May Measurement Month 2018: an analysis of blood pressure screening results from Brazil.

Hypertension is a pathology of high prevalence in the world. In Brazil, it is the main risk factor for the major cause of death in the country, coronary heart disease. The May Measurement Month Campaign in 2018 (MMM18) included a population with representation from all Brazilian states and reflects some of the characteristics of hypertension in Brazil. Questionnaire data were collected and three measures of blood pressure (BP) were performed. The sample consisted of 12 413 individuals, 59.1% were white, 51.3% were women. The average age was 54. ± 16.0 years. Diabetes was present in 11.6%, previous myocardial infarction in 5.9%, and previous stroke in 2.7%. Current smokers were 9.3% and 12.4% were regular drinkers. The average body mass index was 27.3 ± 4.5 kg/m2. After multiple imputations, 67.9% were hypertensive (>140/90 mmHg). Of the individuals who were not taking antihypertensive medication, 27.9% were hypertensive and of those taking antihypertensive medication, 40.3% were uncontrolled. Systolic BP increased with age. The MMM18 campaign demonstrated a large number of unknown hypertensives and a high rate of uncontrolled hypertension in Brazil, unfortunately in keeping with 2017 findings.

IL-6 inhibits apoptosis and retains oxidative DNA lesions in human gastric cancer AGS cells through up-regulation of anti-apoptotic gene mcl-1.

Apoptosis plays a critical role in maintaining genomic integrity by selectively removing the most heavily damaged cells from the population. Reactive oxygen species (ROS) and certain inflammatory cytokines are always elevated during the human carcinogenic process. However, the biological significance of the interplay between ROS and inflammatory cytokine remains elusive. This study demonstrates that interleukin-6 (IL-6) effectively protects gastric cancer cells from the apoptosis induced by hydrogen peroxide (H(2)O(2)). The cell death signaling JNK pathway elicited by H(2)O(2) is also inhibited by IL-6. We further found that Mcl-1, but not other Bcl-2 family members, was up-regulated by IL-6, by a substantial level over 24 h. We further transfected a mcl-1 expression vector, pCMV-mcl-1, into the AGS cells, and successfully obtained several mcl-1-overexpressing clones. Flow cytometric analysis shows that these mcl-1-overexpressing AGS cells are more resistant to the apoptosis induced by H(2)O(2) when compared with the neo control AGS cells. Consistently, the activation of the JNK pathway induced by H(2)O(2) is also blocked in mcl-1-overexpressed cells. These results indicate that the anti-apoptotic effect of IL-6 is, at least in part, due to the up-regulation of mcl-1. To our surprise, either IL-6 exposure or mcl-1 overexpression fails to reduce the level of intracellular peroxides in the AGS cells triggered by H(2)O(2). This study also determined the level of 8-hydroxydeoxyguanosine (8-OH-dGua), an indicator for oxidative DNA lesions in IL-6-treated or mcl-1-overexpressed AGS cells after treatment with H(2)O(2). Notably, our results indicate that a majority of the 8-OH-dGua is efficiently removed in the AGS cells without IL-6 treatment, whereas only approximately 50% of the 8-OH-dGua was repaired in the IL-6-treated AGS cells after 24 h. Similarly, approximately 60-70% of the 8-OH-dGua also failed to repair and was retained in the genomic DNA of the mcl-1 transfectants. Results in this study provide a novel mechanism by which up-regulation of the Mcl-1 protein by IL-6 may enhance the susceptibility to H(2)O(2)-induced oxidative DNA lesions by overriding apoptosis.

A generic model of human lifetime exposure to persistent organic contaminants: development and application to PCB-101.

We have developed a model which successfully reconstructs the lifetime polychlorinated biphenyl (PCB)-101 burden of the UK population for individuals born between 1920 and 1980. It not only follows burdens and clearance of persistent organic contaminants throughout a human lifetime--taking changes in age and body composition into account--but also, importantly, incorporates changing environmental concentrations of the compound of interest. Predicted results agree well with available measured lipid concentrations in human tissues. Its unique construction takes into account both changing environmental concentrations of PCBs in principal food groups and changing dietary habits during the time period. Because environmental burdens of persistent organic contaminants have changed over the last 60 years, residues in food will also have mirrored this change. Critically in this respect, the year in which an individual was born determines the shape and magnitude of their exposure profile for a given compound. Observed trends with age represent an historical legacy of exposure and are not simply a function of equal yearly cumulative inputs. We can demonstrate that the release profile of PCB-101 controls levels in the food supply and ultimately the burden of individuals throughout their life. This effect is expected to be similar for other PCB congeners and persistent organic compounds such as polychlorinated dibenzo-p-dioxins/furans (PCDD/Fs). Models of this type have important applications as predictive tools to estimate the likely impact of source-reduction strategies on human tissue concentrations.

Methods for the analysis of PCBs in human food, faeces and serum.

A method was developed to determine trace concentrations of a range of individual PCB congeners in biological samples (serum, food and faeces) using GC-MS, to prepare a mass balance of PCBs in humans. A simple method for the analysis of PCBs in human serum, which excluded an extraction step, was first employed. Results indicated that the recoveries of 13C12 PCB spikes were variable. A soxhlet extraction step was added and was found to be efficient and reproducible. A quality control routine and method validation results are presented. In batch tests of the methods presented it was found that the serum analysis method gave within batch mean 13C12 spike recoveries of 98-120% and standard deviations between 6 and 20%. The food/faeces analysis method gave within-batch mean 13C12 spike recoveries of 88-100%, and within batch standard deviations between 4 and 12%. The batch to batch mean recovery for serum analysis was 100%, with an RSD of 9% for high spikes and 10% for low spikes. For food/faeces analysis the batch to batch average recovery was 110%, with an RSD of 5% for high spikes and 9% for low spikes.