bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Relationship Between Indirect and Physical Aggression on Television and in Real Life
Authors: Coyne Sarah M. , Archer John 
Published: April 2005

AbstractViewing indirect aggression on television has been shown to have negative short‐term effects on a viewer's subsequent aggressive behavior; however, the longer term relationship between viewing indirect aggression on television and in real life has not yet been examined. Three hundred and forty‐seven adolescents, aged 11–14, were asked to list their five favorite television programs. These programs were analyzed for the amount and type of aggression they contained. Peer‐nominated indirect aggression was predicted by other aggressive behavior, sex, and televised indirect aggression. In particular, indirectly aggressive girls viewed more indirect aggression on television than any other group. Peer‐nominated physical aggression was predicted by other aggressive behavior and sex, but not by televised physical or indirect aggression. This study provides a starting point for future long‐term research on the effect of viewing indirect aggression in the media.
Mothers’ Typical and Event‐Specific Positive Expressions Influence Children's Memory for Events
Authors: Dunsmore Julie C. , Halberstadt Amy G. , Eaton Kimberly L. , Robinson Megan L. 
Published: April 2005

AbstractMothers (N=67) taught their preschool children crafts while varying emotional expressions (delight, irritation). Mothers’ typical expressive styles were assessed by questionnaire. After three weeks, children's memory was assessed with a free‐recall interview followed by re‐enactment of craft‐making with an interviewer. Children of mothers high in positive expressiveness had more elaborate recall when mothers expressed delight rather than irritation. Children of mothers low in positive expressiveness re‐enacted more event details when their mothers were less varied in expression rather than expressive of emotion in general or delight in particular, and had more elaborate recall when their mothers expressed irritation rather than delight. Findings suggest that children remember more when their mother's emotional expressions during an event fit her typical style.
Efficiency and total factor productivity in Ukrainian agriculture in transition
Authors: Lissitsa Alexej , Odening Martin 
Published: April 2005

AbstractThis article analyzes efficiency and total factor productivity (TFP) change of large agricultural enterprises during their transition to a market economy in Ukraine. Efficiency is calculated by Data Envelopment Analysis and productivity change is measured by the Malmquist Productivity Change Index in the period between 1990 and 1999. On average, TFP declined by 6% annually, dropping a total 42%. The main reason for the observed TFP decline is a decrease in technical efficiency, which is found to be remarkably significant. At the same time there is a high variation among individual enterprises: the distribution of efficiency scores widens, which indicates that the farms diverge with respect to their economic performance. A Tobit regression analysis is conducted in which efficiency scores are related to factors such as farm type, farm size, initial conditions, and legal form.
Cost‐effective nitrogen leaching reduction as influenced by linkages between farm‐level decisions
Authors: Ekman Sone 
Published: April 2005

AbstractThis article focuses on how the linkages between various farm‐level decisions affect the choice of measures to reduce nitrogen leaching from crop production. A mathematical programming model is developed. The model considers not only management decisions that affect nitrogen leaching directly, but also other decision variables such as scheduling of field operations and machinery investments. A simplified analysis that ignores the latter management decisions, and the linkages between the various decisions, may result in abatement policies that are not cost‐effective because the policies will have other effects than expected. As an example, the empirical results show that subsidies to catch crops and spring ploughing may contribute to increased nitrogen load, quite contrary to the purpose of these subsidies. Further, it is noted that the characteristics of the production system make it costly to change land use, tillage practices, or fertilizer use drastically. Instead, cost‐effective nitrogen abatement includes a mix of various adjustments of farm‐level production practices. The EU set‐aside payment appears to reduce abatement costs.
Technical and scale efficiency of crop and livestock farms in Poland: does specialization matter?
Authors: Latruffe Laure , Balcombe Kelvin , Davidova Sophia , Zawalinska Katarzyna 
Published: April 2005

AbstractThe technical and scale efficiency of Polish farms is analyzed using data envelopment analysis. Efficiency differences are measured according to farm specialization, in crop or livestock, at two points in time during transition, 1996 and 2000. The efficiency results are reviewed in light of confidence intervals provided by bootstrapping. Livestock farms are found to be, on average, more technically and scale efficient than crop farms. Scale efficiency is high for both specializations. Technical inefficiency appears mostly to be due to “pure technical” rather than “scale” inefficiency, and thus attributable to inefficient management practices. The evidence suggests that the low‐educational attainment of people engaged in agriculture is one important reason for these inefficient practices. In 2000, 64% of livestock farms and 86% of crop farms were operating under increasing returns to scale. Improvements in the land lease legislation and changes to the policy support to farmers' pensions could stimulate the land market and remove the incentives to keep a fragmented operational structure.
The demand for selected nutrients by Greek households: an empirical analysis with quantile regressions
Authors: Fousekis Panos , Lazaridis Panagiotis 
Published: April 2005

AbstractThe article uses information from the 1993–1994 Household Consumption Survey and the semiparametric quantile regression approach to analyze the demand for three macronutrients (carbohydrates, proteins, and fats) and three micronutrients (minerals, vitamins, and cholesterol) in Greece. According to the empirical results the age of the household head, the degree of urbanization, the percentage of food expenditure devoted to food away‐from‐home, and the per capita consumption expenditure affect the intakes of nutrients across all the five quantiles considered. The impact, however, of the household head's gender and the impact of his (her) educational achievement are located only at the lower and the higher quantiles, respectively. The expenditure elasticities are substantially lower than unity, suggesting inelastic responses of nutrient intakes to per capita consumption expenditure.
Engagement of specific T-cell surface molecules regulates cytoskeletal polarization in HTLV-1–infected lymphocytes
Authors: Barnard Amanda L. , Igakura Tadahiko , Tanaka Yuetsu , Taylor Graham P. , Bangham Charles R.M. 
Published: April 2005

AbstractCell-cell contact is required for efficient transmission of human T-lymphotropic virus type 1 (HTLV-1). An HTLV-1–infected cell polarizes its microtubule-organizing center (MTOC) toward the cell-cell junction; HTLV-1 core (Gag) complexes and the HTLV-1 genome accumulate at the point of contact and are then transferred to the uninfected cell. However, the mechanisms involved in this cytoskeletal polarization and transport of HTLV-1 complexes are unknown. Here, we tested the hypothesis that engagement of a specific T-cell surface ligand is synergistic with HTLV-1 infection in causing polarization of the MTOC to the cell contact region. We show that antibodies to intercellular adhesion molecule-1 (ICAM-1; CD54) caused MTOC polarization at a higher frequency in HTLV-1–infected cells. ICAM-1 is upregulated on HTLV-1–infected cells, and, in turn, ICAM-1 on the cell surface upregulates HTLV-1 gene expression. We propose that a positive feedback loop involving ICAM-1 and HTLV-1 Tax protein facilitates the formation of the virologic synapse and contributes to the T-cell tropism of HTLV-1. In contrast, MTOC polarization induced in T cells by antibodies to CD3 or CD28 was significantly inhibited by HTLV-1 infection.
Lentiviral delivery of short hairpin RNAs protects CD4 T cells from multiple clades and primary isolates of HIV
Authors: Lee Sang-Kyung , Dykxhoorn Derek M. , Kumar Priti , Ranjbar Shahin , Song Erwei , Maliszewski Laura E. , François-Bongarçon Vanessa , Goldfeld Anne , Swamy N. Manjunath , Lieberman Judy , Shankar Premlata 
Published: April 2005

AbstractViral heterogeneity is a major hurdle for potential therapeutic use of RNA interference (RNAi) against HIV-1. To determine the extent of RNAi tolerance to mutations, we tested 3 viral target sites with differing propensity for mutations: a highly variable rev sequence, a gag sequence conserved only among clade B isolates, and a vif sequence highly conserved across clades. Lentiviral expression of all 3 shRNAs inhibited replication of the homologous HIVIIIB strain. However, they differed in their ability to protect primary CD4 T cells against multiple isolates within and across HIV clades. The least conserved rev sequence inhibited only 2 of 5 clade B isolates. The gag sequence (conserved within clade B) protected 5 of 5 clade B isolates but not other clade viruses with 2 or 3 mutations in the central region. In contrast, the vif sequence, which was conserved across clades except for single mutations at positions 14 and 17, inhibited viruses from 5 different clades. Moreover, siRNAs with introduced mutations at sites of gag sequence polymorphisms showed reduced antiviral activity, whereas mutations in vif siRNA only modestly decreased silencing. Thus, although 1 or 2 mutations at peripheral sites are tolerated, mutations in the central target cleavage region abolish RNAi activity.
Negative regulation of platelet function by a secreted cell repulsive protein, semaphorin 3A
Authors: Kashiwagi Hirokazu , Shiraga Masamichi , Kato Hisashi , Kamae Tsuyoshi , Yamamoto Naoko , Tadokoro Seiji , Kurata Yoshiyuki , Tomiyama Yoshiaki , Kanakura Yuzuru 
Published: April 2005

AbstractSemaphorin 3A (Sema3A) is a secreted disulfide-bound homodimeric molecule that induces growth cone collapse and repulsion of axon growth in the nervous system. Recently, it has been demonstrated that Sema3A is produced by endothelial cells and inhibits integrin function in an autocrine fashion. In this study, we investigated the effects of Sema3A on platelet function by using 2 distinct human Sema3A chimera proteins. We detected expression of functional Sema3A receptors in platelets and dose-dependent and saturable binding of Sema3A to platelets. Sema3A dose-dependently inhibited activation of integrin αIIbβ3byall agonists examined including adenosine diphosphate (ADP), thrombin, convulxin, phorbol 12-myristate 13-acetate, and A23187. Sema3A inhibited not only platelet aggregation induced by thrombin or collagen but also platelet adhesion and spreading on immobilized fibrinogen. Moreover, Sema3A impaired αIIbβ3-independent spreading on glass coverslips and aggregation-independent granular secretion. Sema3A inhibited agonist-induced elevation of filamentous action (F-actin) contents, phosphorylation of cofilin, and Rac1 activation. In contrast, Sema3A did not affect the levels of cyclic nucleotides or agonist-induced increase of intracellular Ca2+ concentrations. Thus, the extensive inhibition of platelet function by Sema3A appears to be mediated, at least in part, through impairment of agonist-induced Rac1-dependent actin rearrangement.
Production and characterization of erythropoietic protoporphyric heterodimeric ferrochelatases
Authors: Najahi-Missaoui Wided , Dailey Harry A. 
Published: April 2005

AbstractMutations resulting in diminished activity of the dimeric enzyme ferrochelatase are a prerequisite for the inherited disorder erythropoietic protoporphyria (EPP). Patients with clinical EPP have only 10% to 30% of normal levels of ferrochelatase activity, and although many patients with EPP have one mutant allele and one “low-expression” normal allele, the possibility remains that, for some, low ferrochelatase activity may result from an EPP mutation that has an impact on both subunits of the wild-type/mutant heterodimer. Here we present data for 12 ferrochelatase wild-type/EPP mutant heterodimers showing that some mutations result in heterodimers with the residual activity anticipated from individual constituents, whereas others result in heterodimers with significantly lower activity than would be predicted. Although the data do not allow an a priori prediction of heterodimeric residual activity based solely on the in vitro activity of EPP homodimers or the position of the mutated residue within ferrochelatase, mutations that affect the dimer interface or [2Fe-2S] cluster have a significantly greater impact on residual activity than would be predicted. These data suggest that some EPP mutations may result in clinically overt EPP in the absence of a low-expression, wild-type allele; this is of potential significance for genetic counseling of patients with EPP.
CD144 (VE-cadherin) is transiently expressed by fetal liver hematopoietic stem cells
Authors: Kim Injune , Yilmaz Ömer H. , Morrison Sean J. 
Published: April 2005

AbstractHematopoietic stem cells (HSCs) and endothelial progenitors arise from a common embryonic precursor. However, these populations diverge prior to the onset of definitive hematopoiesis, as HSCs become CD45+ and are thought to lose the expression of endothelial markers. After the onset of definitive hematopoiesis, CD144 (vascular endothelial [VE]–cadherin) has been considered a specific marker of endothelial cells. In contrast, we found that virtually all HSC activity from embryonic day 13.5 (E13.5) fetal liver was CD144+. CD144 expression declined on E16.5 fetal liver HSCs and was absent from adult bone marrow HSCs. This identified a new marker that is differentially expressed between fetal and adult HSCs, and enhanced the purification of HSCs from the E13.5 fetal liver. These results emphasize the close developmental relationship between hematopoietic and endothelial cells, while indicating that CD144 is not a specific marker of endothelial cells during fetal development.
Acute myeloid leukemia bearing cytoplasmic nucleophosmin (NPMc+ AML) shows a distinct gene expression profile characterized by up-regulation of genes involved in stem-cell maintenance
Authors: Alcalay Myriam , Tiacci Enrico , Bergomas Roberta , Bigerna Barbara , Venturini Elisa , Minardi Simone P. , Meani Natalia , Diverio Daniela , Bernard Loris , Tizzoni Laura , Volorio Sara , Luzi Lucilla , Colombo Emanuela , Lo Coco Francesco , Mecucci Cristina , Falini Brunangelo , Pelicci Pier Giuseppe ,   for the Gruppo Italiano Malattie Ematologiche Maligne dell'Adulto (GIMEMA) Acute Leukemia Working Party
Published: April 2005

AbstractApproximately one third of acute myeloid leukemias (AMLs) are characterized by aberrant cytoplasmic localization of nucleophosmin (NPMc+ AML), consequent to mutations in the NPM putative nucleolar localization signal. These events are mutually exclusive with the major AML-associated chromosomal rearrangements, and are frequently associated with normal karyotype, FLT3 mutations, and multilineage involvement. We report the gene expression profiles of 78 de novo AMLs (72 with normal karyotype; 6 without major chromosomal abnormalities) that were characterized for the subcellular localization and mutation status of NPM. Unsupervised clustering clearly separated NPMc+ from NPMc– AMLs, regardless of the presence of FLT3 mutations or non–major chromosomal rearrangements, supporting the concept that NPMc+ AML represents a distinct entity. The molecular signature of NPMc+ AML includes up-regulation of several genes putatively involved in the maintenance of a stem-cell phenotype, suggesting that NPMc+ AML may derive from a multipotent hematopoietic progenitor.
Resistance to hepcidin is conferred by hemochromatosis-associated mutations of ferroportin
Authors: Drakesmith Hal , Schimanski Lisa M. , Ormerod Emma , Merryweather-Clarke Alison T. , Viprakasit Vip , Edwards Jon P. , Sweetland Emma , Bastin Judy M. , Cowley Diana , Chinthammitr Yingyong , Robson Kathryn J. H. , Townsend Alain R. M. 
Published: April 2005

AbstractFerroportin (FPN) mediates iron export from cells; FPN mutations are associated with the iron overloading disorder hemochromatosis. Previously, we found that the A77D, V162del, and G490D mutations inhibited FPN activity, but that other disease-associated FPN variants retained full iron export capability. The peptide hormone hepcidin inhibits FPN as part of a homeostatic negative feedback loop. We measured surface expression and function of wild-type FPN and fully active FPN mutants in the presence of hepcidin. We found that the Y64N and C326Y mutants of FPN are completely resistant to hepcidin inhibition and that N144D and N144H are partially resistant. Hemochromatosis-associated FPN mutations, therefore, either reduce iron export ability or produce an FPN variant that is insensitive to hepcidin. The former mutation type is associated with Kupffer-cell iron deposition and normal transferrin saturation in vivo, whereas patients with the latter category of FPN mutation have high transferrin saturation and tend to deposit iron throughout the liver parenchyma. FPN-linked hemochromatosis may have a variable pathogenesis depending on the causative FPN mutant.
Nonhemolytic antibody-induced loss of erythrocyte surface antigen
Authors: Zimring James C. , Hair Gregory A. , Chadwick Traci E. , Deshpande Seema S. , Anderson Kimberly M. , Hillyer Christopher D. , Roback John D. 
Published: April 2005

AbstractTransfusion of red blood cells (RBCs) into patients with anti–donor RBC antibodies (crossmatch-incompatible transfusion) can result in lethal antibody-mediated hemolysis. Less well appreciated is the ability of anti-RBC antibodies to specifically remove their target antigen from donor RBCs without compromising cell survival or adversely affecting the transfusion recipient. In an effort to elucidate the mechanistic details of this process, we describe the first animal model of nonhemolytic antibody-induced RBC antigen loss. RBCs from transgenic mHEL mice express surface hen egg lysozyme (HEL) as a transmembrane protein. Transfusion of mHEL RBCs into mice immunized with HEL results in selective loss of HEL antigen from donor RBCs without affecting other blood group antigens or reducing the circulatory life span of the transfused RBCs. While this process does not require the presence of a spleen, it requires both anti-RBC immunoglobulin G (IgG) antibodies and the FcγIII receptor. These studies provide mechanistic insight into the phenomenon of antigen loss during incompatible transfusion in humans.
Subfunctionalization of duplicated genes as a transition state to neofunctionalization
Authors: Rastogi Shruti , Liberles David A 
Published: April 2005

Abstract

Background
Gene duplication has been suggested to be an important process in the generation of evolutionary novelty. Neofunctionalization, as an adaptive process where one copy mutates into a function that was not present in the pre-duplication gene, is one mechanism that can lead to the retention of both copies. More recently, subfunctionalization, as a neutral process where the two copies partition the ancestral function, has been proposed as an alternative mechanism driving duplicate gene retention in organisms with small effective population sizes. The relative importance of these two processes is unclear.

Results
A set of lattice model genes that fold and bind to two peptide ligands with overlapping binding pockets, but not a third ligand present in the cell was designed. Each gene was duplicated in a model haploid species with a small constant population size and no recombination. One set of models allowed subfunctionalization of binding events following duplication, while another set did not allow subfunctionalization. Modeling under such conditions suggests that subfunctionalization plays an important role, but as a transition state to neofunctionalization rather than as a terminal fate of duplicated genes. There is no apparent selective pressure to maintain redundancy.

Conclusion
Subfunctionalization results in an increase in the preservation of duplicated gene copies, including those that are neofunctionalized, but never represents a substantial fraction of duplicate gene copies at any evolutionary time point and ultimately leads to neofunctionalization of those preserved copies. This conclusion also may reflect changes in gene function after duplication with time in real genomes.
Use of adenoviral E1A protein to analyze K18 promoter deregulation in colon carcinoma cells discloses a role for CtBP1 and BRCA1
Authors: Delouis Cécile , Prochasson Philippe , Laithier Madeleine , Brison Olivier 
Published: April 2005

Abstract
Background
The promoter of the keratin 18 (K18) gene is 5- to 10-fold more active in tumorigenic (T-type) cell clones derived from the SW613-S human colon carcinoma cell line than in non-tumorigenic (NT-type) clones. We have reported previously that the mechanism responsible for this differential activity is acting on the minimal K18 promoter (TATA box and initiation site). This mechanism does not require the binding of a factor to a specific site on the DNA but involves the acetylation of a non-histone substrate. To get further insight into this mechanism, we investigated the effect of the adenovirus E1A protein on the activity of the K18 promoter, both in T and NT cells.

Results
Wild type adenovirus E1A protein and C-terminal deletion mutants inhibit the K18 promoter, specifically in T-type cells. The domain responsible for this inhibitory effect is located in the 12–25 region of the viral protein. E1A mutants that have lost this region but retain the PLDLS motif (the C-terminal binding site for CtBP1) stimulate the K18 promoter, specifically in NT cells. The inhibitory or stimulatory effects of the different E1A mutants are not dependent on a particular sequence of the promoter. An E1A N-terminal deletion mutant carrying point mutations in the PLDLS motif cannot stimulate the K18 promoter. CtBP1 interacts with CtIP, which is a known partner of BRCA1, itself a component of the RNA polymerase II holoenzyme. The stimulatory effect of two BRCA1 mutants, specifically in NT cells, implicates a tripartite BRCA1-CtIP-CtBP1 complex in the regulation of the K18 promoter.

Conclusion
Since we have shown previously that the K18 promoter is stimulated by deacetylase inhibitors, specifically in NT cells, we conclude that the activity of the promoter is repressed in NT cells by a mechanism involving the recruitment, by a BRCA1/CtIP complex, of CtBP1 and associated deacetylases to the preinitiation complex. We propose a model depicting the mechanism responsible for the differential activity of the K18 promoter between T and NT cells of the SW613-S cell line.