Should capillary blood glucose measurements be used in population surveys?

Objective
To determine the accuracy and appropriateness of capillary blood glucose testing in population surveys.
Materials and methods
Capillary blood glucose using the Rochec ACCU-CHEK instrument and Advantage 11 Test Strips was compared to a laboratory instrument. Three independent cross-sectional risk factor surveys (n=1432) and baseline individuals from the Greater Green Triangle Diabetes Prevention Project (n=341) provided both fasting plasma and capillary blood glucose measurements. Accuracy of capillary glucoses was assessed using the ISO 15197 standard. The median age of the participants was 71years, ranging from 25 to 84years. There were 799 males and 974 females.
Results
Capillary glucose method had poorer precision at lower concentrations (CV: 9.50%, mean=3.09mmol/L, CV: 4.90%, mean=16.78mmol/L, n=233 replicates). Individual discrepancies were seen across the measuring range (2.8–19.9mmol/L, n=1773). In total, 94.5% of results fell within the minimum acceptable accuracy standards. This was slightly short of the 95% of results required to meet the ISO 15197 standard. The prevalence of diabetes in the study population using glucose 7.0mmol/L was 2.4% (95%CI 1.8–3.3%) according to fasting plasma glucose and 2.8% (2.1–3.8%) according to fasting capillary glucose. The lower WHO-defined cut-off of 6.1mmol/L for capillary blood glucose testing gave a prevalence of 10.7% (9.0–12.5%).
Conclusions
This study of matched capillary and plasma glucose results concludes that while it is appropriate to use fasting capillary glucose levels to determine the prevalence of diabetes in populations, it should not be used to reliably diagnose diabetes in individuals.

Antihypertensive treatments obscure familial contributions to blood pressure variation

The linkage and association between inherent blood pressure and underlying genotype is potentially confounded by antihypertensive treatment. We estimated blood pressure variance components (genetic, shared environmental, individual-specific) in 767 adult volunteer families by using a variety of approaches to adjusting blood pressure of the 244 subjects (8.2%) receiving antihypertensive medications. The additive genetic component of variance for systolic pressure was 73.9 mm Hg(2) (SE, 8.8) when measured pressures (adjusted for age by gender within each generation) were used but fell to 61.4 mm Hg(2) (SE, 8.0) when treated subjects were excluded. When the relevant 95th percentile values were substituted for treated systolic pressures, the additive genetic component was 81.9 mm Hg(2) (SE, 9.5), but individual adjustments in systolic pressure ranged from -53.5 mm Hg to +64.5 mm Hg (mean, +17.2 mm Hg). Instead, when 10 mm Hg was added to treated systolic pressure, the additive genetic component rose to 86.6 mm Hg(2) (SE, 10.1). Similar changes were seen in the shared environment component of variance for systolic pressure and for the combined genetic and shared environmental (ie, familial) components of diastolic pressure. There was little change in the individual-specific variance component across any of the methods. Therefore, treated subjects contribute important information to the familial components of blood pressure variance. This information is lost if treated subjects are excluded and obscured by treatment effects if unadjusted measured pressures are used. Adding back an appropriate increment of pressure restores familial components, more closely reflects the pretreatment values, and should increase the power of genomic linkage and linkage disequilibrium analyses.

Bivariate variance-component analysis, with application to systolic blood pressure and total cholesterol levels in the Framingham Heart Study

Background :
The correlations between systolic blood pressure (SBP) and total cholesterol levels (CHOL) might result from genetic or environmental factors that determine variation in the phenotypes and are shared by family members. Based on 330 nuclear families in the Framingham Heart Study, we used a multivariate normal model, implemented in the software FISHER, to estimate genetic and shared environmental components of variation and genetic and shared environmental correlation between the phenotypes. The natural logarithm of the phenotypes measured at the last visit in both Cohort 1 and 2 was used in the analyses. The antihypertensive treatment effect was corrected before adjustment of the systolic blood pressure for age, sex, and cohort.
Results :
The univariate correlation coefficient was statistically significant for sibling pairs and parent-offspring pairs, but not significant for spouse pairs. In the bivariate analysis, the cross-trait correlation coefficients were not statistically significant for all relative pairs. The shared environmental correlation was statistically significant, but the genetic correlation was not significant.
Conclusion :
There is no significant evidence for a close genetic correlation between systolic blood pressure and total cholesterol levels. However, some shared environmental factors may determine the variation of both phenotypes.

Familial and genomic analyses of postural changes in systolic and diastolic blood pressure

The physiological adaptation to the erect posture involves integrated neural and cardiovascular responses that might be determined by genetic factors. We examined the familial- and individual-specific components of variance for postural changes in systolic and diastolic blood pressure in 767 volunteer nuclear adult families from the Victorian Family Heart Study. In 274 adult sibling pairs, we made a genome-wide scan using 400 markers for quantitative trait loci linked with the postural changes in systolic and diastolic pressures. Overall, systolic pressure did not change on standing, but there was considerable variation in this phenotype (SD=8.1 mm Hg). Familial analyses revealed that 25% of the variance of change in systolic pressure was attributable to genetic factors. In contrast, diastolic pressure increased by 6.3 mm Hg (SD=7.0 mm Hg) on standing and there was no evidence of contributory genetic factors. Multipoint quantitative genome linkage mapping suggested evidence (Z=3.2) of linkage of the postural change in systolic pressure to chromosome 12 but found no genome-wide evidence of linkage for the change in diastolic pressure. These findings suggest that genetic factors determine whether systolic pressure decreases or increases when one stands, possibly as the result of unidentified alleles on chromosome 12. The genetics of postural changes in systolic blood pressure might reflect the general buffering function of the baroreflex; thereby, the predisposition to sudden decreases or increases in systolic pressure might cause postural hypotension or vessel wall disruption, respectively.

Safer injections, fewer infections : management of needles and sharps and occupational blood exposure in rural north Indian health settings

This study investigated injection practices and occupational exposure to blood in rural north Indian health settings. The findings highlighted a range of practices potentially contributing to the transmission of hepatitis and HIV to both patients and staff in these settings. Interventions need to focus on the development of organisational structures to support and facilitate safer practices.

Was there much blood kid? : cadet journalists in Australian media

This thesis established the ways in which novice journalists formulate their own professional ideologies and identified the key influences in this process. The research focused on the dominant oral traditions operating within newsrooms and established the fundamental strengths and weaknesses of the current systems of training young journalists.

Nitric oxide control of lower vertebrate blood vessels

The gas, nitric oxide, plays a critical role in the control of the cardiovascular system of animals, and in particular blood pressure. This thesis demonstrated unique mechanisms by which nitric oxide regulates the blood vessels of various animals, which will alter our understanding of vascular regulation by peripheral nerves.

The natriuretic peptide system of the heart and central blood vessels of the toad, Bufo marinus

This research has established the presence of a natriuretic peptide system in the cardiovascular system of the toad, Bufo marinus. The presence of atrial natriuretic peptide mRNA and the peptide itself were shown in the heart which does not contain natriuretic peptide receptors in contrast to the large arteries and veins. In arteries these receptors mediated vasodilation. Atrial natriuretic peptide released from the heart may act on large arteries to regulate blood flow, but the action does not target the heart.

A new rodent model to assess blood stage immunity to the plasmodium falciparum antigen merozoite surface protein 119 reveals a protective role for invasion inhibitory antibodies

Antibodies capable of inhibiting the invasion of Plasmodium merozoites into erythrocytes are present in individuals that are clinically immune to the malaria parasite. Those targeting the 19-kD COOH-terminal domain of the major merozoite surface protein (MSP)-119 are a major component of this inhibitory activity. However, it has been difficult to assess the overall relevance of such antibodies to antiparasite immunity. Here we use an allelic replacement approach to generate a rodent malaria parasite (Plasmodium berghei) that expresses a human malaria (Plasmodium falciparum) form of MSP-119. We show that mice made semi-immune to this parasite line generate high levels of merozoite inhibitory antibodies that are specific for P. falciparum MSP-119. Importantly, protection from homologous blood stage challenge in these mice correlated with levels of P. falciparum MSP-119–specific inhibitory antibodies, but not with titres of total MSP-119–specific immunoglobulins. We conclude that merozoite inhibitory antibodies generated in response to infection can play a significant role in suppressing parasitemia in vivo. This study provides a strong impetus for the development of blood stage vaccines designed to generate invasion inhibitory antibodies and offers a new animal model to trial P. falciparum MSP-119 vaccines.