A quantitative genetic signature of senescence in a short-lived perennial plant.

The evolution of senescence (the physiological decline of organisms with age) poses an apparent paradox because it represents a failure of natural selection to increase the survival and reproductive performance of organisms. The paradox can be resolved if natural selection becomes less effective with age, because the death of postreproductive individuals should have diminished effects on Darwinian fitness [1, 2]. A substantial body of empirical work is consistent with this prediction for animals, which transmit their genes to progeny via an immortal germline. However, such evidence is still lacking in plants, which lack a germline and whose reproduction is diffuse and modular across the soma. Here, we provide experimental evidence for a genetic basis of senescence in the short-lived perennial plant Silene latifolia. Our pedigree-based analysis revealed a marked increase with age in the additive genetic variance of traits closely associated with fitness. This result thus extends to plants the quantitative genetic support for the evolutionary theory of senescence.

Comparison of the NEO-FFI, the NEO-FFI-R and an alternative short version of the NEO-PI-R (NEO-60) in Swiss and Spanish samples

Three different short versions of the NEO-PI-R were compared: The NEO-FFI, the NEO-FFI-R, and a new short version developed in the current study (NEO-60). This new version is intended to improve the psychometric characteristics of the original NEO-FFI, specially in regard to the factor structure at the item-level. A French version of the NEO-PI-R was given to 1090 Swiss subjects, whereas the Spanish (Castilian) version of the NEO-PI-R was administered to 1006 Spanish subjects. Results replicate the limitations of the NEO-FFI already found in other countries. Compared to the NEO-FFI, reliability coefficients and factor structure was enhanced by the NEO-FFI-R and the NEO-60 in both samples, although substantial differences were not found. The factor structure of the NEO-60 shows the best fit since only three items do not load mainly on their own factor in both samples. Besides, correlations between items and NEO-PI-R domain scores are also higher for the items included in the NEO-60 version. On the other hand, convergent correlations with the NEO-PI-R dimensions were satisfactory irrespective of the version, and confirmatory factor analyses show slight differences among the different models generated after the three short versions.

Short-term therapy with simvastatin reduces inflammatory mediators and heart inflammation during the acute phase of experimental Chagas disease

Trypanosoma cruzi infection induces progressive cardiac inflammation that leads to fibrosis and modifications in the heart architecture and functionality. Statins, such as 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors, have been studied due to their pleiotropic roles in modulating the inflammatory response. Our goal was to evaluate the effects of simvastatin on the cardiac inflammatory process using a cardiotropic strain of T. cruzi in a murine model of Chagas cardiomyopathy. C57BL/6 mice were infected with 500 trypomastigotes of the Colombian strain of T. cruzi and treated with an oral dose of simvastatin (20 mg/Kg/day) for one month and inflammatory and morphometric parameters were subsequently evaluated in the serum and in the heart, respectively. Simvastatin reduced the total cholesterol and inflammatory mediators (interferon-gamma, tumour necrosis factor-alpha, CCL2 and CCL5) in the serum and in the heart tissue at 30 days post-infection. Additionally, a proportional reduction in heart weight and inflammatory infiltration was observed. Simvastatin also reduced epimastigote proliferation in a dose-dependent manner in vitro and was able to reduce blood trypomastigotes and heart amastigote nests during the acute phase of Chagas disease in vivo. Based on these data, we conclude that simvastatin exerts a modulatory effect on the inflammatory mediators that are elicited by the Colombian strain of T. cruzi and ameliorates the heart damage that is observed in a murine model of Chagas disease.