bluuebunny/crossref_metadata_2025_split huggingface dataset:
Bayesian parameter estimation with informative priors for nonlinear systems
Authors: Coleman Matthew C. , Block David E. 
Published: September 2005

AbstractThe estimation of parameters for nonlinear process models is often accomplished through optimization routines that search for a global optimum with respect to a least squares or weighted least squares criterion. While such an approach is often reasonable, it fails to account for all of the information that is available from the data and practitioner. Here we focus on the inclusion of prior knowledge in the estimation of parameters in nonlinear dynamic systems. We use the Bayesian paradigm to define the probability distribution over process model parameters, called the Bayesian posterior. The quantities associated with this posterior distribution (e.g., credible regions, means, modes) are estimated via Markov Chain Monte Carlo (MCMC) integration. We first give a short introduction to Bayesian parameter estimation and the role of MCMC in evaluating arbitrary probability distributions. Bayesian parameter estimation (via MCMC) is then applied to three case studies. The first case study shows the basic methodology of assigning and evaluating a Bayesian posterior to a simple problem that consists of estimating the mean and variance of a sample. The second case study uses prior information that specifies a preference for a particular type of reaction mechanism over another for a simulated fermentation system; the inclusion of such prior information is shown to improve the estimated values of the model parameters in situations where data are sparse or noisy (compared to the more common weighted least squares approach). The third case study develops a hybrid semi‐parametric neural network (NN) model to predict time‐dependent observed state variables (cell and protein concentration) in Escherichia coli fermentations. An integral step in the development of this hybrid model is parameter estimation of a nonlinear dynamic model. A hybrid model developed from the Bayesian parameter estimates is shown to outperform a hybrid model developed from the weighted least squares parameter estimates for predicting the final protein yield of a test set. © 2005 American Institute of Chemical Engineers AIChE J, 2006
Value of accuracy in linear systems
Authors: Bagajewicz Miguel 
Published: September 2005

AbstractA connection between precision and downside expected lost revenue for linear systems was developed in previous work. Having the value of precision and accuracy in economic terms helps justify the upgrade of instrumentation and/or the increase in corrective maintenance repair rate. The connection between accuracy and economic value is extended in this article to the case where biases are present and in the context of existing corrective maintenance capabilities. © 2005 American Institute of Chemical Engineers AIChE J, 2006
Correlation of rheumatoid arthritis severity with the genetic functional variants and circulating levels of macrophage migration inhibitory factor
Authors: Radstake Timothy R. D. J. , Sweep Fred C. G. J. , Welsing Paco , Franke Barbara , Vermeulen Sita H. H. M. , Geurts‐Moespot Anneke , Calandra Thierry , Donn Rachelle , van Riel Piet L. C. M. 
Published: September 2005

AbstractObjectiveTo study whether genetic variants of macrophage migration inhibitory factor (MIF), the MIF −173G>C and CATT5–8 alleles, are associated with disease severity and levels of circulating MIF in patients with rheumatoid arthritis (RA).MethodsGenotyping was performed in patients with early RA and in healthy controls. Demographic data, disease activity, and outcome measurements were compared between patients with and without the MIF variants. MIF −173G>C and CATT5–8 polymorphisms were genotyped, and a newly developed enzyme‐linked immunosorbent assay for human MIF was used. Allele and genotype distributions of the MIF −173G>C and CATT5–8 polymorphisms were compared between patients and controls by chi‐square test. Multiple regression analysis was performed to assess the independence of the MIF functional genetic variants as risk factors for radiologic joint damage.ResultsGenotyping of the −173G>C and CATT5–8 polymorphisms of MIF in RA patients and healthy individuals (n = 277 each) revealed similar frequencies of genotypes and haplotypes in both groups. No significant differences in demographic or clinical features were observed between RA patients carrying the MIF −173C allele or the MIF CATT7 allele or both and noncarrier RA patients. Radiologic joint damage was significantly higher in patients carrying risk alleles of the MIF −173G>C or the MIF CATT5–8 functional variants. No synergistic effects between both genetic variants were observed. Multivariate regression analysis revealed that presence of the MIF −173C/C and MIF CATT7/7 genotypes and having 1 MIF −173C allele were independent prognostic variables. Carriership of the MIF −173C allele (P = 0.002) or MIF CATT7 allele (P = 0.004) was associated with significantly higher circulating MIF levels compared with those in subjects having none of the risk‐conferring alleles, and greater circulating MIF levels correlated with more severe radiologic joint damage (r = 0.64, P = 0.001).ConclusionThe MIF polymorphisms are not associated with RA susceptibility but are associated with high levels of radiologic joint damage. High circulating MIF levels were shown to correlate strongly with radiologic joint damage, suggesting that MIF expression is genetically determined and can be used as a novel prognostic tool in RA.
The relationship between cartilage loss on magnetic resonance imaging and radiographic progression in men and women with knee osteoarthritis
Authors: Amin Shreyasee , LaValley Michael P. , Guermazi Ali , Grigoryan Mikayel , Hunter David J. , Clancy Margaret , Niu Jingbo , Gale Daniel R. , Felson David T. 
Published: September 2005

AbstractObjectiveTo determine the relationship between radiographic progression of joint space narrowing and cartilage loss on magnetic resonance imaging (MRI) in patients with symptomatic knee osteoarthritis (OA), and to investigate the location of MRI‐based cartilage loss in the knee and its relation to radiographic progression.MethodsTwo hundred twenty‐four men and women (mean age 66 years) were studied. Radiographs and MRI of the more symptomatic knee were obtained at baseline and at 15‐ and 30‐month followup. Radiographs of the knee (with weight‐bearing) were read for joint space narrowing (scale 0–3), with progression defined as any worsening in score. We used a semiquantitative method to score cartilage morphology in all 5 regions of the tibiofemoral joint, and defined cartilage loss as an increase in score (scale 0–4) at any region. We examined the relationship between progression of joint space narrowing on radiographic images and cartilage loss on MRI, using a generalized estimating equation proportional odds logistic regression, adjusted for baseline cartilage score, age, body mass index, and sex. The medial and lateral compartments were analyzed separately.ResultsIn the medial compartment, 104 knees (46%) had cartilage loss detected by MRI. The adjusted odds ratio was 3.7 (95% confidence interval 2.2–6.3) for radiographic progression being predictive of cartilage loss on MRI. However, there was still a substantial proportion of knees (80 of 189 [42%]) with cartilage loss visible on MRI when no radiographic progression was apparent. Cartilage loss occurred frequently in the central regions of the femur and tibia as well as the posterior femur region, but radiographic progression was less likely to be observed when posterior femur regions showed cartilage loss. Radiographic progression appeared specific (91%) but not sensitive (23%) for cartilage loss. Overall findings were similar for the lateral compartment.ConclusionWhile our results provide longitudinal evidence that radiographic progression of joint space narrowing is predictive of cartilage loss assessed on MRI, radiography is not a sensitive measure, and if used alone, will miss a substantial proportion of knees with cartilage loss.
Racial/ethnic differences in surgical outcomes in veterans following knee or hip arthroplasty
Authors: Ibrahim Said A. , Stone Roslyn A. , Han Xiaoyan , Cohen Peter , Fine Michael J. , Henderson William G. , Khuri Shukri F. , Kwoh C. Kent 
Published: September 2005

AbstractObjectiveThe utilization of joint arthroplasty for knee or hip osteoarthritis varies markedly by patient race/ethnicity. Because of concerns about surgical risk, black patients are less willing to consider this treatment. There are few published race/ethnicity‐specific data on joint arthroplasty outcomes. The present study was undertaken to examine racial/ethnic differences in mortality and morbidity following elective knee or hip arthroplasty.MethodsUsing information from the Veterans Administration National Surgical Quality Improvement Program database, data on 12,108 patients who underwent knee arthroplasty and 6,703 patients who underwent hip arthroplasty over a 5‐year period were analyzed. Racial/ethnic differences were determined using prospectively collected data on patient characteristics, procedures, and short‐term outcomes. The main outcome measures were risk‐adjusted 30‐day mortality and complication rates.ResultsAdjusted rates of both non–infection‐related and infection‐related complications after knee arthroplasty were higher among black patients compared with white patients (relative risk [RR] 1.50, 95% confidence interval [95% CI] 1.08–2.10 and RR 1.42, 95% CI 1.06–1.90, respectively). Hispanic patients had a significantly higher risk of infection‐related complications after knee arthroplasty (RR 1.64, 95% CI 1.08–2.49) relative to otherwise similar white patients. Race/ethnicity was not significantly associated with the risk of non–infection‐related complications (RR 0.97, 95% CI 0.68–1.38 in blacks; RR 1.18, 95% CI 0.60–2.30 in Hispanics) or infection‐related complications (RR 1.27, 95% CI 0.91–1.78 in blacks; RR 1.22, 95% CI 0.63–2.36 in Hispanics) after hip arthroplasty. The overall 30‐day mortality was 0.6% following knee arthroplasty and 0.7% following hip arthroplasty, with no significant differences by race/ethnicity observed for either procedure.ConclusionAlthough absolute risks of complication are low, our findings indicate that, after adjustment, black patients have significantly higher rates of infection‐related and non–infection‐related complications following knee arthroplasty, compared with white patients. In addition, adjusted rates of infection‐related complications after knee arthroplasty are higher in Hispanic patients than in white patients. Such differences between ethnic groups are not seen following hip arthroplasty. These groups do not appear to differ significantly in terms of post‐arthroplasty mortality rates.
Adalimumab for the treatment of patients with moderately to severely active psoriatic arthritis: Results of a double‐blind, randomized, placebo‐controlled trial
Authors: Mease Philip J. , Gladman Dafna D. , Ritchlin Christopher T. , Ruderman Eric M. , Steinfeld Serge D. , Choy Ernest H.S. , Sharp John T. , Ory Peter A. , Perdok Renee J. , Weinberg Mark A. 
Published: September 2005

AbstractObjectiveAdalimumab, a fully human, anti–tumor necrosis factor monoclonal antibody, was evaluated for its safety and efficacy compared with placebo in the treatment of active psoriatic arthritis (PsA).MethodsPatients with moderately to severely active PsA and a history of inadequate response to nonsteroidal antiinflammatory drugs were randomized to receive 40 mg adalimumab or placebo subcutaneously every other week for 24 weeks. Study visits were at baseline, weeks 2 and 4, and every 4 weeks thereafter. The primary efficacy end points were the American College of Rheumatology 20% improvement (ACR20) response at week 12 and the change in the modified total Sharp score of structural damage at week 24. Secondary end points were measures of joint disease, disability, and quality of life in all patients, as well as the severity of skin disease in those patients with psoriasis involving at least 3% of body surface area.ResultsAt week 12, 58% of the adalimumab‐treated patients (87 of 151) achieved an ACR20 response, compared with 14% of the placebo‐treated patients (23 of 162) (P < 0.001). At week 24, similar ACR20 response rates were maintained and the mean change in the modified total Sharp score was −0.2 in patients receiving adalimumab and 1.0 in those receiving placebo (P < 0.001). Among the 69 adalimumab‐treated patients evaluated with the Psoriasis Area and Severity Index (PASI), 59% achieved a 75% PASI improvement response at 24 weeks, compared with 1% of the 69 placebo‐treated patients evaluated (P < 0.001). Disability and quality of life measures were also significantly improved with adalimumab treatment compared with placebo. Adalimumab was generally safe and well‐tolerated.ConclusionAdalimumab significantly improved joint and skin manifestations, inhibited structural changes on radiographs, lessened disability due to joint damage, and improved quality of life in patients with moderately to severely active PsA.
Deficiency of type I interferon contributes to Sle2‐associated component lupus phenotypes
Authors: Li Jianwei , Liu Yang , Xie Chun , Zhu Jiankun , Kreska Desi , Morel Laurence , Mohan Chandra 
Published: September 2005

AbstractObjectiveStudies in mice and humans have implicated type I interferon (IFN‐I) in the pathogenesis of lupus. Given that the locus for IFN‐I is positioned within the Sle2 murine lupus susceptibility interval on chromosome 4, we undertook this study to investigate whether differences in IFN‐I levels might potentially contribute to the phenotypes ascribed to this locus.MethodsIFN‐I, anti–IFN‐I, isotype control antibody, or phosphate buffered saline was administered to C57BL/6 and B6.Sle2 mice, and the serologic and cellular phenotypes were studied. In addition, B6.Sle2 mice were examined for structural and expression polymorphisms in the IFN‐I gene.ResultsIn both B6.Sle2 congenic mice and C57BL/6 control mice, antibody‐mediated blockade of IFN‐I augmented serum autoantibody levels and boosted B1a cell numbers. Administration of IFN‐I ameliorated these 2 features previously attributed to this disease locus. Importantly, compared with B6 controls, B6.Sle2 mice had reduced levels of IFN‐I in their sera and cell culture supernatants, following stimulation. Although several sequence polymorphisms were noted in the Sle2 alleles of various IFN‐I genes, it was not established whether any of the noted sequence variations were causally related to the observed phenotypes.ConclusionUnexpectedly, reduction of IFN‐I levels reproduced the serologic and cellular phenotypes previously associated with the Sle2 lupus susceptibility interval. Placing these findings in the context of other studies, the effect of IFN‐I on systemic autoimmunity appears to be far more complex than originally perceived.
Analysis of the kinetics of osteoclastogenesis in arthritic rats
Authors: Schett Georg , Stolina Marina , Bolon Brad , Middleton Scot , Adlam Matt , Brown Heather , Zhu Li , Feige Ulrich , Zack Debra J. 
Published: September 2005

AbstractObjectiveTo analyze the kinetics of osteoclastogenesis in 2 models of chronic immune‐mediated arthritis and 1 model of acute arthritis.MethodsAdjuvant‐induced arthritis (AIA) and collagen‐induced arthritis (CIA) in Lewis rats were used as models of chronic arthritis. Acute arthritis was induced in Lewis rats by injecting carrageenan into the hind paw. Osteoclasts were identified by cathepsin K immunohistochemistry at various time points after the onset of arthritis. The location, size, and nucleation of osteoclasts were also analyzed.ResultsIn both AIA and CIA, multinucleated and cathepsin K–positive osteoclasts first were observed on the day of disease onset. Initially, osteoclasts were localized at the periosteum next to the synovial membrane and in subchondral bone channels. The number, size, and nucleation of osteoclasts rapidly increased, leading to severe bone loss within days after disease onset. In addition, numerous mononucleated cathepsin K–positive osteoclast precursor cells emerged in the synovial membrane. All osteoclasts (cathepsin K–positive, multinucleated, attached to bone) and osteoclast precursors (cathepsin K–positive, mononucleated or multinucleated, within synovial tissue) were also positive for a macrophage‐specific marker. Upon induction of acute arthritis with carrageenan, osteoclasts formed transiently in subchondral bone, but regressed 7 days after disease onset.ConclusionFunctional osteoclasts are generated at the earliest stage of arthritis, and new precursors are continuously formed in the synovial membrane to replenish the osteoclast pool. These data indicate that antiresorptive therapies may provide the most effective bone protection, when treatment is started soon after the onset of arthritis.
Tonic activation of hypoxia‐inducible factor 1α in avascular articular cartilage and implications for metabolic homeostasis
Authors: Brucker Peter U. , Izzo Nicholas J. , Chu Constance R. 
Published: September 2005

AbstractObjectiveTo determine whether oxygen‐dependent activation patterns of hypoxia‐inducible factor 1α (HIF‐1α) observed in vascularized tissues are conserved within avascular and hypoxic articular cartilage and whether HIF‐1α affects cartilage matrix synthesis.MethodsExplants of bovine articular cartilage and primary chondrocytes were exposed to normoxia (21% O2), hypoxia (2% O2), and simulated hypoxia (21% O2 plus CoCl2). Western blot and immunofluorescence analyses of HIF‐1α were performed to determine HIF‐1α activation patterns. To simulate cartilage loss from disease or injury, the top layers of cartilage were removed from osteochondral explants, and the residual cartilage was assessed for HIF‐1α immunolocalization and proteoglycan synthesis.ResultsWe demonstrated continuous nuclear translocation of HIF‐1α in deeper layers of intact articular cartilage. HIF‐1α was not completely degraded in chondrocytes exposed to normoxia, but rather, colocalized to the Golgi complex, a finding not previously reported for any cell type. Following alteration of the oxygen gradient by removal of the top layers of cartilage, predominantly perinuclear HIF‐1α was found in the deeper layers. Restoration of intranuclear HIF‐1α to these areas was achieved by hypoxia and simulated hypoxia. Under conditions in which HIF‐1α was inactivated, matrix synthetic activity was altered (P < 0.0001) compared with control cartilage.ConclusionThese findings demonstrate that hypoxia‐dependent activation of HIF‐1α is highly conserved and that changes in oxygen tensions following cartilage loss from injury or disease alter cartilage metabolism in part by changing HIF‐1α activity. The discovery of tonic activation of HIF‐1α within intact articular cartilage underscores its potential importance to cartilage homeostasis.
How much of the increased incidence of heart failure in rheumatoid arthritis is attributable to traditional cardiovascular risk factors and ischemic heart disease?
Authors: Crowson Cynthia S. , Nicola Paulo J. , Kremers Hilal Maradit , O'Fallon W. Michael , Therneau Terry M. , Jacobsen Steven J. , Roger Veronique L. , Ballman Karla V. , Gabriel Sherine E. 
Published: September 2005

AbstractObjectiveTo compare the proportion of the risk for the development of heart failure (HF) that is attributable to traditional cardiovascular (CV) risk factors, ischemic heart disease (IHD), and alcohol abuse between subjects with and subjects without rheumatoid arthritis (RA).MethodsA population‐based inception cohort of RA patients was assembled along with a similar cohort of subjects without RA. All individuals were followed up through their complete medical records, until HF incidence, death, migration, or January 1, 2001. The attributable risk of HF was estimated as the difference between the observed cumulative incidence of HF in each cohort (estimated from multivariable Cox models and adjusted for the competing risk of death) and the predicted cumulative incidence of HF in the absence of risk factors, with results expressed as a percentage of the observed cumulative incidence.ResultsA total of 575 RA subjects and 583 non‐RA subjects (mean age 57 years, 73% women) without HF at incidence/index date had a mean followup of 15.1 and 17.0 years, respectively. During that period, 165 RA and 115 non‐RA subjects had a first episode of HF, with a cumulative incidence of 36.3% and 20.4%, respectively, at age 80 years. Among non‐RA subjects, 77% of the HF at age 80 years was attributable to CV risk factors, IHD, and alcohol abuse combined, whereas among RA subjects, only 54% of the HF at age 80 years was attributable to these factors (P < 0.01).ConclusionThe excess risk of HF among RA patients is not explained by an increased frequency or effect of CV risk factors and IHD.
Genome‐wide analysis of the transcriptional response of murine hybridomas to osmotic shock
Authors: Shen Duan , Sharfstein Susan T. 
Published: September 2005

AbstractHyperosmotic stress has been shown to increase specific antibody productivity in murine hybridoma systems; however, the mechanisms underlying this phenomenon are still poorly understood. To elucidate the mechanisms for this phenomenon as well as other physiological changes that occur in response to hyperosmotic stress, we performed a genome‐wide analysis of the transcriptional response of murine hybridoma OKT3 toward hyperosmotic stress using DNA microarrays. GeneChip® MOE430A from Affymetrix was used to determine the differences in transcription patterns between OKT3 in hyperosmotic culture (∼100 mOsm above control) and control culture. The chip contains 22,690 probe sets for over 14,000 known genes and more than 4,000 ESTs. Signals were normalized using the GC‐RMA algorithm and the effectiveness of hyperosmotic stress in altering the expression of each gene was evaluated using one‐way ANOVA. 2,793 probe sets on the chip were differentially expressed with a P < 0.05. Among them, 349 probe sets exhibited a two‐fold or greater change (with 202 up‐regulated and 147 down‐regulated) at one or more time points. Within the 215 characterized, differentially expressed genes, many are involved in metabolism/catabolism (19 induced, 12 repressed), cell‐cycle regulation (10 induced, 5 repressed) and apoptosis (8 induced, 2 repressed), regulation of transcription (18 induced, 13 repressed) and translation (2 induced, 2 repressed), transport and signaling pathways (24 induced, 12 repressed). Surprisingly, there were very few changes within the stress‐response genes. Interestingly, the transcription levels of both the immunoglobulin kappa and lambda light chains showed a significant change in response to hyperosmotic stress, although there is no detectable lambda chain in the immunoglobulin produced in this cell line. Quantitative PCR assays with TaqMan® probes were applied to selected genes to validate the results obtained from microarray analysis. © 2005 Wiley Periodicals, Inc.