A standardised sampling protocol for robust assessment of reach-scale fish community diversity in wadeable New Zealand streams

The New Zealand fish fauna contains species that are affected not only by river system connectivity, but also by catchment and local-scale changes in landcover, water quality and habitat quality. Consequently, native fish have potential as multi-scale bioindicators of human pressure on stream ecosystems, yet no standardised, repeatable and scientifically defensible methods currently exist for effectively quantifying their abundance or diversity in New Zealand stream reaches. Here we report on the testing of a back-pack electrofishing method, modified from that used by the United States Environmental Protection Agency, on a wide variety of wadeable stream reaches throughout New Zealand. Seventy-three first- to third-order stream reaches were fished with a single pass over 150-345 m length. Time taken to sample a reach using single-pass electrofishing ranged from 1-8 h. Species accumulation curves indicated that, irrespective of location, continuous sampling of 150 stream metres is required to accurately describe reach-scale fish species richness using this approach. Additional species detection beyond 150 m was rare (<10%) with a single additional species detected at only two out of the 17 reaches sampled beyond this distance. A positive relationship was also evident between species detection and area fished, although stream length rather than area appeared to be the better predictor. The method tested provides a standardised and repeatable approach for regional and/or national reporting on the state of New Zealand's freshwater fish communities and trends in richness and abundance over time

Elevated hemostasis markers after pneumonia increases one-year risk of all-cause and cardiovascular deaths

Background: Acceleration of chronic diseases, particularly cardiovascular disease, may increase long-term mortality after community-acquired pneumonia (CAP), but underlying mechanisms are unknown. Persistence of the prothrombotic state that occurs during an acute infection may increase risk of subsequent atherothrombosis in patients with pre-existing cardiovascular disease and increase subsequent risk of death. We hypothesized that circulating hemostasis markers activated during CAP persist at hospital discharge, when patients appear to have recovered clinically, and are associated with higher mortality, particularly due to cardiovascular causes. Methods: In a cohort of survivors of CAP hospitalization from 28 US sites, we measured D-Dimer, thrombin-antithrombin complexes [TAT], Factor IX, antithrombin, and plasminogen activator inhibitor-1 at hospital discharge, and determined 1-year all-cause and cardiovascular mortality. Results: Of 893 subjects, most did not have severe pneumonia (70.6% never developed severe sepsis) and only 13.4% required intensive care unit admission. At discharge, 88.4% of subjects had normal vital signs and appeared to have clinically recovered. D-dimer and TAT levels were elevated at discharge in 78.8% and 30.1% of all subjects, and in 51.3% and 25.3% of those without severe sepsis. Higher D-dimer and TAT levels were associated with higher risk of all-cause mortality (range of hazard ratios were 1.66-1.17, p = 0.0001 and 1.46-1.04, p = 0.001 after adjusting for demographics and comorbid illnesses) and cardiovascular mortality (p = 0.009 and 0.003 in competing risk analyses). Conclusions: Elevations of TAT and D-dimer levels are common at hospital discharge in patients who appeared to have recovered clinically from pneumonia and are associated with higher risk of subsequent deaths, particularly due to cardiovascular disease. © 2011 Yende et al

Trajectory of vitamin D status during pregnancy in relation to neonatal birth size and fetal survival: a prospective cohort study

Background: We investigated the associations between vitamin D status in early and late pregnancy with neonatal small for gestational age (SGA), low birth weight (LBW) and preterm delivery. Furthermore, associations between vitamin D status and pregnancy loss were studied. Methods: Serum 25-hydroxyvitamin D (25OHD) was sampled in gestational week ≤ 16 (trimester 1 (T1), N = 2046) and > 31 (trimester 3 (T3), N = 1816) and analysed using liquid chromatography tandem mass spectrometry. Pregnant women were recruited at antenatal clinics in south-west Sweden at latitude 57–58°N. Gestational and neonatal data were retrieved from medical records. Multiple gestations and terminated pregnancies were excluded from the analyses. SGA was defined as weight and/or length at birth < 2 SD of the population mean and LBW as < 2500 g. Preterm delivery was defined as delivery < 37 + 0 gestational weeks and pregnancy loss as spontaneous abortion or intrauterine fetal death. Associations between neonatal outcomes and 25OHD at T1, T3 and change in 25OHD (T3-T1) were studied using logistic regression. Results: T1 25OHD was negatively associated with pregnancy loss and 1 nmol/L increase in 25OHD was associated with 1% lower odds of pregnancy loss (OR 0.99, p = 0.046). T3 25OHD ≥ 100 nmol/L (equal to 40 ng/ml) was associated with lower odds of SGA (OR 0.3, p = 0.031) and LBW (OR 0.2, p = 0.046), compared to vitamin D deficiency (25OHD < 30 nmol/L, or 12 ng/ml). Women with a ≥ 30 nmol/L increment in 25OHD from T1 to T3 had the lowest odds of SGA, LBW and preterm delivery. Conclusions: Vitamin D deficiency in late pregnancy was associated with higher odds of SGA and LBW. Lower 25OHD in early pregnancy was only associated with pregnancy loss. Vitamin D status trajectory from early to late pregnancy was inversely associated with SGA, LBW and preterm delivery with the lowest odds among women with the highest increment in 25OHD. Thus, both higher vitamin D status in late pregnancy and gestational vitamin D status trajectory can be suspected to play a role in healthy pregnancy

Effect of Global Cardiac Ischemia on Human Ventricular Fibrillation: Insights from a Multi-scale Mechanistic Model of the Human Heart

Acute regional ischemia in the heart can lead to cardiac arrhythmias such as ventricular fibrillation (VF), which in turn compromise cardiac output and result in secondary global cardiac ischemia. The secondary ischemia may influence the underlying arrhythmia mechanism. A recent clinical study documents the effect of global cardiac ischaemia on the mechanisms of VF. During 150 seconds of global ischemia the dominant frequency of activation decreased, while after reperfusion it increased rapidly. At the same time the complexity of epicardial excitation, measured as the number of epicardical phase singularity points, remained approximately constant during ischemia. Here we perform numerical studies based on these clinical data and propose explanations for the observed dynamics of the period and complexity of activation patterns. In particular, we study the effects on ischemia in pseudo-1D and 2D cardiac tissue models as well as in an anatomically accurate model of human heart ventricles. We demonstrate that the fall of dominant frequency in VF during secondary ischemia can be explained by an increase in extracellular potassium, while the increase during reperfusion is consistent with washout of potassium and continued activation of the ATP-dependent potassium channels. We also suggest that memory effects are responsible for the observed complexity dynamics. In addition, we present unpublished clinical results of individual patient recordings and propose a way of estimating extracellular potassium and activation of ATP-dependent potassium channels from these measurements

Routes for breaching and protecting genetic privacy

We are entering the era of ubiquitous genetic information for research, clinical care, and personal curiosity. Sharing these datasets is vital for rapid progress in understanding the genetic basis of human diseases. However, one growing concern is the ability to protect the genetic privacy of the data originators. Here, we technically map threats to genetic privacy and discuss potential mitigation strategies for privacy-preserving dissemination of genetic data.Comment: Draft for comment

Discussing prognosis and end-of-life care in the final year of life: A randomized controlled trial of a nurse-led ommunication support programme for patients and caregivers

Introduction: Timely communication about lifeexpectancy and end-of-life care is crucial forensuring good patient quality-of-life at the end of lifeand a good quality of death. This article describes theprotocol for a multisite randomised controlled trial of anurse-led communication support programme tofacilitate patients' and caregivers' efforts tocommunicate about these issues with theirhealthcare team.Methods and analysis: This NHMRC-sponsored trialis being conducted at medical oncology clinics locatedat/affiliated with major teaching hospitals in Sydney,Australia. Patients with advanced, incurable cancer andlife expectancy of less than 12 months will participatetogether with their primary informal caregiver wherepossible. Guided by the self-determination theory ofhealth-behaviour change, the communication supportprogramme pairs a purpose-designed Question PromptList (QPL-an evidence-based list of questionspatients/caregivers can ask clinicians) with nurse-ledexploration of QPL content, communication challenges,patient values and concerns and the value of earlydiscussion of end-of-life issues. Oncologists are alsocued to endorse patient and caregiver question askingand use of the QPL. Behavioural and self-report datawill be collected from patients/caregivers approximatelyquarterly for up to 2.5 years or until patient death, afterwhich patient medical records will be examined.Analyses will examine the impact of the intervention onpatients' and caregivers' participation in medicalconsultations, their self-efficacy in medical encounters,quality-of-life, end-of-life care receipt and quality-ofdeathindicators.Ethics and dissemination: Approvals have beengranted by the human ethics review committee ofRoyal Prince Alfred Hospital and governance officersat each participating site. Results will be reported inpeer-reviewed publications and conferencepresentations.Trial registration number: Australian New ZealandClinical Trials Registry ACTRN12610000724077

Quantifying Missing Heritability at Known GWAS Loci

Recent work has shown that much of the missing heritability of complex traits can be resolved by estimates of heritability explained by all genotyped SNPs. However, it is currently unknown how much heritability is missing due to poor tagging or additional causal variants at known GWAS loci. Here, we use variance components to quantify the heritability explained by all SNPs at known GWAS loci in nine diseases from WTCCC1 and WTCCC2. After accounting for expectation, we observed all SNPs at known GWAS loci to explain 1.29 X more heritability than GWAS-associated SNPs on average (P = 3.3 X 10[superscript -5]). For some diseases, this increase was individually significant:2.07 X for Multiple Sclerosis (MS) (P = 6.5 X 10 [superscript -9]) and for Crohn's Disease (CD) (P = 1.3 X 10[superscript -3]); all analyses of autoimmune diseases excluded the well-studied MHC region. Additionally, we found that GWAS loci from other related traits also explained significant heritability. The union of all autoimmune disease loci explained 7.15 X more MS heritability than known MS SNPs (P 20,000 Rheumatoid Arthritis (RA) samples typed on ImmunoChip, with 2.37 X more heritability from all SNPs at GWAS loci (P = 2.3 X 10[superscript -6]) and more heritability from all autoimmune disease loci (P < 1 X 10[superscript -16]) compared to known RA SNPs (including those identified in this cohort). Our methods adjust for LD between SNPs, which can bias standard estimates of heritability from SNPs even if all causal variants are typed. By comparing adjusted estimates, we hypothesize that the genome-wide distribution of causal variants is enriched for low-frequency alleles, but that causal variants at known GWAS loci are skewed towards common alleles. These findings have important ramifications for fine-mapping study design and our understanding of complex disease architecture.National Institutes of Health (U.S.) (Grant R03HG006731)National Institutes of Health (U.S.) (Fellowship F32GM106584

Patient perspectives regarding communication about prognosis and end-of-life issues: How can it be optimised?

Objective: To explore patients' perspectives across two cultures (Australia and USA) regarding communication about prognosis and end-of-life care issues and to consider the ways in which these discussions can be optimised. Methods: Fifteen Australian and 11 US patients completed individual semi-structured qualitative interviews. A further 8 US patients participated in a focus group. Interviews and focus group recordings were transcribed verbatim and interpreted using thematic text analysis with an inductive, data-driven approach. Results: Global themes identified included readiness for and outcomes of discussions of prognosis and end-of-life issues. Contributing to readiness were sub themes including patients' adjustment to and acceptance of their condition (together with seven factors promoting this), doctor and patient communication skills, mutual understandings and therapeutic relationship elements. Outcomes included sub themes of achievement of control and ability to move on. A model of the relationships between these factors, emergent cross cultural differences, and how factors may help to optimise these discussions are presented. Conclusion: Identified optimising factors illustrate Australian and US patients' perspectives regarding how prognosis and end-of-life issues can be discussed with minimised negative impact. Practice implications: Recognition of factors promoting adjustment, acceptance and readiness and use of the communication skills and therapeutic relationship elements identified may assist in optimising discussions and help patients plan care, achieve more control of their situation and enjoy an optimal quality-of-life. © 2011 Elsevier Ireland Ltd