METHOD FOR SINGLE CRYSTAL GROWTH OF PHOTOVOLTAIC PEROVSKITE MATERIAL AND DEVICES

Systems and methods for perovskite single crystal growth include using a low temperature solution process that employs a temperature gradient in a perovskite solution in a container , also including at least one small perovskite single crystal , and a substrate in the solution upon which substrate a perovskite crystal nucleates and grows , in part due to the temperature gradient in the solution and in part due to a temperature gradient in the substrate . For example , a top portion of the substrate external to the solution may be cooled

SYSTEMS AND METHODS FOR SCALABLE PEROVSKITE DEVICE FABRICATION

Continuous processes for fabricating a perovskite device are described that include forming a perovskite layer or film on a substrate using a linear deposition device , and optionally using a conductive tape lamination process to form an anode or a cathode layer on the perovskite device

Chloride Incorporation Process in CH\u3csub\u3e3\u3c/sub\u3eNH\u3csub\u3e3\u3c/sub\u3ePbI\u3csub\u3e3-x\u3c/sub\u3eCl\u3csub\u3ex\u3c/sub\u3e Perovskites via Nanoscale Bandgap Maps

CH3NH3PbI3-xClx perovskites enable fabrication of highly efficient solar cells. Chloride ions benefit the morphology, carrier diffusion length and stability of perovskite films; however, whether those benefits stem from the presence of Cl− in the precursor solution or from their incorporation in annealed films is debated. In this work, the photothermal induced resonance (PTIR), an in situ technique with nanoscale resolution, is leveraged to measure the bandgap of CH3NH3PbI3-xClx films obtained by a multicycle coating process that produces high efficiency (≈16 %) solar cells. Because chloride ions modify the perovskite lattice, thereby widening the bandgap, measuring the bandgap locally yields the local chloride content. After a mild annealing (60 min, 60°C) the films consist of Cl-rich (x \u3c 0.3) and Cl-poor phases that, upon further annealing (110 °C), evolve into a homogenous Cl-poorer (x \u3c 0.06) phase, suggesting that methylammonium-chrloride is progressively expelled from the film. Despite the small chloride content, CH3NH3PbI3-xClx films show better thermal stability up to 140 °C with respect CH3NH3PbI3 films fabricated with the same methodology

QUOIN: Incentive Mechanisms for Crowd Sensing Networks

Crowd sensing networks play a critical role in big data generation where a large number of mobile devices collect various kinds of data with large-volume features. Although which information should be collected is essential for the success of crowd-sensing applications, few research efforts have been made so far. On the other hand, an efficient incentive mechanism is required to encourage all crowd-sensing participants, including data collectors, service providers, and service consumers, to join the networks. In this article, we propose a new incentive mechanism called QUOIN, which simultaneously ensures Quality and Usability Of INformation for crowd-sensing application requirements. We apply a Stackelberg game model to the proposed mechanism to guarantee each participant achieves a satisfactory level of profits. Performance of QUOIN is evaluated with a case study, and experimental results demonstrate that it is efficient and effective in collecting valuable information for crowd-sensing applications

An Introduction to Machine Learning in Quantitative Finance

In this book, the authors provide a systematic and rigorous introduction to supervised, unsupervised and reinforcement learning by establishing essential definitions and theorems

SRSF2 Is Essential For Hematopoiesis and Its Mutations Dysregulate Alternative RNA Splicing In MDS

Abstract Myelodysplastic syndromes (MDS) are a group of neoplasms that are ineffective in generating multiple lineages of myeloid cells and have various risks to progress to acute myeloid leukemia. Recent genome-wide sequencing studies reveal that mutations in genes of splicing factors are commonly associated with MDS. However, the importance of these splicing factors in hematopoiesis has been unclear and the causal effect of their mutations on MDS development remains to be determined. One of these newly identified genes is SRSF2, and its mutations have been linked to poor survival among MDS patients. Interestingly, most of SRSF2 mutations occur at proline 95 and the majority of these mutations change this proline to histidine (P95H). Given that SRSF2 is a well-characterized splicing factor involved in both constitutive and regulated splicing, we hypothesize that SRSF2 plays an important role in normal hematopoiesis and the SRSF2 mutations induce specific changes in alternative splicing that favor disease progression. We first examined the role of SRSF2 in hematopoiesis by generating Srsf2 null mutation in mouse blood cells via crossing conditional Srsf2 knockout mice (Srsf2f/f) with blood cell-specific Cre transgenic mice (Vav-Cre). The mutant mice produced significantly fewer definitive blood cells (10% of wild type controls), exhibited increased apoptosis in the remaining blood cells, and died during embryonic development. Importantly, we detected no hematopoietic stem/progenitor cells (lineage-/cKit+) in E14 fetal livers of Vav-Cre/Srsf2f/f mice. These results indicate that SRSF2 is essential for hematopoiesis during embryonic development. We next examined the role of SRSF2 in adult hematopoiesis by injecting polyIC into mice that carry a polyIC inducible Cre expression unit. Unexpectedly, after multiple polyIC treatments, the Srsf2f/f mice stayed alive during several months of observation. Time course genotyping analyses of polyIC treated mice revealed an increased rate of incomplete Srsf2 deletion in peripheral blood cells. These observations suggest that Srsf2 ablation did not cause immediate cell lethality in differentiated blood cells, but the gene is indispensable for the function of blood stem/progenitor cells. Since mutations of splicing factors are generally heterozygous in MDS patients, we also examined mice with Srsf2+/- blood cells. No obvious defect of hematopoiesis was observed under normal conditions or in response to stress with 5-FU treatment and sublethal irradiation. To gain molecular insight into the splicing activity of MDS-associated mutant forms of SRSF2, we performed large-scale alternative splicing surveys by using RNA-mediated oligonucleotide annealing, selection, and ligation coupled with next-generation sequencing (RASL-seq) previously developed in our lab, which offers a robust and cost-effective platform for splicing profiling. Compared to vector transduction controls, we found that overexpression of both wild type and P95H SRSF2 induced many, but distinct changes in alternative splicing in lineage-negative bone marrow cells, and importantly, we noted several changes in genes with known roles in hematopoietic malignancies that were uniquely induced by the mutant SRSF2. To further link the mutations to altered splicing in MDS patients, we also applied RASL-seq to a large number of MDS patient samples with or without mutations in SRSF2 or other splicing regulators. The data revealed a specific set of alternative splicing events that are commonly linked to MDS with splicing factor mutations. These findings strongly suggest that many of these mutations in splicing regulators are gain-of-function mutations that are causal to MDS. In conclusion, we report that SRSF2 plays an essential role in hematopoietic stem/progenitor cells and that the MDS-associated mutations in SRSF2 have a dominant effect on RNA alternative splicing. These findings provide functional information and molecular basis of SRSF2 and its MDS-related mutations in hematopoiesis and related clinical disorders. Disclosures: No relevant conflicts of interest to declare