Kuala Selangor, Malaysia
Kuala Selangor, Malaysia

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Zamanpoor M.,Genetic Medicine Research Center | Zamanpoor M.,University Putra Malaysia | Rosli R.,Genetic Medicine Research Center | Rosli R.,University Putra Malaysia | And 6 more authors.
Journal of Maternal-Fetal and Neonatal Medicine | Year: 2013

Objective: To quantify circulating fetal DNA (fDNA) levels in the second and third trimesters of normal healthy pregnant individuals and pregnant women with the following clinical conditions: gestational diabetes mellitus (GDM), iron deficiency anemia and gestational hypertension (GHT). Methods: The SRY gene located on the Y chromosome was used as a unique fetal marker. The fDNA was extracted from maternal plasma and the SRY gene concentrations were measured by quantitative real-time polymerase chain reaction (PCR) amplification using TaqMan dual labeled probe system. Results: No significant differences were observed in the mean fDNA concentration between normal and GDM pregnancy samples (p>0.05) and also between normal and anemic pregnancy samples (p>0.05) in both trimesters, but significant differences were observed between the third trimester normal and GHT pregnancy samples (p=0.001). GDM and iron deficiency anemia do not affect the levels of fDNA in maternal plasma while GHT significantly elevates the levels of fDNA in maternal plasma. Conclusions: Increased amount of circulating fDNA in maternal plasma could be used for early identification of adverse pregnancies. GDM and anemia do not affect the levels of fDNA in maternal plasma while GHT significantly elevates the levels of fDNA in maternal plasma. Hence, the elevated fDNA values could be used as a potential screening marker in pregnancies complicated with GHT but not with GDM and iron deficiency anemia. © 2013 Informa UK Ltd.


Partridge T.,Genetic Medicine Research Center
Journal of Child Neurology | Year: 2010

Duchenne muscular dystrophy is mainly caused by mutations that disrupt the generation of a translatable mRNA transcript. Most such mutations occur in parts of the gene that are not essential for its function and thus might be eliminated from the transcript to permit translation of a partially functional protein that would convert the disease to a milder clinical form. Two such antisense oligonucleotides of different backbone chemistries have been successful when tested on the mdx mouse, targeting exon 23, containing the nonsense mutation. Subsequently, the morpholino, the more effective of these, has been tested on the dystrophic dog, where it is necessary to skip 2 exons, again with beneficial results. Currently, results of 2 human trials targeting exon 51 have also yielded promising preliminary results. © The Author(s) 2010.


PubMed | Genetic Medicine Research Center
Type: Journal Article | Journal: Journal of child neurology | Year: 2010

Duchenne muscular dystrophy is mainly caused by mutations that disrupt the generation of a translatable mRNA transcript. Most such mutations occur in parts of the gene that are not essential for its function and thus might be eliminated from the transcript to permit translation of a partially functional protein that would convert the disease to a milder clinical form. Two such antisense oligonucleotides of different backbone chemistries have been successful when tested on the mdx mouse, targeting exon 23, containing the nonsense mutation. Subsequently, the morpholino, the more effective of these, has been tested on the dystrophic dog, where it is necessary to skip 2 exons, again with beneficial results. Currently, results of 2 human trials targeting exon 51 have also yielded promising preliminary results.

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