As a pilot study to investigate whether personalized medicine approaches could have value for the reduction of malaria-related mortality in young children, we evaluated questionnaire and biomarker data collected from the Mother Offspring Malaria Study Project birth cohort (Muheza, Tanzania, 2002–2006) at the time of delivery as potential prognostic markers for pediatric severe malarial anemia. Severe malarial anemia, defined here as a Plasmodium falciparum infection accompanied by hemoglobin levels below 50 g/L, is a key manifestation of life-threatening malaria in high transmission regions. For this study sample, a prediction model incorporating cord blood levels of interleukin-1β provided the strongest discrimination of severe malarial anemia risk with a C-index of 0.77 (95% CI 0.70–0.84), whereas a pragmatic model based on sex, gravidity, transmission season at delivery, and bed net possession yielded a more modest C-index of 0.63 (95% CI 0.54–0.71). Although additional studies, ideally incorporating larger sample sizes and higher event per predictor ratios, are needed to externally validate these prediction models, the findings provide proof of concept that risk score-based screening programs could be developed to avert severe malaria cases in early childhood.

Hosts strongly influence parasite fitness. However, it is challenging to disentangle host effects on genetic vs plasticity-driven traits of parasites, since parasites can evolve quickly. It remains especially difficult to determine the causes and magnitude of parasite plasticity. In successive generations, parasites may respond plastically to better infect their current type of host, or hosts may produce generally ‘good’ or ‘bad’ quality parasites. Here, we characterized parasite plasticity by taking advantage of a system in which the parasite (the yeast Metschnikowia bicuspidata, which infects Daphnia) has no detectable heritable variation, preventing rapid evolution. In experimental infection assays, we found an effect of rearing host genotype on parasite infectivity, where host genotypes produced overall high or low quality parasite spores. Additionally, these plastically induced differences were gained or lost in just a single host generation. Together, these results demonstrate phenotypic plasticity in infectivity driven by the within-host rearing environment. Such plasticity is rarely investigated in parasites, but could shape epidemiologically important traits.

Genetic diversity of Trypanosoma cruzi may play a role in pathogenesis of Chagas disease forms. Natural populations are classified into 6 Discrete Typing Units (DTUs) Tc I-VI with taxonomical status. This study aimed to identify T. cruzi DTUs in bloodstream and tissue samples of Argentinean patients with Chagas disease. PCR-based strategies allowed DTU identification in 256 clinical samples from 239 Argentinean patients. Tc V prevailed in blood from both asymptomatic and symptomatic cases and Tc I was more frequent in bloodstream, cardiac tissues and chagoma samples from immunosuppressed patients. Tc II and VI were identified in a minority of cases, while Tc III and Tc IV were not detected in the studied population. Interestingly, Tc I and Tc II/VI sequences were amplified from the same skin biopsy slice from a kidney transplant patient suffering Chagas disease reactivation. Further data also revealed the occurrence of mixed DTU populations in the human chronic infection. In conclusion, our findings provide evidence of the complexity of the dynamics of T. cruzi diversity in the natural history of human Chagas disease and allege the pathogenic role of DTUs I, II, V and VI in the studied population.

Choline is an essential nutrient and can also be obtained by de novo synthesis via an oestrogen responsive pathway. Choline can be oxidised to the methyl donor betaine, with short-term supplementation reported to lower plasma total homocysteine (tHcy); however, the effects of longer-term choline supplementation are less clear. We investigated the effect of choline supplementation on plasma concentrations of free choline, betaine and tHcy and B-vitamin status in postmenopausal women, a group more susceptible to low choline status. We also assessed whether supplementation altered plasma lipid profiles. In this randomised, double-blinded, placebo-controlled study, forty-two healthy postmenopausal women received 1 g choline per d (as choline bitartrate), or an identical placebo supplement with their habitual diet. Fasting blood samples were collected at baseline, week 6 and week 12. Administration of choline increased median choline and betaine concentrations in plasma, with significant effects evident after 6 weeks of supplementation (P < 0·001) and remaining significant at 12 weeks (P < 0·001); no effect was observed on folate status or on plasma lipids. Choline supplementation induced a median (25th, 75th percentile) change in plasma tHcy concentration at week 6 of − 0·9 ( − 1·6, 0·2) μmol, a change which, when compared to that observed in the placebo group 0·6 ( − 0·4, 1·9) μmol, approached statistical significance (P = 0·058). Choline supplementation at a dose of 1 g/d significantly increases the circulating concentration of free choline, and can also significantly increase the concentration of the methyl donor, betaine, thereby potentially enhancing the betaine–homocysteine methyltransferase-mediated remethylation of tHcy. This trial was registered at http://www.controlled-trials.com/ISRCTN82708510.

Interference-enhanced Raman scattering was utilized to characterize strain in ultra-thin strained silicon-germanium (SiGe) and silicon layers on insulator. Strained SiGe and silicon films with thickness ranging from 10 to 30 nm on insulating borophosphorosilicate glass (BPSG) were formed by layer transfer techniques and/or strain manipulation via lateral expansion of strained films. The optical interference of the multiple reflections at the BPSG interfaces can substantially boost the reflectivity at the interfaces. The reflection improves Raman signal from SiGe and/or silicon films by increasing excitation intensity and Raman signal collection in the thin films. With the use of interference-enhanced Raman scattering, strain can be characterized at visible wavelengths for films as thin as 10 nm.

The formation of ultra-shallow junctions (USJs) for future integrated circuit technologies requires preamorphization and high dose boron doping to achieve high activation levels and abrupt profiles. To achieve the challenging targets set out in the semiconductor roadmap, it is crucial to reach a much better understanding of the basic physical processes taking place during USJ processing. In this paper we review current understanding of dopant-defect interactions during thermal processing of device structures – interactions which are at the heart of the dopant diffusion and activation anomalies seen in USJs. First, we recall the formation and thermal evolution of End of Range (EOR) defects upon annealing of preamorphized implants (PAI). It is shown that various types of extended defect can be formed: clusters, {113} defects and dislocation loops. During annealing, these defects exchange Si interstitial atoms and evolve following an Ostwald ripening mechanism. We review progress in developing models based on these concepts, which can accurately predict EOR defect evolution and interstitial transport between the defect layer and the surface. Based on this physically based defect modelling approach, combined with fully coupled multi-stream modelling of dopant diffusion, one can perform highly predictive simulations of boron diffusion and de/re-activation in Ge-PAI boron USJs. Agreement between simulations and experimental data is found over a wide range of experimental conditions, clearly indicating that the driving mechanism that degrades boron junction depth and activation is the dissolution of the interstitial defect band. Finally, we briefly outline some promising methods, such as co-implants and/or vacancy engineering, for further down-scaling of source-drain resistance and junction depth.

Ruminant feeding regimes that include grass finishing are known to increase the n-3 polyunsaturated fatty acid (n-3 PUFA) content of beef and lamb. By contrast, concentrate finishing produces meat with increased n-6 PUFA concentrations. There is strong evidence that increasing the ratio of n-3: n-6 PUFA in the diet has beneficial effects for human health. In Northern Ireland, it is likely that feeding regimes are predominantly grass-based; therefore beef and lamb could contain appreciable amounts of n-3 PUFA. However, an analysis of types of finishing diets used by farms in Northern Ireland has not been done. The aim of this study was to assess the frequency of grass and concentrate finishing in farms in Northern Ireland.

Simultaneous analysis of handedness data from 35 samples of twins (with a combined sample size of 21,127 twin pairs) found a small but significant additive genetic effect accounting for 25.47% of the variance (95% confidence interval [CI] 15.69–29.51%). No common environmental influences were detected (C = 0.00; 95% CI 0.00–7.67%), with the majority of the variance, 74.53%, explained by factors unique to the individual (95% CI 70.49–78.67%). No significant heterogeneity was observed within studies that used similar methods to assess handedness, or across studies that used different methods. At an individual level the majority of studies had insufficient power to reject a purely unique environmental model due to insufficient power to detect familial aggregation. This lack of power is seldom mentioned within studies, and has contributed to the misconception that twin studies of handedness are not informative.