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Search Results: 1 - 10 of 219518 matches for " Derry C. Roopenian "
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B Cell IgD Deletion Prevents Alveolar Bone Loss Following Murine Oral Infection
Pamela J. Baker,Nicole Ryan Boutaugh,Michaela Tiffany,Derry C. Roopenian
Interdisciplinary Perspectives on Infectious Diseases , 2009, DOI: 10.1155/2009/864359
Abstract: Periodontal disease is one of the most common infectious diseases of humans. Immune responses to infection trigger loss of alveolar bone from the jaw and eventual tooth loss. We investigated the contribution of B cell IgD to alveolar bone loss by comparing the response of B cell normal BALB/cJ mice and IgD deficient BALB/c-Igh-5?/?J mice to oral infection with Porphyromonas gingivalis, a gram-negative periodontopathic bacterium from humans. P. gingivalis-infected normal mice lost bone. Specific antibody to P. gingivalis was lower and oral colonization was higher in IgD deficient mice; yet bone loss was completely absent. Infection increased the proportion of CD69
A Mouse Model of Heritable Cerebrovascular Disease
Thomas J. Sproule,John G. Sled,Jill Wentzell,Bing Wang,R. Mark Henkelman,Derry C. Roopenian,Robert W. Burgess
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0015327
Abstract: The study of animal models of heritable cerebrovascular diseases can improve our understanding of disease mechanisms, identify candidate genes for related human disorders, and provide experimental models for preclinical trials. Here we describe a spontaneous mouse mutation that results in reproducible, adult-onset, progressive, focal ischemia in the brain. The pathology is not the result of hemorrhage, embolism, or an anatomical abnormality in the cerebral vasculature. The mutation maps as a single site recessive locus to mouse Chromosome 9 at 105 Mb, a region of shared synteny with human chromosome 3q22. The genetic interval, defined by recombination mapping, contains seven protein-coding genes and one processed transcript, none of which are changed in their expression level, splicing, or sequence in affected mice. Targeted resequencing of the entire interval did not reveal any provocative changes; thus, the causative molecular lesion has not been identified.
Searching QTL by gene expression: analysis of diabesity
Aaron C Brown, William I Olver, Charles J Donnelly, Marjorie E May, Jürgen K Naggert, Daniel J Shaffer, Derry C Roopenian
BMC Genetics , 2005, DOI: 10.1186/1471-2156-6-12
Abstract: We used our novel data mining tool, ExQuest, to select genes within known diabesity QTL showing enriched expression in primary diabesity affected tissues. We then quantified transcripts in adipose, pancreas, and liver tissue from Tally Ho mice, a multigenic model for Type II diabetes (T2D), and from diabesity-resistant C57BL/6J controls. Analysis of the resulting quantitative PCR data using the Global Pattern Recognition analytical algorithm identified a number of genes whose expression is altered, and thus are novel candidates for diabesity QTL and/or pathways associated with diabesity.Transcription-based data mining of genes in QTL-limited intervals followed by efficient quantitative PCR methods is an effective strategy for identifying genes that may contribute to complex pathophysiological processes.Understanding the molecular etiology of disease processes is a pressing goal of 21st century medicine. Completion of the mouse genome holds considerable promise in the discovery of genes responsible for genetically determined complex diseases. Quantitative trait loci (QTL) are allelically variant regions detected by virtue of their contribution to the overall complex disease phenotype and thus are "experiments in nature", which mark chromosomal intervals carrying genes with a proven disease involvement. Since gene expression is a key link between the genome and the plethora of phenotypic traits exhibited, tools that permit the analysis of the tissue expression pattern of genes in their chromosomal context provides a bridge between QTL and the genes responsible.Global microarray gene expression technologies offer a promising, unbiased approach toward this goal in that they reveal gene expression changes, which can be correlated with the disease phenotype. However, such global methods of analysis are not routine analytical tools and can suffer from incomplete gene coverage, as well as lack of sensitivity. Because only a small fraction of the transcriptome is typically i
Molecular Identification of Collagen 17a1 as a Major Genetic Modifier of Laminin Gamma 2 Mutation-Induced Junctional Epidermolysis Bullosa in Mice
Thomas J. Sproule,Jason A. Bubier,Fiorella C. Grandi,Victor Z. Sun,Vivek M. Philip,Caroline G. McPhee,Elisabeth B. Adkins,John P. Sundberg,Derry C. Roopenian
PLOS Genetics , 2014, DOI: doi/10.1371/journal.pgen.1004068
Abstract: Epidermolysis Bullosa (EB) encompasses a spectrum of mechanobullous disorders caused by rare mutations that result in structural weakening of the skin and mucous membranes. While gene mutated and types of mutations present are broadly predictive of the range of disease to be expected, a remarkable amount of phenotypic variability remains unaccounted for in all but the most deleterious cases. This unexplained variance raises the possibility of genetic modifier effects. We tested this hypothesis using a mouse model that recapitulates a non-Herlitz form of junctional EB (JEB) owing to the hypomorphic jeb allele of laminin gamma 2 (Lamc2). By varying normally asymptomatic background genetics, we document the potent impact of genetic modifiers on the strength of dermal-epidermal adhesion and on the clinical severity of JEB in the context of the Lamc2jeb mutation. Through an unbiased genetic approach involving a combination of QTL mapping and positional cloning, we demonstrate that Col17a1 is a strong genetic modifier of the non-Herlitz JEB that develops in Lamc2jeb mice. This modifier is defined by variations in 1–3 neighboring amino acids in the non-collagenous 4 domain of the collagen XVII protein. These allelic variants alter the strength of dermal-epidermal adhesion in the context of the Lamc2jeb mutation and, consequentially, broadly impact the clinical severity of JEB. Overall the results provide an explanation for how normally innocuous allelic variants can act epistatically with a disease causing mutation to impact the severity of a rare, heritable mechanobullous disorder.
Age Dependence of the Menstrual Cycle Correlation Dimension  [PDF]
Gregory N. Derry, Paula S. Derry
Open Journal of Biophysics (OJBIPHY) , 2012, DOI: 10.4236/ojbiphy.2012.22006
Abstract: Time series analysis, based on the idea that female reproductive endocrine physiology can be construed as a nonlinear dynamical system in a chaotic trajectory, is performed to measure the correlation dimension of the menstrual cycle data from subjects in two different age cohorts. The dimension is computed using a method proposed by Judd (Physica D, vol. 56, 1992, pp. 216-228) that does not assume the correlation dimension to be necessarily constant for all appropriate time scales of the system’s strange attractor. Significant time scale differences are found in the behavior of the dimension between the two age cohorts, but at the shortest time scales the correlation dimension converges to the same value, approximately 5.5, in both cases.
Characterization of chaotic dynamics in the human menstrual cycle
Derry GN,Derry PS
Nonlinear Biomedical Physics , 2010, DOI: 10.1186/1753-4631-4-5
Abstract: Background The human menstrual cycle is known to exhibit a significant amount of unexplained variability. This variation is typically dismissed as random fluctuations in an otherwise periodic and predictable system. Given the many delayed nonlinear feedbacks in the multiple levels of the reproductive endocrine system, however, the menstrual cycle can properly be construed as the output of a nonlinear dynamical system, and such a system has the possibility of being in a chaotic trajectory. We hypothesize that this is in fact the case and that it accounts for the observed variability. Results Here, we test this hypothesis by performing time series analyses on data for 7749 menstrual cycles from 40 women in the 20-40 year age range, using the database maintained by the Tremin Research Program on Women's Health. Both raw menstrual cycle length data and a formal time series constructed from this data are utilized in these analyses. Employing phase space reconstruction techniques with a maximum embedding dimension of 12, we find appropriate scaling behavior in the correlation sums for these data, indicating low dimensional deterministic dynamics. A correlation dimension of Dc ≈ 5.2 is measured in the scaling regime. This result is confirmed by recalculation using the Takens estimator and by surrogate data tests. We interpret this result as an approximation to the fractal dimension of a strange attractor governing chaotic dynamics in the menstrual cycle. We also use the time series to calculate the correlation entropy (K2 ≈ 0.008/τ) and the maximal Lyapunov exponent (λ ≈ 0.005/τ) for the system, where τ is the sampling time of the series. Conclusions Taken collectively, these results constitute significant evidence that the menstrual cycle is the result of chaos in a nonlinear dynamical system. This view of the menstrual cycle has potential implications for clinical practice, modelling of the endocrine system, and the interpretation of the perimenopausal transition.
Reporting of adverse drug reactions in randomised controlled trials – a systematic survey
Yoon Loke, Sheena Derry
BMC Pharmacology and Toxicology , 2001, DOI: 10.1186/1472-6904-1-3
Abstract: Literature review to determine whether the definition, recording and reporting of adverse drug reactions in clinical trials were in accordance with published recommendations on structured reporting.Of the 185 trials reviewed, 25 (14%) made no mention of adverse drug reactions. Data in a further 60 (32%) could not be fully evaluated, either because numbers were not given for each treatment arm (31 trials), or because a generic statement was made without full details (29 trials). When adverse drug reactions such as clinical events or patient symptoms were mentioned in the reports, details on how they had been recorded were given in only 14/95 (15%) and 18/104 (17%) trials respectively. Of the 86 trials that mentioned severity of adverse drug reactions, only 42 (49%) stated how severity had been defined. The median amount of space used for safety data in the Results and Discussion sections was 5.8%.Trial reports often failed to provide details on how adverse drug reactions were defined or recorded. The absence of such methodological information makes comparative evaluation of adverse reaction rates potentially unreliable. Authors and journals should adopt recommendations on the structured reporting of adverse effects.Although drug safety information is of vital importance, evidence is now emerging that adverse drug reactions (ADRs) are often inadequately reported in randomised, controlled trials [1,2]. Lack of consistency in ADR reporting has important implications – it makes systematic reviews of ADR data extremely difficult and also hinders comparisons of ADR rates between trials. For example, the authors of a recent systematic review of beta-blockers in myocardial infarction were able to draw conclusions on the efficacy of treatment, but not safety, because "different definitions and reporting made comparisons between trials problematic" [3].Two aspects of reporting are particularly important when comparing rates of ADRs in different trials [4]. Firstly, adverse eve
Atypical antipsychotics in bipolar disorder: systematic review of randomised trials
Sheena Derry, R Andrew Moore
BMC Psychiatry , 2007, DOI: 10.1186/1471-244x-7-40
Abstract: We examined efficacy in randomised trials of bipolar disorder where the presenting episode was either depression, or manic/mixed, comparing atypical antipsychotic with placebo or active comparator, examined withdrawals for any cause, or due to lack of efficacy or adverse events, and combined all phases for adverse event analysis. Studies were found through systematic search (PubMed, EMBASE, Cochrane Library), and data combined for analysis where there was clinical homogeneity, with especial reference to trial duration.In five trials (2,206 patients) participants presented with a depressive episode, and in 25 trials (6,174 patients) the presenting episode was manic or mixed.In 8-week studies presenting with depression, quetiapine and olanzapine produced significantly better rates of response and symptomatic remission than placebo, with NNTs of 5–6, but more adverse event withdrawals (NNH 12). With mania or mixed presentation atypical antipsychotics produced significantly better rates of response and symptomatic remission than placebo, with NNTs of about 5 up to six weeks, and 4 at 6–12 weeks, but more adverse event withdrawals (NNH of about 22) in studies of 6–12 weeks. In comparisons with established treatments, atypical antipsychotics had similar efficacy, but significantly fewer adverse event withdrawals (NNT to prevent one withdrawal about 10). In maintenance trials atypical antipsychotics had significantly fewer relapses to depression or mania than placebo or active comparator.In placebo-controlled trials, atypical antipsychotics were associated with higher rates of weight gain of ≥7% (mainly olanzapine trials), somnolence, and extrapyramidal symptoms. In active controlled trials, atypical antipsychotics were associated with lower rates of extrapyramidal symptoms, but higher rates of weight gain and somnolence.Atypical antipsychotics are effective in treating both phases of bipolar disorder compared with placebo, and as effective as established drug therapies. A
Systematic review and meta-analysis of randomised trials and cohort studies of mycophenolate mofetil in lupus nephritis
R Andrew Moore, Sheena Derry
Arthritis Research & Therapy , 2006, DOI: 10.1186/ar2093
Abstract: The prevalence of systemic lupus erythematosus (SLE) varies with age, gender, and ethnicity, and the highest rates occur in young adult women, particularly of Afro-Caribbean origin, who are in peak childbearing years [1-4]. Nephritis complicates SLE in a significant minority of patients and is associated with renal failure and increased mortality. The tendency for people of Afro-Caribbean origin to have a worse prognosis may be due, at least in part, to poor socio-economic status [5]. In the 1950s, patients with class IV nephritis rarely lived longer than 5 years, whereas now more than 80% survive with good renal function for more than 10 years [6].The World Health Organization (WHO) classification for lupus nephritis is based on the histological appearance, with progressive changes to the glomerulus and tubulo-interstitium with increasing severity (Additional file 1). Milder disease (WHO classes II and IIIa) affects approximately 35% to 50%, whereas more serious classes IIIb, IV, and V affect 45% to 60% [7]. A significant minority of patients with class III disease (focal segmental proliferative glomerulonephritis) show worsening renal function and may progress to class IV lupus nephritis. Class IV (diffuse proliferative glomerulonephritis) usually presents with clinical evidence of renal disease, including oedema, hypertension, sediment, and worsening renal function with proteinuria. Class V (diffuse membranous glomerulonephritis) involves patients with laboratory and clinical features of nephrotic syndrome.The aim of treatment is first to stop disease progression (induction phase) and then prevent recurrence (maintenance) while minimising the adverse effects. More specifically with lupus nephritis, the aims of treatment are to reduce the risk of end-stage renal disease, reduce renal and extra-renal lupus activity or symptoms, and reduce the mortality risk.Treatment with immunosuppressive therapy is better than prednisolone monotherapy at preserving renal function
Does anybody read "evidence-based" articles?
Yoon K Loke, Sheena Derry
BMC Medical Research Methodology , 2003, DOI: 10.1186/1471-2288-3-14
Abstract: Narrative reviews and editorials are accessed more frequently than primary research papers or systematic reviews in the first week after their publication. These findings may disappoint those who believe that it is important for readers to critically appraise the primary research data.Although the technical quality of journal articles may have been helped by recommendations on structured reporting, the readability of such articles has received little attention. Authors and journal editors must take steps to make research articles and systematic reviews more attractive to readers. This may involve using simpler language, as well as innovative use of web resources to produce shorter, snappier papers, with the methodological or technical details made available elsewhere.Primary research and "evidence-based" papers seem to be less attractive to readers than narrative reviews and editorials in the first week after publication. Authors and editors should try to improve the early appeal of primary research papers.One of the benefits of publishing on the Internet is that the numbers of visitors to a particular article can be easily recorded and displayed. The electronic British Medical Journal (eBMJ) website has a unique "Hit Parade" section, with web access statistics for every online article dating back to 1999.[1] This "Hit Parade" records the number of electronic visits ("hits") in the first week of the article's publication.We were disappointed to find, for instance, that the editorial accompanying a meta-analysis we published in 2000 had been viewed nearly 4000 times whereas the paper itself had received only 1236 visitors.[2,3] This prompted us to ask what people read when they visit the eBMJ. Do they prefer narrative-style articles to original research or evidence-based publications?We assessed the viewing figures in the Hit Parade for all issues, except the Christmas edition, of the eBMJ published in the year 2001. We divided the journal articles into the following
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