Modeling High-Efficiency Rear Junction Photovoltaic Devices

Solar cells are a renewable energy technology that has begun to supply energy in many regions of the world at a utility scale. Nonetheless, further improvements in solar technology are still needed to help reduce costs and increase adoption. Many researchers have been particularly interested in demonstrating higher efficiencies through new materials and designs. Some of the most efficient technologies are made from III-V materials, which feature strong absorption and radiative recombination. Rear junction III-V solar cell devices are of particular interest, as they have been proven to provide higher efficiencies compared to traditionally structured devices. This is believed to be caused by reduced bulk recombination and enhanced photon recycling. However, their performance is not fully understood at this time. In particular, previous studies produced a discrepancy between previous simulated literature and experimental fitted values, at odds with prior independent measurements of the material properties. To help develop a better understanding of these cells, we have developed a tool to examine the parameters that properly fit experimental data sets. Our tool features a web-enabled graphical user interface that allows the user to set the range of parameters to sweep. It then outputs contour plots to determine which ranges of values are most consistent with experimental results. This simulation tool will provide a more accurate understanding of the behavior of GaInP rear-junction solar cells, and more generally, will help advance our understanding of how unconventional solar cell architectures and materials can help achieve higher efficiencies. Future benefits may include improved design techniques for single-junction photovoltaics for terrestrial use, as well as multi-junction high-performance cells for aerospace applications

Characterization of the Positivity of the Density Matrix in Terms of the Coherence Vector Representation

A parameterization of the density operator, a coherence vector representation, which uses a basis of orthogonal, traceless, Hermitian matrices is discussed. Using this parameterization we find the region of permissible vectors which represent a density operator. The inequalities which specify the region are shown to involve the Casimir invariants of the group. In particular cases, this allows the determination of degeneracies in the spectrum of the operator. The identification of the Casimir invariants also provides a method of constructing quantities which are invariant under {\it local} unitary operations. Several examples are given which illustrate the constraints provided by the positivity requirements and the utility of the coherence vector parameterization.Comment: significantly rewritten and submitted for publicatio

Neural Indices of Vowel Discrimination in Monolingual and Bilingual Infants and Children

Objectives: To examine maturation of neural discriminative responses to an English vowel contrast from infancy to 4 years of age and to determine how biological factors (age and sex) and an experiential factor (amount of Spanish versus English input) modulate neural discrimination of speech. Design: Event-related potential (ERP) mismatch responses (MMRs) were used as indices of discrimination of the American English vowels [ε] versus [I] in infants and children between 3 months and 47 months of age. A total of 168 longitudinal and cross-sectional data sets were collected from 98 children (Bilingual Spanish–English: 47 male and 31 female sessions; Monolingual English: 48 male and 42 female sessions). Language exposure and other language measures were collected. ERP responses were examined in an early time window (160 to 360 msec, early MMR [eMMR]) and late time window (400 to 600 msec, late MMR). Results: The eMMR became more negative with increasing age. Language experience and sex also influenced the amplitude of the eMMR. Specifically, bilingual children, especially bilingual females, showed more negative eMMR compared with monolingual children and with males. However, the subset of bilingual children with more exposure to English than Spanish compared with those with more exposure to Spanish than English (as reported by caretakers) showed similar amplitude of the eMMR to their monolingual peers. Age was the only factor that influenced the amplitude of the late MMR. More negative late MMR was observed in older children with no difference found between bilingual and monolingual groups. Conclusions: Consistent with previous studies, our findings revealed that biological factors (age and sex) and language experience modulated the amplitude of the eMMR in young children. The early negative MMR is likely to be the mismatch negativity found in older children and adults. In contrast, the late MMR amplitude was influenced only by age and may be equivalent to the Nc in infants and to the late negativity observed in some auditory passive oddball designs

Myocardial-specific R-spondin3 drives proliferation of the coronary stems primarily through the Leucine Rich Repeat G Protein coupled receptor LGR4

Coronary artery anomalies are common congenital disorders with serious consequences in adult life. Coronary circulation begins when the coronary stems form connections between the aorta and the developing vascular plexus. We recently identified the WNT signaling modulator R-spondin 3 (Rspo3), as a crucial regulator of coronary stem proliferation. Using expression analysis and tissue-specific deletion we now demonstrate that Rspo3 is primarily produced by cardiomyocytes. Moreover, we have employed CRISPR/Cas9 technology to generate novel Lgr4-null alleles that showed a significant decrease in coronary stem proliferation and thus phenocopied the coronary artery defects seen in Rspo3 mutants. Interestingly, Lgr4 mutants displayed slightly hypomorphic right ventricles, an observation also made after myocardial specific deletion of Rspo3. These results shed new light on the role of Rspo3 in heart development and demonstrate that LGR4 is the principal Rspondin 3 receptor in the heart

The adrenal capsule is a signaling center controlling cell renewal and zonation through <i>Rspo3</i>

Adrenal glands are zonated endocrine organs that are essential in controlling body homeostasis. How zonation is induced and maintained and how renewal of the adrenal cortex is ensured remain a mystery. Here we show that capsular RSPO3 signals to the underlying steroidogenic compartment to induce β-catenin signaling and imprint glomerulosa cell fate. Deletion of RSPO3 leads to loss of SHH signaling and impaired organ growth. Importantly, Rspo3 function remains essential in adult life to ensure replenishment of lost cells and maintain the properties of the zona glomerulosa. Thus, the adrenal capsule acts as a central signaling center that ensures replacement of damaged cells and is required to maintain zonation throughout life

TREM2 expression in the brain and biological fluids in prion diseases

Triggering receptor expressed on myeloid cells 2 (TREM2) is an innate immune cell surface receptor that regulates microglial function and is involved in the pathophysiology of several neurodegenerative diseases. Its soluble form (sTREM2) results from shedding of the TREM2 ectodomain. The role of TREM2 in prion diseases, a group of rapidly progressive dementias remains to be elucidated. In the present study, we analysed the expression of TREM2 and its main sheddase ADAM10 in the brain of sporadic Creutzfeldt-Jakob disease (sCJD) patients and evaluated the role of CSF and plasma sTREM2 as a potential diagnostic marker of prion disease. Our data indicate that, compared to controls, TREM2 is increased in sCJD patient brains at the mRNA and protein levels in a regional and subtype dependent fashion, and expressed in a subpopulation of microglia. In contrast, ADAM10 is increased at the protein, but not the mRNA level, with a restricted neuronal expression. Elevated CSF sTREM2 is found in sCJD, genetic CJD with mutations E200K and V210I in the prion protein gene (PRNP), and iatrogenic CJD, as compared to healthy controls (HC) (AUC = 0.78-0.90) and neurological controls (AUC = 0.73-0.85), while CSF sTREM2 is unchanged in fatal familial insomnia. sTREM2 in the CSF of cases with Alzheimer's disease, and multiple sclerosis was not significantly altered in our series. CSF sTREM2 concentrations in sCJD are PRNP codon 129 and subtype-related, correlate with CSF 14-3-3 positivity, total-tau and YKL-40, and increase with disease progression. In plasma, sTREM2 is increased in sCJD compared with HC (AUC = 0.80), displaying positive correlations with plasma total-tau, neurofilament light, and YKL-40. We conclude that comparative study of TREM2 in brain and biological fluids of prion diseases reveals TREM2 to be altered in human prion diseases with a potential value in target engagement, patient stratification, and disease monitoring

Recommendations for defining preventable HIV-related mortality for public health monitoring in the era of Getting to Zero: an expert consensus

Getting to Zero is a commonly cited strategic aim to reduce mortality due to both HIV and avoidable deaths among people with HIV. However, no clear definitions are attached to these aims with regard to what constitutes HIV-related or preventable mortality, and their ambition is limited. This Position Paper presents consensus recommendations to define preventable HIV-related mortality for a pragmatic approach to public health monitoring by use of national HIV surveillance data. These recommendations were informed by a comprehensive literature review and agreed by 42 international experts, including clinicians, public health professionals, researchers, commissioners, and community representatives. By applying the recommendations to 2019 national HIV surveillance data from the UK, we show that 30% of deaths among people with HIV were HIV-related or possibly HIV-related, and at least 63% of these deaths were preventable or potentially preventable. The application of these recommendations by health authorities will ensure consistent monitoring of HIV elimination targets and allow for the identification of inequalities and areas for intervention

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts

Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN