Structural, magnetic and optical properties of disordered double perovskite Gd2CoCrO6 nanoparticles.

We have synthesized disordered double perovskite Gd2CoCrO6 (GCCO) nanoparticles with an average particle size of 71 ± 3 nm by adopting a citrate sol-gel method to investigate their structural, magnetic, and optical properties. Rietveld refinement of the X-ray diffraction pattern showed that GCCO is crystallized in a monoclinic structure with space group P21/n, which is further confirmed by Raman spectroscopic analysis. The absence of perfect long-range ordering between Co and Cr ions is confirmed by the mixed valence states of Co and Cr. A Néel transition was observed at a higher temperature of TN = 105 K compared to that of an analogous double perovskite Gd2FeCrO6 due to a greater degree of magnetocrystalline anisotropy of Co than Fe. Magnetization reversal (MR) behavior with a compensation temperature of Tcomp = 30 K was also observed. The hysteresis loop obtained at 5 K exhibited the presence of both ferromagnetic (FM) and antiferromagnetic (AFM) domains. Super-exchange and Dzyaloshinskii-Moriya (DM) interactions between various cations via oxygen ligands are responsible for the observed FM or AFM ordering in the system. Furthermore, UV-visible and photoluminescence spectroscopy demonstrated the semiconducting nature of GCCO with a direct optical bandgap of 2.25 eV. The Mulliken electronegativity approach revealed the potential applicability of GCCO nanoparticles in photocatalytic H2 and O2 evolution from water. Due to a favorable bandgap and potentiality as a photocatalyst, GCCO can be a promising new member of double perovskite materials for photocatalytic and related solar energy applications.

Identification of Variants and Mutational Analyses of Cardiac Myosin-binding Protein C (MYBPC3) Gene of Adult Bangladeshi Patients with Hypertrophic Cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is the most prevalent genetic hereditary cardiomyopathy characterized by sudden cardiac death. Mutations in the MYBPC3 gene are often the most prevalent genetic abnormality in HCM with a prevalence ranging from 20.0 to 42.0%. The mutation spectrum is available for different countries, but such studies are lacking in the Asian population including Bangladeshi patients. A cross-sectional descriptive study was conducted for mutation analysis of the whole MYBPC3 gene on a cohort of 75 HCM Bengali Bangladeshi probands through Next Generation Sequencing at the Genetic Research Lab of Bangabandhu Sheikh Mujib Medical University from 2016 to 2019. The structural and functional impact of the mutations was further analyzed by in silico process. We analyzed the data and found 103 variants in 102 locations in the MYBPC3 gene. Variants were identified in both the coding region and the non-coding region. We found one possibly novel variant in the MYBPC3 gene. The findings of this research will help to develop a genetic database of HCM which will help in the early diagnosis and proper management of HCM patients in Bangladesh. One pathogenic splice donor variant (47356592 C >T) was found in the intronic region. Among the variants in the coding region, one missense mutation was pathogenic (NP₋000247.2: p.Asp770Asn) which was found in seven patients and another one is of conflicting interpretations of pathogenicity (NP₋000247.2: p.Ser217Gly) which was found in two patients. We have identified one in-frame deletion (NP₋000247.2: p.Ala433del) that is possible a novel variant responsible for the development of HCM.