We have produced thin film samples of cubic ZnS by the chemical bath method. These samples were synthesized using zinc chloride, thiourea, sodium citrate and ammonia solutions at varied deposition time from 24h to 96h. X-ray diffraction (XRD), transmittance and photoluminescence (PL) analyses provided the physical characteristics of cubic ZnS films with crystal plane orientations (2 0 0) and (2 2 2), lattice parameters of 5.648 Å and an atomic plane distance d=1.412 Å. The grain size calculed are 16.53 nm and 17.12 nm. PL revealed deep defects in the gap with peaks in the visible, with prominent emissions at 430 nm (blue) and 510 nm (green). The measured transmittance of the films is 88.6%.

Glassy materials yield under large external mechanical solicitations. Under oscillatory shear, yielding shows a well-known rheological fingerprint, common to samples with widely different microstructures. At the microscale, this corresponds to a transition between slow, solid-like dynamics and faster liquid-like dynamics, which can coexist at yielding in a finite range of strain amplitudes. Here, we capture this phenomenology in a lattice model with two main parameters: glassiness and disorder, describing the average coupling between adjacent lattice sites, and their variance, respectively. In absence of disorder, our model yields a law of correspondent states equivalent to trajectories on a cusp catastrophe manifold, a well-known class of problems including equilibrium liquid-vapour phase transitions. Introducing a finite disorder in our model entails a qualitative change, to a continuous and rounded transition, whose extent is controlled by the magnitude of the disorder. We show that a spatial correlation length ξ emerges spontaneously from the coupling between disorder and bifurcating dynamics. With vanishing disorder, ξ diverges and yielding becomes discontinuous, suggesting that the abruptness of yielding can be rationalized in terms of a lengthscale of dynamic heterogeneities

Inborn errors of immunity (IEIs) are genetic disorders that underlie susceptibility to infection, autoimmunity, autoinflammation, allergy and/or malignancy1. Incomplete penetrance is common among IEIs despite their monogenic basis2. Here we investigate the contribution of autosomal random monoallelic expression (aRMAE), a somatic commitment to the expression of one allele3,4, to phenotypic variability observed in families with IEIs. Using a clonal primary T cell system to assess aRMAE status of genes in healthy individuals, we find that 4.30% of IEI genes and 5.20% of all genes undergo aRMAE. Perturbing H3K27me3 and DNA methylation alters allele expression commitment, in support of two proposed mechanisms5,6 for the regulation of aRMAE. We tested peripheral blood mononuclear cells from individuals with IEIs with shared genetic lesions but discordant clinical phenotypes for aRMAE. Among two relatives who were heterozygous for a mutation in PLCG2 (delEx19), an antibody deficiency phenotype corresponds to selective mutant allele expression in B cells. By contrast, among relatives who were heterozygous for a mutation in JAK1 (c.2099G>A; p.S700N), the unaffected carrier T cells predominantly expressed the wild-type JAK1 allele, whereas the affected carrier T cells exhibited biallelic expression. Allelic expression bias was also documented in phenotypically discordant family members with mutations in STAT1 and CARD11. This study highlights the importance of considering both the genotype and the ‘transcriptotype’ in analyses of the penetrance and expressivity of monogenic disorders.