Samples were shipped to the laboratory in randomly ordered boxes, with no identifiers other than a barcode

Samples were shipped to the laboratory in randomly ordered boxes, with no identifiers other than a barcode. were used for these analyses. A cardiovascular death was defined as a death where the underlying cause of death belonged to codes I10CI79 inclusive and a cancer death to codes C00CC97. The cardiovascular codes were selected to reflect postulated CMV pathogenetic mechanisms and included causes of death such as hypertensive heart disease, atherosclerosis including coronary and cerebrovascular disease, heart failure, aortic aneurysms, and thrombosis [22]. CMV Measurements CMV-specific IgG measurements were performed on sera from 13 090 participants, by the Cambridge University Hospitals Virology Laboratory, using an indirect chemiluminescence immunoassay (Liaison, Diasorin, Saluggia, Italy). The amount of isoluminol-antibody conjugate is usually measured by a photomultiplier as relative light units (RLUs). The machine, using an internal algorithm, converts RLUs to antibody levels. The coefficient of variation for the assay is usually 8%, specificity 99.65%, sensitivity 99.88%, and repeatability 98%. The assay compares favorably to other CMV IgG assays for confirmation of past CMV infections [23]. Samples were shipped to the laboratory in randomly ordered boxes, with no identifiers other than a barcode. A Epifriedelanol sample was defined as Epifriedelanol being unfavorable, equivocal, or positive for CMV IgG antibody using the clinical antibody cutoffs of the assay ( 0.4 IU/mL, 0.4C0.6 IU/mL, and 0.6 IU/mL, respectively). Ninety-one participants had equivocal test results and were excluded. Because of low variable missingness ( 5% for all those variables), no other exclusions were applied and models were performed on the maximum number possible. Results from 7113 women and 5886 men were available for analysis. Statistical Analyses RLUs were standardized by calculating the difference from the mean and dividing by the standard deviation within the day of measurement, to account for any differences in assay performance from day to day. Standardized RLUs among participants with positive assessments only were grouped into thirds of the distribution. We summarized baseline characteristics within the cohort using means and standard deviations for continuous variables with an approximately symmetric distribution, medians and interquartile ranges for continuous variables with a skewed distribution (Townsend deprivation index, alcohol consumption, fibrinogen, ferritin, plasma glucose, cholesterol, low-density lipoprotein, high-density lipoprotein, triglycerides), and percentages for binary variables. Among participants with positive assessments, a value for linear trend in the baseline characteristic across thirds of the distribution was calculated using linear regression (continuous variables) or logistic regression (binary variables), adjusted for age and sex. Continuous variables with skewed distributions were log transformed. Comparable methods were used to test the difference between participants with positive and negative assessments. We used Cox proportional hazards regression models to estimate age- and sex-adjusted mortality rates (using the age/sex distribution of our dataset as the standard population) and hazard ratios of death, comparing seropositive vs seronegative individuals, and also comparing thirds of RLU values, with seronegative individuals as the reference group. We also estimated the effect of each exposure on cardiovascular death, cancer-related death, and noncancer, noncardiovascular-related death, separately. The assumption of proportional hazards was tested by plotting and inspecting the relevant Kaplan-Meier survival curves. Within the Cox model we tested for interactions between the exposure of interest (either seropositive vs seronegative or thirds of RLU values) and sex, age at time of entry to the study (continuous), socioeconomic status (manual vs nonmanual employment), physical activity, body mass index (BMI; continuous), and inflammatory markers (ferritin, fibrinogen, and CRP, all continuous). We fit multivariable models adjusting for various potential confounders. We did not assume any mediation effects. Covariates were chosen as possible confounders (age, sex, Townsend deprivation index, smoking, educational level, physical activity, social class, BMI, waist-to-hip ratio [WHR], total cholesterol, CRP) based on a priori hypotheses only. We additionally performed all of the above analyses (1) including the 91 participants with the equivocal results initially in the seronegative and subsequently in the seropositive group (lower Epifriedelanol antibody category), and (2) excluding all seronegative people and repeating all of Mst1 the analyses inside the seropositive group just, using the low antibody group as the baseline. All statistical analyses had been performed using Stata/SE 12.0 (StataCorp, University Station, Tx). RESULTS A complete of 59% from the individuals had been seropositive for CMV, with seropositivity becoming slightly more prevalent in ladies (60%) in comparison to males (57%, 2 .001) with older age groups. Higher CMV IgG antibody amounts among seropositive individuals were.