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The degree to which self-reports of health and functioning reflect negativity (NA), a dispositional tendency to emphasize the negative, was examined with data from a 7-year longitudinal study of adaptation to rheumatoid arthritis. Principal component analyses performed on each of 8 waves of data consistently indicated that the dominant factor in these data was defined by measures of pain and functional impairment. In the final wave, Disease Impact, a scale derived from this component, was directly compared to NA. The 2 scales demonstrated considerable discriminant validity, and most of the significant intercorrelations among Disease Impact and the other variables examined remained statistically significant after the influence of NA was partialed out. These results suggest that reports of pain, impairment, and associated variables reflected disease-related outcomes and processes and not simply NA.
OBJECTIVES - To evaluate the responsiveness of whole blood activated partial thromboplastin time (aPTT) to varying heparin doses in vitro and to examine the ex vivo relationship of whole blood aPTT to plasma heparin concentration.
DESIGN - Prospective, controlled laboratory study.
SETTING - Surgical suites and laboratory at a tertiary center.
PATIENTS - Surgical patients and volunteers at a tertiary center were eligible for inclusion in this study. In vitro evaluation was performed using specimens obtained from each of five, healthy volunteers. Ex vivo evaluation was performed using specimens obtained from 30 cardiac surgical patients before and after systemic administration of heparin for extracorporeal circulation.
INTERVENTIONS - Blood specimens were obtained from volunteers and added to syringes containing varying amounts of unfractionated porcine heparin for in vitro evaluation. For ex vivo evaluation, blood specimens were obtained from patients before and after systemic administration of 20 U/kg of heparin.
MEASUREMENTS AND MAIN RESULTS - For the in vitro evaluation, specimens were divided into two aliquots after mixing with varying amounts of unfractionated porcine heparin. One aliquot was used to measure whole blood aPTT using a whole blood coagulation monitor immediately after blood collection and 3 mins later, and a second aliquot was used to determine plasma aPTT with a conventional, laboratory-based assay. Linear regression analysis demonstrated a high correlation (r = .94; r2 = .88) between aPTT assay systems and bias analysis demonstrated a mean aPTT measurement difference of 1.6 secs with +/- 2 SD limits of -15 to +18.2 secs. As indicated by comparable regression slopes, the in vitro aPTT responsiveness to increasing heparin concentration was similar with the two assay systems among individual subjects. Whole blood aPTT measurements after 3 mins of blood specimen storage were similar to immediate measurements. For ex vivo evaluation, blood specimens obtained from patients before and after systemic administration of heparin were divided into two aliquots. One aliquot was used to measure whole blood aPTT in duplicate and a second aliquot was used to measure plasma heparin concentration with an antifactor X active chromogenic assay. A high correlation (r = .89; r2 = .79) between whole blood aPTT and plasma heparin concentration was observed.
CONCLUSIONS - Heparin responsiveness of whole blood aPTT, measured with a portable whole blood coagulation monitor, is similar to that of conventional laboratory aPTT over a clinically relevant range of heparin concentrations in vitro and ex vivo. On-site whole blood aPTT measurements should be useful in clinical situations requiring rapid aPTT results.
As part of a study of patient-centered care outcomes that requires the ability to be interviewed by telephone after hospitalization, 4,600 adult patients on 118 medical-surgical units in 17 midwestern hospitals selected by stratified random sampling were identified as potential subjects. This article describes response-rate differences and reasons for nonparticipation by gender, age, ethnicity, and race. Issues related to understanding and reporting response rates, reducing losses due to ineligibility, dealing with refusals, and tailoring survey approaches to special populations are discussed.
Evidence is presented for the utilization of a shortened version of the Arthritis Impact Measurement Scales. The results confirmed that the shortened versions retained adequate internal consistencies, test-retest reliabilities, and both concurrent and predictive validities over a 2 year period which were similar to the original longer versions.
The analysis and interpretation of the data collected in SUPPORT provide great potential for understanding the relationships among treatment choices, patient and physician values and preferences, perceptions about the risks and benefits of treatments, institutional characteristics, and outcomes (as measured by quality of life, survival, and satisfaction). The complicated analyses required to elucidate these relationships will pose many technical challenges in dealing with longitudinal observational data collected from seriously ill patients at multiple sites. Major challenges include the handling of incomplete data, proper parameterization of treatment effects, strategies to avoid various potential biases, validating predictive models, and constructing endpoints that combine survival with quality of life. Within the structure of the SUPPORT study, mechanisms have been established to guide the analyses and to ensure their quality and validity.
To assess the use of Doppler echocardiographic screening for abnormal pulmonary vasoreactivity, we measured pulmonary artery pressure in 10 adult patients and 11 normal subjects while recording Doppler right ventricular outflow acceleration time, pre-ejection period, and ejection time. In the normal subjects we also measured the changes in each parameter after 10 minutes of hypoxic breathing (FIO2 = 0.12). Mean pulmonary artery pressure increased by 39% during hypoxia (13 +/- 4.3 to 18 +/- 5.4 mm Hg). In the patients and normal subjects at rest, mean pulmonary artery-pressure correlated well with acceleration time (r = -0.84; standard error of the estimate, 6.6 mm Hg; p = 0.0001). Over the narrow range of mean pulmonary artery pressure in normal subjects at rest, mean pulmonary artery pressure did not correlate well with acceleration time, acceleration time/pre-ejection period, or acceleration time/right ventricular ejection time. However, changes in mean pulmonary artery pressure induced by hypoxic breathing did correlate with changes in acceleration time/right ventricular ejection time (r = 0.73; standard error of the estimate, 2.3 mm Hg; p = 0.01). Doppler ultrasound may offer a noninvasive means for detecting abnormal pulmonary vasoreactivity in asymptomatic individuals at risk for developing pulmonary hypertension.
PURPOSE - To determine which clinical characteristics obtained by a physician during an initial clinical examination are important for estimating the likelihood of severe coronary artery disease, and to determine whether estimates based on these characteristics remain valid when applied prospectively and in different patient groups.
PATIENTS AND METHODS - We examined clinical characteristics predictive of severe disease in 6,435 consecutive symptomatic patients referred for suspected coronary artery disease between 1969 and 1983.
RESULTS - Eleven of 23 characteristics were important for estimating the likelihood of severe coronary artery disease. A model using these characteristics accurately estimated the likelihood of severe disease in an independent sample of 2,342 patients referred since 1983. The model also accurately estimated the prevalence of severe disease in large series of patients reported in the literature.
CONCLUSIONS - These findings suggest that the clinician's initial evaluation can identify patients at high or low risk of anatomically severe coronary artery disease. Cost-conscious quality care is encouraged by identifying patients at higher risk for severe coronary artery disease who are most likely to benefit from further evaluation.
Selected factors have been evaluated in order to determine their influences on the plasma lipoprotein proton NMR spectra of normal and cancer patients. The variables were donor's diet (fasting/non-fasting), temperature and time of sample storage, processing procedure, centrifugation speed, and water pre-saturation time. Plasma samples from fasting individuals that were placed immediately on ice, spun at 1,000 and 3,000 g for 15 minutes, and the proton NMR spectrum acquired with the Carr-Purcell Meiboom-Gill (CPMG) pulse sequence, using a two-second water pre-saturation time, consistently gave reproducible results. Resonances attributed to lactate were minimized under these processing conditions. Centrifugation speed and pre-saturation time did not affect the average line width; however, donor fasting state, processing temperature, and storage time did alter the line width. Most important, blood chemistry analysis revealed an inverse correlation between triglyceride levels and average methyl and methylene line widths. Thus, these factors alone caution against the indiscriminate use of proton NMR spectra to differentiate plasma from normal and cancer patients.
Proteolysis of elastic fibers is central to the development of emphysema, and a simple, noninvasive assay of elastin degradation would be useful in diagnosis and in therapeutic monitoring. We have adapted an indirect enzyme-linked immunosorbent assay (ELISA) to determine plasma, urine, and bronchoalveolar lavage fluid (BALF) elastin peptide concentrations in nonsmokers, healthy smokers, and patients with chronic obstructive pulmonary disease (COPD). Plasma elastin peptide concentrations were significantly higher in subjects with COPD (66.8 +/- 5.8 ng/ml, n = 10) compared with nonsmokers (23.4 +/- 4.6 ng/ml, n = 12), and healthy smokers had intermediate values (36.0 +/- 6.8, n = 6), p less than 0.05. Urine values (both unadjusted and normalized to urine creatinine concentration) were approximately 10-fold higher than plasma in all subject groups, and the relative differences among groups were the same as for plasma with values of 910.8 +/- 105.6, 358.1 +/- 101.2, and 281.0 +/- 67.8 ng/ml for subjects with COPD (n = 10), healthy smokers (n = 6), and healthy nonsmokers (n = 12), respectively. Poor recovery of BALF in COPD subjects reduced differences in the BALF elastin peptide concentrations among subjects groups, although the healthy smokers and COPD subjects tended to have higher amounts. Assuming some dilution due to lavage technique, elastin peptide concentrations were estimated to be substantially higher in epithelial lining fluid than in plasma, suggesting lung as a significant source of elastin peptides in COPD. This is the first application of elastin peptide measurement to human urine or BALF, and we conclude that this assay in urine is useful in characterizing elastin turnover in patients with or at risk for emphysema.
Two colour flow cytometry was used to analyse in situ cytokine expression by human monocytes. Whole blood was cultured in siliconised glass bottles, with or without E. coli lipopolysaccharide (LPS), for various times, and the mononuclear cells (MNCs) then exposed to a variety of permeabilisation procedures prior to flow cytometric analysis. Paraformaldehyde (PF)/saponin fixation preserved cellular morphology, and caused a reproducible degree of permeabilisation (estimated by propidium iodide inclusion: mean 94%, range 86-99% (n = 33)). After fixation with 4% PF and permeabilisation with 1% saponin at 0 degrees C in PBS containing 20% human serum, MNCs were incubated with phycoerythrin(PE)-conjugated mouse anti-CD14 (monocyte phenotype) and polyclonal rabbit anti-human interleukin-1 alpha (IL-1 alpha), IL-1 beta, tumour necrosis factor alpha (TNF-alpha), or control rabbit IgG. Binding of rabbit antibodies was detected using goat anti-rabbit IgG fluorescein isothiocyanate (FITC). FITC fluorescence was increased in CD14 PE positive cells with the three anti-cytokine antibodies following LPS stimulation, compared with controls. There was a reproducible dose related response in monocyte IL-1 beta and TNF-alpha expression following LPS stimulation, with early peaks in TNF-alpha (2 h), compared with IL-1 beta (4 h), and IL-1 alpha (12 h). Specificity of this cytokine detection system was confirmed by inhibition studies using the corresponding recombinant human cytokines, by an absence of staining in CD14 negative or unpermeabilised MNCs, and by the characteristic cytoplasmic localisation of the different cytokines visualised with UV immunochemistry. Hence, the methods described here provide a reproducible, semiquantitative and specific assay for the detection of cell associated monokines. The technique may be applicable to the analysis of a variety of different cytokines in other phenotypically defined cell populations.