Silicon materials task of the low cost solar array project. Phase 3: Effect of impurities and processing on silicon solar cells

The 13th quarterly report of a study entitled an Investigation of the Effects of Impurities and Processing on Silicon Solar Cells is given. The objective of the program is to define the effects of impurities, various thermochemical processes and any impurity-process interactions on the performance of terrestrial silicon solar cells. The Phase 3 program effort falls in five areas: (1) cell processing studies; (2) completion of the data base and impurity-performance modeling for n-base cells; (3) extension of p-base studies to include contaminants likely to be introduced during silicon production, refining or crystal growth; (4) anisotropy effects; and (5) a preliminary study of the permanence of impurity effects in silicon solar cells. The quarterly activities for this report focus on tasks (1), (3) and (4)

Effect of impurities and processing on silicon solar cells. Volume 1: Characterization methods for impurities in silicon and impurity effects data base

Two major topics are treated: methods to measure and evaluate impurity effects in silicon and comprehensive tabulations of data derived during the study. Discussions of deep level spectroscopy, detailed dark I-V measurements, recombination lifetime determination, scanned laser photo-response, conventional solar cell I-V techniques, and descriptions of silicon chemical analysis are presented and discussed. The tabulated data include lists of impurity segregation coefficients, ingot impurity analyses and estimated concentrations, typical deep level impurity spectra, photoconductive and open circuit decay lifetimes for individual metal-doped ingots, and a complete tabulation of the cell I-V characteristics of nearly 200 ingots

Characterization of potential biomarkers of reactogenicity of licensed antiviral vaccines: randomized controlled clinical trials conducted by the BIOVACSAFE consortium

Funding text The authors are grateful for the vital contributions of the participating study volunteers, clinicians, nurses, and laboratory technicians at the Surrey study site. The work by Roberto Leone, laboratory technician at Humanitas Clinical and Research Center, is gratefully acknowledged. Finally, they thank Ellen Oe (GSK) for scientific writing assistance. The research leading to these results has received support from the Innovative Medicines Initiative Joint Undertaking under grant agreement n°115308, resources of which are composed of financial contribution from the European Union’s Seventh Framework Programme (FP7/2007–2013) and EFPIA companies’ in-kind contribution. The contribution of the European Commission to the Advanced Immunization Technologies (ADITEC) project (grant agreement n° 280873) is also gratefully acknowledged. Publisher Copyright: © 2019, The Author(s).Biomarkers predictive of inflammatory events post-vaccination could accelerate vaccine development. Within the BIOVACSAFE framework, we conducted three identically designed, placebo-controlled inpatient/outpatient clinical studies (NCT01765413/NCT01771354/NCT01771367). Six antiviral vaccination strategies were evaluated to generate training data-sets of pre-/post-vaccination vital signs, blood changes and whole-blood gene transcripts, and to identify putative biomarkers of early inflammation/reactogenicity that could guide the design of subsequent focused confirmatory studies. Healthy adults (N = 123; 20–21/group) received one immunization at Day (D)0. Alum-adjuvanted hepatitis B vaccine elicited vital signs and inflammatory (CRP/innate cells) responses that were similar between primed/naive vaccinees, and low-level gene responses. MF59-adjuvanted trivalent influenza vaccine (ATIV) induced distinct physiological (temperature/heart rate/reactogenicity) response-patterns not seen with non-adjuvanted TIV or with the other vaccines. ATIV also elicited robust early (D1) activation of IFN-related genes (associated with serum IP-10 levels) and innate-cell-related genes, and changes in monocyte/neutrophil/lymphocyte counts, while TIV elicited similar but lower responses. Due to viral replication kinetics, innate gene activation by live yellow-fever or varicella-zoster virus (YFV/VZV) vaccines was more suspended, with early IFN-associated responses in naïve YFV-vaccine recipients but not in primed VZV-vaccine recipients. Inflammatory responses (physiological/serum markers, innate-signaling transcripts) are therefore a function of the vaccine type/composition and presence/absence of immune memory. The data reported here have guided the design of confirmatory Phase IV trials using ATIV to provide tools to identify inflammatory or reactogenicity biomarkers.Peer reviewe

Developmental transcriptome of resting cell formation in Mycobacterium smegmatis

Functional classification of gene numbers up- and down-regulated during shock starvation in PBS. (PDF 1796 kb

Short-term mucosal disruption enables colibactin-producing E. coli to cause long-term perturbation of colonic homeostasis

Colibactin, a bacterial genotoxin produced by E. coli strains harboring the pks genomic island, induces cytopathic effects, such as DNA breaks, cell cycle arrest, and apoptosis. Patients with inflammatory bowel diseases, such as ulcerative colitis, display changes in their microbiota with the expansion of E. coli. Whether and how colibactin affects the integrity of the colonic mucosa and whether pks+ E. coli contributes to the pathogenesis of colitis is not clear. Using a gnotobiotic mouse model, we show that under homeostatic conditions, pks+ E. coli do not directly interact with the epithelium or affect colonic integrity. However, upon short-term chemical disruption of mucosal integrity, pks+ E. coli gain direct access to the epithelium, causing epithelial injury and chronic colitis, while mice colonized with an isogenic ΔclbR mutant incapable of producing colibactin show a rapid recovery. pks+ E. coli colonized mice are unable to reestablish a functional barrier. In turn, pks+ E. coli remains in direct contact with the epithelium, perpetuating the process and triggering chronic mucosal inflammation that morphologically and transcriptionally resembles human ulcerative colitis. This state is characterized by impaired epithelial differentiation and high proliferative activity, which is associated with high levels of stromal R-spondin 3. Genetic overexpression of R-spondin 3 in colon myofibroblasts is sufficient to mimic barrier disruption and expansion of E. coli. Together, our data reveal that pks+ E. coli are pathobionts that promote severe injury and initiate a proinflammatory trajectory upon contact with the colonic epithelium, resulting in a chronic impairment of tissue integrity

Modelling Chlamydia and HPV co-infection in patient-derived ectocervix organoids reveals distinct cellular reprogramming

Coinfections with pathogenic microbes continually confront cervical mucosa, yet their implications in pathogenesis remain unclear. Lack of in-vitro models recapitulating cervical epithelium has been a bottleneck to study coinfections. Using patient-derived ectocervical organoids, we systematically modeled individual and coinfection dynamics of Human papillomavirus (HPV)16 E6E7 and Chlamydia, associated with carcinogenesis. The ectocervical stem cells were genetically manipulated to introduce E6E7 oncogenes to mimic HPV16 integration. Organoids from these stem cells develop the characteristics of precancerous lesions while retaining the self-renewal capacity and organize into mature stratified epithelium similar to healthy organoids. HPV16 E6E7 interferes with Chlamydia development and induces persistence. Unique transcriptional and post-translational responses induced by Chlamydia and HPV lead to distinct reprogramming of host cell processes. Strikingly, Chlamydia impedes HPV-induced mechanisms that maintain cellular and genome integrity, including mismatch repair in the stem cells. Together, our study employing organoids demonstrates the hazard of multiple infections and the unique cellular microenvironment they create, potentially contributing to neoplastic progression

Sources of antibiotic resistance: zoonotic, human, environment

Antibiotic resistance is a global problem that must be managed under the One Health perspective. Retrospectively, it is assumed that microbial populations able to cope with compounds with antimicrobial activity and susceptible bacteria lived in equilibrium for a thousand years. This situation would change in the middle 1940s of the twentieth century when one of the most important revolutions of modern medicine started - the use of a natural antimicrobial compound, the penicillin, to treat infectious bacterial diseases. Over the years, the massive use of antibiotics in human and animal medicine, as well as in animal production for both growth promotion and infection prophylaxis/metaphylaxis, accelerated and shaped one of the most successful evolutionary case studies. As a result of an impressive combination of genome and community dynamics, bacteria with acquired antibiotic resistance are nowadays widespread across different environmental compartments (water, soil, wildlife) as well as in the human food chain (poultry, livestock, aquaculture, produce). Hence, the evolutionary success of these bacteria turned to represent a major threat to the human health. This review discusses some of the drivers and paths of antibiotic resistance dissemination across zoonotic, human, and environmental sources.info:eu-repo/semantics/acceptedVersio