and new product success.This article describes in detail the changes that a Fortune 500 company made to its product development process to foster synergy between marketing and R&D. The modified process formalized the roles of marketing and R&D at both the front and back ends of the product development process, increasing productive interaction between the groups. The company found that at the front end, marketing and R&D needed to work together (1) to clarify the market requirements implicit in the market attack plan and (2) to develop a technical strategy that responded to the market requirements and that consequently implemented the market attack plan. At the back end, the groups needed to work together (3) to formulate the value messages used to market the company's products. The synergy created between marketing and R&D through the new process is credited for enabling the company to compete successfully in a market it never before had entered.
Novel classical MHC class I alleles identified in horses by sequencing clones of reverse transcription‐PCR products
Authors: Chung C. , Leib S. R. , Fraser D. G. , Ellis S. A. , McGuire T. C. 
Published: December 2003

SummaryImproved typing of horse classical MHC class I is required to more accurately define these molecules and to extend the number identified further than current serological assays. Defining classical MHC class I alleleic polymorphism is important in evaluating cytotoxic T lymphocyte (CTL) responses in horses. In this study, horse classical MHC class I genes were analyzed based on reverse transcription (RT)‐PCR amplification of sequences encoding the polymorphic peptide binding region and the more conserved alpha 3, transmembrane and cytoplasmic regions followed by cloning and sequencing. Primer sets included a horse classical MHC class I‐specific reverse primer and a forward primer conserved in all known horse MHC class I genes. Sequencing at least 25 clones containing MHC class I sequences from each of 13 horses identified 25 novel sequences and three others which had been described. Of these, nine alleles were identified from different horses or different RT‐PCR and 19 putative alleles were identified in multiple clones from the same RT‐PCR. The primer pairs did not amplify putative non‐classical MHC class I genes as only classical MHC class I and related pseudogenes were found in 462 clones. This method also identified classical MHC class I alleles shared between horses by descent, and defined differences in alleles between horses varying in equine leukocyte antigen (ELA)‐A haplotype as determined by serology. However, horses sharing ELA‐A haplotypes defined by serotyping did not always share cDNA sequences, suggesting subhaplotypic variations within serologically defined ELA‐A haplotypes. The 13 horses in this study had two to five classical MHC class I sequences, indicating that multiple loci code for these genes. Sequencing clones from RT‐PCR with classical MHC class I‐specific primers should be useful for selection of haplotype matched and mismatched horses for CTL studies, and provides sequence information needed to develop easier and more discriminating typing procedures.
Two novel somatic mutations in the human interleukin 6 promoter region in a patient with sporadic breast cancer
Authors: Saha A. , Bairwa N. K. , Ranjan A. , Gupta V. , Bamezai R. 
Published: December 2003

SummaryTwo new single nucleotide mutations were observed within the promoter region of human interleukin‐6 gene (IL‐6) in the tumour sample of a patient with sporadic breast cancer, which was a somatic change. Both mutations, one at −125 (C > G) and the other at position −173 (G > T) from the translation start site, were transversions observed at new positions, not reported earlier. In addition to these two novel mutations in this patient, a known somatic polymorphism was also observed at position −174 (G > C) (from the transcription initiation site, redesignated as −236 from the translational initiation site as per the HUGO nomenclature). Further, a preliminary comparative analysis of the studied promoter region by the ‘ConsInspector 3.0’ program, where the mutated sequence (AF362378) was compared with the sequence existing in the database (Y00081), depicted the presence of the variations in putative binding sites for transcription factors such as glucocorticoid response element (GRE) and nuclear factor kappa‐B (NFκ‐B), which could lead to differential expression of this gene.
Human platelet alloantigens (HPAs): PCR‐SSP genotyping of a UK population for 15 HPA alleles
Authors: Jones D. C. , Bunce M. , Fuggle S. V. , Young N. T. , Marshall S. E. 
Published: December 2003

SummaryAlloimmunization to human platelet alloantigens (HPAs) is responsible for neonatal alloimmune thrombocytopenia (NAIT), post‐transfusional purpura (PTP) and platelet transfusion refractoriness. HPAs may also have a role as histocompatibility antigens in transplantation as well as associations with cardiac disease. We have developed a polymerase chain reaction–sequence‐specific primer (PCR‐SSP) assay capable of detecting 15 HPA allelic variants. As part of the validation of the assay, 134 UK renal donors were genotyped to determine HPA allele frequencies in the UK population. The HPA allele frequencies obtained are consistent with those of the other European studies: GP1A*1 (HPA‐5a) and GP1A*2 (HPA‐5b), 0.914 and 0.086, respectively; GP1BA*1 (HPA‐2a) and GP1BA*2 (HPA‐2b), 0.925 and 0.075; GP2B*1 (HPA‐3a) and GP2B*2 (HPA‐3b), 0.627 and 0.373; GP3A*1 (HPA‐1a) and GP3A*2 (HPA‐1b), 0.840 and 0.161. The rare alleles GP2B*3 (HPA‐9bw) and GP3A*3 to *8 (HPA‐4b, ‐6b, ‐7bw, ‐8bw, ‐10bw and ‐11bw, respectively) were all absent. This comprehensive HPA genotyping assay allows rapid, accurate and reproducible results at low cost.
IL12B and IRF1 gene polymorphisms and susceptibility to celiac disease
Authors: Seegers D. , Borm M. E. A. , Van Belzen M. J. , Mulder C. J. J. , Bailing J. , Crusius J. B. A. , Meijer J. W. R. , Wijmenga C. , Peña A. S. , Bouma G. 
Published: December 2003

SummaryCeliac disease (CD) is a common gastro‐intestinal disorder resulting from permanent intolerance to wheat gliadins and related proteins in rye and barley. In addition to the strong genetic association with HLA‐DQ2 and HLA‐DQ8, a genetic region on chromosomes 5 (CELIAC2) has been identified that harbours a susceptibility gene for CD. The gene(s) responsible for this association, however, remains to be identified. In the present study we evaluated polymorphisms in the genes encoding interleukin‐12 p40 (IL12B) and interferon regulatory factor 1 (IRF1). Both genes are located in the celiac2 region, and have key roles in inducing interferon (IFN)‐γ secreting T helper 1 (Th1) cells, one of the immunological hallmarks of CD. The frequencies of a TaqI gene polymorphism in the 3′ UTR of IL12B and a HinfI gene polymorphism in the 3′ UTR of IRF1 were studied in 258 Dutch CD patients and 237 ethnically matched healthy controls. The transmission of the polymorphic variants from parents to affected child was determined in 123 families with at least one affected child. The frequencies of the IL12B TaqI gene polymorphism and the IRF1 HinfI gene polymorphism did not differ significantly between patients and controls. In addition, in the family study, no deviation from the expected transmission from parents to affected child of any of the polymorphic variants was found. The IL12B TaqI and the IRF1 HinfI gene polymorphisms do not appear to be involved in susceptibility to CD. Further studies on the factors that drive the Th1 immunopathology in CD are required.
Immunogenetics of a new HLA‐B null allele, HLA‐B*4423N
Authors: Hammond L. , Street J. , Downing J. , Thompson J. , Darke C. 
Published: December 2003

SummaryThe second example of an HLA‐B*44 null allele (B*4423N) was identified by discrepancies between serological and polymerase chain reaction–sequence‐specific primer (PCR‐SSP) typing in two north‐western European Caucasoid unrelated stem cell donor volunteers. HLA‐B*4423N was identical to B*440201 except for a single nucleotide substitution at position 493 in exon 3, resulting in a premature stop codon at bases 493–495 (TAG rather than CAG at codon 141). As expected, comprehensive serological testing using 54 antisera, directed towards B44 or Bw4, failed to identify the HLA‐B44 (Bw4) specificity. The B*4423N‐bearing haplotype was identified as A*0201, Cw*0501, DRB1*0408, DRB4*01, DQA1*03, DQB1*0304 and the frequency of B*4423N estimated as 0.00006 (carriage frequency 0.0121%) in 16 533 subjects resident in Wales.
1214 ± 5 Ma dyke from the Darling Range, southwestern Yilgarn Craton, Western Australia
Authors: Pidgeon R. T. , Cook T. J. F. 
Published: December 2003

High thorium euhedral, twinned and elongate zircons from the felsic part of a mafic dyke located in the Archaean Yilgarn Craton approximately 30 km northeast of Perth and approximately 2 km east of the Darling Fault, have consistent 207Pb/206Pb ages of 1214 ± 5 Ma. This age is interpreted as the age of dyke emplacement and is identical, within the uncertainties, with other U–Pb dyke ages reported for the southwest Yilgarn Craton. The present result extends the known occurrence of ca 1210 Ma dykes to the western margin of the Yilgarn Craton and confirms earlier conclusions that a major mafic dyke emplacement occurred throughout the southern Yilgarn Craton during a short‐lived magmatic pulse at ca 1210 Ma.
Bookshelf 2003
Authors: Greene Anne‐marie 
Published: December 2003

Books reviewed:Wolfgang Lecher, Bernhard Nagel and Hans‐Wolfgang Platzer. The Establishment of European Works Councils: From information committee to social actor.Wolfgang Lecher, Hans‐Wolfgang Platzer, Stefan Rüb and Klaus‐Peter Weiner. European Works Councils: Developments, types and networking.Wolfgang Lecher, Hans‐Wolfgang Platzer, Stefan Rüb and Klaus‐Peter Weiner. European Works Councils: Negotiated Europeanisation. Between statutory framework and social dynamic.Gregor Murray, Jacques Bélanger, Anthony Giles and Paul‐André Lapointe (eds). Work and Employment Relations in the High‐Performance Workplace.Bob Hancké. Large Firms and Institutional Change: Industrial Renewal and Economic Restructuring in France.Daryl D’Art and Thomas Turner (eds). Irish Employment Relations in the New Economy.Margaret Linehan, Michael J. Morley and James S. Walsh. International Human Resource Management and Expatriate Transfers: Irish Experiences.
Generation and Characterization of Closely Related Epizootic and Enzootic Infectious cDNA Clones for Studying Interferon Sensitivity and Emergence Mechanisms of Venezuelan Equine Encephalitis Virus
Authors: Anishchenko Michael , Paessler Slobodan , Greene Ivorlyne P. , Aguilar Patricia V. , Carrara Anne-Sophie , Weaver Scott C. 
Published: December 2003

ABSTRACT
Venezuelan equine encephalitis virus (VEEV) is a reemerging pathogen and a continuing threat to humans and equines in the Americas. Identification of the genetic determinants that enable epizootic VEEV strains to arise and exploit equines as amplification hosts to cause widespread human disease is pivotal to understanding VEE emergence. The sensitivity to murine alpha/beta interferon-mediated antiviral activity was previously correlated to the epizootic phenotype of several VEEV strains. Infectious cDNA clones were generated from an epizootic subtype IC VEEV strain (SH3) isolated during the 1992 Venezuelan outbreak and a closely related enzootic, sympatric subtype ID strain (ZPC738). These VEEV strains had low-cell-culture-passage histories and differed by only 12 amino acids in the nonstructural and structural proteins. Rescued viruses showed similar growth kinetics to their parent viruses in several cell lines, and murine infections resulted in comparable viremia and disease. Unlike what was found in other studies of epizootic and enzootic VEEV strains, the sensitivities to murine alpha/beta interferon did not differ appreciably between these epizootic versus enzootic strains, calling into question the reliability of interferon sensitivity as a marker of epizootic potential.
Inhibition of S-Phase Cyclin-Dependent Kinase Activity Blocks Expression of Epstein-Barr Virus Immediate-Early and Early Genes, Preventing Viral Lytic Replication
Authors: Kudoh Ayumi , Daikoku Tohru , Sugaya Yutaka , Isomura Hiroki , Fujita Masatoshi , Kiyono Tohru , Nishiyama Yukihiro , Tsurumi Tatsuya 
Published: December 2003

ABSTRACTThe induction of lytic replication of the Epstein-Barr virus (EBV) completely arrests cell cycle progression, in spite of elevation of S-phase cyclin-dependent kinase (CDK) activity, thereby causing accumulation of hyperphosphorylated forms of retinoblastoma (Rb) protein (A. Kudoh, M. Fujita, T. Kiyono, K. Kuzushima, Y. Sugaya, S. Izuta, Y. Nishiyama, and T. Tsurumi, J. Virol.77:851-861, 2003). Thus, the EBV lytic program appears to promote specific cell cycle-associated activity involved in the progression from G1to S phase. We have proposed that this provides a cellular environment that is advantageous for EBV productive infection. Purvalanol A and roscovitine, inhibitors of S-phase CDKs, blocked the viral lytic replication when cells were treated at the early stage of lytic infection, while well-characterized inhibitors of enzymes, such as mitogen-activated protein kinase, phosphatidylinositol 3-kinase, and protein kinase C, known to be involved in BZLF1 gene expression did not. Inhibition of CDK activity resulted in the accumulation of the hypophosphorylated form of Rb protein and inhibition of expression of EBV immediate-early and early proteins. Cycloheximide block-and-release experiments clearly demonstrated that even in the presence of enough amounts of the BZLF1 protein, purvalanol A blocked expression of lytic viral proteins at transcription level. Furthermore, reporter gene experiments confirmed that BZLF1-induced activation of early EBV promoters was impaired in the presence of the CDK inhibitor. We conclude here that the EBV lytic program promotes specific cell cycle-associated activity involved in the progression from G1to S phase because the S-phase-like cellular environment is essential for the expression of immediate-early and early genes supplying the viral replication proteins and hence for lytic viral replication.
Vaccination of Rabbits with an Adenovirus Vector Expressing the Papillomavirus E2 Protein Leads to Clearance of Papillomas and Infection
Authors: Brandsma Janet L. , Shlyankevich Mark , Zhang Lixin , Slade Martin D. , Goodwin Edward C. , Peh Woei , Deisseroth Albert B. 
Published: December 2003

ABSTRACT
Cervical cancer arises from lesions caused by infection with high-risk types of human papillomavirus (HPV). Therefore, vaccination against HPV could prevent carcinogenesis by preventing HPV infection or inducing lesion regression. HPV E2 protein is an attractive candidate for vaccine development because it is required for papilloma formation, is involved in all stages of the virus life cycle, and is expressed in all premalignant lesions as well as some cancers. This study reports vaccination against E2 protein using a rabbit model of papillomavirus infection. A recombinant adenovirus (Ad) vector expressing the E2 protein of cottontail rabbit papillomavirus (CRPV) was tested for therapeutic efficacy in CRPV-infected rabbits. Primary immunization with the Ad-E2 vaccine, compared to immunization with a control Ad vector, reduced the number of papilloma-forming sites from 17 of 45 to 4 of 45. After booster immunization, vaccinated rabbits formed no new papillomas versus an additional 23 papillomas in rabbits that received the control vector. Papillomas in the Ad-E2 vaccinees were significantly smaller than those in the control rabbits, and all four papillomas in the Ad-E2 vaccinated rabbits regressed. No CRPV DNA was detected either in the regression sites or in sites that did not form papillomas, indicating that the vaccination led to clearance of CRPV from all infected sites.
Role for Bovine Viral Diarrhea Virus E
rns
Glycoprotein in the Control of Activation of Beta Interferon by Double-Stranded RNA
Authors: Iqbal Munir , Poole Emma , Goodbourn Stephen , McCauley John W. 
Published: December 2003

ABSTRACT

Production of alpha/beta interferon in response to viral double-stranded RNA (dsRNA) produced during viral replication is a first line of defense against viral infections. Here we demonstrate that the E
rns
glycoprotein of the pestivirus bovine viral diarrhea virus can act as an inhibitor of dsRNA-induced responses of cells. This effect is seen whether E
rns
is constitutively expressed in cells or exogenously added to the culture medium. The E
rns
effect is specific to dsRNA since activation of NF-κB in cells infected with Semliki Forest virus or treated with tumor necrosis factor alpha was not affected. We also show that E
rns
contains a dsRNA-binding activity, and its RNase is active against dsRNA at a low pH. Both the dsRNA binding and RNase activities are required for the inhibition of dsRNA signaling, and we discuss here a model to account for these observations.
A Single Injection of Recombinant Measles Virus Vaccines Expressing Human Immunodeficiency Virus (HIV) Type 1 Clade B Envelope Glycoproteins Induces Neutralizing Antibodies and Cellular Immune Responses to HIV
Authors: Lorin Clarisse , Mollet Lucile , Delebecque Frédéric , Combredet Chantal , Hurtrel Bruno , Charneau Pierre , Brahic Michel , Tangy Frédéric 
Published: December 2003

ABSTRACT

The anchored and secreted forms of the human immunodeficiency virus type 1 (HIV-1) 89.6 envelope glycoprotein, either complete or after deletion of the V3 loop, were expressed in a cloned attenuated measles virus (MV) vector. The recombinant viruses grew as efficiently as the parental virus and expressed high levels of the HIV protein. Expression was stable during serial passages. The immunogenicity of these recombinant vectors was tested in mice susceptible to MV and in macaques. High titers of antibodies to both MV and HIV-Env were obtained after a single injection in susceptible mice. These antibodies neutralized homologous SHIV89.6p virus, as well as several heterologous HIV-1 primary isolates. A gp160 mutant in which the V3 loop was deleted induced antibodies that neutralized heterologous viruses more efficiently than antibodies induced by the native envelope protein. A high level of CD8
+
and CD4
+
cells specific for HIV gp120 was also detected in MV-susceptible mice. Furthermore, recombinant MV was able to raise immune responses against HIV in mice and macaques with a preexisting anti-MV immunity. Therefore, recombinant MV vaccines inducing anti-HIV neutralizing antibodies and specific T lymphocytes responses deserve to be tested as a candidate AIDS vaccine.
Residues of Human Cytomegalovirus DNA Polymerase Catalytic Subunit UL54 That Are Necessary and Sufficient for Interaction with the Accessory Protein UL44
Authors: Loregian Arianna , Appleton Brent A. , Hogle James M. , Coen Donald M. 
Published: December 2003

ABSTRACT

The human cytomegalovirus DNA polymerase contains a catalytic subunit, UL54, and an accessory protein, UL44. Recent studies suggested that UL54 might interact via its extreme C terminus with UL44 (A. Loregian, R. Rigatti, M. Murphy, E. Schievano, G. Palu', and H. S. Marsden, J. Virol. 77:8336-8344, 2003). To address this hypothesis, we quantitatively measured the binding of peptides corresponding to the extreme C terminus of UL54 to UL44 by using isothermal titration calorimetry. A peptide corresponding to the last 22 residues of UL54 was sufficient to bind specifically to UL44 in a 1:1 complex with a dissociation constant of ca. 0.7 μM. To define individual residues in this segment that are crucial for interacting with UL44, we engineered a series of mutations in the C-terminal region of
UL54
. The UL54 mutants were tested for their ability to interact with UL44 by glutathione
S
-transferase pulldown assays, for basal DNA polymerase activity, and for long-chain DNA synthesis in the presence of UL44. We observed that deletion of the C-terminal segment or substitution of alanine for Leu1227 or Phe1231 in UL54 greatly impaired both the UL54-UL44 interaction in pulldown assays and long-chain DNA synthesis without affecting basal polymerase activity, identifying these residues as important for subunit interaction. Thus, like the herpes simplex virus UL30-UL42 interaction, a few specific side chains in the C terminus of UL54 are crucial for UL54-UL44 interaction. However, the UL54 residues important for interaction with UL44 are hydrophobic and not basic. This information might aid in the rational design of new drugs for the treatment of human cytomegalovirus infection.