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Search Results: 1 - 10 of 8659 matches for " Elizabeth Costenbader "
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Empiricism and Theorizing in Epidemiology and Social Network Analysis
Richard Rothenberg,Elizabeth Costenbader
Interdisciplinary Perspectives on Infectious Diseases , 2011, DOI: 10.1155/2011/157194
Abstract: The connection between theory and data is an iterative one. In principle, each is informed by the other: data provide the basis for theory that in turn generates the need for new information. This circularity is reflected in the notion of abduction, a concept that focuses on the space between induction (generating theory from data) and deduction (testing theory with data). Einstein, in the 1920s, placed scientific creativity in that space. In the field of social network analysis, some remarkable theory has been developed, accompanied by sophisticated tools to develop, extend, and test the theory. At the same time, important empirical data have been generated that provide insight into transmission dynamics. Unfortunately, the connection between them is often tenuous and the iterative loop is frayed. This circumstance may arise both from data deficiencies and from the ease with which data can be created by simulation. But for whatever reason, theory and empirical data often occupy different orbits. Fortunately, the relationship, while frayed, is not broken, to which several recent analyses merging theory and extant data will attest. Their further rapprochement in the field of social network analysis could provide the field with a more creative approach to experimentation and inference. 1. Introduction Theory and empirical data are in principle intimately interwoven. Yet in the practice of social network analysis, there appears to be a disconnect: theorizing and empiricism often seem to occupy separate orbits, and these separate discussions may be difficult to relate to each other. The root of the problem may lie in the different skill sets required by each, or perhaps in the substantial obstacles to collection of human network data. The following exploration of the distance between theory and empiricism suggests that a rapprochement would be of considerable benefit to the field. The mid-19th Century American philosopher Charles Peirce coined the term “abduction” (which he also called “retroduction”) to fill a gap he perceived in the territory occupied by induction and deduction. As distilled by Professor Burch [1], Peirce used syllogisms to explain this term, substituting Rule, Case, and Result for the more familiar Major Premise, Minor Premise, and Conclusion. But perhaps more interesting to epidemiologists and social network analysts, he related this logical process to sampling. As Professor Burch explains it, a standard valid syllogism would progress as follows.Rule: All balls in this urn are red.Case: All balls in this particular random sample are
Epstein–Barr virus and rheumatoid arthritis: is there a link?
Karen H Costenbader, Elizabeth W Karlson
Arthritis Research & Therapy , 2005, DOI: 10.1186/ar1893
Abstract: Rheumatoid arthritis (RA) is a chronic inflammatory polyarthritis that progressively destroys synovial joints and can cause systemic complications. RA affects about 1% of the world's population [1], and its prevalence in women is twofold to fourfold that in men [2,3]. RA has enormous personal, social, and economic impact [4,5]; women with RA have overall mortality rates 2.3-fold those in age-matched controls [6]. New biologic therapies, based on an increasing understanding of the molecular mechanisms involved in RA, afford a more normal life to many, but the burden of disease remains high. At present there is no known cure. Despite improved therapy, the long-term prognosis remains poor and average life expectancy is reduced by 3 to 18 years [7]. Both the direct costs of treatment of RA and the indirect costs of disability and loss from the workplace are high [8,9].RA is marked by extensive synovial hyperplasia and infiltration by lymphocytes, monocytes, macrophages, and fibroblasts. RA is a predominantly CD4+ T helper type 1 (Th1)-driven disease [10]. Aberrant T cell activation is one of the earliest events in the development of RA, with CD4+ T cells stimulating monocytes and macrophages to produce inflammatory cytokines, including interleukin (IL)-1, IL-6, and tumor necrosis factor-α (TNF-α), as well as proteolytic enzymes, destroying synovium, cartilage, and underlying bone [11]. The T cells infiltrating the rheumatoid synovium are oligoclonal, implicating an antigen-driven process [12,13], but the inciting antigen or antigens remain unidentified. Activated T cells also signal B cells to produce increased levels of immunoglobulins, including rheumatoid factor (RF). Autoreactive B cells also have a central role in the development of RA, producing autoantibodies that might be involved in tissue damage in RA [14].Genetic factors are important in disease susceptibility, but environmental exposures are probably crucial as well. Many exposures have been investigated as
Genetic polymorphisms in PTPN22, PADI-4, and CTLA-4 and risk for rheumatoid arthritis in two longitudinal cohort studies: evidence of gene-environment interactions with heavy cigarette smoking
Karen H Costenbader, Shun-Chiao Chang, Immaculata De Vivo, Robert Plenge, Elizabeth W Karlson
Arthritis Research & Therapy , 2008, DOI: 10.1186/ar2421
Abstract: We studied RA risk associated with PTPN22 (rs2476601), PADI-4 (rs2240340), and CTLA-4 (rs3087243) in the Nurses' Health Study (NHS) and NHSII. Participants in NHS were aged 30 to 55 years at entry in 1976; those in NHSII were aged 25 to 42 years at entry in 1989. We confirmed incident RA cases through to 2002 in NHS and to 2003 in NHSII by questionnaire and medical record review. We excluded reports not confirmed as RA. In a nested case-control design involving participants for whom there were samples for genetic analyses (45% of NHS and 25% of NHSII), each incident RA case was matched to a participant without RA by year of birth, menopausal status, and postmenopausal hormone use. Genotyping was performed using Taqman single nucleotide polymorphism allelic discrimination on the ABI 7900 HT (Applied Biosystems, 850 Lincoln Centre Drive, Foster City, CA 94404 USA) with published primers. Human leukocyte antigen shared epitope (HLA-SE) genotyping was performed at high resolution. We employed conditional logistic regression analyses, adjusting for smoking and reproductive factors. We tested for additive and multiplicative interactions between each genotype and smoking.A total of 437 incident RA cases were matched to healthy female control individuals. Mean (± standard deviation) age at RA diagnosis was 55 (± 10), 57% of RA cases were rheumatoid factor (RF) positive, and 31% had radiographic erosions at diagnosis. PTPN22 was associated with increased RA risk (pooled odds ratio in multivariable dominant model = 1.46, 95% confidence interval [CI] = 1.02 to 2.08). The risk was stronger for RF-positive than for RF-negative RA. A significant multiplicative interaction between PTPN22 and smoking for more than 10 pack-years was observed (P = 0.04). CTLA-4 and PADI-4 genotypes were not associated with RA risk in the pooled results (pooled odds ratios in multivariable dominant models: 1.27 [95% CI = 0.88 to 1.84] for CTLA-4 and 1.04 [95% CI = 0.77 to 1.40] for PADI-4). No gene-ge
Dietary intake of vitamin D during adolescence and risk of adult onset systemic lupus erythematosus and rheumatoid arthritis
Hiraki Linda T,Costenbader Karen H,Munger Kassandra L,Karlson Elizabeth W
Pediatric Rheumatology , 2012, DOI: 10.1186/1546-0096-10-s1-a30
Abstract:
Genetic Risk Score Predicting Risk of Rheumatoid Arthritis Phenotypes and Age of Symptom Onset
Lori B. Chibnik, Brendan T. Keenan, Jing Cui, Katherine P. Liao, Karen H. Costenbader, Robert M. Plenge, Elizabeth W. Karlson
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0024380
Abstract: Background Cumulative genetic profiles can help identify individuals at high-risk for developing RA. We examined the impact of 39 validated genetic risk alleles on the risk of RA phenotypes characterized by serologic and erosive status. Methods/Principal Findings We evaluated single nucleotide polymorphisms at 31 validated RA risk loci and 8 Human Leukocyte Antigen alleles among 542 Caucasian RA cases and 551 Caucasian controls from Nurses' Health Study and Nurses' Health Study II. We created a weighted genetic risk score (GRS) and evaluated it as 7 ordinal groups using logistic regression (adjusting for age and smoking) to assess the relationship between GRS group and odds of developing seronegative (RF? and CCP?), seropositive (RF+ or CCP+), erosive, and seropositive, erosive RA phenotypes. In separate case only analyses, we assessed the relationships between GRS and age of symptom onset. In 542 RA cases, 317 (58%) were seropositive, 163 (30%) had erosions and 105 (19%) were seropositive with erosions. Comparing the highest GRS risk group to the median group, we found an OR of 1.2 (95% CI = 0.8–2.1) for seronegative RA, 3.0 (95% CI = 1.9–4.7) for seropositive RA, 3.2 (95% CI = 1.8–5.6) for erosive RA, and 7.6 (95% CI = 3.6–16.3) for seropositive, erosive RA. No significant relationship was seen between GRS and age of onset. Conclusions/Significance Results suggest that seronegative and seropositive/erosive RA have different genetic architecture and support the importance of considering RA phenotypes in RA genetic studies.
A prospective study of androgen levels, hormone-related genes and risk of rheumatoid arthritis
Elizabeth W Karlson, Lori B Chibnik, Monica McGrath, Shun-Chiao Chang, Brendan T Keenan, Karen H Costenbader, Patricia A Fraser, Shelley Tworoger, Susan E Hankinson, I-Min Lee, Julie Buring, Immaculata De Vivo
Arthritis Research & Therapy , 2009, DOI: 10.1186/ar2742
Abstract: We genotyped AR, ESR2, CYP19, PGR SNPs and the AR CAG repeat in RA case–control studies nested within the Nurses' Health Study (NHS), NHS II (449 RA cases, 449 controls) and the Women's Health Study (72 cases, and 202 controls). All controls were matched on cohort, age, Caucasian race, menopausal status, and postmenopausal hormone use. We measured plasma dehydroepiandrosterone sulfate (DHEAS), testosterone, and sex hormone binding globulin in 132 pre-RA samples and 396 matched controls in the NHS cohorts. We used conditional logistic regression models adjusted for potential confounders to assess RA risk.Mean age of RA diagnosis was 55 years in both cohorts; 58% of cases were rheumatoid factor positive at diagnosis. There was no significant association between plasma DHEAS, total testosterone, or calculated free testosterone and risk of future RA. There was no association between individual variants or haplotypes in any of the genes and RA or seropositive RA, nor any association for the AR CAG repeat.Steroid hormone levels measured at a single time point prior to RA onset were not associated with RA risk in this study. Our findings do not suggest that androgens or the AR, ESR2, PGR, and CYP19 genes are important to RA risk in women.Women are two to four times more likely than men to develop rheumatoid arthritis (RA) [1,2], and sex hormones including androgens, estrogen, and progesterone may be related to this disparity [3,4]. In women and men the age-related increased incidence of RA parallels the decline in androgen production [5]. Cross-sectional studies of serum androgen levels demonstrate low serum testosterone levels and dehydroepiandrosterone sulfate (DHEAS) in RA patients compared with healthy individuals [6-10]. Serum testosterone levels are inversely correlated with RA disease activity [11], and DHEAS levels are inversely correlated with both disease duration and clinical severity of RA [12]. Androgen receptor expression is significantly higher in RA synovia
SLE - Practical and theoretical barriers to the prevention of accelerated atherosclerosis in systemic lupus erythematosus
Karen H Costenbader, Matthew H Liang
Arthritis Research & Therapy , 2003, DOI: 10.1186/ar773
Abstract: Aggressive and accelerated atherosclerosis is a major problem in systemic lupus erythematosus (SLE) and is one of its major causes of death, an observation first made more than 20 years ago by Urowitz [1]. Coronary artery disease develops in 6–9% of SLE patients and accounts for up to 36.4% of deaths in SLE. High rates of atherosclerotic vascular disease (ASVD) are particularly striking in young women with SLE, normally at low risk. The incidence of myocardial infarction in women with SLE aged 35–44 years is 50-fold greater than in women of similar ages from a population-based sample [2]. Non-invasive methods of demonstrating atherosclerotic disease, such as carotid duplex ultrasound, electron-beam computed tomography, and thallium perfusion scanning, and one autopsy study, suggest that symptomatic disease might be the tip of the iceberg. The true incidence could be as high as 74% [3-10].The pathophysiology of SLE-associated atherosclerosis is unknown, but the emerging picture is that many of the same risk factors as those observed in normal individuals are also involved. This has motivated authorities in both rheumatology and preventive cardiology to advocate more aggressive risk factor assessment and management of risk factors [11-17]. There are theoretical and practical barriers to improving atherosclerosis-related outcomes in SLE suggesting that this approach will be challenging, and the potential benefit is yet unknown.First, when risk factors are examined quantitatively, SLE and/or its treatment (most probably with corticosteroids) are the most important risk factors. Indeed, data from Esdaile and colleagues suggest that even after adjusting for 'normal risk', SLE and/or its treatment increases the risk of coronary artery disease 5–10-fold [18]. This suggests that even if physicians were perfectly virtuous, sought out risk factors aggressively and followed guidelines scrupulously; and patients were tolerant, compliant, and responsive to lipid-lowering strategi
Prevalence and demographics of systemic lupus erythematosus and lupus nephritis among US children with Medicaid coverage, 2002-2004
Hiraki Linda T,Shaykevich Tamara,Winkelmayer Wolfgang C,Costenbader Karen H
Pediatric Rheumatology , 2012, DOI: 10.1186/1546-0096-10-s1-a104
Abstract:
Family Structure and Psychological Health in Young Adults  [PDF]
Tony Cassidy, Elizabeth Wright, Elizabeth Noon
Psychology (PSYCH) , 2014, DOI: 10.4236/psych.2014.510129
Abstract:

This study explored the effect of the gendered structure of siblings in intact and non-intact families, on family relations, social support, perceived control, and psychological distress in a sample of 708 young adults (294 males and 414 females) aged between 18 - 21 years. Of the sample 96 were singletons, 208 had both a brother and sister, 206 had a brother and no sister, and 198 had a sister and no brother. While the results show that both the gender of the participants and the gender of the sibling seem to impact on distress and its mediators; the more important factor is the gender of siblings. In essence the presence of a female sibling is associated with more perceived support, control and optimism, and with lower pessimism and psychological distress. The presence of a female is also associated with better family relations overall and it is suggested that the main mechanism for this positive impact of female siblings is through the lowered conflict and increased expressiveness and cohesion experienced in female versus male dominated sibling groups.

Design of Sharp 2D Multiplier-Less Circularly Symmetric FIR Filter Using Harmony Search Algorithm and Frequency Transformation  [PDF]
Manju Manuel, Elizabeth Elias
Journal of Signal and Information Processing (JSIP) , 2012, DOI: 10.4236/jsip.2012.33044
Abstract: In this paper, we present a novel and efficient method for the design of a sharp, two dimensional (2D) wideband, circularly symmetric, FIR filter. First of all, a sharp one dimensional (1D) infinite precision FIR filter is designed using the Frequency Response Masking (FRM) technique. This filter is converted into a multiplier-less filter by representing it in the Canonic Signed Digit (CSD) space. The design of the FRM filter in the CSD space calls for the use of a discrete optimization technique. To this end, a new optimization approach is proposed using a modified Harmony Search Algorithm (HSA). HSA is modified in such a way that, in every exploitation and exploration phase, the candidate solutions turns out to be integers. The 1D FRM multiplier-less filter, is in turn transformed to the 2D equivalent using the recently proposed multiplier-less transformations namely, T1 and T2. These transformations are successful in generating circular contours even for wideband filters. Since multipliers are the most power consuming elements in a 2D filter, the multiplier-less realization calls for reduced power consumption as well as computation time. Significant reduction in the computational complexity and computation time are the highlights of our proposed design technique. Besides, the proposed discrete optimization using modified HSA can be used to solve optimization problems in other engineering disciplines, where the search space consists of integers.
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