Influence of root and leaf traits on the uptake of nutrients in cover crops

Aims: Cover crops play an important role in soil fertility as they can accumulate large amounts of nutrients. This study aimed at understanding the nutrient uptake capacity of a wide range of cover crops and at assessing the relevance of acquisition strategies. Methods: A field experiment was conducted to characterize 20 species in terms of leaf and root traits. Plant traits were related to nutrient concentration and shoot biomass production with a redundancy analysis. Acquisition strategies were identified using a cluster analysis. Results: Root systems varied greatly among cover crop species. Five nutrient acquisition strategies were delineated. Significant amounts of nutrients (about 120 kg ha−1 of nitrogen, 30 kg ha−1 of phosphorus and 190 kg ha−1 of potassium) were accumulated by the species in a short period. Nutrient acquisition strategies related to high accumulations of nutrients consisted in either high shoot biomass and root mass and dense tissues, or high nutrient concentrations and root length densities. Species with high root length densities showed lower C/N ratios. Conclusions: The same amounts of nutrients were accumulated by groups with different acquisition strategies. However, their nutrient concentrations offer different perspectives in terms of nutrient release for the subsequent crop and nutrient cycling improvement

The M235T Polymorphism in the AGT Gene and CHD Risk: Evidence of a Hardy-Weinberg Equilibrium Violation and Publication Bias in a Meta-Analysis

BACKGROUND: The M235T polymorphism in the AGT gene has been related to an increased risk of hypertension. This finding may also suggest an increased risk of coronary heart disease (CHD). METHODOLOGY/PRINCIPAL FINDINGS: A case-cohort study was conducted in 1,732 unrelated middle-age women (210 CHD cases and 1,522 controls) from a prospective cohort of 15,236 initially healthy Dutch women. We applied a Cox proportional hazards model to study the association of the polymorphism with acute myocardial infarction (AMI) (n = 71) and CHD. In the case-cohort study, no increased risk for CHD was found under the additive genetic model (hazard ratio [HR] = 1.20; 95% confidence interval [CI], 0.86 to 1.68; P = 0.28). This result was not changed by adjustment (HR = 1.17; 95% CI, 0.83 to 1.64; P = 0.38) nor by using dominant, recessive and pairwise genetic models. Analyses for AMI risk under the additive genetic model also did not show any statistically significant association (crude HR = 1.14; 95% CI, 0.93 to 1.39; P = 0.20). To evaluate the association, a comprehensive systematic review and meta-analysis were undertaken of all studies published up to February 2007 (searched through PubMed/MEDLINE, Web of Science and EMBASE). The meta-analysis (38 studies with 13284 cases and 18722 controls) showed a per-allele odds ratio (OR) of 1.08 (95% CI, 1.01 to 1.15; P = 0.02). Moderate to large levels of heterogeneity were identified between studies. Hardy-Weinberg equilibrium (HWE) violation and the mean age of cases were statistically significant sources of the observed variation. In a stratum of non-HWE violation studies, there was no effect. An asymmetric funnel plot, the Egger's test (P = 0.066), and the Begg-Mazumdar test (P = 0.074) were all suggestive of the presence of publication bias. CONCLUSIONS/SIGNIFICANCE: The pooled OR of the present meta-analysis, including our own data, presented evidence that there is an increase in the risk of CHD conferred by the M235T variant of the AGT gene. However, the relevance of this weakly positive overall association remains uncertain because it may be due to various residual biases, including HWE-violation and publication biases

Bayesian methods for meta-analysis of causal relationships estimated using genetic instrumental variables.

Genetic markers can be used as instrumental variables, in an analogous way to randomization in a clinical trial, to estimate the causal relationship between a phenotype and an outcome variable. Our purpose is to extend the existing methods for such Mendelian randomization studies to the context of multiple genetic markers measured in multiple studies, based on the analysis of individual participant data. First, for a single genetic marker in one study, we show that the usual ratio of coefficients approach can be reformulated as a regression with heterogeneous error in the explanatory variable. This can be implemented using a Bayesian approach, which is next extended to include multiple genetic markers. We then propose a hierarchical model for undertaking a meta-analysis of multiple studies, in which it is not necessary that the same genetic markers are measured in each study. This provides an overall estimate of the causal relationship between the phenotype and the outcome, and an assessment of its heterogeneity across studies. As an example, we estimate the causal relationship of blood concentrations of C-reactive protein on fibrinogen levels using data from 11 studies. These methods provide a flexible framework for efficient estimation of causal relationships derived from multiple studies. Issues discussed include weak instrument bias, analysis of binary outcome data such as disease risk, missing genetic data, and the use of haplotypes.This is the accepted manuscript version. The final published version is available from Wiley at http://onlinelibrary.wiley.com/doi/10.1002/sim.3843/abstract;jsessionid=D83E836311AE8220A26CB4E7BFBF3DF1.f01t01

Refining the accuracy of validated target identification through coding variant fine-mapping in type 2 diabetes

We aggregated coding variant data for 81,412 type 2 diabetes cases and 370,832 controls of diverse ancestry, identifying 40 coding variant association signals (P &lt; 2.2 × 10-7); of these, 16 map outside known risk-associated loci. We make two important observations. First, only five of these signals are driven by low-frequency variants: even for these, effect sizes are modest (odds ratio ≤1.29). Second, when we used large-scale genome-wide association data to fine-map the associated variants in their regional context, accounting for the global enrichment of complex trait associations in coding sequence, compelling evidence for coding variant causality was obtained for only 16 signals. At 13 others, the associated coding variants clearly represent 'false leads' with potential to generate erroneous mechanistic inference. Coding variant associations offer a direct route to biological insight for complex diseases and identification of validated therapeutic targets; however, appropriate mechanistic inference requires careful specification of their causal contribution to disease predisposition.</p

WSES guidelines for management of Clostridium difficile infection in surgical patients

In the last two decades there have been dramatic changes in the epidemiology of Clostridium difficile infection (CDI), with increases in incidence and severity of disease in many countries worldwide. The incidence of CDI has also increased in surgical patients. Optimization of management of C difficile, has therefore become increasingly urgent. An international multidisciplinary panel of experts prepared evidenced-based World Society of Emergency Surgery (WSES) guidelines for management of CDI in surgical patients.Peer reviewe

Renin gene MboI dimorphism is a discriminator for hypertension in hyperlipidaemic subjects

As renin is the key enzyme of the renin-angiotensin-aldosterone system, the renin gene (REN) represents a good candidate quantitative trait locus for investigations aimed at uncovering the molecular and genetic influences implicated in the molecular etiology of essential hypertension. Among the various polymorphic markers that are available at the REN gene locus, an MboI dimorphic site located in the ninth intron of the REN gene has previously been shown to be significantly associated with a family history of hypertension in a Japanese population and with direct clinical diagnosis of essential hypertension in a Gulf population. We determined MboI allele and genotype distributions in a sample population of 349 (178 men, 171 women) hyperlipidaemic US Caucasians (mean age 55.4 +/- 13.1 yr), comprising 122 hypertensive and 227 normotensive subjects. A statistically significant association was found between alleles on which the MboI site was present [MboI(+)] and clinical diagnosis of hypertension. REN MboI(+) alleles are thus in linkage disequilibrium with genetic influences that contribute to increased individual susceptibility to hypertension of hyperlipidaemic patients (with an associated odds ratio of 2.15, 95% CI: 1.34-3.45). This positive association does not seem to occur through the effect of classical risks factors represented by lipid, lipoprotein and apolipoprotein levels