البحث والنشر العلمي

1

Qadah T, Finlayson J, Ghassemifar R: In vitro characterization of the α-thalassemia point mutation HBA2:c.95+1G>A (α2IVS1-1(G>A)). Hemoglobin, 2012, 36(1):38–46.

http://www.ncbi.nlm.nih.gov/pubmed/21967524

2

Qadah T, Finlayson J, Newbound C, Pell N, Jennens M, Holmes P, Grey D, Beilby J, Ghassemifar R.: A molecular tool to assess the pathological relevance of alpha-globin DNA variants. Pathology. 2012, 44(4):337-341.

http://www.ncbi.nlm.nih.gov/pubmed/22531344

3

Qadah T, Finlayson J, Newbound C, Pell N, Pascoe M, Greenwood L, Holmes P, Grey D, Beilby J, Ghassemifar R: Molecular and cellular characterization of a new α-thalassemia mutation (HBA2:c.94A>C) generating an alternative splice site and a premature stop codon. Hemoglobin. 2012, 36(3):244-52.

http://www.ncbi.nlm.nih.gov/pubmed/22524210

4

Ghassemifar R, Forster L, Qadah T, Finlayson J: Identification and Characterization of Two Novel and Differentially Expressed Isoforms of Human α2- and α1-Globin Genes. Hemoglobin. 2012, 36(3): p. 244-252.

http://www.ncbi.nlm.nih.gov/pubmed/22738435

5

Qadah T, Finlayson J, Dennis M, Ghassemifar R. Molecular and cellular analysis of three novel α2-globin gene promoter mutations [HBA2:c.-59C>T], [HBA2:c.-81C>A] and [HBA2:c.-91G>A] reveal varying patterns of transcriptional and translational activities. Pathology. 2014, 46(1):46-52.

http://www.ncbi.nlm.nih.gov/pubmed/24300714

6

Qadah T, Joly P, Finlayson J, Ghassemifar R Molecular and cellular analysis of a novel α2-globin mutation [HBA2:c.94A>G] shows activation of a cryptic splice site and generation of a premature termination codon. Hemoglobin. 2014, 38(1):13-8

http://www.ncbi.nlm.nih.gov/pubmed/24274170

7

Qadah T, Finlayson J, Emma N, Ghassemifar R: Molecular characterization of Hb Hamilton Hill (HBA2:c.388delC), a novel HBA2 variant generating a premature termination codon and truncated HBA2 chain. Hemoglobin, 2015; 39(2):88-94.

http://www.ncbi.nlm.nih.gov/pubmed/25791745

8

Qadah T, Finlayson J, Newbound C, Ghassemifar R: Experimental characterization of Hb Flurlingen (HBA2:c.177C>G,p.His>Gln) and Hb Boghé (HBA2:c.177C>A,p.His>Gln), reveals contradictory HBA2 expression and translation patterns despite identical amino acid substitutions.

Hemoglobin, 2015; 39(5):340-5.

https://www.ncbi.nlm.nih.gov/pubmed/26193975

9

Forster L, Ardakani RM, Qadah T, Finlayson J, Ghassemifar R: The effect of nonsense mediated decay on transcriptional activity within the novel β-thalassaemia mutation Hemoglobin Yala (HBB:c.129delT).

Hemoglobin, 2015;39(5):334-9.

https://www.ncbi.nlm.nih.gov/pubmed/26207313

10

Khojah A, Faidah H, Sami I, Qadah T: The Effect of Fetal Hemoglobin on RBC Parameters among Sickle Cell Anemia Patients: A Cross Sectional Study from Makkah City; Western Saudi Arabia.

Hematol Transfus Int J, 2016; 3(1): 00059. DOI: 10.15406/htij.2016.03.00059

http://medcraveonline.com/HTIJ/HTIJ-03-00059.php