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Risk Estimation (risk + estimation)
Selected AbstractsConfidence Bands for Low-Dose Risk Estimation with Quantal Response DataBIOMETRICS, Issue 4 2003Obaid M. Al-Saidy Summary. We study the use of simultaneous confidence bands for low-dose risk estimation with quantal response data, and derive methods for estimating simultaneous upper confidence limits on predicted extra risk under a multistage model. By inverting the upper bands on extra risk, we obtain simultaneous lower bounds on the benchmark dose (BMD). Monte Carlo evaluations explore characteristics of the simultaneous limits under this setting, and a suite of actual data sets are used to compare existing methods for placing lower limits on the BMD. [source] Blurring Emotional Safety With Physical Safety in AIDS and STD Risk Estimations: The Casual/Regular Partner Distinction,JOURNAL OF APPLIED SOCIAL PSYCHOLOGY, Issue 12 2000Lisa K. Comer Research on the sexual behavior of young adults has documented a casual/regular partner distinction in terms of condom use and perceived risk of contracting sexually transmitted diseases (STDs). How this population distinguishes between the 2 partner types has not been known, making it impossible to assess the rationality of this strategy. In the present study, college students' conceptions of casual vs. regular partners were explored and used to create 3 sexual partner scenarios: casual, regular with insufficient risk information (regular emotionally safe), and regular with sufficient risk information (regular objectively safe). Participants rated the target partner in terms of emotional safety, AIDS/STD risk, and likelihood of condom use. Results showed participants to be blurring emotional with physical safety; i. e., employing an emotionally based strategy in rating perceived risk. [source] Benchmark dose estimation based on epidemiologic cohort dataENVIRONMETRICS, Issue 5 2005Knashawn H. Morales Abstract Risk assessments based on epidemiologic studies are becoming increasingly common in evaluating environmental health risks and setting health standards. This article will discuss and compare some of the available methods for exposure,response modeling and risk estimation based on environmental epidemiologic studies with age-specific incidence and mortality data. Recommendations will be made regarding approaches that can be used in practice. Copyright © 2005 John Wiley & Sons, Ltd. [source] Advanced glycation end-products and the kidneyEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 8 2010Martin Busch Eur J Clin Invest 2010; 40 (8): 742,755 Abstract Background, Advanced glycation end-products (AGEs) are increased in situations with hyperglycemia and oxidative stress such as diabetes mellitus. They are products of nonenzymatic glycation and oxidation of proteins and lipids. The kidney plays an important role in clearance and metabolism of AGEs. Methods, Medline© and other relevant databases were searched. In addition, key review articles were scanned for relevant original publication. Finally, original data from our research group were also included. Results, Kidney podocytes and endothelial cells express specific receptors for AGEs. Their activation leads to multiple pathophysiological effects including hypertrophy with cell cycle arrest and apoptosis, altered migration, and generation of proinflammatory cytokines. AGEs have been primarily implicated in the pathophysiology of diabetic nephropathy and diabetic microvascular complications. AGEs are also involved in other primary renal diseases as well as in the development and progression of atherosclerosis. However, serum or plasma concentrations of AGEs do not correlate well with cardiovascular events in patients with chronic kidney disease (CKD). This is likely due to the fact that serum concentrations failed to correlate with AGEs deposited in target tissues. Several inhibitors of the AGE-RAGE axis are currently tested for various indications. Conclusion, AGEs and their receptors are involved in the pathogenesis of vascular and kidney disease. The role of circulating AGEs as biomarkers for cardiovascular risk estimation is questionable. Whether putative inhibitors of AGEs will get the maturity for its therapeutic use in the future remains open. [source] Estimating haplotype relative risks in complex disease from unphased SNPs data in families using a likelihood adjusted for ascertainmentGENETIC EPIDEMIOLOGY, Issue 8 2006J. Carayol Abstract The understanding of complex diseases and insights to improve their medical management may be achieved through the deduction of how specific haplotypes may play a joint effect to change relative risk information. In this paper we describe an ascertainment adjusted likelihood-based method to estimate haplotype relative risks using pooled family data coming from association and/or linkage studies that were used to identify specific haplotypes. Haplotype-based analysis tends to require a large amount of parameters to capture all the information that leads to efficiency problems. An adaptation of the Stochastic Expectation Maximization algorithm is used for haplotypes inference from genotypic data and to reduce the number of nuisance parameters for risk estimation. Using different simulations, we show that this method provides unbiased relative risk estimates even in case of departure from Hardy-Weinberg equilibrium. Genet. Epidemiol. 2006. © 2006 Wiley-Liss, Inc. [source] Optimal designs for estimating penetrance of rare mutations of a disease-susceptibility geneGENETIC EPIDEMIOLOGY, Issue 3 2003Gail Gong Abstract Many clinical decisions require accurate estimates of disease risks associated with mutations of known disease-susceptibility genes. Such risk estimation is difficult when the mutations are rare. We used computer simulations to compare the performance of estimates obtained from two types of designs based on family data. In the first (clinic-based designs), families are ascertained because they meet certain criteria concerning multiple disease occurrences among family members. In the second (population-based designs), families are sampled through a population-based registry of affected individuals called probands, with oversampling of probands whose families are more likely to segregate mutations. We generated family structures, genotypes, and phenotypes using models that reflect the frequencies and penetrances of mutations of the BRCA1/2 genes. We studied the effects of risk heterogeneity due to unmeasured, shared risk factors by including risk variation due to unmeasured genotypes of another gene. The simulations were chosen to mimic the ascertainment and selection processes commonly used in the two types of designs. We found that penetrance estimates from both designs are nearly unbiased in the absence of unmeasured shared risk factors, but are biased upward in the presence of such factors. The bias increases with increasing variation in risks across genotypes of the second gene. However, it is small compared to the standard error of the estimates. Standard errors from population-based designs are roughly twice those from clinic-based designs with the same number of families. Using the root-mean-square error as a measure of performance, we found that in all instances, the clinic-based designs gave more accurate estimates than did the population-based designs with the same numbers of families. Rough variance calculations suggest that clinic-based designs give more accurate estimates because they include more identified mutation carriers. Genet Epidemiol 24:173,180, 2003. © 2003 Wiley-Liss, Inc. [source] Unstructured grid generation using LiDAR data for urban flood inundation modellingHYDROLOGICAL PROCESSES, Issue 11 2010Ryota Tsubaki Abstract Inundation disasters, caused by sudden water level rise or rapid flow, occur frequently in various parts of the world. Such catastrophes strike not only in thinly populated flood plains or farmland but also in highly populated villages or urban areas. Inundation of the populated areas causes severe damage to the economy, injury, and loss of life; therefore, a proper management scheme for the disaster has to be developed. To predict and manage such adversity, an understanding of the dynamic processes of inundation flow is necessary because risk estimation is performed based on inundation flow information. In this study, we developed a comprehensive method to conduct detailed inundation flow simulations for a populated area with quite complex topographical features using LiDAR (Light Detection and Ranging) data. Detailed geospatial information including the location and shape of each building was extracted from the LiDAR data and used for the grid generation. The developed approach can distinguish buildings from vegetation and treat them differently in the flow model. With this method, a fine unstructured grid can be generated representing the complicated urban land features precisely without exhausting labour for data preparation. The accuracy of the generated grid with different grid spacing and grid type is discussed and the optimal range of grid spacing for direct representation of urban topography is investigated. The developed method is applied to the estimation of inundation flows, which occurred in the basin of the Shin-minato River. A detailed inundation flow structure is represented by the flow model, and the flow characteristics with respect to topographic features are discussed. Copyright © 2010 John Wiley & Sons, Ltd. [source] Coherence and correspondence criteria for rationality: experts' estimation of risks of sexually transmitted infectionsJOURNAL OF BEHAVIORAL DECISION MAKING, Issue 3 2005Mary B. Adam Abstract The aim of this study is to examine both coherence and correspondence criteria for rationality in experts' judgments of risk. We investigated biases in risk estimation for sexually transmitted infections (STIs) predicted by fuzzy-trace theory, i.e., that specific errors would occur despite experts' knowledge of correct responses. One hundred twenty professionals with specific knowledge of STI risks in adolescents were administered a survey questionnaire to test predictions concerning: knowledge deficits (producing underestimation of risks); gist-based representation of risk categories (producing overestimation of condom effectiveness); retrieval failure for risk knowledge (producing lower risk estimates); and processing interference in combining risk estimates (producing biases in post-test diagnosis of infection). Retrieval was manipulated by asking estimation questions that "unpacked" the STI category into infection types or did not specify infection types. Other questions differentiated processing biases from knowledge deficits or retrieval failure by directly providing requisite knowledge. Experts' knowledge of STI transmission and infection risks was verified empirically. Nevertheless, under predictable conditions, they misestimated risk, overestimated the effectiveness of condoms, and also suffered from processing biases. When questions provided better retrieval supports (unpacked format), risk estimates improved. Biases were linked to gist representations, retrieval failures, and processing errors, as opposed to knowledge about STIs. Results support fuzzy-trace theory's dual-process assumptions that different types of errors are dissociated from one another, and separate failures of coherence and correspondence among the same sample of experts. Copyright © 2005 John Wiley & Sons, Ltd. [source] The evolution of fracture risk estimationJOURNAL OF BONE AND MINERAL RESEARCH, Issue 10 2010Neil Binkley No abstract is available for this article. [source] Alterations of DNA methylation and clinicopathological diversity of human cancersPATHOLOGY INTERNATIONAL, Issue 9 2008Yae Kanai Alterations of DNA methylation can account for the histological heterogeneity, reflected in the stepwise progression and complex biological characteristics of human cancers, that genetic alterations alone cannot explain. Analysis of DNA methylation status in tissue samples can be an aid to understanding the molecular mechanisms of multistage carcinogenesis. Human cancer cells show a drastic change in DNA methylation status, that is, overall DNA hypomethylation and regional DNA hypermethylation, which results in chromosomal instability and silencing of tumor-suppressor genes. Overexpression of DNA methyltransferase (DNMT) 1 is not a secondary result of increased cell proliferative activity but may underline the CpG island methylator phenotype of cancers. Splicing alteration of DNMT3B may result in chromosomal instability through DNA hypomethylation of pericentromeric satellite regions. Alterations of DNA methylation are observed even in the precancerous stage frequently associated with chronic inflammation and/or persistent viral infection or with cigarette smoking. Precancerous conditions showing alterations of DNA methylation may generate more malignant cancers. Aberrant DNA methylation is significantly associated with aggressiveness of cancers and poorer outcome of cancer patients. Genome-wide analysis of DNA methylation status based on array-based technology may identify DNA methylation profiles that can be used as appropriate indicators for carcinogenetic risk estimation and prognostication. [source] Semi-automated risk estimation using large databases: quinolones and clostridium difficile associated diarrhea,PHARMACOEPIDEMIOLOGY AND DRUG SAFETY, Issue 6 2010Robertino M. Mera Abstract Purpose The availability of large databases with person time information and appropriate statistical methods allow for relatively rapid pharmacovigilance analyses. A semi-automated method was used to investigate the effect of fluoroquinolones on the incidence of C. difficile associated diarrhea (CDAD). Methods Two US databases, an electronic medical record (EMR) and a large medical claims database for the period 2006,2007 were evaluated using a semi-automated methodology. The raw EMR and claims datasets were subject to a normalization procedure that aligns the drug exposures and conditions using ontologies; Snowmed for medications and MedDRA for conditions. A retrospective cohort design was used together with matching by means of the propensity score. The association between exposure and outcome was evaluated using a Poisson regression model after taking into account potential confounders. Results A comparison between quinolones as the target cohort and macrolides as the comparison cohort produced a total of 564,797 subjects exposed to a quinolone in the claims data and 233,090 subjects in the EMR. They were matched with replacement within six strata of the propensity score. Among the matched cohorts there were a total of 488 and 158 outcomes in the claims and the EMR respectively. Quinolones were found to be twice more likely to be significantly associated with CDAD than macrolides adjusting for risk factors (IRR 2.75, 95%CI 2.18,3.48). Conclusions Use of a semi-automated method was successfully applied to two observational databases and was able to rapidly identify a potential for increased risk of developing CDAD with quinolones. Copyright © 2010 John Wiley & Sons, Ltd. [source] Value of anti,modified citrullinated vimentin and third-generation anti,cyclic citrullinated peptide compared with second-generation anti,cyclic citrullinated peptide and rheumatoid factor in predicting disease outcome in undifferentiated arthritis and rheumatoid arthritisARTHRITIS & RHEUMATISM, Issue 8 2009Michael P. M. van der Linden Objective Autoantibodies such as rheumatoid factor (RF) and anti,citrullinated protein autoantibodies (ACPAs) determined by testing with second-generation anti,cyclic citrullinated peptide (anti,CCP-2) are frequently measured in clinical practice because of their association with disease outcome in undifferentiated arthritis (UA) and rheumatoid arthritis (RA). Recently, 2 new ACPA tests were developed: third-generation anti-CCP (anti,CCP-3) and anti,modified citrullinated vimentin (anti-MCV) autoantibody tests. To facilitate the decision on which autoantibody to test in daily practice, this study evaluated the capability of these autoantibodies and combinations of them to predict 3 outcome measures: progression from UA to RA, the rate of joint destruction in RA, and the chance of achieving sustained disease-modifying antirheumatic drug (DMARD),free remission in RA. Methods Patients with UA (n = 625) were studied for whether UA progressed to RA after 1 year. Patients with RA (n = 687) were studied for whether sustained DMARD-free remission was achieved and for the rate of joint destruction during a median followup of 5 years. Positive predictive values (PPVs) for RA development and for associations with the disease course in RA were compared between single tests (anti,CCP-2, anti,CCP-3, anti-MCV, and RF) and between combinations of these tests. Results Among the single tests performed in patients with UA, anti,CCP-2 tended to have the highest PPV for RA development (67.1%), but the 95% confidence intervals of the other tests overlapped. Among the single tests in patients with RA, all 4 tests showed comparable associations with the rate of joint destruction and with the achievement of remission. In both ACPA-positive and ACPA-negative RA, the presence of RF was not associated with more joint destruction. For all outcome measures, performing combinations of 2 or 3 autoantibody tests did not increase the predictive accuracy compared with performing a single test. Conclusion For clinical practice, a single autoantibody test is sufficient for risk estimation in UA and RA. [source] A Method for Estimating Penetrance from Families Sampled for Linkage AnalysisBIOMETRICS, Issue 4 2006Yuanjia Wang Summary When a gene variant is discovered to segregate with a disease, it may be of interest to estimate the risk (or the age-specific risk) of the disease to carriers of the variant. The families that contributed to the discovery of the variant would typically contain multiple carriers, and so, especially if the variant is rare, might prove a valuable source of study subjects for estimation of the risk. These families, by virtue of having brought the gene in question to the attention of researchers, however, may not be representative of the relationship between carrier status and the risk of the disease in the population. Using these families for risk estimation could bias the observed association between the variant and the risk. The purpose here is to present an approach to adjusting for the potential bias while using the families from linkage analysis to estimate the risk. [source] Confidence Bands for Low-Dose Risk Estimation with Quantal Response DataBIOMETRICS, Issue 4 2003Obaid M. Al-Saidy Summary. We study the use of simultaneous confidence bands for low-dose risk estimation with quantal response data, and derive methods for estimating simultaneous upper confidence limits on predicted extra risk under a multistage model. By inverting the upper bands on extra risk, we obtain simultaneous lower bounds on the benchmark dose (BMD). Monte Carlo evaluations explore characteristics of the simultaneous limits under this setting, and a suite of actual data sets are used to compare existing methods for placing lower limits on the BMD. [source] Evolution of NCEP guidelines: ATP1-ATPIII risk estimation for coronary heart disease in 2002CLINICAL CARDIOLOGY, Issue 3 2002C. Richard Conti M.D., M.A.C.C. Editor-in-Chief No abstract is available for this article. [source] |