Graphene nanoplatelets/CeO2 nanotiles nanocomposites as effective antibacterial material for multiple drug-resistant bacteria.

Antibacterial agents with low toxicity to normal cells, redox activity and free radical scavenging property are urgently needed to address the global health crisis. The phenomenal conducting nature of graphene is a best fit to enhance the antibacterial properties of metal oxides. In this work, CeO2 nanotiles and graphene nanoplatelets/CeO2 nanotiles nanocomposites (G/CeO2) have been synthesized by a solvothermal method. The prepared materials have been characterized using XRD, FE-SEM, EDX, and UV-visible spectroscopy techniques to investigate their crystallinity, morphology, composition, and optical bandgap energies. The CeO2 and G/CeO2 nanocomposites have also been tested for antibacterial applications. The neat CeO 2 nanotiles sample inhibits the bacterial growth of Pseudomonas aeruginosa and Staphylococcus aureus up to 14.21% and 39.53% respectively. The antibacterial activity was tremendously enhanced using 25% graphene-loaded sample (G/CeO2-II) i.e., approximately 83% loss of P. aeruginosa and 89% in case of S. aureus has been observed. This can be attributed to the unique nano-architecture, oxidative stress due to the excellent ability of reversible conversion between the two electronic states of CeO2 and the stress exerted by the planar graphene and CeO2 nanotiles. Therefore, the G/CeO2 nanocomposites can find potential application as nano-antibiotics for controlling pathogens.

SnO2nanorods/graphene nanoplatelets nanocomposites: towards fast removal of malachite green and pathogen control.

The world is facing alarming challenges of environmental pollution due to uncontrolled water contamination and multiple drug resistance of pathogens. However, these challenges can be addressed by using novel nanocomposites materials such as, SnO2/graphene nanopaletelets (GNPs) nanocomposites remarkably. In this work, we have prepared SnO2nanorods and SnO2/GNPs nanocomposites (GS-I and GS-II) with size of 25 ± 6 nm in length and 4 ± 2 nm in diameter. The optical bandgap energies change from 3.14 eV to 2.80 eV in SnO2and SnO2/GNPs nanocomposite. We found that SnO2/GNPs nanocomposite (GS-II) completely removes (99.11%) malachite green in 12 min, under UV light exposure, while under same conditions, SnO2nanorods removes only 37% dye. Moreover, visible light exposure resulted in 99.01% removal of malachite green in 15 min by GSII as compared to 24.7% removal by SnO2. In addition, GS-II nanocomposite inhibits 79.57% and 78.51% growth ofP. aeruginosaandS. aureusrespectively. A synchronized contribution of SnO2and GNPs makes SnO2/GNPs nanocomposites (GS-II) an innovative multifunctional material for simultaneous fast and complete removal of malachite green and inhibition of drug resistant pathogens.

Screening of 31 genes involved in monogenic forms of obesity in 23 Pakistani probands with early-onset childhood obesity: a case report.

BACKGROUND: Consanguine families display a high degree of homozygosity which increases the risk of family members suffering from autosomal recessive disorders. Thus, homozygous mutations in monogenic obesity genes may be a more frequent cause of childhood obesity in a consanguineous population. METHODS: We identified 23 probands from 23 Pakistani families displaying autosomal recessive obesity. We have previously excluded mutations in MC4R, LEP and LEPR in all probands. Using a chip-based, target-region capture array, 31 genes involved in monogenic forms of obesity, were screened in all probands. RESULTS: We identified 31 rare non-synonymous possibly pathogenic variants (28 missense and three nonsense) within the 31 selected genes. All variants were heterozygous, thus no homozygous pathogenic variants were found. Two of the rare heterozygous nonsense variants identified (p.R75X and p.R481X) were found in BBS9 within one proband, suggesting that obesity is caused by compound heterozygosity. Sequencing of the parents supported the compound heterozygous nature of obesity as each parent was carrying one of the variants. Subsequent clinical investigation strongly indicated that the proband had Bardet-Biedl syndrome. CONCLUSIONS: Mutation screening in 31 genes among probands with severe early-onset obesity from Pakistani families did not reveal the presence of homozygous obesity causing variants. However, a compound heterozygote carrier of BBS9 mutations was identified, indicating that compound heterozygosity must not be overlooked when investigating the genetic etiology of severe childhood obesity in populations with a high degree of consanguinity.

Increased frequency of rare missense PPP1R3B variants among Danish patients with type 2 diabetes.

BACKGROUND: PPP1R3B has been suggested as a candidate gene for monogenic forms of diabetes as well as type 2 diabetes (T2D) due to its association with glycaemic trait and its biological role in glycogen synthesis. OBJECTIVES: To study if rare missense variants in PPP1R3B increase the risk of maturity onset diabetes of the young (MODY), T2D or affect measures of glucose metabolism. METHOD: Targeted resequencing of PPP1R3B was performed in 8,710 samples; MODY patients with unknown etiology (n = 54), newly diagnosed patients with T2D (n = 2,930) and population-based control individuals (n = 5,726, of whom n = 4,569 had normal glucose tolerance). All population-based sampled individuals were examined using an oral glucose tolerance test. RESULTS: Among n = 396 carriers, we identified twenty-three PPP1R3B missense mutations, none of which segregated with MODY. The burden of likely deleterious PPP1R3B variants was significantly increased with a total of 17 carriers among patients with T2D (0.58% (95% CI: 0.36-0.93)) compared to 18 carriers among non-diabetic individuals (0.31% (95% CI: 0.20-0.49)), resulting in an increased risk of T2D (OR (95% CI) = 2.57 (1.14-5.79), p = 0.02 (age and sex adjusted)). Furthermore, carriers with diabetes had less abdominal fat and a higher serum concentration of LDL-cholesterol compared to patients with T2D without rare missense PPP1R3B variants. In addition, non-diabetic carriers had a higher birth weight compared to non-carriers. CONCLUSION: Rare missense PPP1R3B variants may predispose to T2D.

Identification of novel LEPR mutations in Pakistani families with morbid childhood obesity.

BACKGROUND: Mutations in the genes encoding leptin (LEP), the leptin receptor (LEPR), and the melanocortin 4 receptor (MC4R) are known to cause severe early-onset childhood obesity. The aim of the current study was to examine the prevalence of damaging LEP, LEPR, and MC4R mutations in Pakistani families having a recessive heritance of early-onset obesity. METHODS: Using targeted resequencing, the presence of rare mutations in LEP, LEPR, and MC4R, was investigated in individuals from 25 families suspected of having autosomal recessive early-onset obesity. Segregation patterns of variants were assessed based on chip-based genotyping. RESULTS: Homozygous LEPR variants were identified in two probands. One carried a deletion (c.3260AG) resulting in the frameshift mutation p.Ser1090Trpfs*6, and the second carried a substitution (c.2675C > G) resulting in the missense mutation p.Pro892Arg. Both mutations were located within regions of homozygosity shared only among affected individuals. Both probands displayed early-onset obesity, hyperphagia and diabetes. No mutations were found in LEP and MC4R. CONCLUSIONS: The current study highlights the implication of LEPR mutations in cases of severe early-onset obesity in consanguineous Pakistani families. Through targeted resequencing, we identified novel damaging mutations, and our approach may therefore be utilized in clinical testing or diagnosis of known forms of monogenic obesity with the aim of optimizing obesity treatment.