Temperature and pH define the realised niche space of arbuscular mycorrhizal fungi.

The arbuscular mycorrhizal (AM) fungi are a globally distributed group of soil organisms that play critical roles in ecosystem function. However, the ecological niches of individual AM fungal taxa are poorly understood. We collected > 300 soil samples from natural ecosystems worldwide and modelled the realised niches of AM fungal virtual taxa (VT; approximately species-level phylogroups). We found that environmental and spatial variables jointly explained VT distribution worldwide, with temperature and pH being the most important abiotic drivers, and spatial effects generally occurring at local to regional scales. While dispersal limitation could explain some variation in VT distribution, VT relative abundance was almost exclusively driven by environmental variables. Several environmental and spatial effects on VT distribution and relative abundance were correlated with phylogeny, indicating that closely related VT exhibit similar niche optima and widths. Major clades within the Glomeraceae exhibited distinct niche optima, Acaulosporaceae generally had niche optima in low pH and low temperature conditions, and Gigasporaceae generally had niche optima in high precipitation conditions. Identification of the realised niche space occupied by individual and phylogenetic groups of soil microbial taxa provides a basis for building detailed hypotheses about how soil communities respond to gradients and manipulation in ecosystems worldwide.

[Angiotensin converting enzyme gene polymorphisms and coronary risk in a Portuguese population].

BACKGROUND: A family history of coronary heart disease (CHD) is a strong risk marker for the disease, independently of classical risk factors. It could be decoded by recognizing the polymorphisms associated with increased risk. Renin-angiotensin system genes are candidate genes in CHD and the deletion allele of the angiotensin converting enzyme (ACE) has been reported as deleterious. However, there is disagreement as to the role of the insertion/deletion polymorphism of the ACE gene in coronary risk. AIM: To evaluate whether ACE gene polymorphisms constitute a CHD risk factor. METHODS: We conducted a population-based case-control study of 301 subjects with a history of myocardial infarction or angiographic evidence of coronary heart disease and 510 age- and gender-matched controls, without CHD, living in a region with high CHD mortality rates. Blood samples were taken, DNA extracted and genotypes determined by the polymerase chain reaction (PCR). Amplification products were identified by agarose gel electrophoresis. STATISTICAL ANALYSIS: The Data were evaluated by SPSS for Windows, using the Student's t test, the chi-square test, odds ratios and 95% confidence intervals. RESULTS: The prevalence of the DD, ID and II genotype was 41.2%, 46.3%, 12.5% in the cases and 28.1%, 55.2% and 16.7% in the control group. The frequency of the DD genotype was significantly higher in the cases than in the controls (41.2% vs. 28.1%, odds ratio 1.79, 95% CI 1.31 to 2.4, p < 0.0001). By contrast, the ID and II genotypes' prevalence was higher in the control group (55.2% vs. 46.3%, p = 0.002 and 16.7 vs. 12.5%, p = NS, respectively) compared to the case group. CONCLUSIONS: This study clearly shows that the ACE DD polymorphism is strongly linked to CHD, and if our data are confirmed in a larger population sample, more aggressive vascular prevention could be justified in patients carrying the DD genotype.

Polymorphism of the ACE gene is associated with extent and severity of coronary disease.

BACKGROUND: The progression and extent of coronary heart disease (CHD) are extremely variable and in many instances independent of conventional risk factors. The differences may be partly explained by less favorable genetic polymorphisms that are associated with them. The polymorphisms of the angiotensin I converting enzyme (ACE) gene have been thoroughly evaluated, but the connection between them and the extent of CHD is unknown. AIMS: Our study is aimed at determining whether any or all of the polymorphisms of the ACE gene are markers of the extent and severity of CHD. METHODS: This was a descriptive study of 296 patients with a history of myocardial infarction or with coronary disease confirmed by coronary angiography. The severity of CHD was quantified according to Leaman's score (based on the number of arteries with more than 75% reduction in diameter and the number of affected coronary segments). The ACE genotypes were determined by specific polymerase chain reaction amplification and the segments were subjected to polyacrylamide gel electrophoresis. The mean coronary score and standard deviation of the three polymorphisms were calculated and the values statistically compared using the Student's t test for independent samples. RESULTS: 296 patients with a mean age of 55.103 years, 234 male, were evaluated. CONCLUSION: The study clearly shows that the DD genotype is linked to the extent of CHD, with a high level of significance. If this is confirmed, careful secondary prevention is indicated in patients with this genotype.