bluuebunny/crossref_metadata_2025_split huggingface dataset:
The evolutionary diversification of LSF and Grainyhead transcription factors preceded the radiation of basal animal lineages
Authors: Traylor-Knowles Nikki , Hansen Ulla , Dubuc Timothy Q , Martindale Mark Q , Kaufman Les , Finnerty John R 
Published: April 2010

AbstractBackgroundThe transcription factors of the LSF/Grainyhead (GRH) family are characterized by the possession of a distinctive DNA-binding domain that bears no clear relationship to other known DNA-binding domains, with the possible exception of the p53 core domain. In triploblastic animals, the LSF and GRH subfamilies have diverged extensively with respect to their biological roles, general expression patterns, and mechanism of DNA binding. For example,Grainyhead(GRH) homologs are expressed primarily in the epidermis, and they appear to play an ancient role in maintaining the epidermal barrier. By contrast, LSF homologs are more widely expressed, and they regulate general cellular functions such as cell cycle progression and survival in addition to cell-lineage specific gene expression.ResultsTo illuminate the early evolution of this family and reconstruct the functional divergence of LSF and GRH, we compared homologs from 18 phylogenetically diverse taxa, including four basal animals (Nematostella vectensis,Vallicula multiformis,Trichoplax adhaerens, andAmphimedon queenslandica), a choanoflagellate (Monosiga brevicollis) and several fungi. Phylogenetic and bioinformatic analyses of these sequences indicate that (1) the LSF/GRH gene family originated prior to the animal-fungal divergence, and (2) the functional diversification of the LSF and GRH subfamilies occurred prior to the divergence between sponges and eumetazoans. Aspects of the domain architecture of LSF/GRH proteins are well conserved between fungi, choanoflagellates, and metazoans, though within the Metazoa, the LSF and GRH families are clearly distinct. We failed to identify a convincing LSF/GRH homolog in the sequenced genomes of the algaeVolvox carteriandChlamydomonas reinhardtiior the amoebozoanDictyostelium purpureum. Interestingly, the ancestral GRH locus has become split into two separate loci in the sea anemoneNematostella, with one locus encoding a DNA binding domain and the other locus encoding the dimerization domain.ConclusionsIn metazoans, LSF and GRH proteins play a number of roles that are essential to achieving and maintaining multicellularity. It is now clear that this protein family already existed in the unicellular ancestor of animals, choanoflagellates, and fungi. However, the diversification of distinct LSF and GRH subfamilies appears to be a metazoan invention. Given the conserved role of GRH in maintaining epithelial integrity in vertebrates, insects, and nematodes, it is noteworthy that the evolutionary origin of Grh appears roughly coincident with the evolutionary origin of the epithelium.
High-throughput analysis of candidate imprinted genes and allele-specific gene expression in the human term placenta
Authors: Daelemans Caroline , Ritchie Matthew E , Smits Guillaume , Abu-Amero Sayeda , Sudbery Ian M , Forrest Matthew S , Campino Susana , Clark Taane G , Stanier Philip , Kwiatkowski Dominic , Deloukas Panos , Dermitzakis Emmanouil T , Tavaré Simon , Moore Gudrun E , Dunham Ian 
Published: April 2010

AbstractBackgroundImprinted genes show expression from one parental allele only and are important for development and behaviour. This extreme mode of allelic imbalance has been described for approximately 56 human genes. Imprinting status is often disrupted in cancer and dysmorphic syndromes. More subtle variation of gene expression, that is not parent-of-origin specific, termed 'allele-specific gene expression' (ASE) is more common and may give rise to milder phenotypic differences. Using two allele-specific high-throughput technologies alongside bioinformatics predictions, normal term human placenta was screened to find new imprinted genes and to ascertain the extent of ASE in this tissue.ResultsTwenty-three family trios of placental cDNA, placental genomic DNA (gDNA) and gDNA from both parents were tested for 130 candidate genes with the Sequenom MassArray system. Six genes were found differentially expressed but none imprinted. The Illumina ASE BeadArray platform was then used to test 1536 SNPs in 932 genes. The array was enriched for the human orthologues of 124 mouse candidate genes from bioinformatics predictions and 10 human candidate imprinted genes from EST database mining. After quality control pruning, a total of 261 informative SNPs (214 genes) remained for analysis. Imprinting with maternal expression was demonstrated for the lymphocyte imprinted geneZNF331in human placenta. Two potential differentially methylated regions (DMRs) were found in the vicinity ofZNF331. None of the bioinformatically predicted candidates tested showed imprinting except for a skewed allelic expression in a parent-specific manner observed forPHACTR2, a neighbour of the imprintedPLAGL1gene. ASE was detected for two or more individuals in 39 candidate genes (18%).ConclusionsBoth Sequenom and Illumina assays were sensitive enough to study imprinting and strong allelic bias. Previous bioinformatics approaches were not predictive of new imprinted genes in the human term placenta.ZNF331is imprinted in human term placenta and might be a new ubiquitously imprinted gene, part of a primate-specific locus. Demonstration of partial imprinting ofPHACTR2calls for re-evaluation of the allelic pattern of expression for thePHACTR2-PLAGL1locus. ASE was common in human term placenta.
Comparative gene expression in toxic versus non-toxic strains of the marine dinoflagellate Alexandrium minutum
Authors: Yang Ines , John Uwe , Beszteri Sára , Glöckner Gernot , Krock Bernd , Goesmann Alexander , Cembella Allan D 
Published: April 2010

Abstract

Background
The dinoflagellate Alexandrium minutum typically produces paralytic shellfish poisoning (PSP) toxins, which are known only from cyanobacteria and dinoflagellates. While a PSP toxin gene cluster has recently been characterized in cyanobacteria, the genetic background of PSP toxin production in dinoflagellates remains elusive.

Results
We constructed and analysed an expressed sequence tag (EST) library of A. minutum, which contained 15,703 read sequences yielding a total of 4,320 unique expressed clusters. Of these clusters, 72% combined the forward-and reverse reads of at least one bacterial clone. This sequence resource was then used to construct an oligonucleotide microarray. We analysed the expression of all clusters in three different strains. While the cyanobacterial PSP toxin genes were not found among the A. minutum sequences, 192 genes were differentially expressed between toxic and non-toxic strains.

Conclusions
Based on this study and on the lack of identified PSP synthesis genes in the two existent Alexandrium tamarense EST libraries, we propose that the PSP toxin genes in dinoflagellates might be more different from their cyanobacterial counterparts than would be expected in the case of a recent gene transfer. As a starting point to identify possible PSP toxin-associated genes in dinoflagellates without relying on a priori sequence information, the sequences only present in mRNA pools of the toxic strain can be seen as putative candidates involved in toxin synthesis and regulation, or acclimation to intracellular PSP toxins.
GPR30, but not estrogen receptor-α, is crucial in the treatment of experimental autoimmune encephalomyelitis by oral ethinyl estradiol
Authors: Yates Melissa A , Li Yuexin , Chlebeck Peter J , Offner Halina 
Published: April 2010

AbstractBackgroundRemission of multiple sclerosis during periods of high ovarian hormone secretion (such as pregnancy) has led to a great deal of interest in the potential for estrogens to treat autoimmune disease. Previous work has established that 17β-estradiol can inhibit onset of experimental autoimmune encephalomyelitis (EAE), while ethinyl estradiol (EE) can reduce the severity of established disease. In the current study, the influence of estrogen receptor-α (ERα) and the G-protein coupled estrogen receptor (GPR30 or GPER) on EE's ability to treat EAE was explored.ResultsEE reduced disease severity in wild-type and ERα knockout (ERKO) mice, but did not alter disease in the GPR30KO group. Production of anti-inflammatory IL-10 increased in EE-ERKO mice (which showed reduced disease) but not in EE-GPR30KO mice (who did not have improved disease).ConclusionsDifferential production of IL-10 following EE treatment in ERKO and GPR30KO animals may be responsible for the distinctly different effects on disease severity. Increased IL-10 in ERKO-EE compared to ERKO-Controls is likely to be an important factor in reducing established disease. The inability of EE to reduce disease in GPR30KO mice indicates an important but still undefined role for GPR30 in regulating immune reactivity.
Transcriptional profiles underlying parent-of-origin effects in seeds of Arabidopsis thaliana
Authors: Tiwari Sushma , Spielman Melissa , Schulz Reiner , Oakey Rebecca J , Kelsey Gavin , Salazar Andres , Zhang Ke , Pennell Roger , Scott Rod J 
Published: April 2010

Abstract

Background
Crossing plants of the same species but different ploidies can have dramatic effects on seed growth, but little is known about the alterations to transcriptional programmes responsible for this. Parental genomic imbalance particularly affects proliferation of the endosperm, with an increased ratio of paternally to maternally contributed genomes ('paternal excess') associated with overproliferation, while maternal excess inhibits endosperm growth. One interpretation is that interploidy crosses disrupt the balance in the seed of active copies of parentally imprinted genes. This is supported by the observation that mutations in imprinted FIS-class genes of Arabidopsis thaliana share many features of the paternal excess phenotype. Here we investigated gene expression underlying parent-of-origin effects in Arabidopsis through transcriptional profiling of siliques generated by interploidy crosses and FIS-class mutants.

Results
We found that fertilized fis1 mutant seeds have similar profiles to seeds with paternal excess, showing that the shared phenotypes are underpinned by similar patterns of gene expression. We identified genes strongly associated with enhanced or inhibited seed growth; this provided many candidates for further investigation including MADS-box transcription factors, cell cycle genes, and genes involved in hormone pathways.

Conclusions
The work presented here is a step towards understanding the effects on seed development of the related phenomena of parental genome balance and imprinting.
Essential role of the N-terminal region of TFII-I in viability and behavior
Authors: Lucena Jaume , Pezzi Susana , Aso Ester , Valero Maria C , Carreiro Candelas , Dubus Pierre , Sampaio Adriana , Segura Maria , Barthelemy Isabel , Zindel Marc Y , Sousa Nuno , Barbero José L , Maldonado Rafael , Pérez-Jurado Luis A , Campuzano Victoria 
Published: April 2010

AbstractBackgroundGTF2Icodes for a general intrinsic transcription factor and calcium channel regulator TFII-I, with high and ubiquitous expression, and a strong candidate for involvement in the morphological and neuro-developmental anomalies of the Williams-Beuren syndrome (WBS). WBS is a genetic disorder due to a recurring deletion of about 1,55-1,83 Mb containing 25-28 genes in chromosome band 7q11.23 includingGTF2I. Completed homozygous loss of either theGtf2iorGtf2ird1function in mice provided additional evidence for the involvement of both genes in the craniofacial and cognitive phenotype. Unfortunately nothing is now about the behavioral characterization of heterozygous mice.MethodsBy gene targeting we have generated a mutant mice with a deletion of the first 140 amino-acids of TFII-I. mRNA and protein expression analysis were used to document the effect of the study deletion. We performed behavioral characterization of heterozygous mutant mice to documentin vivoimplications of TFII-I in the cognitive profile of WBS patients.ResultsHomozygous and heterozygous mutant mice exhibit craniofacial alterations, most clearly represented in homozygous condition. Behavioral test demonstrate that heterozygous mutant mice exhibit some neurobehavioral alterations and hyperacusis or odynacusis that could be associated with specific features of WBS phenotype. Homozygous mutant mice present highly compromised embryonic viability and fertility. Regarding cellular model, we documented a retarded growth in heterozygous MEFs respect to homozygous or wild-type MEFs.ConclusionOur data confirm that, although additive effects of haploinsufficiency at several genes may contribute to the full craniofacial or neurocognitive features of WBS, correct expression ofGTF2Iis one of the main players. In addition, these findings show that the deletion of the fist 140 amino-acids of TFII-I altered it correct function leading to a clear phenotype, at both levels, at the cellular model and at thein vivomodel.
Increased expression of urokinase plasminogen activator and its cognate receptor in human seminomas
Authors: Ulisse Salvatore , Baldini Enke , Mottolese Marcella , Sentinelli Steno , Gargiulo Patrizia , Valentina Brancato , Sorrenti Salvatore , Di Benedetto Anna , De Antoni Enrico , D'Armiento Massimino 
Published: April 2010

Abstract

Background
The urokinase plasminogen activating system (uPAS) is implicated in neoplastic progression and high tissue levels of uPAS components correlate with a poor prognosis in different human cancers. Despite that, relative few studies are available on the expression and function of the uPAS components in human seminomas. In the present study we characterized the expression of the urokinase plasminogen activator (uPA), its cognate receptor (uPAR) and the uPA inhibitors PAI-1 and PAI-2 in normal human testis and seminomas.

Methods
The expression of the above genes was evaluated by means of quantitative RT-PCR, western blot, zymographic analysis and immunohistochemistry.

Results
Quantitative RT-PCR analysis of 14 seminomas demonstrated that uPA and uPAR mRNAs were, with respect to control tissues, increased in tumor tissues by 3.80 ± 0.74 (p < 0.01) and 6.25 ± 1.18 (p < 0.01) fold, respectively. On the other hand, PAI-1 mRNA level was unchanged (1.02 ± 0.24 fold), while that of PAI-2 was significantly reduced to 0.34 ± 0.18 (p < 0.01) fold. Western blot experiments performed with protein extracts of three seminomas and normal tissues from the same patients showed that uPA protein levels were low or undetectable in normal tissues and induced in tumor tissues. On the same samples, zymographic analysis demonstrated increased uPA activity in tumor tissue extracts. Western blot experiments showed that also the uPAR protein was increased in tumor tissues by 1.83 ± 0.15 fold (p < 0.01). The increased expression of uPA and uPAR was further confirmed by immunohistochemical staining performed in 10 seminomas and autologous uninvolved peritumoral tissues. Finally, variation in the mRNA level of PAI-1 significantly correlated with tumor size.

Conclusions
We demonstrated the increased expression of uPA and uPAR in human seminomas with respect to normal testis tissues, which may be relevant in testicular cancer progression.
A simple fluorescence based assay for quantification of human immunodeficiency virus particle release
Authors: Hermle Johannes , Anders Maria , Heuser Anke-Mareil , Müller Barbara 
Published: April 2010

Abstract

Background
The assembly and release of human immunodeficiency virus (HIV) particles from infected cells represent attractive, but not yet exploited targets for antiretroviral therapy. The availability of simple methods to measure the efficiency of these replication steps in tissue culture would facilitate the identification of host factors essential for these processes as well as the screening for lead compounds acting as specific inhibitors of particle formation. We describe here the development of a rapid cell based assay for quantification of human immunodeficiency virus type 1 (HIV-1) particle assembly and/or release.

Results
Using a fluorescently labelled HIV-derivative, which carries an eYFP domain within the main viral structural protein Gag in the complete viral protein context, the release of virus like particles could be monitored by directly measuring the fluorescence intensity of the tissue culture supernatant. Intracellular Gag was quantitated in parallel by direct fluorescence analysis of cell lysates, allowing us to normalize for Gag expression efficiency. The assay was validated by comparison with p24 capsid ELISA measurements, a standard method for quantifying HIV-1 particles. Optimization of conditions allowed the robust detection of particle amounts corresponding to 50 ng p24/ml in medium by fluorescence spectroscopy. Further adaptation to a multi-well format rendered the assay suitable for medium or high throughput screening of siRNA libraries to identify host cell factors involved in late stages of HIV replication, as well as for random screening approaches to search for potential inhibitors of HIV-1 assembly or release.

Conclusions
The fast and simple fluorescence based quantification of HIV particle release yielded reproducible results which were comparable to the well established ELISA measurements, while in addition allowing the parallel determination of intracellular Gag expression. The protocols described here can be used for screening of siRNA libraries or chemical compounds, respectively, for inhibition of HIV in a 96-well format.
Socio-demographic disparity in oral health among the poor: a cross sectional study of early adolescents in Kilwa district, Tanzania
Authors: Mashoto Kijakazi O , Astrom Anne N , Skeie Marit S , Masalu Joyce R 
Published: April 2010

Abstract

Background
There is a lack of studies considering social disparity in oral health emanating from adolescents in low-income countries. This study aimed to assess socio-demographic disparities in clinical- and self reported oral health status and a number of oral health behaviors. The extent to which oral health related behaviors might account for socio-demographic disparities in oral health status was also examined.

Methods
A cross-sectional study was conducted in Kilwa district in 2008. One thousand seven hundred and forty five schoolchildren completed an interview and a full mouth clinical examination. Caries experience was recorded using WHO criteria, whilst type of treatment need was categorized using the ART approach.

Results
The majority of students were caries free (79.8%) and presented with a low need for dental treatment (89.3%). Compared to their counterparts in opposite groups, rural residents and those from less poor households presented more frequently with caries experience (DMT>0), high need for dental treatment and poor oral hygiene behavior, but were less likely to report poor oral health status. Stepwise logistic regressions revealed that social and behavioral variables varied systematically with caries experience, high need for dental treatment and poor self reported oral health. Socio-demographic disparities in oral health outcomes persisted after adjusting for oral health behaviors.

Conclusions
Socio-demographic disparities in oral health outcomes and oral health behaviors do exist. Socio-demographic disparities in oral health outcomes were marginally accounted for by oral health behaviors. Developing policies and programs targeting both social and individual determinants of oral health should be an urgent public health strategy in Tanzania.
Alpha-tocopherol transfer protein disruption confers resistance to malarial infection in mice
Authors: Herbas Maria S , Ueta Yoshiko Y , Ichikawa Chie , Chiba Mayumi , Ishibashi Kana , Shichiri Mototada , Fukumoto Shinya , Yokoyama Naoaki , Takeya Motohiro , Xuan Xuenan , Arai Hiroyuki , Suzuki Hiroshi 
Published: April 2010

Abstract

Background
Various factors impact the severity of malaria, including the nutritional status of the host. Vitamin E, an intra and extracellular anti-oxidant, is one such nutrient whose absence was shown previously to negatively affect Plasmodium development. However, mechanisms of this Plasmodium inhibition, in addition to means by which to exploit this finding as a therapeutic strategy, remain unclear.

Methods
α-TTP knockout mice were infected with Plasmodium berghei NK65 or Plasmodium yoelii XL-17, parasitaemia, survival rate were monitored. In one part of the experiments mice were fed with a supplemented diet of vitamin E and then infected. In addition, parasite DNA damage was monitored by means of comet assay and 8-OHdG test. Moreover, infected mice were treated with chloroquine and parasitaemia and survival rate were monitored.

Results
Inhibition of α-tocopherol transfer protein (α-TTP), a determinant of vitamin E concentration in circulation, confers resistance to malarial infection as a result of oxidative damage to the parasites. Furthermore, in combination with the anti-malarial drug chloroquine results were even more dramatic.

Conclusion
Considering that these knockout mice lack observable negative impacts typical of vitamin E deficiency, these results suggest that inhibition of α-TTP activity in the liver may be a useful strategy in the prevention and treatment of malaria infection. Moreover, a combined strategy of α-TTP inhibition and chloroquine treatment might be effective against drug resistant parasites.
School-based participatory health education for malaria control in Ghana: engaging children as health messengers
Authors: Ayi Irene , Nonaka Daisuke , Adjovu Josiah K , Hanafusa Shigeki , Jimba Masamine , Bosompem Kwabena M , Mizoue Tetsuya , Takeuchi Tsutomu , Boakye Daniel A , Kobayashi Jun 
Published: April 2010

Abstract

Background
School children have been increasingly recognized as health messengers for malaria control. However, little evidence is available. The objective of this study was to determine the impact of school-based malaria education intervention on school children and community adults.

Methods
This study was conducted in the Dangme-East district of the Greater Accra Region, Ghana, between 2007 and 2008. Trained schoolteachers designed participatory health education activities and led school children to disseminate messages related to malaria control to their communities. Three schools and their respective communities were chosen for the study and assigned to an intervention group (one school) and a control group (two schools). Questionnaire-based interviews and parasitological surveys were conducted before and after the intervention, with the intervention group (105 children, 250 community adults) and the control group (81 children, 133 community adults). Chi-square and Fisher's Exact tests were used to analyse differences in knowledge, practices, and parasite prevalence between pre- and post-intervention.

Results
After the intervention, the misperception that malaria has multiple causes was significantly improved, both among children and community adults. Moreover, the community adults who treated a bed net with insecticide in the past six months, increased from 21.5% to 50.0% (p < 0.001). Parasite prevalence in school children decreased from 30.9% to 10.3% (p = 0.003). These positive changes were observed only in the intervention group.

Conclusions
This study suggests that the participatory health education intervention contributed to the decreased malaria prevalence among children. It had a positive impact not only on school children, but also on community adults, through the improvement of knowledge and practices. This strategy can be applied as a complementary approach to existing malaria control strategies in West African countries where school health management systems have been strengthened.