Population genetics of trypanosoma brucei rhodesiense: clonality and diversity within and between foci

African trypanosomes are unusual among pathogenic protozoa in that they can undergo their complete morphological life cycle in the tsetse fly vector with mating as a non-obligatory part of this development. Trypanosoma brucei rhodesiense, which infects humans and livestock in East and Southern Africa, has classically been described as a host-range variant of the non-human infective Trypanosoma brucei that occurs as stable clonal lineages. We have examined T. b. rhodesiense populations from East (Uganda) and Southern (Malawi) Africa using a panel of microsatellite markers, incorporating both spatial and temporal analyses. Our data demonstrate that Ugandan T. b. rhodesiense existed as clonal populations, with a small number of highly related genotypes and substantial linkage disequilibrium between pairs of loci. However, these populations were not stable as the dominant genotypes changed and the genetic diversity also reduced over time. Thus these populations do not conform to one of the criteria for strict clonality, namely stability of predominant genotypes over time, and our results show that, in a period in the mid 1990s, the previously predominant genotypes were not detected but were replaced by a novel clonal population with limited genetic relationship to the original population present between 1970 and 1990. In contrast, the Malawi T. b. rhodesiense population demonstrated significantly greater diversity and evidence for frequent genetic exchange. Therefore, the population genetics of T. b. rhodesiense is more complex than previously described. This has important implications for the spread of the single copy T. b. rhodesiense gene that allows human infectivity, and therefore the epidemiology of the human disease, as well as suggesting that these parasites represent an important organism to study the influence of optional recombination upon population genetic dynamics

Influence of short and long term processes on SAR11 communities in open ocean and coastal systems

SAR11 bacteria dominate the surface ocean and are major players in converting fixed carbon back to atmospheric carbon dioxide. The SAR11 clade is comprised of niche-specialized ecotypes that display distinctive spatiotemporal transitions. We analyzed SAR11 ecotype seasonality in two long-term 16S rRNA amplicon time series representing different North Atlantic regimes: the Sargasso Sea (subtropical ocean-gyre; BATS) and the temperate coastal Western English Channel (WEC). Using phylogenetically resolved amplicon sequence variants (ASVs), we evaluated seasonal environmental constraints on SAR11 ecotype periodicity. Despite large differences in temperature and nutrient availability between the two sites, at both SAR11 succession was defined by summer and winter clusters of ASVs. The summer cluster was dominated by ecotype Ia.3 in both sites. Winter clusters were dominated by ecotypes Ib and IIa.A at BATS and Ia.1 and IIa.B at WEC. A 2-year weekly analysis within the WEC time series showed that the response of SAR11 communities to short-term environmental fluctuations was variable. In 2016, community shifts were abrupt and synchronized to environmental shifts. However, in 2015, changes were gradual and decoupled from environmental fluctuations, likely due to increased mixing from strong winds. We demonstrate that interannual weather variability disturb the pace of SAR11 seasonal progression

Lack of association between HLA antigen DR3 and α<inf>1</inf> deficiency in liver transplant recipients

The relationship between α1-antitrypsin deficiency (α-ATD) and the HLA antigen system was studied in 32 liver transplant recipients. Despite previous reports of an association of HLA antigen DR3 with homozygosity for α-AT ZZ, no such association was seen in this population of α-ATD homozygous ZZ patients with advanced hepatic disease. Thus, the reported association of HLA class II antigens and homozygosity for the Z allele for α-AT may be an artifact of either a small study population or geographic inbreeding and a coincidental association of certain HLA antigens with the presence of homozygosity for the Z allele of α-AT. © 1993 Plenum Publishing Corporation

Elucidation on the Effect of Operating Temperature to the Transport Properties of Polymeric Membrane Using Molecular Simulation Tool

Existing reports of gas transport properties within polymeric membrane as a direct consequence of operating temperature are in a small number and have arrived in diverging conclusion. The scarcity has been associated to challenges in fabricating defect free membranes and empirical investigations of gas permeation performance at the laboratory scale that are often time consuming and costly. Molecular simulation has been proposed as a feasible alternative of experimentally studied materials to provide insights into gas transport characteristic. Hence, a sequence of molecular modelling procedures has been proposed to simulate polymeric membranes at varying operating temperatures in order to elucidate its effect to gas transport behaviour. The simulation model has been validated with experimental data through satisfactory agreement. Solubility has shown a decrement in value when increased in temperature (an average factor of 1.78), while the opposite has been observed for gas diffusivity (an average factor of 1.32) when the temperature is increased from 298.15Â K to 323.15Â K. In addition, it is found that permeability decreases by 1.36 times as the temperature is increased

Increased ventral striatal volume in college-aged binge drinkers

BACKGROUND Binge drinking is a serious public health issue associated with cognitive, physiological, and anatomical differences from healthy individuals. No studies, however, have reported subcortical grey matter differences in this population. To address this, we compared the grey matter volumes of college-age binge drinkers and healthy controls, focusing on the ventral striatum, hippocampus and amygdala. METHOD T1-weighted images of 19 binge drinkers and 19 healthy volunteers were analyzed using voxel-based morphometry. Structural data were also covaried with Alcohol Use Disorders Identification Test (AUDIT) scores. Cluster-extent threshold and small volume corrections were both used to analyze imaging data. RESULTS Binge drinkers had significantly larger ventral striatal grey matter volumes compared to controls. There were no between group differences in hippocampal or amygdalar volume. Ventral striatal, amygdalar, and hippocampal volumes were also negatively related to AUDIT scores across groups. CONCLUSIONS Our findings stand in contrast to the lower ventral striatal volume previously observed in more severe forms of alcohol use disorders, suggesting that college-age binge drinkers may represent a distinct population from those groups. These findings may instead represent early sequelae, compensatory effects of repeated binge and withdrawal, or an endophenotypic risk factor

Fully spray-coated triple-cation perovskite solar cells

We use ultrasonic spray-coating to sequentially deposit thin films of tin oxide, a triple-cation perovskite and spiro-OMeTAD, allowing us fabricate perovskite solar cells (PSCs) with a champion reverse scan power conversion efficiency (PCE) of 19.4% on small-area substrates. We show that the use of spray-deposition permits us to rapidly (>80 mm s−1) coat 25 mm × 75 mm substrates that were divided into a series of devices each with an active area of 15.4 mm2, yielding an average PCE of 10.3% and a peak PCE of 16.3%. By connecting seven 15.4 mm2 devices in parallel on a single substrate, we create a device having an effective active area of 1.08 cm2 and a PCE of 12.7%. This work demonstrates the possibility for spray-coating to fabricate high efficiency and low-cost perovskite solar cells at speed

Profiling of the perturbed metabolomic state of mouse spleen during acute and chronic toxoplasmosis

Background Toxoplasma gondii, a common opportunistic protozoan, is a leading cause of illness and mortality among immunosuppressed individuals and during congenital infections. Current therapeutic strategies for toxoplasmosis are not fully effective at curtailing disease progression in these cases. Given the parasite ability to influence host immunity and metabolism, understanding of the metabolic alterations in the host’s immune organs during T. gondii infection may enhance the understanding of the molecular mechanisms that define the pathophysiology of T. gondii infection. Methods We investigated the global metabolic changes in the spleen of BALB/c mice at early and late stage of infection with T. gondii using LC-MS/MS-based metabolomics. Multivariate data analysis methods, principal components analysis (PCA) and partial least squares discriminant analysis (PLS-DA), were used to identify metabolites that are influenced by T. gondii infection. Results Multivariate analyses clearly separated the metabolites of spleen of infected and control mice. A total of 132 differential metabolites were identified, 23 metabolites from acutely infected versus control mice and 109 metabolites from chronically infected versus control mice. Lipids, hormones, lactones, acids, peptides, antibiotics, alkaloids and natural toxins were the most influenced chemical groups. There were 12 shared differential metabolites between acutely infected versus control mice and chronically infected versus control mice, of which 4,4-Dimethyl-5alpha-cholesta-8,14,24-trien-3beta-ol was significantly upregulated and ubiquinone-8 was significantly downregulated. Major perturbed metabolic pathways included primary bile acid biosynthesis, steroid hormone biosynthesis, biotin metabolism, and steroid biosynthesis, with arachidonic acid metabolism being the most significantly impacted pathway. These metabolic changes suggest a multifactorial nature of the immunometabolic responses of mouse spleen to T. gondii infection. Conclusions This study demonstrated that T. gondii infection can cause significant metabolomic alterations in the spleen of infected mice. These findings provide new insights into the molecular mechanisms that underpin the pathogenesis of T. gondii infection