bluuebunny/crossref_metadata_2025_split huggingface dataset:
High levels of the BCR/ABL oncoprotein are required for the MAPK-hnRNP-E2–dependent suppression of C/EBPα-driven myeloid differentiation
Authors: Chang Ji Suk , Santhanam Ramasamy , Trotta Rossana , Neviani Paolo , Eiring Anna M. , Briercheck Edward , Ronchetti Mattia , Roy Denis C. , Calabretta Bruno , Caligiuri Michael A. , Perrotti Danilo 
Published: May 2007

AbstractThe inability of myeloid chronic myelogenous leukemia blast crisis (CML-BC) progenitors to undergo neutrophil differentiation depends on suppression of C/EBPα expression through the translation inhibitory activity of the RNA-binding protein hnRNP-E2. Here we show that “oncogene dosage” is a determinant factor for suppression of differentiation in CML-BC. In fact, high levels of p210-BCR/ABL are required for enhanced hnRNP-E2 expression, which depends on phosphorylation of hnRNP-E2 serines 173, 189, and 272 and threonine 213 by the BCR/ABL-activated MAPKERK1/2. Serine/threonine to alanine substitution abolishes hnRNP-E2 phosphorylation and markedly decreases its stability in BCR/ABL-expressing myeloid precursors. Similarly, pharmacologic inhibition of MAPKERK1/2 activity decreases hnRNP-E2 binding to the 5′UTR of C/EBPα mRNA by impairing hnRNP-E2 phosphorylation and stability. This, in turn, restores in vitro and/or in vivo C/EBPα expression and G-CSF–driven neutrophilic maturation of differentiation-arrested BCR/ABL+ cell lines, primary CML-BCCD34+ patient cells and lineage-negative mouse bone marrow cells expressing high levels of p210-BCR/ABL. Thus, increased BCR/ABL oncogenic tyrosine kinase activity is essential for suppression of myeloid differentiation of CML-BC progenitors as it is required for sustained activation of the MAPKERK1/2-hnRNP-E2-C/EBPα differentiation-inhibitory pathway. Furthermore, these findings suggest the inclusion of clinically relevant MAPK inhibitors in the therapy of CML-BC.
Anti-inflammatory properties of desipramine and fluoxetine
Authors: Roumestan Caroline , Michel Alain , Bichon Florence , Portet Karine , Detoc Maëlle , Henriquet Corinne , Jaffuel Dany , Mathieu Marc 
Published: May 2007

AbstractBackgroundAntidepressants are heavily prescribed drugs and have been shown to affect inflammatory signals. We examined whether these have anti-inflammatory properties in animal models of septic shock and allergic asthma. We also analysed whether antidepressants act directly on peripheral cell types that participate in the inflammatory response in these diseases.MethodsThe antidepressants desipramine and fluoxetine were compared in vivo to the glucocorticoid prednisolone, an anti-inflammatory drug of reference. In a murine model of lipopolysaccharides (LPS)-induced septic shock, animals received the drugs either before or after injection of LPS. Circulating levels of tumour necrosis factor (TNF)-α and mortality rate were measured. In ovalbumin-sensitized rats, the effect of drug treatment on lung inflammation was assessed by counting leukocytes in bronchoalveolar lavages. Bronchial hyperreactivity was measured using barometric plethysmography. In vitro production of TNF-α and Regulated upon Activation, Normal T cell Expressed and presumably Secreted (RANTES) from activated monocytes and lung epithelial cells, respectively, was analysed by immunoassays. Reporter gene assays were used to measure the effect of antidepressants on the activity of nuclear factor-κB and activator protein-1 which are involved in the control of TNF-α and RANTES expression.ResultsIn the septic shock model, all three drugs given preventively markedly decreased circulating levels of TNF-α and mortality (50% mortality in fluoxetine treated group, 30% in desipramine and prednisolone treated groups versus 90% in controls). In the curative trial, antidepressants had no statistically significant effect, while prednisolone still decreased mortality (60% mortality versus 95% in controls). In ovalbumin-sensitized rats, the three drugs decreased lung inflammation, albeit to different degrees. Prednisolone and fluoxetine reduced the number of macrophages, lymphocytes, neutrophils and eosinophils, while desipramine diminished only the number of macrophages and lymphocytes. However, antidepressants as opposed to prednisolone did not attenuate bronchial hyperreactivity. In vitro, desipramine and fluoxetine dose-dependently inhibited the release of TNF-α from LPS-treated monocytes. In lung epithelial cells, these compounds decreased TNF-α-induced RANTES expression as well as the activity of nuclear factor-κB and activator protein-1.ConclusionDesipramine and fluoxetine reduce the inflammatory reaction in two animal models of human diseases. These antidepressants act directly on relevant peripheral cell types to decrease expression of inflammatory mediators probably by affecting their gene transcription. Clinical implications of these observations are discussed.
Positive role of cell wall anchored proteinase PrtP in adhesion of lactococci
Authors: Habimana Olivier , Le Goff Carine , Juillard Vincent , Bellon-Fontaine Marie-Noëlle , Buist Girbe , Kulakauskas Saulius , Briandet Romain 
Published: May 2007

Abstract

Background
The first step in biofilm formation is bacterial attachment to solid surfaces, which is dependent on the cell surface physico-chemical properties. Cell wall anchored proteins (CWAP) are among the known adhesins that confer the adhesive properties to pathogenic Gram-positive bacteria. To investigate the role of CWAP of non-pathogen Gram-positive bacteria in the initial steps of biofilm formation, we evaluated the physico-chemical properties and adhesion to solid surfaces of Lactococcus lactis. To be able to grow in milk this dairy bacterium expresses a cell wall anchored proteinase PrtP for breakdown of milk caseins.

Results
The influence of the anchored cell wall proteinase PrtP on microbial surface physico-chemical properties, and consequently on adhesion, was evaluated using lactococci carrying different alleles of prtP. The presence of cell wall anchored proteinase on the surface of lactococcal cells resulted in an increased affinity to solvents with different physico-chemical properties (apolar and Lewis acid-base solvents). These properties were observed regardless of whether the PrtP variant was biologically active or not, and were not observed in strains without PrtP. Anchored PrtP displayed a significant increase in cell adhesion to solid glass and tetrafluoroethylene surfaces.

Conclusion
Obtained results indicate that exposure of an anchored cell wall proteinase PrtP, and not its proteolytic activity, is responsible for greater cell hydrophobicity and adhesion. The increased bacterial affinity to polar and apolar solvents indicated that exposure of PrtP on lactococcal cell surface could enhance the capacity to exchange attractive van der Waals interactions, and consequently increase their adhesion to different types of solid surfaces and solvents.
Promoter methylation of RASSF1A and DAPK and mutations of K-ras, p53, and EGFR in lung tumors from smokers and never-smokers
Authors: Liu Yang , Gao Weimin , Siegfried Jill M , Weissfeld Joel L , Luketich James D , Keohavong Phouthone 
Published: May 2007

Abstract

Background
Epidemiological studies indicate that some characteristics of lung cancer among never-smokers significantly differ from those of smokers. Aberrant promoter methylation and mutations in some oncogenes and tumor suppressor genes are frequent in lung tumors from smokers but rare in those from never-smokers. In this study, we analyzed promoter methylation in the ras-association domain isoform A (RASSF1A) and the death-associated protein kinase (DAPK) genes in lung tumors from patients with primarily non-small cell lung cancer (NSCLC) from the Western Pennsylvania region. We compare the results with the smoking status of the patients and the mutation status of the K-ras, p53, and EGFR genes determined previously on these same lung tumors.

Methods
Promoter methylation of the RASSF1A and DAPK genes was analyzed by using a modified two-stage methylation-specific PCR. Data on mutations of K-ras, p53, and EGFR were obtained from our previous studies.

Results
The RASSF1A gene promoter methylation was found in tumors from 46.7% (57/122) of the patients and was not significantly different between smokers and never-smokers, but was associated significantly in multiple variable analysis with tumor histology (p = 0.031) and marginally with tumor stage (p = 0.063). The DAPK gene promoter methylation frequency in these tumors was 32.8% (40/122) and did not differ according to the patients' smoking status, tumor histology, or tumor stage. Multivariate analysis adjusted for age, gender, smoking status, tumor histology and stage showed that the frequency of promoter methylation of the RASSF1A or DAPK genes did not correlate with the frequency of mutations of the K-ras, p53, and EGFR gene.

Conclusion
Our results showed that RASSF1A and DAPK genes' promoter methylation occurred frequently in lung tumors, although the prevalence of this alteration in these genes was not associated with the smoking status of the patients or the occurrence of mutations in the K-ras, p53 and EGFR genes, suggesting each of these events may represent independent event in non-small lung tumorigenesis.
Inhibition of the alternative complement activation pathway in traumatic brain injury by a monoclonal anti-factor B antibody: a randomized placebo-controlled study in mice
Authors: Leinhase Iris , Rozanski Michal , Harhausen Denise , Thurman Joshua M , Schmidt Oliver I , Hossini Amir M , Taha Mohy E , Rittirsch Daniel , Ward Peter A , Holers V Michael , Ertel Wolfgang , Stahel Philip F 
Published: May 2007

AbstractBackgroundThe posttraumatic response to traumatic brain injury (TBI) is characterized, in part, by activation of the innate immune response, including the complement system. We have recently shown that mice devoid of a functional alternative pathway of complement activation (factor B-/- mice) are protected from complement-mediated neuroinflammation and neuropathology after TBI. In the present study, we extrapolated this knowledge from studies in genetically engineered mice to a pharmacological approach using a monoclonal anti-factor B antibody. This neutralizing antibody represents a specific and potent inhibitor of the alternative complement pathway in mice.MethodsA focal trauma was applied to the left hemisphere of C57BL/6 mice (n= 89) using a standardized electric weight-drop model. Animals were randomly assigned to two treatment groups: (1) Systemic injection of 1 mg monoclonal anti-factor B antibody (mAb 1379) in 400 μl phosphate-buffered saline (PBS) at 1 hour and 24 hours after trauma; (2) Systemic injection of vehicle only (400 μl PBS), as placebo control, at identical time-points after trauma. Sham-operated and untreated mice served as additional negative controls. Evaluation of neurological scores and analysis of brain tissue specimens and serum samples was performed at defined time-points for up to 1 week. Complement activation in serum was assessed by zymosan assay and by murine C5a ELISA. Brain samples were analyzed by immunohistochemistry, terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) histochemistry, and real-time RT-PCR.ResultsThemAb 1379leads to a significant inhibition of alternative pathway complement activity and to significantly attenuated C5a levels in serum, as compared to head-injured placebo-treated control mice. TBI induced histomorphological signs of neuroinflammation and neuronal apoptosis in the injured brain hemisphere of placebo-treated control mice for up to 7 days. In contrast, the systemic administration of an inhibitory anti-factor B antibody led to a substantial attenuation of cerebral tissue damage and neuronal cell death. In addition, the posttraumatic administration of themAb 1379induced a neuroprotective pattern of intracerebral gene expression.ConclusionInhibition of the alternative complement pathway by posttraumatic administration of a neutralizing anti-factor B antibody appears to represent a new promising avenue for pharmacological attenuation of the complement-mediated neuroinflammatory response after head injury.
Drosophilaas a genetic and cellular model for studies on axonal growth
Authors: Sánchez-Soriano Natalia , Tear Guy , Whitington Paul , Prokop Andreas 
Published: May 2007

AbstractOne of the most fascinating processes during nervous system development is the establishment of stereotypic neuronal networks. An essential step in this process is the outgrowth and precise navigation (pathfinding) of axons and dendrites towards their synaptic partner cells. This phenomenon was first described more than a century ago and, over the past decades, increasing insights have been gained into the cellular and molecular mechanisms regulating neuronal growth and navigation. Progress in this area has been greatly assisted by the use of simple and genetically tractable invertebrate model systems, such as the fruit fly Drosophila melanogaster. This review is dedicated to Drosophila as a genetic and cellular model to study axonal growth and demonstrates how it can and has been used for this research. We describe the various cellular systems of Drosophila used for such studies, insights into axonal growth cones and their cytoskeletal dynamics, and summarise identified molecular signalling pathways required for growth cone navigation, with particular focus on pathfinding decisions in the ventral nerve cord of Drosophila embryos. These Drosophila-specific aspects are viewed in the general context of our current knowledge about neuronal growth.
Evolution of the core and pan-genome of Streptococcus: positive selection, recombination, and genome composition
Authors: Lefébure Tristan , Stanhope Michael J 
Published: May 2007

Abstract
Background
The genus Streptococcus is one of the most diverse and important human and agricultural pathogens. This study employs comparative evolutionary analyses of 26 Streptococcus genomes to yield an improved understanding of the relative roles of recombination and positive selection in pathogen adaptation to their hosts.

Results
Streptococcus genomes exhibit extreme levels of evolutionary plasticity, with high levels of gene gain and loss during species and strain evolution. S. agalactiae has a large pan-genome, with little recombination in its core-genome, while S. pyogenes has a smaller pan-genome and much more recombination of its core-genome, perhaps reflecting the greater habitat, and gene pool, diversity for S. agalactiae compared to S. pyogenes. Core-genome recombination was evident in all lineages (18% to 37% of the core-genome judged to be recombinant), while positive selection was mainly observed during species differentiation (from 11% to 34% of the core-genome). Positive selection pressure was unevenly distributed across lineages and biochemical main role categories. S. suis was the lineage with the greatest level of positive selection pressure, the largest number of unique loci selected, and the largest amount of gene gain and loss.

Conclusion
Recombination is an important evolutionary force in shaping Streptococcus genomes, not only in the acquisition of significant portions of the genome as lineage specific loci, but also in facilitating rapid evolution of the core-genome. Positive selection, although undoubtedly a slower process, has nonetheless played an important role in adaptation of the core-genome of different Streptococcus species to different hosts.
Gene expression analysis of nuclear factor I-A deficient mice indicates delayed brain maturation
Authors: Wong Yong Wee , Schulze Christian , Streichert Thomas , Gronostajski Richard M , Schachner Melitta , Tilling Thomas 
Published: May 2007

Abstract
Background
Nuclear factor I-A (NFI-A), a phylogenetically conserved transcription/replication protein, plays a crucial role in mouse brain development. Previous studies have shown that disruption of the Nfia gene in mice leads to perinatal lethality, corpus callosum agenesis, and hydrocephalus.

Results
To identify potential NFI-A target genes involved in the observed tissue malformations, we analyzed gene expression in brains from Nfia-/- and Nfia+/+ littermate mice at the mRNA level using oligonucleotide microarrays. In young postnatal animals (postnatal day 16), 356 genes were identified as being differentially regulated, whereas at the late embryonic stage (embryonic day 18) only five dysregulated genes were found. An in silico analysis identified phylogenetically conserved NFI binding sites in at least 70 of the differentially regulated genes. Moreover, assignment of gene function showed that marker genes for immature neural cells and neural precursors were expressed at elevated levels in young postnatal Nfia-/- mice. In contrast, marker genes for differentiated neural cells were downregulated at this stage. In particular, genes relevant for oligodendrocyte differentiation were affected.

Conclusion
Our findings suggest that brain development, especially oligodendrocyte maturation, is delayed in Nfia-/- mice during the early postnatal period, which at least partly accounts for their phenotype. The identification of potential NFI-A target genes in our study should help to elucidate NFI-A dependent transcriptional pathways and contribute to enhanced understanding of this period of brain formation, especially with regard to the function of NFI-A.
The role of the β-glucan receptor Dectin-1 in control of fungal infection
Authors: Dennehy Kevin M , Brown Gordon D 
Published: May 2007

AbstractDuring fungal infection, a variety of receptors initiates immune responses, including TLR and the β-glucan receptor Dectin-1. TLR recognition of fungal ligands and subsequent signaling through the MyD88 pathway were thought to be the most important interactions required for the control of fungal infection. However, recent papers have challenged this view, highlighting the role of Dectin-1 in induction of cytokine responses and the respiratory burst. Two papers, using independently derived, Dectin-1-deficient mice, address the role of Dectin-1 in control of fungal infection. Saijo et al. [1] argue that Dectin-1 plays a minor role in control of Pneumocystis carinii by direct killing and that TLR-mediated cytokine production controls P. carinii and Candida albicans. By contrast, Taylor et al. [2] argue that Dectin-1-mediated cytokine and chemokine production, leading to efficient recruitment of inflammatory cells, is required for control of fungal infection. In this review, we argue that collaborative responses induced during infection may partially explain these apparently contradictory results. We propose that Dectin-1 is the first of many pattern recognition receptors that can mediate their own signaling, as well as synergize with TLR to initiate specific responses to infectious agents.
Optimal Stocking Densities of Walleye Fingerlings in Minnesota Lakes
Authors: Jacobson Peter C. , Anderson Charles S. 
Published: May 2007

Abstract
A generalized additive model was developed that described the effects of fingerling stocking density on the abundance of walleyes Sander vitreus in 551 lakes in Minnesota. Walleye abundance was measured as a catch per effort (CPE) from 1,511 standard Minnesota Department of Natural Resources gill-net assessments conducted during 1986–2004. In addition to fingerling stocking, the effects of lake morphometry, productivity, and fish community variables on walleye CPE were also described using a generalized additive model. Lake morphometry variables had sharply nonlinear effects on walleye abundance. Walleye abundance declined in lakes with areas less than 1,000 acres and increased rapidly in lakes with depths of less than 30 ft. The lake productivity variable, total alkalinity, was positively related to walleye abundance. Abundance of northern pike Esox lucius had a negative effect and abundance of yellow perch Perca flavescens a positive effect on walleye abundance. The response of walleye abundance to fingerling stocking was asymptotic: peak walleye abundance occurred at stocking densities greater than 0.65 lb·littoral acre−1·year−1. A fingerling stocking density of 0.50 lb·littoral acre−1·year−1 is recommended as a balance between increased abundance and relative costs of stocking for most lakes in Minnesota.
Production of External Fluorescent Marks on Golden Perch Fingerlings through Osmotic Induction Marking with Alizarin Red S
Authors: Crook David A. , O'Mahony Damien , Gillanders Bronwyn M. , Munro Andrew R. , Sanger Andrew C. 
Published: May 2007

Abstract
Osmotic induction marking trials with alizarin red S (ARS) were conducted on golden perch Macquaria ambigua to evaluate the use of ARS as a lower-cost alternative to osmotic induction marking with calcein for producing external fluorescent marks on hatchery-produced fish. After a 10-min immersion in a 5% solution of salt, experimental groups of golden perch were rinsed for 5 s in freshwater and immersed for 10 min in either a 0.1% or 0.5% solution of ARS, whereas control groups were either left untreated or immersed in a 0.1% solution of ARS for 10 min without prior immersion in the salt solution. All fish treated in the 0.5% solution of ARS died within 5 min of immersion, but no mortalities were observed in any of the controls or fish treated with the 0.1% solution of ARS. External fluorescent marks were observed on both the osmotic induction-marked fish and the direct ARS immersion-marked fish 100 d after treatment, but the osmotic induction-marked fish possessed more intense marks. Clear marks remained visible on fish marked by osmotic induction 9 months after treatment. This study indicates that highly visible external marks can be produced through osmotic induction with ARS at a substantially lower cost than marks produced through osmotic induction with calcein. Although further refinement and testing are needed, we conclude that the method has considerable potential for use in the mass marking of fish.
Precision of Hard Structures Used to Estimate Age of Riverine Catostomids and Cyprinids in the Upper Colorado River Basin
Authors: Quist Michael C. , Jackson Zachary J. , Bower Michael R. , Hubert Wayne A. 
Published: May 2007

Abstract
Understanding the population dynamics of native and nonnative fishes is critical for guiding and evaluating management activities, but obtaining information on population dynamics is often dependent on identifying structures that provide precise estimates of age. We examined age estimation using various hard structures for native bluehead suckers Catostomus discobolus, flannelmouth suckers C. latipinnis, and roundtail chub Gila robusta, and nonnative white suckers C. commersonii, creek chub Semotilus atromaculatus, white sucker × bluehead sucker hybrids, and white sucker × flannelmouth sucker hybrids in a small headwater stream of the upper Colorado River basin (UCRB) in Wyoming. We evaluated between-reader precision (i.e., between two readers) and agreement of otolith age estimates with estimates from scales, fin rays, cleithra, and opercular bones. Exact agreement between readers was highest for otoliths (66–96% among species) and fin rays (61–92%) and lowest for opercles (25–69%), cleithra (21–41%), and scales (15–48%). Age estimates from fin rays were almost exactly the same as those from otoliths for all species except creek chub, for which fin ray estimates were consistently lower than otolith estimates. Age estimates from scales were generally 1–4 years lower than those from otoliths for most species, and most discrepancies occurred when otolith ages were greater than 5 years. We recommend that fin rays be used to estimate age of native catostomids and roundtail chub in the UCRB because fin rays provide accurate estimates of otolith age and can be obtained without sacrificing fish. We further recommend that otoliths be used to estimate age of creek chub in the UCRB because accuracy of fin rays was poor and because sacrificing this nonnative species may benefit native fishes of the UCRB.