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Search Results: 1 - 10 of 169527 matches for " Jill E Larsen "
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Expression profiling identifies genes involved in emphysema severity
Santiyagu Francis, Jill E Larsen, Sandra J Pavey, Rayleen V Bowman, Nicholas K Hayward, Kwun M Fong, Ian A Yang
Respiratory Research , 2009, DOI: 10.1186/1465-9921-10-81
Abstract: Gene expression profiling was performed on total RNA extracted from non-tumor lung tissue from 30 smokers with emphysema. Class comparison analysis based on gas transfer measurement was performed to identify differentially expressed genes. Genes were then selected for technical validation by quantitative reverse transcriptase-PCR (qRT-PCR) if also represented on microarray platforms used in previously published emphysema studies. Genes technically validated advanced to tests of biological replication by qRT-PCR using an independent test set of 62 lung samples.Class comparison identified 98 differentially expressed genes (p < 0.01). Fifty-one of those genes had been previously evaluated in differentiation between normal and severe emphysema lung. qRT-PCR confirmed the direction of change in expression in 29 of the 51 genes and 11 of those validated, remaining significant at p < 0.05. Biological replication in an independent cohort confirmed the altered expression of eight genes, with seven genes differentially expressed by greater than 1.3 fold, identifying these as candidate determinants of emphysema severity.Gene expression profiling of lung from emphysema patients identified seven candidate genes associated with emphysema severity including COL6A3, SERPINF1, ZNHIT6, NEDD4, CDKN2A, NRN1 and GSTM3.Chronic obstructive pulmonary disease (COPD) is a major health burden worldwide [1]. Smoking is the primary cause of COPD, with up to 50% of smokers developing the disease [2]. It is frequently under-diagnosed and under-treated [3] since its early stages are often asymptomatic. COPD patients are classified into mild, moderate and severe based on the degree of airflow limitation, which is a result of damage in the large airways (bronchitis), small airways (bronchiolitis) and or alveoli (emphysema). Emphysema affects 40% of heavy smokers [4] and causes loss of elastic recoil, leading to abnormal gas exchange and breathlessness. Despite smoking cessation, some individuals con
Genes and Gene Ontologies Common to Airflow Obstruction and Emphysema in the Lungs of Patients with COPD
Santiyagu M. Savarimuthu Francis,Jill E. Larsen,Sandra J. Pavey,Edwina E. Duhig,Belinda E. Clarke,Rayleen V. Bowman,Nick K. Hayward,Kwun M. Fong,Ian A. Yang
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0017442
Abstract: Chronic obstructive pulmonary disease (COPD) is a major public health problem with increasing prevalence worldwide. The primary aim of this study was to identify genes and gene ontologies associated with COPD severity. Gene expression profiling was performed on total RNA extracted from lung tissue of 18 former smokers with COPD. Class comparison analysis on mild (n = 9, FEV1 80–110% predicted) and moderate (n = 9, FEV1 50–60% predicted) COPD patients identified 46 differentially expressed genes (p<0.01), of which 14 genes were technically confirmed by quantitative real-time-PCR. Biological replication in an independent test set of 58 lung samples confirmed the altered expression of ten genes with increasing COPD severity, with eight of these genes (NNMT, THBS1, HLA-DPB1, IGHD, ETS2, ELF1, PTGDS and CYRBD1) being differentially expressed by greater than 1.8 fold between mild and moderate COPD, identifying these as candidate determinants of COPD severity. These genes belonged to ontologies potentially implicated in COPD including angiogenesis, cell migration, proliferation and apoptosis. Our secondary aim was to identify gene ontologies common to airway obstruction, indicated by impaired FEV1 and KCO. Using gene ontology enrichment analysis we have identified relevant biological and molecular processes including regulation of cell-matrix adhesion, leukocyte activation, cell and substrate adhesion, cell adhesion, angiogenesis, cell activation that are enriched among genes involved in airflow obstruction. Exploring the functional significance of these genes and their gene ontologies will provide clues to molecular changes involved in severity of COPD, which could be developed as targets for therapy or biomarkers for early diagnosis.
MicroRNA-218 Is Deleted and Downregulated in Lung Squamous Cell Carcinoma
Morgan R. Davidson,Jill E. Larsen,Ian A. Yang,Nicholas K. Hayward,Belinda E. Clarke,Edwina E. Duhig,Linda H. Passmore,Rayleen V. Bowman,Kwun M. Fong
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0012560
Abstract: MicroRNAs (miRNAs) are a family of small, non-coding RNA species functioning as negative regulators of multiple target genes including tumour suppressor genes and oncogenes. Many miRNA gene loci are located within cancer-associated genomic regions. To identify potential new amplified oncogenic and/or deleted tumour suppressing miRNAs in lung cancer, we inferred miRNA gene dosage from high dimensional arrayCGH data. From miRBase v9.0 (http://microrna.sanger.ac.uk), 474 human miRNA genes were physically mapped to regions of chromosomal loss or gain identified from a high-resolution genome-wide arrayCGH study of 132 primary non-small cell lung cancers (NSCLCs) (a training set of 60 squamous cell carcinomas and 72 adenocarcinomas). MiRNAs were selected as candidates if their immediately flanking probes or host gene were deleted or amplified in at least 25% of primary tumours using both Analysis of Copy Errors algorithm and fold change (≥±1.2) analyses. Using these criteria, 97 miRNAs mapped to regions of aberrant copy number. Analysis of three independent published lung cancer arrayCGH datasets confirmed that 22 of these miRNA loci showed directionally concordant copy number variation. MiR-218, encoded on 4p15.31 and 5q35.1 within two host genes (SLIT2 and SLIT3), in a region of copy number loss, was selected as a priority candidate for follow-up as it is reported as underexpressed in lung cancer. We confirmed decreased expression of mature miR-218 and its host genes by qRT-PCR in 39 NSCLCs relative to normal lung tissue. This downregulation of miR-218 was found to be associated with a history of cigarette smoking, but not human papilloma virus. Thus, we show for the first time that putative lung cancer-associated miRNAs can be identified from genome-wide arrayCGH datasets using a bioinformatics mapping approach, and report that miR-218 is a strong candidate tumour suppressing miRNA potentially involved in lung cancer.
When Children Draw vs When Children Don’t: Exploring the Effects of Observational Drawing in Science  [PDF]
Jill E. Fox, Joohi Lee
Creative Education (CE) , 2013, DOI: 10.4236/ce.2013.47A1002
Abstract:

The purpose of this study was to investigate how kindergarten children’s observational drawings impact their information retention. This research was conducted in an urban school in a large metropolitan area in the southwestern United States. Forty-two kindergarten children participated in this study; approximately 97% of them qualified for free and/or reduced lunch. For this study, children’s retention of factual information was compared using a paired t-test of when they drew and when they didn’t. Children scored higher on all 7 items—descriptions of observation, location, action, color, size, shape, and sound—when they drew than when they didn’t. Findings were statistically significant for descriptions of observation (t = 3.08, p = .00) and location (t = 2.36, p = .02).

Occupational Noise Levels in Two Fish Rearing Buildings at an Aquaculture Facility  [PDF]
Jill Voorhees, Michael E. Barnes
Occupational Diseases and Environmental Medicine (ODEM) , 2017, DOI: 10.4236/odem.2017.52006
Abstract: Occupational noise is commonly encountered during aquaculture. This study documented noise levels in two buildings at a production fish hatchery, a tank room with 32, 1.8-m diameter tanks, and a rearing pavilion with 32, 6.1-m diameter tanks. With water flowing to all of the tanks in the tank room, mean noise levels were 68.4 dB, and significantly increased to 73.0 dB during tank cleaning and 73.2 dB when intermittent automatic feeders were running. The highest tank room values of 77.1 dB were recorded directly next to individual tanks during cleaning. With water flowing to all of the tanks in the rearing pavilion, mean noise levels were 70.2 dB. A significant increase to 76.1 dB was observed when the pavilion tanks were being power washed, with the highest value of 83.2 dB recorded immediately adjacent to the power washer. Although none of the noise levels exceeded regulatory limits, the use of techniques to reduce occupational noise in aquaculture environments is recommended.
Array-Comparative Genomic Hybridization Reveals Loss of SOCS6 Is Associated with Poor Prognosis in Primary Lung Squamous Cell Carcinoma
Krishna B. Sriram, Jill E. Larsen, Santiyagu M. Savarimuthu Francis, Casey M. Wright, Belinda E. Clarke, Edwina E. Duhig, Kevin M. Brown, Nicholas K. Hayward, Ian A. Yang, Rayleen V. Bowman, Kwun M. Fong
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0030398
Abstract: Background Primary tumor recurrence commonly occurs after surgical resection of lung squamous cell carcinoma (SCC). Little is known about the genes driving SCC recurrence. Methods We used array comparative genomic hybridization (aCGH) to identify genes affected by copy number alterations that may be involved in SCC recurrence. Training and test sets of resected primary lung SCC were assembled. aCGH was used to determine genomic copy number in a training set of 62 primary lung SCCs (28 with recurrence and 34 with no evidence of recurrence) and the altered copy number of candidate genes was confirmed by quantitative PCR (qPCR). An independent test set of 72 primary lung SCCs (20 with recurrence and 52 with no evidence of recurrence) was used for biological validation. mRNA expression of candidate genes was studied using qRT-PCR. Candidate gene promoter methylation was evaluated using methylation microarrays and Sequenom EpiTYPER analysis. Results 18q22.3 loss was identified by aCGH as being significantly associated with recurrence (p = 0.038). Seven genes within 18q22.3 had aCGH copy number loss associated with recurrence but only SOCS6 copy number was both technically replicated by qPCR and biologically validated in the test set. SOCS6 copy number loss correlated with reduced mRNA expression in the study samples and in the samples with copy number loss, there was a trend for increased methylation, albeit non-significant. Overall survival was significantly poorer in patients with SOCS6 loss compared to patients without SOCS6 loss in both the training (30 vs. 43 months, p = 0.023) and test set (27 vs. 43 months, p = 0.010). Conclusion Reduced copy number and mRNA expression of SOCS6 are associated with disease recurrence in primary lung SCC and may be useful prognostic biomarkers.
Some Methods to Maximize Extraction of Scientific Knowledge from Parallel Group Randomized Trials  [PDF]
Anders M. Gall?e, Carsten T. Larsen
World Journal of Cardiovascular Diseases (WJCD) , 2015, DOI: 10.4236/wjcd.2015.51003
Abstract: The amount of scientific knowledge from randomized parallel group trials have been improved by the CONSORT Guideline, but important intelligence with important clinical implications remains to be extracted. This may though be obtained if the conventional statistical significance testing is supplied by 1) Addition of an unbiased and reproducible quantification of the magnitude or size of the clinical significance/importance of a difference in treatment outcome; 2) Addition of a quantification of the credulity of statements on any possible effect size and finally; 3) Addition of a quantification of the risk of committing an error when the null hypothesis is either accepted or rejected. These matters are crucial to proper conversion of trial results into good usage in every-day clinical practice and may produce immediate therapeutic consequence in quite opposite direction to the usual ones. In our drug eluting stent trial “SORT OUT II”, the implementation of our suggestions would have led to immediate cessation of use of the paclitaxel-eluting stent, which the usual Consort like reporting did not lead to. Consequently harm to subsequent patients treated by this stent might have been avoided. Our suggestions are also useful in cancer treatment trials and in fact generally so in most randomized trial. Therefore increased scientific knowledge with immediate and potentially altered clinical consequence may be the result if hypothesis testing is made complete and the corresponding adjustments are added to the CONSORT Guideline—first of all— for the potential benefit of future patients.
Antigen-Specific T Cells: Analyses of the Needles in the Haystack
Jill E. Slansky
PLOS Biology , 2012, DOI: 10.1371/journal.pbio.0000078
Abstract:
Antigen-Specific T Cells: Analyses of the Needles in the Haystack
Jill E Slansky
PLOS Biology , 2003, DOI: 10.1371/journal.pbio.0000078
Abstract:
Pneumothorax as a predatory goal for the sabertooth cat (Smilodon fatalis)  [PDF]
Ted Wilson, Dirk E. Wilson, Jill M. Zimanske
Open Journal of Animal Sciences (OJAS) , 2013, DOI: 10.4236/ojas.2013.31006
Abstract:

Smilodon fatalis was a large extinct felid distinguished by their two impressive maxillary canines and surprisingly low canine fracture rates. Previous theories regarding their attack strategy have suggested delivering damage by a bite with their maxillary canines. It has also been previously suggested that the canines could have been used to deliver a non-biting stab with an open jaw. It has been generally hypothesized that the attack was delivered to the neck of their large herbivore prey. Smilodon fatalis could have used their canines in a non-biting stab delivered with a closed jaw for the sole purpose of creating a pneumothorax. Creation of a pneumothorax would maximize immediate attack lethality, and minimize exposure of its canines to fracture.

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