Evolutionary Instability of Symbiotic Function in Bradyrhizobium japonicum

Bacterial mutualists are often acquired from the environment by eukaryotic hosts. However, both theory and empirical work suggest that this bacterial lifestyle is evolutionarily unstable. Bacterial evolution outside of the host is predicted to favor traits that promote an independent lifestyle in the environment at a cost to symbiotic function. Consistent with these predictions, environmentally-acquired bacterial mutualists often lose symbiotic function over evolutionary time. Here, we investigate the evolutionary erosion of symbiotic traits in Bradyrhizobium japonicum, a nodulating root symbiont of legumes. Building on a previous published phylogeny we infer loss events of nodulation capability in a natural population of Bradyrhizobium, potentially driven by mutation or deletion of symbiosis loci. Subsequently, we experimentally evolved representative strains from the symbiont population under host-free in vitro conditions to examine potential drivers of these loss events. Among Bradyrhizobium genotypes that evolved significant increases in fitness in vitro, two exhibited reduced symbiotic quality, but no experimentally evolved strain lost nodulation capability or evolved any fixed changes at six sequenced loci. Our results are consistent with trade-offs between symbiotic quality and fitness in a host free environment. However, the drivers of loss-of-nodulation events in natural Bradyrhizobium populations remain unknown

Item level characterization of mm-wave indoor propagation

According to the current prospect of allocating next generation wireless systems in the underutilized millimeter frequency bands, a thorough characterization of mm-wave propagation represents a pressing necessity. In this work, an “item level” characterization of radiowave propagation at 70 GHz is carried out. The scattering properties of several, different objects commonly present in indoor environment are investigated by means of measurements carried out in an anechoic chamber. The measured data have been also exploited to tune some parameters of a 3D ray tracing model

Phytoscreening and phytoextraction of heavy metals at Danish polluted sites using willow and poplar trees

The main purpose of this study was to determine typical concentrations of heavy metals (HM) in wood from willows and poplars, in order to test the feasibility of phytoscreening and phytoextraction of HM. Samples were taken from one strongly, one moderately, and one slightly polluted site and from three reference sites. Wood from both tree species had similar background concentrations at 0.5 mg kg(−1) for cadmium (Cd), 1.6 mg kg(−1) for copper (Cu), 0.3 mg kg(−1) for nickel (Ni), and 25 mg kg(−1) for zinc (Zn). Concentrations of chromium (Cr) and lead (Pb) were below or close to detection limit. Concentrations in wood from the highly polluted site were significantly elevated, compared to references, in particular for willow. The conclusion from these results is that tree coring could be used successfully to identify strongly heavy metal-polluted soil for Cd, Cu, Ni, Zn, and that willow trees were superior to poplars, except when screening for Ni. Phytoextraction of HMs was quantified from measured concentration in wood at the most polluted site. Extraction efficiencies were best for willows and Cd, but below 0.5 % over 10 years, and below 1 ‰ in 10 years for all other HMs. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11356-013-2085-z) contains supplementary material, which is available to authorized users

Towards the clinical implementation of pharmacogenetics in bipolar disorder.

BackgroundBipolar disorder (BD) is a psychiatric illness defined by pathological alterations between the mood states of mania and depression, causing disability, imposing healthcare costs and elevating the risk of suicide. Although effective treatments for BD exist, variability in outcomes leads to a large number of treatment failures, typically followed by a trial and error process of medication switches that can take years. Pharmacogenetic testing (PGT), by tailoring drug choice to an individual, may personalize and expedite treatment so as to identify more rapidly medications well suited to individual BD patients.DiscussionA number of associations have been made in BD between medication response phenotypes and specific genetic markers. However, to date clinical adoption of PGT has been limited, often citing questions that must be answered before it can be widely utilized. These include: What are the requirements of supporting evidence? How large is a clinically relevant effect? What degree of specificity and sensitivity are required? Does a given marker influence decision making and have clinical utility? In many cases, the answers to these questions remain unknown, and ultimately, the question of whether PGT is valid and useful must be determined empirically. Towards this aim, we have reviewed the literature and selected drug-genotype associations with the strongest evidence for utility in BD.SummaryBased upon these findings, we propose a preliminary panel for use in PGT, and a method by which the results of a PGT panel can be integrated for clinical interpretation. Finally, we argue that based on the sufficiency of accumulated evidence, PGT implementation studies are now warranted. We propose and discuss the design for a randomized clinical trial to test the use of PGT in the treatment of BD

Dual Role of Ribosome-Binding Domain of NAC as a Potent Suppressor of Protein Aggregation and Aging-Related Proteinopathies

The nascent polypeptide-associated complex (NAC) is a conserved ribosome-associated protein biogenesis factor. Whether NAC exerts chaperone activity and whether this function is restricted to de novo protein synthesis is unknown. Here, we demonstrate that NAC directly exerts chaperone activity toward structurally diverse model substrates including polyglutamine (PolyQ) proteins, firefly luciferase, and Aβ40. Strikingly, we identified the positively charged ribosome-binding domain in the N terminus of the βNAC subunit (N-βNAC) as a major chaperone entity of NAC. N-βNAC by itself suppressed aggregation of PolyQ-expanded proteins in vitro, and the positive charge of this domain was critical for this activity. Moreover, we found that NAC also exerts a ribosome-independent chaperone function in vivo. Consistently, we found that a substantial fraction of NAC is non-ribosomal bound in higher eukaryotes. In sum, NAC is a potent suppressor of aggregation and proteotoxicity of mutant PolyQ-expanded proteins associated with human diseases like Huntington’s disease and spinocerebellar ataxias

Regional disparities in infant mortality in Canada: a reversal of egalitarian trends

<p>Abstract</p> <p>Background</p> <p>Although national health insurance plans and social programs introduced in the 1960s led to reductions in regional disparities in infant mortality in Canada, it is unclear if such patterns prevailed in the 1990s when the health care and related systems were under fiscal duress. This study examined regional patterns of change in infant mortality in Canada in recent decades.</p> <p>Methods</p> <p>We analysed regional changes in crude infant mortality rates and in infant mortality rates among live births with a birth weight ≥ 500 g and ≥ 1,000 g in Canada from 1945 to 2002. Associations between baseline infant mortality rates in the provinces and territories (e.g., in 1985–89) and the change observed in infant mortality rates over the subsequent period (e.g., between 1985–89 and 1995–99) were assessed using Spearman's rank correlation coefficient. Trends in regional disparities were also assessed by calculating period-specific rate ratios between provinces/territories with the highest versus the lowest infant mortality.</p> <p>Results</p> <p>Provincial/territorial infant mortality rates in 1945–49 were not correlated with changes in infant mortality over the next 10 years (rho = 0.01, P = 0.99). However, there was a strong negative correlation between infant mortality rates in 1965–69 and the subsequent decline in infant mortality (rho = - 0.85, P = 0.002). Provinces/territories with higher infant mortality rates in 1965–69 (Northwest Territories 64.7 vs British Columbia 20.7 per 1,000 live births) experienced relatively larger reductions in infant mortality between 1965–69 and 1975–79 (53.7% decline in the Northwest Territories vs a 36.6% decline in British Columbia). This pattern was reversed in the more recent decades. Provinces/territories with higher infant mortality rates ≥ 500 g in 1985–89 experience relatively smaller reductions in infant mortality between 1985–89 and 2000–02 (rho = 0.82, P = 0.004). The infant mortality ≥ 500 g rate ratio (contrasting the province/territory with the highest versus lowest infant mortality) was 3.2 in 1965–69, 2.4 in 1975–79, 2.2 in 1985–89, 3.1 in 1995–99 and 4.1 in 2000–02.</p> <p>Conclusion</p> <p>Fiscal constraints in the 1990s led to a reversal of provincial/territorial patterns of change in infant mortality in Canada and to an increase in regional health disparities.</p

Malaria in rural Mozambique. Part I: Children attending the outpatient clinic

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