Socioeconomic determinants of health, traditional risk factors and cardiovascular outcomes in Australia

Background: Cardiovascular disease burden is decreasing, but these reductions have not been distributed equally amongst socioeconomic groups. Objectives: The aim of this study was to define the relationships between different domains of socioeconomic health, traditional cardiovascular risk factors and cardiovascular events. Methods: This was a cross-sectional study of local government areas (LGAs) in Victoria, Australia. We used data from a population health survey combined with cardiovascular event data derived from hospital and government data. Four socioeconomic domains: educational attainment, financial wellbeing, remoteness, and psychosocial health, were generated from 22 variables. The primary outcome was a composite of non-STEMI, STEMI, heart failure and cardiovascular deaths per 10,000 persons. Linear regression and cluster analysis were used to assess the relationships between risk factors and events. Results: Across 79 LGAs there were 33,654 interviews conducted. All socioeconomic domains were associated with burden of traditional risk factors, including hypertension, smoking, poor diet, diabetes, and obesity. Financial wellbeing, educational attainment and remoteness were all correlated with cardiovascular events on univariate analysis. After multivariate adjustment for age and sex, financial wellbeing, psychosocial wellbeing, and remoteness were associated with cardiovascular events, while educational attainment was not. After including traditional risk factors only financial wellbeing and remoteness remained correlated with cardiovascular events. Conclusions: Financial wellbeing and remoteness independently be associated with cardiovascular events, while educational attainment and psychosocial wellbeing are attenuated by traditional cardiovascular risk factors. Poor socioeconomic health is clustered in certain areas, which have high cardiovascular event rates

Does addition of a diagnostic contrast-enhanced CT to a contemporaneous PET/CT provide incremental value in patients for restaging of colorectal carcinoma?

Abstract Background Both constrast-enhanced computed tomography (ceCT) and 18F-Fluorodeoxyglucose positron emission tomography (PET) are widely used for evaluation of colorectal cancer. Not infrequently patients undergo both tests, increasing cost and radiation burden. Whether this combination provides useful incremental diagnostic information remains unclear. Our purpose was to determine whether the addition of ceCT to PET/CT results in an appropriate change in the N or M stage in patients with colorectal cancer. Methods This was a single centre, retrospective study in a tertiary referral hospital. Over 9 months, 74 consecutive patients with colorectal carcinoma were referred for PET with a recent ceCT scan and adequate follow-up were analysed. The N and M stage of each modality was compared. Management was determined according to institutional guidelines with incremental impact of ceCT results on management categorised as appropriate, inappropriate or unchanged, based on pathological results, clinical or imaging follow-up of discrepant findings. Results Of 74 patients, PET/CT and ceCT N and M stages were concordant in 56 patients (76%) but PET/CT and ceCT identified additional abnormalities in 9 cases each respectively. Of the 18 discordant cases, accepting the ceCT result would have appropriately changed management in only 2 patients and inappropriately in 1 with most management plans unchanged. When comparing PET/CT and ceCT, kappa agreement (95% confidence interval) for N and M stage was 0.58 (0.20–0.95) and 0.60(0.41–0.79) respectively reflecting moderate agreement. Conclusions Whole-body ceCT probably has limited management impact in colorectal cancer patients who are also undergoing PET/CT and therefore may possibly be omitted from routine use. Targeted regional MRI or ceCT should, however, be considered based on clinical suspicion or when high-resolution anatomical information is required for treatment planning

LPS structure of meningococcal strain H44/76.

<p>(A) The genes disrupted in this study are indicated and this resulted in truncated glycoforms of different lengths. Disruption of <i>lpxL1</i> prevented the addition of the final acyl chain which is indicated by the dotted line. Key: Gal – galactose, GlcNAc – N-acetyl glucosamine, Glc – glucose, Hep – heptose, PEtn – phosphoethanolamine, NeuNAc – <i>N</i>-acetyl neuraminic acid, KDO – 2-keto-3-deoxyoctulosonic acid. (B) LPS profiles of H44/76 mutants obtained by electrophoresis using 16.5% acrylamide Tris-Tricine gels and silver staining. LPS from cell lysates from strains (1) H44/76-IcsB, (3) H44/76-LgtE and (5) H44/76-LgtB migrate slightly slower than LPS from OMVs of strains (2) H44/76-IcsB-LpxL1, (4) H44/76-LgtE-LpxL1 (6) H44/76-LgtB-LpxL1, as the latter each lack an acyl chain. LPS from strain H44/76 (7) was run for comparison.</p

ELISA against (A) rPorA P1.7-2,4 and (B) BZ198 OMVs.

<p>Mouse groups 1-5 received 5 µg rPorA P1.7-2,4 adjuvanted with the following: 1) no adjuvant, 2) Alhydrogel, 3) H44/76-LgtB-LpxL1 nOMV, 4) H44/76-LgtE-LpxL1 nOMV, 5) H44/76-IcsB-LpxL1 nOMV. Groups 6-9 did not contain any rPorA and were immunized with the following nOMVs: 6) H44/76-LgtB-LpxL1, 7) H44/76-LgtE-LpxL1, 8) H44/76-IcsB-LpxL1. Group 9 received Alhydrogel alone. Mice were immunized twice at 4 and 8 weeks and serum samples were taken 2 weeks after the last injection. Each symbol represents an individual animal; the horizontal bar represents the mean of the group. Statistical differences observed between groups containing rPorA are noted on the graphs (*: p<0.05). Statistical differences between rPorA-immunized groups of mice and control groups (nOMVs only or no antigen) are not shown.</p

Bactericidal titres of pooled murine sera obtained after immunisation with rPorA P1.7-2,4 adjuvated with Alhydrogel or various nOMVs.

<p>Bactericidal titres of pooled murine sera obtained after immunisation with rPorA P1.7-2,4 adjuvated with Alhydrogel or various nOMVs.</p

Characterization of recombinant rPorA protein.

<p>(A) rPorA protein was purified on a metal chelate affinity column, the SDS-PAGE patterns of elution fractions 1 to 7 are shown. M indicates the molecular weight marker. (B) Circular dichroism spectrum indicating correctly folded rPorA P1.7-2,4.</p

Immunization schedules.

<p>Immunization schedules.</p

Genotype of strains used and constructed.

<p>Genotype of strains used and constructed.</p

Schematic representation of the construction strategy showing PCR products and plasmid construction.

<p>Separate amplification of the 5′ and 3′ ends of the MC58 <i>lpxL1</i> gene, introduction of a novel <i>XmaI</i> restriction enzyme site by fusion PCR, and introduction of the <i>tetR</i> resistance gene to disrupt lpxL1 with cloning of the resulting <i>ΔlpxL1</i> into pCR2 plasmid, which was then used for <i>N. meningitidis</i> strain transformation. The numbers indicate the size of the fragments in Kbp.</p