Reduced Graphene Oxide-Zinc Sulfide Nanocomposite Decorated with Silver Nanoparticles for Wastewater Treatment by Adsorption, Photocatalysis and Antimicrobial Action.

Reduced graphene oxide nanosheets decorated with ZnS and ZnS-Ag nanoparticles are successfully prepared via a facile one-step chemical approach consisting of reducing the metal precursors on a rGO surface. Prepared rGO-ZnS nanocomposite is employed as an adsorbent material against two model dyes: malachite green (MG) and ethyl violet (EV). The adsorptive behavior of the nanocomposite was tuned by monitoring some parameters, such as the time of contact between the dye and the adsorbent, and the adsorbent dose. Experimental data were also simulated with kinetic models to evaluate the adsorption behavior, and the results confirmed that the adsorption of both dyes followed a pseudo 2nd order kinetic mode. Moreover, the adsorbent was also regenerated in a suitable media for both dyes (HCl for MG and ethanol for EV), without any significant loss in removal efficiency. Ag doped rGO-ZnS nanocomposite was also utilized as a photocatalyst for the degradation of the selected organic contaminant, resorcinol. The complete degradation of the phenolic compound was achieved after 60 min with 200 mg of rGO-ZnS-Ag nanocomposite under natural sunlight irradiation. The photocatalytic activity was studied considering some parameters, such as the initial phenol concentration, the photocatalyst loading, and the pH of the solution. The degradation kinetics of resorcinol was carefully studied and found to follow a linear Langmuir-Hinshelwood model. An additional advantage of rGO-ZnS and rGO-ZnS-Ag nanocomposites was antibacterial activity against Gram-negative bacterium, E. coli, and the results confirmed the significant performance of the nanocomposites in destroying harmful pathogens.

Effects of Multivitamin-Mineral Supplementation on Chronic Stress-Induced Oxidative Damage in Swiss Albino Mice.

OBJECTIVE: Stress is a hazardous occurrence that causes a variety of physiological and behavioral responses in a person. It increases energy metabolism and enhances oxidative stress, both of which are implicated in the pathophysiology of several diseases. Numerous vitamins and minerals have the ability to modulate oxidative stress. The present investigation aimed to evaluate the effectiveness of a multivitamin-mineral (MM) supplement in addressing oxidative imbalances caused by chronic stress in the plasma, hepatic, and renal tissues of Swiss albino mice. METHODS: Thirty healthy male Swiss albino mice were randomly assigned to one of the three groups, with 10 animals each: control, unpredictable chronic stress (UCS), and MM + UCS. The experiment lasted for four weeks, after which all the animals underwent cervical decapitation, and samples of their blood, liver, and kidney were taken for biochemical studies. DNA damage analysis was performed on lymphocytes. RESULTS: Exposure to UCS negatively affected all biochemical markers, as indicated by reduced levels of antioxidants (superoxide dismutase, catalase, glutathione S-transferase, glutathione reductase, and reduced glutathione) in the plasma, liver, and kidney tissues, along with enhanced levels of lipid peroxidation and marker enzymes. MM supplementation normalized the deranged biochemical markers in stress-exposed mice. The results of DNA damage supported the biochemical findings mentioned above. CONCLUSION: The findings suggest that MM supplementation could help reduce oxidative disturbances caused by stress in both healthy and diseased conditions.

Genome-wide CNV analysis uncovers novel pathogenic regions in cohort of five multiplex families with neurodevelopmental disorders.

Structural reorganization of chromosomes by genomic duplications and/or deletions are known as copy number variations (CNVs). Pathogenic and disease susceptible CNVs alter gene dosage and its phenotypic expression that often leads to human genetic diseases including Neurological disorders. CNVs affecting same common genes in multiple neurodevelopmental disorders can better explain the shared clinical and genetic aetiology across brain diseases. Our study presents the novel copy number variations in a cohort of five multiplex consanguineous families with intellectual disability, microcephaly, ASD, epilepsy, and neurological syndromic features. Cytoscan HD microarray suite has revealed genome wide deletions, duplications and LOH regions which are co-segregating in the family members for the rare neurodevelopmental syndromic phenotypes. This study identifies 1q21.1 microduplication, 16p11.2 microduplication, Xp11.22 microduplication, 4p12 microdeletion and Xq21.1 microdeletion that significantly contribute to primary disease onset and its progression for the first time in Pakistani families. Our study has potential impact on the understanding of pathogenic genetic predisposition for appearance of complex and heterogeneous neurodevelopmental disorders with otherwise unexplained syndromic features. Identification of altered gene dosage across the genome is helpful in improved diagnosis, better disease management in day-to-day life activities of patients with cognitive impairment and genetic counselling of families where consanguinity is a tradition. Our study will contribute to expand the knowledge of genotype-phenotype expression and future gateways in therapeutics and precision medicine research will be open in Pakistan.