Dr Saad Salem

Associate Lecturer

School of Biomedical Sciences and Pharmacy

Career Summary

Biography

Dr Saad Salem graduated with a Doctor of Pharmacy (PharmD) degree with a strong clinical focus; he appreciates the importance of understanding the mechanism of action of medicines in order to develop and optimise pharmacotherapeutic plans and make sound clinical judgements. Saad completed a PhD at The University of Melbourne investigating the role of transforming growth factor-beta (TGF-β) in modulating the cellular responses of glucocorticoids, an important class of medicines used to treat asthma and inflammatory conditions.  Dr Salem’s research was awarded multiple prizes including best oral presentation at the Thoracic Society of Australia and New Zealand (TSANZ) annual scientific meeting and Neville Percy prize for best poster presentation at the Australasian Society of Clinical and Experimental Pharmacologists and Toxicologists (ASCEPT) annual scientific meeting. He was invited by the British Pharmacological Society (BPS) to present his research at the BPS annual winter scientific meeting in London for which he was awarded a travel grant. He is a member of the translational research program at the Hunter Medical Research Institute (HMRI) focusing on viruses, infections/immunity, vaccines and asthma (VIVA).  

Dr Salem is a pharmacist registered with the Pharmacy Board of Australia and the Australian Health Practitioner Regulation Agency (AHPRA). He incorporates his experience as a community pharmacist into his teaching of pharmacotherapy and pharmacy practice and strives to equip students with the knowledge and skills to become future leaders in pharmacy.


Qualifications

  • Doctor of Philosophy, University of Melbourne
  • Doctor of Pharmacy, Jordan University of Science & Technology - Jordan

Professional Experience

UON Appointment

Title Organisation / Department
Associate Lecturer University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia

Awards

Prize

Year Award
2011 The British Pharmacological Society Travel Bursary
The British Pharmacological Society (BPS)
2010 Neville Percy Prize for Best Poster Presentation at The Australasian Society of Clinical and Experimental Pharmacologists and Toxicologists
Australian Society of Clinical and Experimental Pharmacologists and Toxicologists
2010 The Thoracic Society of Australia and New Zealand Best Oral Presentation
The Thoracic Society of Australia and New Zealand

Scholarship

Year Award
2011 The Australasian Society of Clinical and Experimental Pharmacologists and Toxicologists International Travel Scholarship
Australasian Society of Clinical and Experimental Pharmacologists and Toxicologists
2011 The University of Melbourne Abroad Travel Scholarship
The University of Melbourne
2011 M.A. Bartlett Research Scholarship Fund
The University of Melbourne
2011 The Department of Pharmacology, The University of Melbourne Abroad Travelling Scholarship
The University of Melbourne

Invitations

Speaker

Year Title / Rationale
2011 TGF-beta Impairs Glucocorticoid Responses in Airway Epithelial Cells
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Publications

For publications that are currently unpublished or in-press, details are shown in italics.


Journal article (5 outputs)

Year Citation Altmetrics Link
2014 Keenan CR, Mok JSL, Harris T, Xia Y, Salem S, Stewart AG, 'Bronchial epithelial cells are rendered insensitive to glucocorticoid transactivation by transforming growth factor-ß1', Respiratory Research, 15 (2014) [C1]

Background: We have previously shown that transforming growth factor-beta (TGF-beta) impairs glucocorticoid (GC) function in pulmonary epithelial cell-lines. However, the signalli... [more]

Background: We have previously shown that transforming growth factor-beta (TGF-beta) impairs glucocorticoid (GC) function in pulmonary epithelial cell-lines. However, the signalling cascade leading to this impairment is unknown. In the present study, we provide the first evidence that TGF-beta impairs GC action in differentiated primary air-liquid interface (ALI) human bronchial epithelial cells (HBECs). Using the BEAS-2B bronchial epithelial cell line, we also present a systematic examination of the known pathways activated by TGF-beta, in order to ascertain the molecular mechanism through which TGF-beta impairs epithelial GC action.Methods: GC transactivation was measured using a Glucocorticoid Response Element (GRE)-Secreted embryonic alkaline phosphatase (SEAP) reporter and measuring GC-inducible gene expression by qRT-PCR. GC transrepression was measured by examining GC regulation of pro-inflammatory mediators. TGF-beta signalling pathways were investigated using siRNA and small molecule kinase inhibitors. GRa level, phosphorylation and sub-cellular localisation were determined by western blotting, immunocytochemistry and localisation of GRa-Yellow Fluorescent Protein (YFP). Data are presented as the mean ± SEM for n independent experiments in cell lines, or for experiments on primary HBEC cells from n individual donors. All data were statistically analysed using GraphPad Prism 5.0 (Graphpad, San Diego, CA). In most cases, two-way analyses of variance (ANOVA) with Bonferroni post-hoc tests were used to analyse the data. In all cases, P < 0.05 was considered to be statistically significant.Results: TGF-beta impaired Glucocorticoid Response Element (GRE) activation and the GC induction of several anti-inflammatory genes, but did not broadly impair the regulation of pro-inflammatory gene expression in A549 and BEAS-2B cell lines. TGF-beta-impairment of GC transactivation was also observed in differentiated primary HBECs. The TGF-beta receptor (ALK5) inhibitor SB431541 fully prevented the GC transactivation impairment in the BEAS-2B cell line. However, neither inhibitors of the known downstream non-canonical signalling pathways, nor knocking down Smad4 by siRNA prevented the TGF-beta impairment of GC activity.Conclusions: Our results indicate that TGF-beta profoundly impairs GC transactivation in bronchial epithelial cells through activating ALK5, but not through known non-canonical pathways, nor through Smad4-dependent signalling, suggesting that TGF-beta may impair GC action through a novel non-canonical signalling mechanism. © 2014 Keenan et al.; licensee BioMed Central Ltd.

DOI 10.1186/1465-9921-15-55
Citations Scopus - 12Web of Science - 15
2012 Salem S, Harris T, Mok JSL, Li MYS, Keenan CR, Schuliga MJ, Stewart AG, 'Transforming growth factor-ß impairs glucocorticoid activity in the A549 lung adenocarcinoma cell line', British Journal of Pharmacology, 166 2036-2048 (2012) [C1]
DOI 10.1111/j.1476-5381.2012.01885.x
Citations Scopus - 24Web of Science - 29
Co-authors Michael Schuliga
2012 Keenan CR, Salem S, Fietz ER, Gualano RC, Stewart AG, 'Glucocorticoid-resistant asthma and novel anti-inflammatory drugs', Drug Discovery Today, 17 1031-1038 (2012) [C1]
DOI 10.1016/j.drudis.2012.05.011
Citations Scopus - 31Web of Science - 33
2009 Alzoubi KH, Mhaidat N, azzam SA, Khader Y, Salem S, Issaifan H, Haddadin R, 'Prevalence of migraine and tension-type headache among adults in Jordan', The Journal of Headache and Pain, 10 265-270 (2009)
DOI 10.1007/s10194-009-0122-6
2002 El-Gindy GA, Mohammed FA, Salem SY, 'Preparation, pharmacokinetic and pharmacodynamic evaluation of carbamazepine inclusion complexes with cyclodextrins', S.T.P. Pharma Sciences, 12 369-378 (2002)

In an attempt to improve the solubility, bioavailability and anti-convulsion activity of carbamazepine (CBZ), inclusion complexes of CBZ were prepared with a-CD, ß-CD and di-O-me... [more]

In an attempt to improve the solubility, bioavailability and anti-convulsion activity of carbamazepine (CBZ), inclusion complexes of CBZ were prepared with a-CD, ß-CD and di-O-methyl-ß-cyclodextrin (DM-ß-CD). This report investigates the study of CBZ's phase diagram, preparation of the inclusion complexes and characterization of the physicochemical properties of the complexes. The bioavailability, and anti-convulsion activity of CBZ were determined in animals following oral administration of the prepared complexes, and compared with the sole drug, as well as physical and ground mixtures with different types of cyclodextrins. The solubility curves of CBZ with a-CD, ß-CD and DM-ß-CD were typical AL type curves, and apparent stability constants, K c , were calculated from the slope and intercept of the solubility, diagrams as 1000, 2400 and 4333 M -1 , respectively. The inclusion complexation, in aqueous solution and in solid phases, was confirmed by the solubility method, X-ray diffractometry, infrared spectroscopy (IR) and differential scanning calorimetry (DSC). The dissolution rate of CBZ in ground mixtures and inclusion complexes was much more rapid than that of CBZ alone or the corresponding physical mixtures. The bioavailability studies indicated faster absorption of CBZ from its complex and ground mixtures with DM-ß-CD, compared to a-CD and ß-CD, or the corresponding physical mixtures as indicated by the t max and the C max values. Administration of the CBZ-DM-ß-CD complex produced the highest protection percentage for mice from death (66%) by maximum electroshock-induced convulsion (MES). The onset of convulsion was markedly delayed in mice pretreated with the CBZ-DM-ß-CD complex. Based on the obtained results, preparation of CBZ complexes with DM-ß-CD should markedly improve the solubility, bioavailability and anticonvulsion activity of CBZ.

Citations Scopus - 7
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Conference (5 outputs)

Year Citation Altmetrics Link
2013 Keenan C, Lopez-Campos G, Salem S, Harris T, Schuliga M, Johnstone C, Stewart A, 'RNA-seq analysis of transforming growth factor-beta-induced glucocorticoid resistance in human bronchial epithelial cells', EUROPEAN RESPIRATORY JOURNAL (2013)
Co-authors Michael Schuliga
2013 Keenan CR, Salem S, Harris T, Schuliga M, Stewart AG, 'TRANSFORMING GROWTH FACTOR-beta INDUCES GLUCOCORTICOID RESISTANCE IN HUMAN BRONCHIAL EPITHELIAL CELLS', RESPIROLOGY (2013)
Co-authors Michael Schuliga
2011 Salem S, Harris T, Schuliga M, Mok J, Stewart A, 'Transforming Growth Factor Beta (TGFBeta) Induces Glucocorticoid-Resistance In A549 Adenocarcinoma Cell Line By Reducing Glucocorticoid Receptor Nuclear Localisation', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2011)
Co-authors Michael Schuliga
2010 Stewart A, Salem S, Lian JMS, Schuliga M, Harris T, 'Glucocorticoid resistance in human airway epithelial cells: a potential role for Transforming Growth Factor-beta', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2010)
Co-authors Michael Schuliga
2009 Stewart AG, Schuliga M, Mok J, Salem S, Harris T, 'TGF-Induces Glucocorticoid Resistance beta.', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE (2009)
Co-authors Michael Schuliga
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Dr Saad Salem

Position

Associate Lecturer
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Contact Details

Email saad.salem@newcastle.edu.au
Phone (02) 4985 4380

Office

Room MS110
Building Medical Science Building
Location Callaghan
University Drive
Callaghan, NSW 2308
Australia
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