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- 저자 : Furhan Iqbal (검색결과 2 건)
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Biocompatibility of cobalt iron oxide magnetic nanoparticles in male rabbits
Furhan Iqbal,Tanveer Ahmad Tabish,Muhammad Naeem Ashiq,Muhammad Azeem Ullah,Shahid Iqbal,Muhammad Latif,Muhammad Ali,Muhammad Fahad Ehsan 한국화학공학회 2016 Korean Journal of Chemical Engineering Vol.33 No.7
Present study was conducted to study the in vivo biocompatibility of cobalt iron oxide magnetic nano-particles (CoFe2O4 MNPs) in rabbits. CoFe2O4 MNPs were synthesized by the conventional micro emulsion technique in crystallite size range of 30 to 50 nm. The lattice constant (a) and cell volume were found to be 8.386 Å and 589.75 Å3, respectively, revealed by XRD. Subject animals were divided in three groups--low dose, high dose and control group without nanoparticles implantation for biocompatibility evaluation. CoFe2O4 was intraperitoneally implanted in rabbits: low dose (1mg CoFe2O4/Kg body weight) and high dose (10mg CoFe2O4/Kg body weight). Blood, serum and histological study of vital organs (liver, heart, kidney and spleen) were carried out in seven days of time protocol after sacrificing of animals. Results indicated that CoFe2O4 had drastically affected the blood chemistry in a dose-dependent manner as RDWa (P=0.01), Platelet (P<0.001) and Plateletcrit (P<0.001) concentrations reduced significantly in low dose and high dose CoFe2O4 treatments as compared to sham treated control group. Histological analysis revealed that CoFe2O4 exposure resulted in disordered and abnormal histology of liver, kidney and that of muscles at surgical site. It is concluded that CoFe2O4 has low biocompatibility and higher toxicity levels in living system at the applied doses.
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Saima Mustafa,Zafrin Akhtar,Muhammad Latif,Mubashir Hassan,Muhammad Faisal,Furhan Iqbal 한국유전학회 2020 Genes & Genomics Vol.42 No.8
Background Acromesomelic dysplasia, type Maroteaux (AMDM) is a rare skeletal dysplasia following autosomal recessive mode of inheritance and characterized by abnormal growth plates, short and abnormal bones in the extremities and spine. Objective Present study was designed to report the molecular basis of AMDM in enrolled consanguineous family from Pakistan. Methods A consanguineous family from Vehari District in Pakistan having multiple siblings suffering from AMDM was enrolled in present study. Whole exome sequencing (WES) approach was adopted to identify causative agent of AMDM. Human full length NPR2 gene and sequence with nonsense mutation was amplified by using Myc-tagged pXN vector and transformed in E. coli DH5α cells to confirm mutation. SDS-PAGE and Western blotting were done to confirm the production of truncated protein. Computational three dimensional structure generation through homology modeling approach was done to compare protein structure between patients and controls. Results WES reveled a nonsense mutation (c.613 C>T, p.R205X) in exon 1 of NPR2 gene leading to premature termination codon in mRNA of NPR2 gene resulting in a truncated protein with 204 amino acid residues that was confirmed by SDSPAGE and Western blotting. Sanger sequencing confirmed that mutation in all subjects and mutation followed Mendalian pattern of inheritance. Multiple sequence alignment by ClustalW revealed that mutated domain of NPR2 is conserved region. Proetin structure comparison revealed a significant structural part of NPR2 was missing in truncated protein as compared to control. Conclusion We are reporting that a novel nonsense mutation (c.613 C>T, p.R205X) in exon 1 of NPR2 gene is causing AMDM in a consanguineous Pakistani family.
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