bluuebunny/crossref_metadata_2025_split huggingface dataset:
Competitive Interactions of Attentional Resources in Early Visual Cortex during Sustained Visuospatial Attention within or between Visual Hemifields: Evidence for the Different-hemifield Advantage
Authors: Walter Sabrina , Quigley Cliodhna , Mueller Matthias M. 
Published: December 2013

Abstract
Performing a task across the left and right visual hemifields results in better performance than in a within-hemifield version of the task, termed the different-hemifield advantage. Although recent studies used transient stimuli that were presented with long ISIs, here we used a continuous objective electrophysiological (EEG) measure of competitive interactions for attentional processing resources in early visual cortex, the steady-state visual evoked potential (SSVEP). We frequency-tagged locations in each visual quadrant and at central fixation by flickering light-emitting diodes (LEDs) at different frequencies to elicit distinguishable SSVEPs. Stimuli were presented for several seconds, and participants were cued to attend to two LEDs either in one (Within) or distributed across left and right visual hemifields (Across). In addition, we introduced two reference measures: one for suppressive interactions between the peripheral LEDs by using a task at fixation where attention was withdrawn from the periphery and another estimating the upper bound of SSVEP amplitude by cueing participants to attend to only one of the peripheral LEDs. We found significantly greater SSVEP amplitude modulations in Across compared with Within hemifield conditions. No differences were found between SSVEP amplitudes elicited by the peripheral LEDs when participants attended to the centrally located LEDs compared with when peripheral LEDs had to be ignored in Across and Within trials. Attending to only one LED elicited the same SSVEP amplitude as Across conditions. Although behavioral data displayed a more complex pattern, SSVEP amplitudes were well in line with the predictions of the different-hemifield advantage account during sustained visuospatial attention.
The Changing Landscape of Total Laryngectomy Surgery
Authors: Verma Sunil P. , Mahboubi Hossein 
Published: December 2013

ObjectiveTo determine if the number of total laryngectomies (TL) performed in California has changed over a 15‐year period from 1996 to 2010. We also sought to investigate if the location of surgery, length of stay, use of rotational/free flaps, cost, and complications changed over this period.Study DesignCross‐sectional.SettingCalifornia Hospital Inpatient Discharge Data sets.Subjects and MethodsAll patient records enlisting International Classification of Diseases, Ninth Revision, Clinical Modification procedural codes for total/radical laryngectomy were extracted from 1996 to 2010 data sets. Patients’ demographics were evaluated. Hospitals were coded as university medical centers (UMCs) vs others. Population‐adjusted surgery rates, percentage of surgeries with rotational/free flap and/or percutaneous endoscopic gastrostomy (PEG), length of stay, total charges, and disposition status were then analyzed and compared between UMCs and non‐UMCs.ResultsA total of 4145 TLs were performed in California during 1996 to 2010. The overall number of surgeries declined from 1.3 to 0.6 per 100,000 California residents (P <. 001). The number of surgeries performed in non‐UMCs dropped by 70% during this period (P <. 001). The median length of stay increased from 10 to 12 days, and the median total charges increased from $45,000 to $192,000 over the 15‐year period. The use of rotational/free flaps more than doubled, and the use of PEG tubes increased 7‐fold.ConclusionThe total number of TLs in California has declined and surgeries are currently being performed equally at UMCs and non‐UMCs. The use of rotational/free flaps, costs, hospital stay length, and complications have increased over the past 15 years.
Effects of Freeze–Thaw Cycle with and without Proteolysis Inhibitors and Cryopreservant on the Biochemical and Biomechanical Properties of Articular Cartilage
Authors: Qu Chengjuan , Hirviniemi Mikko , Tiitu Virpi , Jurvelin Jukka S. , Töyräs Juha , Lammi Mikko J. 
Published: December 2013

Objective: We investigated the effects of freeze-thawing on the properties of articular cartilage. Design: The reproducibility of repeated biomechanical assay of the same osteochondral sample was first verified with 11 patellar plugs from 3 animals. Then, 4 osteochondral samples from 15 bovine patellae were divided into 4 groups. The reference samples were immersed in phosphate-buffered saline (PBS) containing proteolysis inhibitors and biomechanically tested before storage for further analyses. Samples of group 1 were biomechanically tested before and after freeze-thawing in PBS in the absence and those of group 2 in the presence of inhibitors. Samples of the group 3 were biomechanically tested in PBS-containing inhibitors, but frozen in 30% dimethyl sulfoxide/PBS and subsequently tested in PBS supplemented with the inhibitors. Glycosaminoglycan contents of the samples and immersion solutions were analyzed, and proteoglycan structures examined with SDS-agarose gel electrophoresis. Results: Freeze-thawing decreased slightly dynamic moduli in all 3 groups. The glycosaminoglycan contents and proteoglycan structures of the cartilage were similar in all experimental groups. Occasionally, the diffused proteoglycans were partly degraded in group 1. Digital densitometry revealed similar staining intensities for the glycosaminoglycans in all groups. Use of cryopreservant had no marked effect on the glycosaminoglycan loss during freeze-thawing. Conclusion: The freeze-thawed cartilage samples appear suitable for the biochemical and biomechanical studies.
Network-based differential gene expression analysis suggests cell cycle related genes regulated by E2F1 underlie the molecular difference between smoker and non-smoker lung adenocarcinoma
Authors: Wu Chao , Zhu Jun , Zhang Xuegong 
Published: December 2013

Abstract

Background
Differential gene expression (DGE) analysis is commonly used to reveal the deregulated molecular mechanisms of complex diseases. However, traditional DGE analysis (e.g., the t test or the rank sum test) tests each gene independently without considering interactions between them. Top-ranked differentially regulated genes prioritized by the analysis may not directly relate to the coherent molecular changes underlying complex diseases. Joint analyses of co-expression and DGE have been applied to reveal the deregulated molecular modules underlying complex diseases. Most of these methods consist of separate steps: first to identify gene-gene relationships under the studied phenotype then to integrate them with gene expression changes for prioritizing signature genes, or vice versa. It is warrant a method that can simultaneously consider gene-gene co-expression strength and corresponding expression level changes so that both types of information can be leveraged optimally.

Results
In this paper, we develop a gene module based method for differential gene expression analysis, named network-based differential gene expression (nDGE) analysis, a one-step integrative process for prioritizing deregulated genes and grouping them into gene modules. We demonstrate that nDGE outperforms existing methods in prioritizing deregulated genes and discovering deregulated gene modules using simulated data sets. When tested on a series of smoker and non-smoker lung adenocarcinoma data sets, we show that top differentially regulated genes identified by the rank sum test in different sets are not consistent while top ranked genes defined by nDGE in different data sets significantly overlap. nDGE results suggest that a differentially regulated gene module, which is enriched for cell cycle related genes and E2F1 targeted genes, plays a role in the molecular differences between smoker and non-smoker lung adenocarcinoma.

Conclusions
In this paper, we develop nDGE to prioritize deregulated genes and group them into gene modules by simultaneously considering gene expression level changes and gene-gene co-regulations. When applied to both simulated and empirical data, nDGE outperforms the traditional DGE method. More specifically, when applied to smoker and non-smoker lung cancer sets, nDGE results illustrate the molecular differences between smoker and non-smoker lung cancer.
The early phase transcriptome of bovine monocyte-derived macrophages infected with Staphylococcus aureus in vitro
Authors: Lewandowska-Sabat Anna Monika , Boman Guro Margrethe , Downing Alison , Talbot Richard , Storset Anne Kristine , Olsaker Ingrid 
Published: December 2013

Abstract

Background
In the mammary gland, local recruitment and action of macrophages is a key immunological defence mechanism against infection. Macrophages are members of the innate immune system, serve as the first line of the defence against invading pathogens and are critical effectors and regulators of inflammation. We have examined the early phase response of bovine macrophages to infection with live Staphylococcus aureus. Genome-wide transcript profiling of blood monocyte-derived macrophages from six Norwegian Red heifers infected with live S. aureus for 2 and 6 hours in vitro was performed.

Results
About 420 of the 17 000 genes on the ARK-Genomics bovine cDNA array were differentially regulated at 6 hours post infection. Approximately 70% of the responding genes had a known identity (Entrez Gene ID) and were used in the identification of overrepresented pathways and biological functions in the dataset.
Analysis of a subset of differentially regulated genes (List eQG) obtained by comparison with data from genome-wide association mapping in Norwegian Red cattle identified anti-inflammatory cytokines interleukin 4 and interleukin 13 as putative expression quantitative trait loci, suggesting that S. aureus infection triggers alternative activation of macrophages. Moreover, several classical activation pathways were found, mainly cellular immune response and cytokine signaling pathways, i.e. triggering receptor expressed on myeloid cells 1 (TREM1) and nucleotide-binding and oligomerization domain-like receptor (NLR) pathways. Tumor necrosis factor receptor superfamily member 5 (CD40 ligand) was identified as an upstream regulator which points toward CD40 likely acting as a co-stimulatory receptor during Toll-like receptor 2(TLR2)-mediated inflammatory response of bovine macrophages to S. aureus infection. Furthermore, peptidoglycan was identified as an upstream regulator in the List eQG, which indicates that this bacterial cell-wall component might be pivotal in macrophage intracellular bacterial recognition during early inflammation.

Conclusions
Here we have shown that in vitro infection of bovine macrophages with live S. aureus induced both alternative and classical activation pathways. Alternative activation of macrophages may be a mechanism contributing to intracellular persistence of S. aureus in the course of inflammation such as during mastitis in dairy cattle.
OnPLS integration of transcriptomic, proteomic and metabolomic data shows multi-level oxidative stress responses in the cambium of transgenic hipI- superoxide dismutase Populus plants
Authors: Srivastava Vaibhav , Obudulu Ogonna , Bygdell Joakim , Löfstedt Tommy , Rydén Patrik , Nilsson Robert , Ahnlund Maria , Johansson Annika , Jonsson Pär , Freyhult Eva , Qvarnström Johanna , Karlsson Jan , Melzer Michael , Moritz Thomas , Trygg Johan , Hvidsten Torgeir R , Wingsle Gunnar 
Published: December 2013

AbstractBackgroundReactive oxygen species (ROS) are involved in the regulation of diverse physiological processes in plants, including various biotic and abiotic stress responses. Thus, oxidative stress tolerance mechanisms in plants are complex, and diverse responses at multiple levels need to be characterized in order to understand them. Here we present system responses to oxidative stress inPopulusby integrating data from analyses of the cambial region of wild-type controls and plants expressing high-isoelectric-point superoxide dismutase (hipI-SOD) transcripts in antisense orientation showing a higher production of superoxide. The cambium, a thin cell layer, generates cells that differentiate to form either phloem or xylem and is hypothesized to be a major reason for phenotypic perturbations in the transgenic plants. Data from multiple platforms including transcriptomics (microarray analysis), proteomics (UPLC/QTOF-MS), and metabolomics (GC-TOF/MS, UPLC/MS, and UHPLC-LTQ/MS) were integrated using the most recent development of orthogonal projections to latent structures called OnPLS. OnPLS is a symmetrical multi-block method that does not depend on the order of analysis when more than two blocks are analysed. Significantly affected genes, proteins and metabolites were then visualized in painted pathway diagrams.ResultsThe main categories that appear to be significantly influenced in the transgenic plants were pathways related to redox regulation, carbon metabolism and protein degradation, e.g. the glycolysis and pentose phosphate pathways (PPP). The results provide system-level information on ROS metabolism and responses to oxidative stress, and indicate that some initial responses to oxidative stress may share common pathways.ConclusionThe proposed data evaluation strategy shows an efficient way of compiling complex, multi-platform datasets to obtain significant biological information.
Phylogenetic relationship and virulence inference of Streptococcus Anginosus Group: curated annotation and whole-genome comparative analysis support distinct species designation
Authors: Olson Adam B , Kent Heather , Sibley Christopher D , Grinwis Margot E , Mabon Philip , Ouellette Claude , Tyson Shari , Graham Morag , Tyler Shaun D , Van Domselaar Gary , Surette Michael G , Corbett Cindi R 
Published: December 2013

AbstractBackgroundThe Streptococcus Anginosus Group (SAG) represents three closely related species of the viridans group streptococci recognized as commensal bacteria of the oral, gastrointestinal and urogenital tracts. The SAG also cause severe invasive infections, and are pathogens during cystic fibrosis (CF) pulmonary exacerbation. Little genomic information or description of virulence mechanisms is currently available for SAG. We conducted intra and inter species whole-genome comparative analyses with 59 publically availableStreptococcusgenomes and seven in-house closed high quality finished SAG genomes;S. constellatus(3),S. intermedius(2), andS. anginosus(2). For each SAG species, we sequenced at least one numerically dominant strain from CF airways recovered during acute exacerbation and an invasive, non-lung isolate. We also evaluated microevolution that occurred within two isolates that were cultured from one individual one year apart.ResultsThe SAG genomes were most closely related toS. gordoniiandS. sanguinis, based on shared orthologs and harbor a similar number of proteins within each COG category as otherStreptococcusspecies. Numerous characterized streptococcus virulence factor homologs were identified within the SAG genomes including; adherence, invasion, spreading factors, LPxTG cell wall proteins, and two component histidine kinases known to be involved in virulence gene regulation. Mobile elements, primarily integrative conjugative elements and bacteriophage, account for greater than 10% of the SAG genomes.S. anginosuswas the most variable species sequenced in this study, yielding both the smallest and the largest SAG genomes containing multiple genomic rearrangements, insertions and deletions. In contrast, within theS. constellatusandS. intermediusspecies, there was extensive continuous synteny, with only slight differences in genome size between strains. WithinS. constellatuswe were able to determine important SNPs and changes in VNTR numbers that occurred over the course of one year.ConclusionsThe comparative genomic analysis of the SAG clarifies the phylogenetics of these bacteria and supports the distinct species classification. Numerous potential virulence determinants were identified and provide a foundation for further studies into SAG pathogenesis. Furthermore, the data may be used to enable the development of rapid diagnostic assays and therapeutics for these pathogens.
Assessment of hematopoietic failure due to Rpl11 deficiency in a zebrafish model of Diamond-Blackfan anemia by deep sequencing
Authors: Zhang Zhaojun , Jia Haibo , Zhang Qian , Wan Yang , Zhou Yang , Jia Qiong , Zhang Wanguang , Yuan Weiping , Cheng Tao , Zhu Xiaofan , Fang Xiangdong 
Published: December 2013

Abstract

Background
Diamond–Blackfan anemia is a rare congenital red blood cell dysplasia that develops soon after birth. RPL11 mutations account for approximately 4.8% of human DBA cases with defective hematopoietic phenotypes. However, the mechanisms by which RPL11 regulates hematopoiesis in DBA remain elusive. In this study, we analyzed the transcriptome using deep sequencing data from an Rpl11-deficient zebrafish model to identify Rpl11-mediated hematopoietic failure and investigate the underlying mechanisms.

Results
We characterized hematological defects in Rpl11-deficient zebrafish embryos by identifying affected hematological genes, hematopoiesis-associated pathways, and regulatory networks. We found that hemoglobin biosynthetic and hematological defects in Rpl11-deficient zebrafish were related to dysregulation of iron metabolism-related genes, including tfa, tfr1b, alas2 and slc25a37, which are involved in heme and hemoglobin biosynthesis. In addition, we found reduced expression of the hematopoietic stem cells (HSC) marker cmyb and HSC transcription factors tal1 and hoxb4a in Rpl11-deficient zebrafish embryos, indicating that the hematopoietic defects may be related to impaired HSC formation, differentiation, and proliferation. However, Rpl11 deficiency did not affect the development of other blood cell lineages such as granulocytes and myelocytes.

Conclusion
We identified hematopoietic failure of Rpl11-deficient zebrafish embryos using transcriptome deep sequencing and elucidated potential underlying mechanisms. The present analyses demonstrate that Rpl11-deficient zebrafish may serve as a model of DBA and may provide insights into the pathogenesis of mutant RPL11-mediated human DBA disease.
Epigenetic regulation of MDR1 gene through post-translational histone modifications in prostate cancer
Authors: Henrique Rui , Oliveira Ana Isabel , Costa Vera L , Baptista Tiago , Martins Ana Teresa , Morais António , Oliveira Jorge , Jerónimo Carmen 
Published: December 2013

Abstract

Background
Multidrug resistance 1 (MDR1) gene encodes for an ATP binding cassette transporter - P-glycoprotein (P-gp) - involved in chemoresistance to taxanes. MDR1 promoter methylation is frequent in prostate carcinoma (PCa), suggesting an epigenetic regulation but no functional correlation has been established. We aimed to elucidate the epigenetic mechanisms involved in MDR1 deregulation in PCa.

Results

MDR1 promoter methylation and P-gp expression were assessed in 121 PCa, 39 high-grade prostatic intraepithelial neoplasia (HGPIN), 28 benign prostatic hyperplasia (BPH) and 10 morphologically normal prostate tissue (NPT) samples, using quantitative methylation specific PCR and immunohistochemistry, respectively. PCa cell lines were exposed to a DNA methyltransferases inhibitor 5-aza-2′deoxycytidine (DAC) and histone deacetylases inhibitor trichostatin A (TSA). Methylation and histone posttranscriptional modifications status were characterized and correlated with mRNA and protein expression. MDR1 promoter methylation levels and frequency significantly increased from NPTs, to HGPIN and to PCa. Conversely, decreased or absent P-gp immunoexpression was observed in HGPIN and PCa, inversely correlating with methylation levels. Exposure to DAC alone did not alter significantly methylation levels, although increased expression was apparent. However, P-gp mRNA and protein re-expression were higher in cell lines exposed to TSA alone or combined with DAC. Accordingly, histone active marks H3Ac, H3K4me2, H3K4me3, H3K9Ac, and H4Ac were increased at the MDR1 promoter after exposure to TSA alone or combined with DAC.

Conclusion
Our data suggests that, in prostate carcinogenesis, MDR1 downregulation is mainly due to histone post-translational modifications. This occurs concomitantly with aberrant promoter methylation, substantiating the association with P-gp decreased expression.
Differential regulation of the rainbow trout (Oncorhynchus mykiss) MT-A gene by nuclear factor interleukin-6 and activator protein-1
Authors: Kling Peter , Modig Carina , Mujahed Huthayfa , Khalaf Hazem , von Hofsten Jonas , Olsson Per-Erik 
Published: December 2013

Abstract

Background
Previously we have identified a distal region of the rainbow trout (Oncorhynchus mykiss) metallothionein-A (rtMT-A) enhancer region, being essential for free radical activation of the rtMT-A gene. The distal promoter region included four activator protein 1 (AP1) cis-acting elements and a single nuclear factor interleukin-6 (NF-IL6) element. In the present study we used the rainbow trout hepatoma (RTH-149) cell line to further examine the involvement of NF-IL6 and AP1 in rtMT-A gene expression following exposure to oxidative stress and tumour promotion.

Results
Using enhancer deletion studies we observed strong paraquat (PQ)-induced rtMT-A activation via NF-IL6 while the AP1 cis-elements showed a weak but significant activation. In contrast to mammals the metal responsive elements were not activated by oxidative stress. Electrophoretic mobility shift assay (EMSA) mutation analysis revealed that the two most proximal AP1 elements, AP11,2, exhibited strong binding to the AP1 consensus sequence, while the more distal AP1 elements, AP13,4 were ineffective. Phorbol-12-myristate-13-acetate (PMA), a known tumor promoter, resulted in a robust induction of rtMT-A via the AP1 elements alone. To determine the conservation of regulatory functions we transfected human Hep G2 cells with the rtMT-A enhancer constructs and were able to demonstrate that the cis-elements were functionally conserved. The importance of NF-IL6 in regulation of teleost MT is supported by the conservation of these elements in MT genes from different teleosts. In addition, PMA and PQ injection of rainbow trout resulted in increased hepatic rtMT-A mRNA levels.

Conclusions
These studies suggest that AP1 primarily is involved in PMA regulation of the rtMT-A gene while NF-IL6 is involved in free radical regulation. Taken together this study demonstrates the functionality of the NF-IL6 and AP-1 elements and suggests an involvement of MT in protection during pathological processes such as inflammation and cancer.