Back Contact Engineering for Increased Performance in Kesterite Solar Cells

The thin‐film photovoltaic absorber Cu₂ZnSn(S,Se)₄ (CZTSSe) holds considerable promise for large scale conversion of sunlight into electricity. CZTSSe is composed of Earth‐abundant elements that exhibit low‐toxicities, but improvements in device efficiency have been hampered by difficulties in increasing open circuit voltages (V_OC) due, at least in part, to disorder induced band tailing. We present a method to increase V_OC through direct modification of the back contact; our approach involves the separation of fully functioning devices from their Mo/glass substrate to reveal the back CZTSSe surface. Formation of a new back contact consisting of a thermally deposited high work function material (MoO₃), together with a higly reflective (Au) capping layer, creates an electrostatic field that drives electrons to the front p‐n junction and leads to a decrease in electron‐hole recombination. Model simulations indicating an increase in V_OC with decreasing absorber thickness are borne out by experiments with devices of varying thicknesses (0.7–2.0 μm). We report V_OC increases of up to 49 mV for a 1 μm thick absorber, with even greater increases up to 61 mV when the back CZTSSe surface is etched with bromine‐methanol.     

Characterization of suppressible mutations in the viomycin phosphotransferase gene of the Streptomyces enteric plasmid pVE138.

The viomycin phosphotransferase gene (vph) is expressed and confers resistance to viomycin in both Streptomyces spp. and members of the family Enterobacteriaceae. We report the isolation of UGA (opal) and UAG (amber) mutations in the vph gene of shuttle plasmid pVE138. We found that the five UGA mutations in vph resulted in a temperature-sensitive phenotype in Salmonella typhimurium. Su- strains are Vior at 28 degrees C and Vios at 37 degrees C, whereas Su+UGA strains are Vior at both 28 and 37 degrees C. The single amber mutation isolated was not temperature sensitive and resulted in the expected Vios phenotype in Su- strains and Vior in Su+UAG strains.     

Geographical features are the predominant driver of molecular diversification in widely distributed North American whipsnakes

Allopatric divergence following the formation of geographical features has been implicated as a major driver of evolutionary diversification. Widespread species complexes provide opportunities to examine allopatric divergence across varying degrees of isolation in both time and space. In North America, several geographical features may play such a role in diversification, including the Mississippi River, Pecos River, Rocky Mountains, Cochise Filter Barrier, Gulf of California and Isthmus of Tehuantepec. We used thousands of nuclear single nucleotide polymorphisms (SNPs) and mitochondrial DNA from several species of whipsnakes (genera Masticophis and Coluber) distributed across North and Central America to investigate the role that these geographical features have played on lineage divergence. We hypothesize that these features restrict gene flow and separate whipsnakes into diagnosable genomic clusters. We performed genomic clustering and phylogenetic reconstructions at the species and population levels using Bayesian and likelihood analyses and quantified migration levels across geographical features to assess the degree of genetic isolation due to allopatry. Our analyses suggest that (i) major genetic divisions are often consistent with isolation by geographical features, (ii) migration rates between clusters are asymmetrical across major geographical features, and (iii) areas that receive proportionally more migrants possess higher levels of genetic diversity. Collectively, our findings suggest that multiple features of the North American landscape contributed to allopatric divergence in this widely distributed snake group.     

Limitations of Climatic Data for Inferring Species Boundaries: Insights from Speckled Rattlesnakes

Phenotypes, DNA, and measures of ecological differences are widely used in species delimitation. Although rarely defined in such studies, ecological divergence is almost always approximated using multivariate climatic data associated with sets of specimens (i.e., the “climatic niche”); the justification for this approach is that species-specific climatic envelopes act as surrogates for physiological tolerances. Using identical statistical procedures, we evaluated the usefulness and validity of the climate-as-proxy assumption by comparing performance of genetic (nDNA SNPs and mitochondrial DNA), phenotypic, and climatic data for objective species delimitation in the speckled rattlesnake (Crotalus mitchellii) complex. Ordination and clustering patterns were largely congruent among intrinsic (heritable) traits (nDNA, mtDNA, phenotype), and discordance is explained by biological processes (e.g., ontogeny, hybridization). In contrast, climatic data did not produce biologically meaningful clusters that were congruent with any intrinsic dataset, but rather corresponded to regional differences in atmospheric circulation and climate, indicating an absence of inherent taxonomic signal in these data. Surrogating climate for physiological tolerances adds artificial weight to evidence of species boundaries, as these data are irrelevant for that purpose. Based on the evidence from congruent clustering of intrinsic datasets, we recommend that three subspecies of C. mitchellii be recognized as species: C. angelensis, C. mitchellii, and C. Pyrrhus.     

Genetic control of glutamine synthetase in Klebiella aerogenes.

Mutations at two sites, glnA and glnB, of the Klebsiella aerogenes chromosome result in the loss of glutamine synthetase. The locations of these sites on the chromosome were established by complementation by episomes of Escherichia coli and by determination of their linkage to other genetic sites by transduction with phage P1. The glnB gene is located at a position corresponding to 48 min on the Taylor map of the E. coli chromosome; it is linked to tryA, nadB, and GUA. The glnA gene is at a position corresponding to 77 min on the Taylor map and is linked to rha and metB; it is also closely linked to rbs, located in E. coli at 74 min, indicating a difference in this chromosomal region between E. coli and K. aerogenes. Mutations in the glnA site can also lead to nonrepressible synthesis of active glutamine synthetase. The examination of the fine genetic structure of glnA revealed that one such mutation is located between two mutations leading to the loss of enzymatic activity. This result, together with evidence that the structural gene for glutamine synthetase is at glnA, suggests that glutamine synthetase controls expression of its own structural gene by repression.     

Remarkable ancient divergences amongst neglected lorisiform primates

Lorisiform primates (Primates: Strepsirrhini: Lorisiformes) represent almost 10% of the living primate species and are widely distributed in sub‐Saharan Africa and South/South‐East Asia; however, their taxonomy, evolutionary history, and biogeography are still poorly understood. In this study we report the largest molecular phylogeny in terms of the number of represented taxa. We sequenced the complete mitochondrial cytochrome b gene for 86 lorisiform specimens, including ～80% of all the species currently recognized. Our results support the monophyly of the Galagidae, but a common ancestry of the Lorisinae and Perodicticinae (family Lorisidae) was not recovered. These three lineages have early origins, with the Galagidae and the Lorisinae diverging in the Oligocene at about 30 Mya and the Perodicticinae emerging in the early Miocene. Our mitochondrial phylogeny agrees with recent studies based on nuclear data, and supports Euoticus as the oldest galagid lineage and the polyphyletic status of Galagoides. Moreover, we have elucidated phylogenetic relationships for several species never included before in a molecular phylogeny. The results obtained in this study suggest that lorisiform diversity remains substantially underestimated and that previously unnoticed cryptic diversity might be present within many lineages, thus urgently requiring a comprehensive taxonomic revision of this primate group. © 2015 The Linnean Society of London     

Simulation of lower limb axial arterial length change during locomotion

The effect of external forces on axial arterial wall mechanics has conventionally been regarded as secondary to hemodynamic influences. However, arteries are similar to muscles in terms of the manner in which they traverse joints, and their three-dimensional geometrical requirements for joint motion. This study considers axial arterial shortening and elongation due to motion of the lower extremity during gait, ascending stairs, and sitting-to-standing motion. Arterial length change was simulated by means of a graphics based anatomic and kinematic model of the lower extremity. This model estimated the axial shortening to be as much as 23% for the femoropopliteal arterial region and as much as 21% for the iliac artery. A strong correlation was observed between femoropopliteal artery shortening and maximum knee flexion angle (r2=0.8) as well as iliac artery shortening and maximum hip angle flexion (r2=0.9). This implies a significant mechanical influence of locomotion on arterial behavior in addition to hemodynamics factors. Vascular tissue has high demands for axial compliance that should be considered in the pathology of atherosclerosis and the design of vascular implants.     

Model for studying virus attachment. II. Binding of biotinylated human T cell leukemia virus type I to human blood mononuclear cells potential targets for human T cell leukemia virus type I infection.

Purified human T cell leukemia virus type I (HTLV-I) was biotinylated and used to study its attachment to human PBMC. The use of biotinylated HTLV-I (biot-HTLV-I) in conjunction with mouse mAb specific for selected cell-surface molecules and flow cytometric analysis allowed us to positively identify virus-binding cells among a heterogeneous blood mononuclear cell population. Biot-HTLV-I efficiently bound not only to T cells, but also to B cells and monocytes. Preincubation of monocytes with excess of unlabeled HTLV-I significantly reduced the attachment of biot-HTLV-I. HTLV-I not only bound to, but also infected, B cells, as suggested by: i) in situ hybridization of a 35S-labeled full length HTLV-I DNA probe with EBV-transformed B cells, previously cocultured with HTLV-I-producing (G11MJ) T cells, and ii) hybridization of the same nick-translated 32P-labeled DNA probe with blotted DNA from similar HTLV-I-infected EBV-transformed B cells. HTLV-I infection did not affect the ability of B cells to secrete IgG. These findings suggest that HTLV-I cannot only infect cells of the T lineage, but can also infect B cells.     

Programmatically Selected Multidrug-Resistant Strains Drive the Emergence of Extensively Drug-Resistant Tuberculosis in South Africa

Background

South Africa shows one of the highest global burdens of multidrug-resistant (MDR) and extensively drug-resistant (XDR) tuberculosis (TB). Since 2002, MDR-TB in South Africa has been treated by a standardized combination therapy, which until 2010 included ofloxacin, kanamycin, ethionamide, ethambutol and pyrazinamide. Since 2010, ethambutol has been replaced by cycloserine or terizidone. The effect of standardized treatment on the acquisition of XDR-TB is not currently known.

Methods

We genetically characterized a random sample of 4,667 patient isolates of drug-sensitive, MDR and XDR-TB cases collected from three South African provinces, namely, the Western Cape, Eastern Cape and KwaZulu-Natal. Drug resistance patterns of a subset of isolates were analyzed for the presence of commonly observed resistance mutations.

Results

Our analyses revealed a strong association between distinct strain genotypes and the emergence of XDR-TB in three neighbouring provinces of South Africa. Strains predominant in XDR-TB increased in proportion by more than 20-fold from drug-sensitive to XDR-TB and accounted for up to 95% of the XDR-TB cases. A high degree of clustering for drug resistance mutation patterns was detected. For example, the largest cluster of XDR-TB associated strains in the Eastern Cape, affecting more than 40% of all MDR patients in this province, harboured identical mutations concurrently conferring resistance to isoniazid, rifampicin, pyrazinamide, ethambutol, streptomycin, ethionamide, kanamycin, amikacin and capreomycin.

Conclusions

XDR-TB associated genotypes in South Africa probably were programmatically selected as a result of the standard treatment regimen being ineffective in preventing their transmission. Our findings call for an immediate adaptation of standard treatment regimens for M/XDR-TB in South Africa.