
Dr Fatemeh Moheimani
Conjoint Lecturer
School of Biomedical Sciences and Pharmacy
- Email:fatemeh.moheimani@newcastle.edu.au
- Phone: (02) 40420363
At the top of our lungs
Dr Fatemeh Moheimani is investigating how the structure and function of airway epithelium contribute to respiratory disease, with the end goal of developing novel interventions for asthma.
Considerable experience in cardio-vascular research employing different techniques across several laboratories has furnished Dr Fatemeh Moheimani with the skills needed to excel in her most recent area of focus in respiratory disease research, in particular, the airway epithelial cells in asthma.
Fatemeh is looking at what is happening at tissue and molecular level inside the lungs of asthma sufferers.
“Since the air we breathe is common between people who suffer from asthma and those who don’t, there should be underlying mechanisms at tissue and molecular level, responsible for asthma development,” Fatemeh explains.
“I am interested in understanding these mechanisms.”
“If we understand the mechanism involved, we can then offer an approach to manage the disease.”
Coming from RMIT in 2013 to establish Professor Darryl Knight’s Airway Cell Biology Laboratory and lead asthma research program in this laboratory at the Hunter Medical Research Institute (HMRI), Fatemeh has quickly proven she is more than capable of rising to the challenge of mastering a new area of focus whilst running a world-class research facility.
TRANSFORMING CELLS
The epithelium is the thin tissue lining the outer layer of the airway surface and is the first protective barrier between inhaled particles, for example allergens and viruses, and the internal environment of the lung.
“The airway epithelium has a pseudostratified structure,” Fatemeh says, “meaning although airway epithelium comprises a single layer of cells which are resting on a basement membrane, the nuclei of these cells are positioned in a manner suggestive of a multilayer structure of cell populations.”
“Some of these cells are like stem cells, we call them basal cells - they are able to divide and produce more cells. They can stay as basal cells or they can differentiate to different types of cells.”
Some cells produce mucus which lubricates the surface for protection against scratches from foreign particles. Other cells develop cilia, tiny hairs that aid in the removal of the foreign particles through a constant pulsing.
The balance between these cell populations is essential for normal function of the epithelium in the lung. Unfortunately, this balance isn’t always achieved in asthmatics.
ENTER ASTHMA
In asthmatics, cells predominantly stay in the stem cell or basal cell mode. These abnormalities in asthmatic epithelium prevent normal regeneration after epithelial wounding, resulting in a cycle of inflammatory and detrimental effects.
“The focus of the lab is trying to understand further what is happening during the whole process of epithelial cell proliferation and differentiation, so we can identify why asthmatic epithelium behave in a divergent manner,” Fatemeh clarifies.
“We also assess the effect of viral infections on airway epithelial cells.”
“We know that there are different cellular mechanisms that determine the fate of cells, and whether they remain undifferentiated or differentiate to more mature cells.”
These mechanisms are being investigated with a focus on identifying the precise roles of epigenetic factors which is defined as how environmental factors can influence gene expression.
“I’m particularly looking at microRNAs, they are biological regulatory factors and they are silencing RNA and post-transcriptionally regulating gene expression,” Fatemeh says.
Proteins are also an important part of the equation in the structure of cells and connect the epithelial cells to each other and their underlying structure. Each microRNA targets different proteins.
“If we can find out, for example, that a particular cell is lacking or overexpressing a specific (or group) of microRNA with essential targets important in the process of epithelial cells homeostatic, that would be a breakthrough.”
“Then we could work on a proper intervention for asthma.”
COMING FULL CIRCLE
Fatemeh’s journey to her current position has been long and impressive.
After completing a doctorate degree in pharmacy in Iran (Pharm-D), she migrated to Australia to follow her passion for research.
Moving to the University of Adelaide in 2003, after working briefly for the University of Newcastle, she completed a Masters of Medical Science by research, investigating the effect of a novel polyunsaturated fatty acid on the development of atherosclerosis in apoE deficient mice.
A short stint at the Flinders Medical Centre followed before Fatemeh was offered an APA scholarship from the University of Sydney to undertake a PhD.
“My PhD was about cardiovascular disease in people with diabetes. I looked at the molecular mechanism linking diabetes with atherosclerosis,” she affirms.
Joining RMIT’s Thrombosis and Vascular Diseases Laboratory as a postdoctoral researcher in 2010, Fatemeh focused on the role of different regulatory mechanisms of platelets during thrombosis formation. Here, she also gained invaluable experience in co-supervising and mentoring postgraduate students.
Fatemeh returned to Newcastle in 2013 as a postdoctoral fellow to work with Professor Darryl Knight, a preeminent expert on airway epithelium and respiratory diseases.
LAB IMITATES LIFE
Clearly fascinated by the mechanisms she is studying, Fatemeh animatedly describes a protocol developed by Professor Knight and other scientists to create a mimic in vitro epithelium for study.
“We use an air liquid interface technique (ALI) here in the lab where we can grow the primary epithelial cells in a pseudostratified structure,” she divulges.
“A special media then helps epithelial cells to develop different population of the cells and differentiate - we can see the cilia beating, and the mucus production.”
“We can use this to look at the different targets, because we already have those differentiated cells in the tissue culture in the lab.”
“We can also assess how viral infections affect airway epithelium. It is amazing!”
Much lauded and with a history of varied research behind her, one is left to wonder what body part Fatemeh will become expert in next.
“At the moment I am focusing on understanding the underlying mechanisms responsible for respiratory diseases, particularly at airway epithelium level,” she states.
“Airway epithelium is the first barrier, first defense of your body, between inside and outside. In any lung disease it plays a very important role.”
“But,” she says, smiling, “the human body is complex, just one layer, one part, one tissue is not the entire thing. There is so much to discover and learn.”
SURPRISE PATHS
Ever humble, Fatemeh laughs away any suggestion that her dedication and achievements are awe-inspiring.
“I am telling you, the whole way through I have always worked with passionate and fabulous people,” Fatemeh attests.
One of her roles in the lab is supervising/mentoring of students and junior staff. Experience has afforded Fatemeh a philosophical approach to her research that she shares with her mentees.
“It is good to have a goal and then find your way towards it,” she observes.
“But sometimes it doesn't always go as you expect, that is the beauty of research. If one thing doesn't work, you try to find a reason for that, and you may go in a completely different direction and find something important there.”
“It is not easy, and it is not a one person job. But the people, the equipment and the technology at HMRI are not like anywhere else, it is remarkable,” she asserts solemnly.
“There is not a day that I walk in here and I don't want to be here. It is such an amazing feeling that my research may contribute in easing the pain of asthma sufferers one day.”
Related links
At the top of our lungs
Dr Fatemeh Moheimani is investigating how the structure and function of airway epithelium contribute to respiratory disease, with the end goal of developing nov
Career Summary
Biography
Fatemeh graduated from Faculty of Pharmacy, Shiraz, Iran with the Doctorate degree in Pharmacy (Pharm-D). She then moved to Australia to pursue her research career. Fatemeh completed her Master of Medical Science (by research: the effect of a novel polyunsaturated fatty acid on development of atherosclerosis in apoE deficient mice) at University of Adelaide in 2005 and her PhD (molecular mechanisms linking diabetes with atherosclerosis) at University of Sydney in 2009. She was offered various scholarships, travel grants and postgraduate grants, e.g. GlaxoSmithKline postgraduate grant (2007-2008: $25,000) during her postgraduate trainings. She also worked as a researcher and taught in various Medical Institutes and Universities.
Fatemeh was offered her postdoctoral research fellow at RMIT University in 2010 where she was investigating molecular mechanisms that regulate platelet thrombus formation. During her position at RMIT, Fatemeh co-supervised several Masters and PhD students, acted as postdoctoral representative in school of medical sciences, was successful in obtaining several travel grants and attended prestigious national and international conferences such as Australian Vascular Biology Society (AVBS) meeting (2012), the Gordon Research Conference-Haemostasis, New Hampshire, USA (2012) and the International Society on Thrombosis and Haemostasis, Kyoto, Japan (2011).
Fatemeh was then offered her postdoctoral fellow position in Respiratory Cell and Molecular Biology area at School of Biomedical Sciences and Pharmacy, University of Newcastle, in 2013, under the supervision of Prof Knight. She has established Prof Knight’s laboratory and collaborated closely with expertise in the field, including Prof Peter Wark and Prof Philip Hansbro to investigate the importance of tissue and cell specific mechanisms that contribute to the respiratory diseases, particularly asthma. Fatemeh is addressing how the structure and function of epithelial cells contribute to asthma.
Research ExpertiseFatemeh is a research scientist with background in Biochemistry/Pharmacy and extensive medical research experience in cardiovascular field. The outcomes of her research have revealed essential molecular mechanisms linking diabetes with atherosclerosis. Fatemeh has expanded her research expertise to the respiratory field since 2013. She is particularly interested in asthma and investigating the importance of tissue and cell specific mechanisms that contribute to the disease. Fatemeh is addressing how the structure and function of epithelial cells contribute to asthma.
Teaching Expertise
Fatemeh’s has acted as co-supervisor of Masters and PhD students. She also acted as academic supervisor of 8 undergraduate students of professional practice in Discipline of Laboratory Medicine, RMIT University with 100% and 78% good teaching score in 2013. In addition, she has teaching experience as practical tutor in subjects of ‘Traditional Chinese medicine’, ‘Medical science 1’, ‘Medical science 2’, and ‘Essentials of Pathophysiology’ in UTS from 2006 to 2008 as well as teaching in Microbial control of medicines lab and Industrial pharmacy lab in Faculty of Pharmacy, Shiraz, Iran from 2001 to 2002.
Qualifications
- PhD (Medicine), University of Sydney
- Master of Medical Science, University of Adelaide
Keywords
- Asthma
- Atherosclerosis
- Diabetes
- Haemostasis
- Medical science
- Pharmaceutics
- Pharmacology
- Professional practice in Discipline of Laboratory Medicine, RMIT University
Languages
- Persian (excluding Dari) (Fluent)
Professional Experience
Academic appointment
Dates | Title | Organisation / Department |
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1/12/2001 - 1/10/2002 | Teaching and Research Assistant | Shiraz University of Medical Sciences, Iran Faculty of Pharmacy Iran, Islamic Republic of |
1/7/2006 - 1/6/2008 | Practical Tutor | University of Technology Sydney Department of Medical and Molecular Biosciences Australia |
1/1/2010 - 1/3/2013 | Postdoctoral Research Fellow | RMIT University School of Medical Sciences |
1/9/2005 - 1/1/2006 | Research Assistant | Flinders Medical Centre, SA Department of Medical Biochemistry, School of Medicine Australia |
1/8/2009 - 1/12/2009 | Research Scientist | The Heart Research Institute, Sydney Australia |
1/1/2003 - 1/3/2003 | Research Assistant | University of Newcastle Discipline of Experimental Pharmacology, School of Biomedical Science, Faculty of Health Australia |
1/1/2001 - 31/12/2006 | Membership - Pharmacist Association, Registered Pharmacist | Iranian Pharmacist Association Australia |
1/1/2007 - 31/12/2009 | Membership - Australian Atherosclerosis Society ASM | Australian Atherosclerosis Society ASM Australia |
1/1/2010 - 31/12/2012 | Membership - Australian Vascular Biology Society | Australian Vascular Biology Society Australia |
1/1/2013 - | Membership - The Thoracic Society of Australia and New Zealand | The Thoracic Society of Australia and New Zealand Australia |
1/8/2009 - 1/12/2009 | Research Scientist | The Heart Research Institute, Sydney Australia |
1/1/2010 - 1/3/2013 | Postdoctoral Research Fellow | RMIT University |
1/4/2013 - | Postdoctoral Fellow | University of Newcastle Australia |
Awards
Recipient
Year | Award |
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2014 |
Early Career Researcher Grant Unknown |
Research Award
Year | Award |
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2014 |
New Staff Grant Unknown |
2014 |
John Hunter Hospital Charitable Trust Unknown |
2013 |
Hunter Medical Research Institute PROJECT FUNDING Hunter Medical Research Institute |
2012 |
CASS Foundation Travel Grant Unknown |
2012 |
RMIT Travel Grant RMIT University |
2011 |
Japanese Society on Thrombosis and Haemostasis Asian-Pacific Scholarship (JSTH/APS) Unknown |
2011 |
RMIT Travel Grant Unknown |
2008 |
Postgraduate Research Support Scheme (PRSS) Unknown |
2007 |
GlaxoSmithKline (GSK) Postgraduate Grant Support Unknown |
2007 |
Postgraduate Research Support Scheme (PRSS) Unknown |
2006 |
Australian Postgraduate Award (APA) University of Sydney |
2003 |
Departmental Postgraduate Scholarship University of Adelaide |
Publications
For publications that are currently unpublished or in-press, details are shown in italics.
Journal article (17 outputs)
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2020 |
Reid AT, Nichol KS, Veerati PC, Moheimani F, Kicic A, Stick SM, et al., 'Blocking notch3 signaling abolishes MUC5AC production in airway epithelial cells from individuals with asthma', American Journal of Respiratory Cell and Molecular Biology, 62 513-523 (2020) [C1] Copyright © 2020 by the American Thoracic Society. In asthma, goblet cell numbers are increased within the airway epithelium, perpetuating the production of mucus that is more dif... [more] Copyright © 2020 by the American Thoracic Society. In asthma, goblet cell numbers are increased within the airway epithelium, perpetuating the production of mucus that is more difficult to clear and results in airway mucus plugging. Notch1, Notch2, or Notch3, or a combination of these has been shown to influence the differentiation of airway epithelial cells. How the expression of specific Notch isoforms differs in fully differentiated adult asthmatic epithelium and whether Notch influences mucin production after differentiation is currently unknown. We aimed to quantify different Notch isoforms in the airway epithelium of individuals with severe asthma and to examine the impact of Notch signaling on mucin MUC5AC. Human lung sections and primary bronchial epithelial cells from individuals with and without asthma were used in this study. Primary bronchial epithelial cells were differentiated at the air-liquid interface for 28 days. Notch isoform expression was analyzed by Taqman quantitative PCR. Immunohistochemistry was used to localize and quantify Notch isoforms in human airway sections. Notch signaling was inhibited in vitro using dibenzazepine or Notch3-specific siRNA, followed by analysis of MUC5AC. NOTCH3 was highly expressed in asthmatic airway epithelium compared with nonasthmatic epithelium. Dibenzazepine significantly reduced MUC5AC production in air-liquid interface cultures of primary bronchial epithelial cells concomitantly with suppression of NOTCH3 intracellular domain protein. Specific knockdown using NOTCH3 siRNA recapitulated the dibenzazepine-induced reduction in MUC5AC. We demonstrate that NOTCH3 is a regulator of MUC5AC production. Increased NOTCH3 signaling in the asthmatic airway epithelium may therefore be an underlying driver of excess MUC5AC production.
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2018 |
Reid AT, Veerati PC, Gosens R, Bartlett NW, Wark PA, Grainge CL, et al., 'Persistent induction of goblet cell differentiation in the airways: Therapeutic approaches', Pharmacology and Therapeutics, 185 155-169 (2018) [C1] © 2017 Dysregulated induction of goblet cell differentiation results in excessive production and retention of mucus and is a common feature of several chronic airways diseases. To... [more] © 2017 Dysregulated induction of goblet cell differentiation results in excessive production and retention of mucus and is a common feature of several chronic airways diseases. To date, therapeutic strategies to reduce mucus accumulation have focused primarily on altering the properties of the mucus itself, or have aimed to limit the production of mucus-stimulating cytokines. Here we review the current knowledge of key molecular pathways that are dysregulated during persistent goblet cell differentiation and highlights both pre-existing and novel therapeutic strategies to combat this pathology.
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2018 |
Moheimani F, Koops J, Williams T, Reid AT, Hansbro PM, Wark PA, Knight DA, 'Influenza A virus infection dysregulates the expression of microRNA-22 and its targets; CD147 and HDAC4, in epithelium of asthmatics', Respiratory Research, 19 (2018) [C1]
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2016 |
Hsu ACY, Parsons K, Moheimani F, Knight DA, Hansbro PM, Fujita T, Wark PA, 'Impaired antiviral stress granule and IFN-ß enhanceosome formation enhances susceptibility to influenza infection in chronic obstructive pulmonary disease epithelium', American Journal of Respiratory Cell and Molecular Biology, 55 117-127 (2016) [C1] Chronic obstructive pulmonary disease (COPD) is a serious lung disease that progressively worsens lung function. Those affected are highly susceptible to influenza virus infection... [more] Chronic obstructive pulmonary disease (COPD) is a serious lung disease that progressively worsens lung function. Those affected are highly susceptible to influenza virus infections that result in exacerbations with exaggerated symptoms with increased mortality. The mechanisms underpinning this increased susceptibility to infection in COPD are unclear. In this study, we show that primary bronchial epithelial cells (pBECs) from subjects with COPD have impaired induction of type I IFN (IFN-ß) and lead to heightened viral replication after influenza viral infection. COPD pBECs have reduced protein levels of protein kinase (PK) R and decreased formation of PKR-mediated antiviral stress granules, which are critical in initiating type I IFNinductions. In addition, reduced protein expression of p300 resulted in decreased activation of IFN regulatory factor 3 and subsequent formation of IFN-ß enhanceosome in COPD pBECs. The decreased p300 induction was the result of enhanced levels of microRNA (miR)-132. Ectopic expression of PKR or miR-132 antagomiR alone failed to restore IFN-ß induction, whereas cotreatment increased antiviral stress granule formation, induction of p300, and IFN-ß in COPD pBECs. This study reveals that decreased induction of both PKR and p300 proteins contribute to impaired induction of IFN-ß in COPD pBECs upon influenza infection.
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2016 |
Moheimani F, Hsu AC-Y, Reid AT, Williams T, Kicic A, Stick SM, et al., 'The genetic and epigenetic landscapes of the epithelium in asthma', RESPIRATORY RESEARCH, 17 (2016) [C1]
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2015 |
Hirota JA, Marchant DJ, Singhera GK, Moheimani F, Dorscheid DR, Carlsten C, et al., 'Urban particulate matter increases human airway epithelial cell IL-1 beta secretion following scratch wounding and H1N1 influenza A exposure in vitro', EXPERIMENTAL LUNG RESEARCH, 41 353-362 (2015) [C1]
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2015 |
Sercombe L, Veerati T, Moheimani F, Wu SY, Sood AK, Hua S, 'Advances and challenges of liposome assisted drug delivery', Frontiers in Pharmacology, 6 (2015) [C1] © 2015 Sercombe, Veerati, Moheimani, Wu, Sood and Hua. The application of liposomes to assist drug delivery has already had a major impact on many biomedical areas. They have been... [more] © 2015 Sercombe, Veerati, Moheimani, Wu, Sood and Hua. The application of liposomes to assist drug delivery has already had a major impact on many biomedical areas. They have been shown to be beneficial for stabilizing therapeutic compounds, overcoming obstacles to cellular and tissue uptake, and improving biodistribution of compounds to target sites in vivo. This enables effective delivery of encapsulated compounds to target sites while minimizing systemic toxicity. Liposomes present as an attractive delivery system due to their flexible physicochemical and biophysical properties, which allow easy manipulation to address different delivery considerations. Despite considerable research in the last 50 years and the plethora of positive results in preclinical studies, the clinical translation of liposome assisted drug delivery platforms has progressed incrementally. In this review, we will discuss the advances in liposome assisted drug delivery, biological challenges that still remain, and current clinical and experimental use of liposomes for biomedical applications. The translational obstacles of liposomal technology will also be presented.
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2015 |
Moheimani F, Roth HM, Cross J, Reid AT, Shaheen F, Warner SM, et al., 'Disruption of ß-catenin/CBP signaling inhibits human airway epithelial-mesenchymal transition and repair', International Journal of Biochemistry and Cell Biology, 68 59-69 (2015) [C1] © 2015 Elsevier Ltd. The epithelium of asthmatics is characterized by reduced expression of E-cadherin and increased expression of the basal cell markers ck-5 and p63 that is indi... [more] © 2015 Elsevier Ltd. The epithelium of asthmatics is characterized by reduced expression of E-cadherin and increased expression of the basal cell markers ck-5 and p63 that is indicative of a relatively undifferentiated repairing epithelium. This phenotype correlates with increased proliferation, compromised wound healing and an enhanced capacity to undergo epithelial-mesenchymal transition (EMT). The transcription factor ß-catenin plays a vital role in epithelial cell differentiation and regeneration, depending on the co-factor recruited. Transcriptional programs driven by the ß-catenin/CBP axis are critical for maintaining an undifferentiated and proliferative state, whereas the ß-catenin/p300 axis is associated with cell differentiation. We hypothesized that disrupting the ß-catenin/CBP signaling axis would promote epithelial differentiation and inhibit EMT. We treated monolayer cultures of human airway epithelial cells with TGFß1 in the presence or absence of the selective small molecule ICG-001 to inhibit ß-catenin/CBP signaling. We used western blots to assess expression of an EMT signature, CBP, p300, ß-catenin, fibronectin and ITGß1 and scratch wound assays to assess epithelial cell migration. Snai-1 and -2 expressions were determined using q-PCR. Exposure to TGFß1 induced EMT, characterized by reduced E-cadherin expression with increased expression of a-smooth muscle actin and EDA-fibronectin. Either co-treatment or therapeutic administration of ICG-001 completely inhibited TGFß1-induced EMT. ICG-001 also reduced the expression of ck-5 and -19 independent of TGFß1. Exposure to ICG-001 significantly inhibited epithelial cell proliferation and migration, coincident with a down regulation of ITGß1 and fibronectin expression. These data support our hypothesis that modulating the ß-catenin/CBP signaling axis plays a key role in epithelial plasticity and function.
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2015 |
Makkawi M, Moheimani F, Alserihi R, Howells D, Wright M, Ashman L, Jackson DE, 'A complementary role for tetraspanin superfamily member CD151 and ADP purinergic P2Y12 receptor in platelets.', Thromb Haemost, 114 1004-1019 (2015) [C1]
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Show 14 more journal articles |
Conference (14 outputs)
Year | Citation | Altmetrics | Link | ||
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2018 |
Reid A, Nichol K, Wei L, Moheimani F, Bartlett N, Hansbro P, et al., 'NOTCH3 INHIBITION SIGNIFICANTLY REDUCES MUC5AC IN HUMAN AIRWAY EPITHELIAL CELLS', RESPIROLOGY (2018)
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2018 |
Moheimani F, Williams T, Reid A, Hansbro P, Wark P, Knight D, 'ABNORMAL MIRNA-22 EXPRESSION AFTER INFLUENZA INFECTION FACILITATES EPITHELIUM REMODELING IN ASTHMA', RESPIROLOGY (2018)
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2018 |
Reid AT, Nichol KS, Wei L, Moheimani F, Bartlett NW, Hansbro PM, et al., 'Inhibition of NOTCH3 Signaling Abolishes MUC5AC Production in Human Airway Epithelial Cells', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, San Diego, CA (2018)
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2015 |
Moheimani F, Roth H, Cross J, Reid A, Shaheen F, Warner S, et al., 'SUPPRESSION OF beta-CATENIN/CBP SIGNALING INHIBITS EPITHELIAL-MESENCHYMAL TRANSITION AND MIGRATION OF HUMAN AIRWAY EPITHELIUM', RESPIROLOGY, Queensland, AUSTRALIA (2015) [E3]
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Show 11 more conferences |
Grants and Funding
Summary
Number of grants | 5 |
---|---|
Total funding | $67,512 |
Click on a grant title below to expand the full details for that specific grant.
20171 grants / $5,000
microRNA-22 as a potential epigenetic target to restore the airway epithelium integrity in asthmatics$5,000
Funding body: Thoracic Society of Australia and New Zealand
Funding body | Thoracic Society of Australia and New Zealand |
---|---|
Project Team | Doctor Fatemeh Moheimani |
Scheme | ¿TSANZ/AstraZeneca Grant-In-Aid for Severe Asthma Research |
Role | Lead |
Funding Start | 2017 |
Funding Finish | 2017 |
GNo | G1601341 |
Type Of Funding | C3112 - Aust Not for profit |
Category | 3112 |
UON | Y |
20161 grants / $20,000
A novel approach in restoring the airway epithelium integrity in asthmatics$20,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Doctor Fatemeh Moheimani, Professor Darryl Knight |
Scheme | Project Grant |
Role | Lead |
Funding Start | 2016 |
Funding Finish | 2016 |
GNo | G1600919 |
Type Of Funding | C3120 - Aust Philanthropy |
Category | 3120 |
UON | Y |
20142 grants / $32,512
Mechanisms of dysregulated antiviral signallings to influenza infection in chronic obstructive pulmonary disease$27,512
Funding body: John Hunter Hospital Charitable Trust
Funding body | John Hunter Hospital Charitable Trust |
---|---|
Project Team | Doctor Alan Hsu, Doctor Fatemeh Moheimani, Professor Darryl Knight, Conjoint Professor Peter Wark |
Scheme | Research Grant |
Role | Investigator |
Funding Start | 2014 |
Funding Finish | 2014 |
GNo | G1400435 |
Type Of Funding | Other Public Sector - State |
Category | 2OPS |
UON | Y |
Role of the transcriptional co-activator p300 in resetting epithelial differentiation: A potential pathway involved in asthma prevention and therapy$5,000
Funding body: University of Newcastle
Funding body | University of Newcastle |
---|---|
Project Team | Doctor Fatemeh Moheimani |
Scheme | New Staff Grant |
Role | Lead |
Funding Start | 2014 |
Funding Finish | 2014 |
GNo | G1301262 |
Type Of Funding | Internal |
Category | INTE |
UON | Y |
20131 grants / $10,000
Role of the transcriptional co-activator p300 in resetting epithelial differentiation: A potential pathway involved in asthma prevention and therapy$10,000
Funding body: University of Newcastle
Funding body | University of Newcastle |
---|---|
Project Team | Doctor Fatemeh Moheimani, Professor Darryl Knight, Ms Kirsty Wark, Doctor Alan Hsu, Doctor Malcolm Starkey |
Scheme | Early Career Researcher Grant |
Role | Lead |
Funding Start | 2013 |
Funding Finish | 2013 |
GNo | G1301174 |
Type Of Funding | Internal |
Category | INTE |
UON | Y |
Research Supervision
Number of supervisions
Past Supervision
Year | Level of Study | Research Title | Program | Supervisor Type |
---|---|---|---|---|
2015 | Masters | MicroRNAs: potential links between dysregulated regeneration and impaired anti-viral responses in asthmatic airway epithelium? | Pharmacy, University of Groningen | Principal Supervisor |
2015 | PhD | Tyrosine kinase inhibitors modulate platelet reactivity and platelet function | Medical Science, RMIT University | Co-Supervisor |
2014 | PhD | Investigating novel platelet immunoreceptors ‘CEACAM2’ in contact-dependent events that modulate platelet thrombus formation | Medical Science, RMIT University | Co-Supervisor |
2012 | Masters | Physical association of ADP purinergic receptor, P2Y12, with tetraspanin CD151 on human platelets | Medical Science, RMIT University | Co-Supervisor |
Research Collaborations
The map is a representation of a researchers co-authorship with collaborators across the globe. The map displays the number of publications against a country, where there is at least one co-author based in that country. Data is sourced from the University of Newcastle research publication management system (NURO) and may not fully represent the authors complete body of work.
Country | Count of Publications | |
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Australia | 30 | |
Canada | 15 | |
Netherlands | 4 | |
United States | 4 | |
Japan | 1 |
Dr Fatemeh Moheimani
Position
Conjoint Lecturer
The Priority Research Centre for Asthma and Respiratory Diseases
School of Biomedical Sciences and Pharmacy
College of Health, Medicine and Wellbeing
Contact Details
fatemeh.moheimani@newcastle.edu.au | |
Phone | (02) 40420363 |
Office
Room | HMRI 2101 |
---|---|
Building | The Hunter Medical Research Institute |
Location | The University of Newcastle , |