31 research outputs found

    Raman spectroscopy insights into the a- and d-phases of formamidinium lead iodide (FAPbI3)

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    Solar perovskites have received phenomenal attention and success over the past decade, due to their high power conversion efficiencies (PCE), ease of fabrication and low cost which has enabled the prospect of them being a real commercial contender to the traditional silicon technology. In one of the several developments on the archetypal MAPbI3perovskite absorber layer, FAPbI3was found to obtain a higher PCE, likely due to its more optimum band gap, with doping strategies focusing on the inclusion of MA+/Cs+cations to avoid the unfavourable phase transformation to a photoinactive phase. To better understand the phase change from the photoactive cubic (Pm3¯m) black (a) phase to the unwanted photoinactive (P63/mmc) yellow (d) phase, we make use of variable temperature Raman spectroscopy to probe the molecular species and its relationship to the inorganic framework. We show for the first time there to be no Raman active modes for the a phase up to 4000 cm-1, which can be correlated to thePm3¯mcubic symmetry of that phase. Our detailed studies suggest that previous reports of the observation of Raman peaks for this phase are likely associated with degradation reactions from the localised laser exposure and the formation of Raman active lead oxide. In addition, we have identified water as a contributing factor to the transformation, and observed a corresponding signal in the Raman spectra, although confirmation of its exact role still remains inconclusive

    ZMYND11‐related syndromic intellectual disability: 16 patients delineating and expanding the phenotypic spectrum

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    Pathogenic variants in ZMYND11, which acts as a transcriptional repressor, have been associated with intellectual disability, behavioural abnormalities and seizures. Only 11 affected individuals have been reported to‐date, and the phenotype associated with pathogenic variants in this gene have not been fully defined. Here, we present 16 additional patients with predicted pathogenic heterozygous variants in ZMYND11, including four individuals from the same family, to further delineate and expand the genotypic and phenotypic spectrum of ZMYND11‐related syndromic intellectual disability. The associated phenotype includes developmental delay, particularly affecting speech, mild‐moderate intellectual disability, significant behavioural abnormalities, seizures, and hypotonia. There are subtle shared dysmorphic features, including prominent eyelashes and eyebrows, depressed nasal bridge with bulbous nasal tip, anteverted nares, thin vermilion of the upper lip and wide mouth. Novel features include brachydactyly and tooth enamel hypoplasia. Most identified variants are likely to result in premature truncation and/or nonsense mediated decay. Two ZMYND11 variants located in the final exon ‐ p.(Gln586*) (likely escaping nonsense‐mediated decay) and p.(Cys574Arg) ‐ are predicted to disrupt the MYND‐type zinc finger motif and likely interfere with binding to its interaction partners. Hence, the homogeneous phenotype likely results from a common mechanism of loss‐of‐function
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