bluuebunny/crossref_metadata_2025_split huggingface dataset:
Paralytic Shellfish Poisoning Toxin-Producing CyanobacteriumAphanizomenon gracilein Northeast Germany
Authors: Ballot Andreas , Fastner Jutta , Wiedner Claudia 
Published: January 2010

ABSTRACTNeurotoxic paralytic shellfish poisoning (PSP) toxins, anatoxin-a (ATX), and hepatotoxic cylindrospermopsin (CYN) have been detected in several lakes in northeast Germany during the last 2 decades. They are produced worldwide by members of the nostocalean generaAnabaena,Cylindrospermopsis, andAphanizomenon. Although no additional sources of PSP toxins and ATX have been identified in German water bodies to date, the observed CYN concentrations cannot be produced solely byAphanizomenon flos-aquae, the only known CYN producer in Germany. Therefore, we attempted to identify PSP toxin, ATX, and CYN producers by isolating and characterizing 92Anabaena, Aphanizomenon, andAnabaenopsisstrains from five lakes in northeast Germany. In a polyphasic approach, all strains were morphologically and phylogenetically classified and then tested for PSP toxins, ATX, and CYN by liquid chromatography-tandem mass spectrometry (LC-MS/MS) and enzyme-linked immunosorbent assay (ELISA) and screened for the presence of PSP toxin- and CYN-encoding gene fragments. As demonstrated by ELISA and LC-MS, 14Aphanizomenon gracilestrains from Lakes Melang and Scharmützel produced four PSP toxin variants (gonyautoxin 5 [GTX5], decarbamoylsaxitoxin [dcSTX], saxitoxin [STX], and neosaxitoxin [NEO]). GTX5 was the most prevalent PSP toxin variant among the seven strains from Lake Scharmützel, and NEO was the most prevalent among the seven strains from Lake Melang. ThesxtAgene, which is part of the saxitoxin gene cluster, was found in the 14 PSP toxin-producingA. gracilestrains and in 11 non-PSP toxin-producingAphanizomenon issatschenkoi,A. flos-aquae,Anabaena planktonica, andAnabaenopsis elenkiniistrains. ATX and CYN were not detected in any of the isolated strains. This study is the first confirming the role ofA. gracileas a PSP toxin producer in German water bodies.
Pseudomonas aeruginosaAlginate PromotesBurkholderia cenocepaciaPersistence in Cystic Fibrosis Transmembrane Conductance Regulator Knockout Mice
Authors: Chattoraj Sangbrita S. , Murthy Rachana , Ganesan Shyamala , Goldberg Joanna B. , Zhao Ying , Hershenson Marc B. , Sajjan Umadevi S. 
Published: January 2010

ABSTRACTPseudomonas aeruginosa, a major respiratory pathogen in cystic fibrosis (CF) patients, facilitates infection by other opportunistic pathogens.Burkholderia cenocepacia, which normally infects adolescent patients, encounters alginate elaborated by mucoidP. aeruginosa. To determine whetherP. aeruginosaalginate facilitatesB. cenocepaciainfection in mice, cystic fibrosis transmembrane conductance regulator knockout mice were infected withB. cenocepaciastrain BC7 suspended in either phosphate-buffered saline (BC7/PBS) orP. aeruginosaalginate (BC7/alginate), and the pulmonary bacterial load and inflammation were monitored. Mice infected with BC7/PBS cleared all of the bacteria within 3 days, and inflammation was resolved by day 5. In contrast, mice infected with BC7/alginate showed persistence of bacteria and increased cytokine levels for up to 7 days. Histological examination of the lungs indicated that there was moderate to severe inflammation and pneumonic consolidation in isolated areas at 5 and 7 days postinfection in the BC7/alginate group. Further, alginate decreased phagocytosis ofB. cenocepaciaby professional phagocytes bothin vivoandin vitro. P. aeruginosaalginate also reduced the proinflammatory responses of CF airway epithelial cells and alveolar macrophages toB. cenocepaciainfection. The observed effects are specific toP. aeruginosaalginate, because enzymatically degraded alginate or other polyuronic acids did not facilitate bacterial persistence. These observations suggest thatP. aeruginosaalginate may facilitateB. cenocepaciainfection by interfering with host innate defense mechanisms.
ATP-Dependent Carboxylation of Acetophenone by a Novel Type of Carboxylase
Authors: Jobst Björn , Schühle Karola , Linne Uwe , Heider Johann 
Published: January 2010

ABSTRACT

Anaerobic ethylbenzene metabolism in the betaproteobacterium
Aromatoleum aromaticum
is initiated by anaerobic oxidation to acetophenone via (
S
)-1-phenylethanol. The subsequent carboxylation of acetophenone to benzoylacetate is catalyzed by an acetophenone-induced enzyme, which has been purified and studied. The same enzyme is involved in acetophenone metabolism in the absence of ethylbenzene. Acetophenone carboxylase consists of five subunits with molecular masses of 70, 15, 87, 75, and 34 kDa, whose genes (
apcABCDE
) form an apparent operon. The enzyme is synthesized at high levels in cells grown on ethylbenzene or acetophenone, but not in cells grown on benzoate. During purification, acetophenone carboxylase dissociates into inactive subcomplexes consisting of the 70-, 15-, 87-, and 75-kDa subunits (
apcABCD
gene products) and the 34-kDa subunit (
apcE
gene product), respectively. Acetophenone carboxylase activity was restored by mixing the purified subcomplexes. The enzyme contains 1 Zn
2+
ion per αβγδ core complex and is dependent on the presence of Mg
2+
or Mn
2+
. In spite of the presence of Zn in the enzyme, it is strongly inhibited by Zn
2+
ions. Carboxylation of acetophenone is dependent on ATP hydrolysis to ADP and P
i
, exhibiting a stoichiometry of 2 mol ATP per mol acetophenone carboxylated. The enzyme shows uncoupled ATPase activity with either bicarbonate or acetophenone in the absence of the second substrate. These observations indicate that both substrates may be phosphorylated, which is consistent with isotope exchange activity observed with deuterated acetophenone and inhibition by carbamoylphosphate, a structural analogue of carboxyphosphate. A potential mechanism of ATP-dependent acetophenone carboxylation is suggested.
Measuring and guaranteeing quality of barrier coverage for general belts with wireless sensors
Authors: Chen Ai , Lai Ten H. , Xuan Dong 
Published: January 2010

Sensors may fail due to various reasons such as heat, malicious activity, environmental hazards, extended use, and lack of power. As more and more sensors fail, certain desired properties such as barrier coverage will diminish and eventually fall below a desired level. In such a case, the network will have to be repaired. It is therefore desirable to have mechanisms to monitor network properties. In this article, we are interested in measuring the quality of barrier coverage, which is known to be an appropriate model of coverage for movement detection applications such as intrusion detection.
In the literature, researchers only consider whether or not a sensor network provides barrier coverage. This is equivalent to measuring its quality as either 0 or 1. We believe quality of barrier coverage is not binary and propose a metric for measuring it. If the measured quality is short of a desired value, we further identify all local regions that need to be repaired. The identified regions are minimal in the sense that if one of them is not repaired then the resulting network will still be short of quality. We also discuss how to actually repair a region.
Strategic Approach to Validating Methylated Genes as Biomarkers for Breast Cancer
Authors: Wang Wendy , Srivastava Sudhir 
Published: January 2010

AbstractAlthough the potential of biomarkers to aid in the early detection, diagnosis, prevention, and treatment of breast cancer is broadly recognized and numerous biomarker candidates have been reported in the literature, few molecular markers have been adopted into clinical use to date. To address this lack of translation of biomarkers from the bench to clinical practice, the Cancer Biomarkers Research Group in the Division of Cancer Prevention of the National Cancer Institute organized a meeting, “Strategic Discussion on Biomarkers for Breast Cancer,” which was held at the Fred Hutchinson Cancer Research Center on September 14, 2008. Participants included industry leaders, basic and physician scientists, and National Cancer Institute program staff. The objectives of this strategic discussion were to define clinical uses and needed performance characteristics of biomarkers; to identify novel approaches to discover and validate breast cancer biomarkers, particularly those with improved chances of being clinically useful; and to identify candidate DNA methylation markers that could be taken forward for validation. Participants presented and recommended methylation biomarkers suitable for initiating collaborative projects to evaluate the markers for future clinical application. This commentary summarizes their discussions and recommendations and the rationale for initiating specific projects to validate DNA methylation biomarkers of breast cancer. Cancer Prev Res; 3(1); 16–24
Sulindac and Sulindac Metabolites in Nipple Aspirate Fluid and Effect on Drug Targets in a Phase I Trial
Authors: Thompson Patricia A. , Hsu Chiu-Hsieh , Green Sylvan , Stopeck Alison T. , Johnson Karen , Alberts David S. , Chow H-H. Sherry 
Published: January 2010

Abstract
Regular use of nonsteroidal anti-inflammatory drugs (NSAID) has been associated with reduced risk of breast cancer. Sulindac, a nonselective NSAID with both cyclooxygenase-2–dependent and –independent activities, is a candidate for breast chemoprevention. We conducted a phase Ib trial in 30 women at increased risk for breast cancer to evaluate the breast tissue distribution of sulindac at two dose levels (150 mg daily and 150 mg twice daily for 6 weeks), using nipple aspirate fluid (NAF) as a surrogate of breast tissue drug exposure. We also explored the effect of sulindac on drug-induced biomarkers in NAF. We show that sulindac and its metabolites partition to human breast as measured by NAF levels. Sulindac intervention did not decrease 13,14-dihydro-15-keto prostaglandin A2, a stable derivative of prostaglandin E2, in NAF, but exposure was associated with a significant trend towards higher levels of growth differentiation factor 15 in NAF in women receiving 150 mg twice daily (P = 0.038). These results are the first to show partitioning of sulindac and metabolites to human breast tissue and the first evidence for a potential dose-dependent effect of sulindac on growth differentiation factor 15 levels in NAF. Cancer Prev Res; 3(1); 101–7
Beyond the Scalpel: Targeting Hedgehog in Skin Cancer Prevention
Authors: Rudin Charles M. 
Published: January 2010

Abstract
This perspective places the article by Tang et al. in this issue of the journal (beginning on page 25) in the context of recent work defining the hedgehog signaling pathway as a central etiologic factor and as a therapeutic target in basal cell cancer. Tang et al. show that inhibition of cyclooxygenase activity, either genetically (in a relevant mouse model) or pharmacologically (in the mouse and in patients highly predisposed to develop basal cell skin cancers), may suppress basal cell carcinogenesis. This new study of cyclooxygenase inhibition, together with recent data on the efficacy of hedgehog pathway inhibition, offers new hope for patients at a high risk for basal cell cancer. Cancer Prev Res; 3(1); 1–3
Translating Cyclooxygenase Signaling in Patch Heterozygote Mice into a Randomized Clinical Trial in Basal Cell Carcinoma
Authors: Arbiser Jack L. 
Published: January 2010

Abstract
This different perspective on Tang et al. (beginning on p. 25 in this issue of the journal) discusses the pivotal role of cyclooxygenase (COX) signaling in the pathogenesis of basal cell carcinoma (BCC). These investigators conducted elegant experiments showing increased BCC burden in patch heterozygous mice overexpressing COX-2 in the epidermis. Genetic deletion of COX-1 or COX-2 resulted in a robust decrease in BCC burden in patch heterozygote mice. They then studied pharmacologic COX inhibition in mice and humans with loss of patch, finding a trend in humans toward decreased BCC burden. This finding has implications for public health. Cancer Prev Res; 3(1); 4–7
A computational screen for site selective A-to-I editing detects novel sites in neuron specific Hu proteins
Authors: Ensterö Mats , Åkerborg Örjan , Lundin Daniel , Wang Bei , Furey Terrence S , Öhman Marie , Lagergren Jens 
Published: January 2010

Abstract

Background
Several bioinformatic approaches have previously been used to find novel sites of ADAR mediated A-to-I RNA editing in human. These studies have discovered thousands of genes that are hyper-edited in their non-coding intronic regions, especially in alu retrotransposable elements, but very few substrates that are site-selectively edited in coding regions. Known RNA edited substrates suggest, however, that site selective A-to-I editing is particularly important for normal brain development in mammals.

Results
We have compiled a screen that enables the identification of new sites of site-selective editing, primarily in coding sequences. To avoid hyper-edited repeat regions, we applied our screen to the alu-free mouse genome. Focusing on the mouse also facilitated better experimental verification. To identify candidate sites of RNA editing, we first performed an explorative screen based on RNA structure and genomic sequence conservation. We further evaluated the results of the explorative screen by determining which transcripts were enriched for A-G mismatches between the genomic template and the expressed sequence since the editing product, inosine (I), is read as guanosine (G) by the translational machinery. For expressed sequences, we only considered coding regions to focus entirely on re-coding events. Lastly, we refined the results from the explorative screen using a novel scoring scheme based on characteristics for known A-to-I edited sites. The extent of editing in the final candidate genes was verified using total RNA from mouse brain and 454 sequencing.

Conclusions
Using this method, we identified and confirmed efficient editing at one site in the Gabra3 gene. Editing was also verified at several other novel sites within candidates predicted to be edited. Five of these sites are situated in genes coding for the neuron-specific RNA binding proteins HuB and HuD.
Complete genome sequence of the fire blight pathogen Erwinia pyrifoliae DSM 12163T and comparative genomic insights into plant pathogenicity
Authors: Smits Theo HM , Jaenicke Sebastian , Rezzonico Fabio , Kamber Tim , Goesmann Alexander , Frey Jürg E , Duffy Brion 
Published: January 2010

Abstract

Background

Erwinia pyrifoliae is a newly described necrotrophic pathogen, which causes fire blight on Asian (Nashi) pear and is geographically restricted to Eastern Asia. Relatively little is known about its genetics compared to the closely related main fire blight pathogen E. amylovora.

Results
The genome of the type strain of E. pyrifoliae strain DSM 12163T, was sequenced using both 454 and Solexa pyrosequencing and annotated. The genome contains a circular chromosome of 4.026 Mb and four small plasmids. Based on their respective role in virulence in E. amylovora or related organisms, we identified several putative virulence factors, including type III and type VI secretion systems and their effectors, flagellar genes, sorbitol metabolism, iron uptake determinants, and quorum-sensing components. A deletion in the rpoS gene covering the most conserved region of the protein was identified which may contribute to the difference in virulence/host-range compared to E. amylovora. Comparative genomics with the pome fruit epiphyte Erwinia tasmaniensis Et1/99 showed that both species are overall highly similar, although specific differences were identified, for example the presence of some phage gene-containing regions and a high number of putative genomic islands containing transposases in the E. pyrifoliae DSM 12163T genome.

Conclusions
The E. pyrifoliae genome is an important addition to the published genome of E. tasmaniensis and the unfinished genome of E. amylovora providing a foundation for re-sequencing additional strains that may shed light on the evolution of the host-range and virulence/pathogenicity of this important group of plant-associated bacteria.
Analysis of newly established EST databases reveals similarities between heart regeneration in newt and fish
Authors: Borchardt Thilo , Looso Mario , Bruckskotten Marc , Weis Patrick , Kruse Julia , Braun Thomas 
Published: January 2010

AbstractBackgroundThe newtNotophthalmus viridescenspossesses the remarkable ability to respond to cardiac damage by formation of new myocardial tissue. Surprisingly little is known about changes in gene activities that occur during the course of regeneration. To begin to decipher the molecular processes, that underlie restoration of functional cardiac tissue, we generated an EST database from regenerating newt hearts and compared the transcriptional profile of selected candidates with genes deregulated during zebrafish heart regeneration.ResultsA cDNA library of 100,000 cDNA clones was generated from newt hearts 14 days after ventricular injury. Sequencing of 11520 cDNA clones resulted in 2894 assembled contigs. BLAST searches revealed 1695 sequences with potential homology to sequences from the NCBI database. BLAST searches to TrEMBL and Swiss-Prot databases assigned 1116 proteins to Gene Ontology terms. We also identified a relatively large set of 174 ORFs, which are likely to be unique for urodele amphibians. Expression analysis of newt-zebrafish homologues confirmed the deregulation of selected genes during heart regeneration. Sequences, BLAST results and GO annotations were visualized in a relational web based database followed by grouping of identified proteins into clusters of GO Terms. Comparison of data from regenerating zebrafish hearts identified biological processes, which were uniformly overrepresented during cardiac regeneration in newt and zebrafish.ConclusionWe concluded that heart regeneration in newts and zebrafish led to the activation of similar sets of genes, which suggests that heart regeneration in both species might follow similar principles. The design of the newly established newt EST database allows identification of molecular pathways important for heart regeneration.
Identification of genes differentially expressed during interaction of resistant and susceptible apple cultivars (Malus × domestica) with Erwinia amylovora
Authors: Baldo Angela , Norelli Jay L , Farrell Robert E , Bassett Carole L , Aldwinckle Herb S , Malnoy Mickael 
Published: January 2010

Abstract

Background
The necrogenic enterobacterium, Erwinia amylovora is the causal agent of the fire blight (FB) disease in many Rosaceaespecies, including apple and pear. During the infection process, the bacteria induce an oxidative stress response with kinetics similar to those induced in an incompatible bacteria-plant interaction. No resistance mechanism to E. amylovora in host plants has yet been characterized, recent work has identified some molecular events which occur in resistant and/or susceptible host interaction with E. amylovora: In order to understand the mechanisms that characterize responses to FB, differentially expressed genes were identified by cDNA-AFLP analysis in resistant and susceptible apple genotypes after inoculation with E. amylovora.

Results
cDNA were isolated from M.26 (susceptible) and G.41 (resistant) apple tissues collected 2 h and 48 h after challenge with a virulent E. amylovora strain or mock (buffer) inoculated. To identify differentially expressed transcripts, electrophoretic banding patterns were obtained from cDNAs. In the AFLP experiments, M.26 and G.41 showed different patterns of expression, including genes specifically induced, not induced, or repressed by E. amylovora. In total, 190 ESTs differentially expressed between M.26 and G.41 were identified using 42 pairs of AFLP primers. cDNA-AFLP analysis of global EST expression in a resistant and a susceptible apple genotype identified different major classes of genes. EST sequencing data showed that genes linked to resistance, encoding proteins involved in recognition, signaling, defense and apoptosis, were modulated by E. amylovora in its host plant. The expression time course of some of these ESTs selected via a bioinformatic analysis has been characterized.

Conclusion
These data are being used to develop hypotheses of resistance or susceptibility mechanisms in Malus to E. amylovora and provide an initial categorization of genes possibly involved in recognition events, early signaling responses the subsequent development of resistance or susceptibility. These data also provided potential candidates for improving apple resistance to fire blight either by marker-assisted selection or genetic engineering.
QTLs and candidate genes for desiccation and abscisic acid content in maize kernels
Authors: Capelle Valérie , Remoué Carine , Moreau Laurence , Reyss Agnès , Mahé Aline , Massonneau Agnès , Falque Matthieu , Charcosset Alain , Thévenot Claudine , Rogowsky Peter , Coursol Sylvie , Prioul Jean-Louis 
Published: January 2010

Abstract

Background
Kernel moisture at harvest is an important trait since a low value is required to prevent unexpected early germination and ensure seed preservation. It is also well known that early germination occurs in viviparous mutants, which are impaired in abscisic acid (ABA) biosynthesis. To provide some insight into the genetic determinism of kernel desiccation in maize, quantitative trait loci (QTLs) were detected for traits related to kernel moisture and ABA content in both embryo and endosperm during kernel desiccation. In parallel, the expression and mapping of genes involved in kernel desiccation and ABA biosynthesis, were examined to detect candidate genes.

Results
The use of an intermated recombinant inbred line population allowed for precise QTL mapping. For 29 traits examined in an unreplicated time course trial of days after pollination, a total of 78 QTLs were detected, 43 being related to kernel desiccation, 15 to kernel weight and 20 to ABA content. Multi QTL models explained 35 to 50% of the phenotypic variation for traits related to water status, indicating a large genetic control amenable to breeding. Ten of the 20 loci controlling ABA content colocated with previously detected QTLs controlling water status and ABA content in water stressed leaves. Mapping of candidate genes associated with kernel desiccation and ABA biosynthesis revealed several colocations between genes with putative functions and QTLs. Parallel investigation via RT-PCR experiments showed that the expression patterns of the ABA-responsive Rab17 and Rab28 genes as well as the late embryogenesis abundant Emb5 and aquaporin genes were related to desiccation rate and parental allele effect. Database searches led to the identification and mapping of two zeaxanthin epoxidase (ZEP) and five novel 9-cis-epoxycarotenoid dioxygenase (NCED) related genes, both gene families being involved in ABA biosynthesis. The expression of these genes appeared independent in the embryo and endosperm and not correlated with ABA content in either tissue.

Conclusions
A high resolution QTL map for kernel desiccation and ABA content in embryo and endosperm showed several precise colocations between desiccation and ABA traits. Five new members of the maize NCED gene family and another maize ZEP gene were identified and mapped. Among all the identified candidates, aquaporins and members of the Responsive to ABA gene family appeared better candidates than NCEDs and ZEPs.