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  Curriculum Vitae
Dati Anagrafici
Esperienze
Studi AMINA AHMED



Home Address Temporary Address
15 Ellerslie Gardens First Floor Oudesteenweg 67
Willesden Green Antwerpen
London NW10 3TB Belgium 2060
UK
mobile: +0032 (0) 495 755052 Email address: amina_ciao2003@yahoo.co.uk
Date of birth: 2 April 1977 Nationality: British

Education

2009-2010 University of the West of England, Bristol.
MSc Science Communication (part-time)

2006-2008 Dundee University, School of Life Sciences, Dundee, Scotland.
MSc in Neuroscience. Dissertation: Studies on the Expression of . Endogenous and Recombinant LRRK2. Passed

2000-2005 University of the West of England, Bristol.
BSc (Hons) Biomedical Sciences: upper 2:1
Dissertation: A study of the factors affecting the activity of
mammalian phosphorylase., supervisour: Dr Terry Stygall

1997-2000 Oxford College of Further Education, Oxford.
A-levels: Italian (A), Chemistry (D), Biology (D), GCSE: French (A)
GSCE : English (C), Italian Literature Course, Access Course Science: . Chemistry, Biology, Physics and Maths all passed.

Professional experience

2009 Pharma Publishing and Media Europe, Mol, Belgium.
Editorial assistant.

2005-2006 Flinders University School of Medicine, Adelaide, Australia.
Department of human physiology. Honorary visiting scholar.

2002-2003 Internship at the Central Hospitalier Universitaire, La Tronche.
Laboratory of Neurobiophysique INSERM U 318, Grenoble, France
Research of Parkinson’s disease.

2002-2003 Summer Placement in the Institute of Neurology, Catholic University, Rome, Italy.

Research Techniques used

Electrophysiology
• Stereotaxic surgery in rat and monkeys brain
• I attended deep brain stimulation (DBS) in patients with Parkinson Disease carried by Dr Alim-Louis Benabid and his team..
• I learned histological techniques: performing rat perfusion, fixation, and sectioning brain using a microtome, staining by cresyl violet.

Mammalian cell culture
• Preparation and maintenance of (HEK293, C6, SH-SY5Y, Hela, U-87 MG M059K, M059J, NG108-15 and PC-12 cell lines)

Mammalian cell transfection
• Stable transfection (Lipofectamine 2000)
• Transient transfection (PEI)

Molecular biology
• Gel electrophoresis and immunoblotting
• Immunoprecipitation
• Mass Spectrometry
• Protein Purification (GST- and Flag-tagged proteins)
• ELISA
• Expression and purification of recombinant proteins in E.coli
• In-gel and peptide assay
• PCR & RT-PCR
• Bacterial transformation/ restriction enzyme digest
• DNA Maxi-prep

Other Experience

04/08-present Marks and Spencer, Dundee, Scotland
• Sale assistant

June 2005 Teach English as Foreign Language, Bristol.
TEFL certificate

2004-2005 Marie Curie Cancer Care, Bristol
• Voluntary administration assistant

2002-2003 University Stendhal, Grenoble
French Courses

2001-2002 Knightingales/ Marks and Spencer/ Universal Utilities,
Bristol.
• Sale Assistant
• Telesale

Summer 1999 Churchill Hospital and Radcliffe Hospitals, Oxford.
• Volunteer helper/work experience ( assisting nurses and patients)
• Work experience (virology and cardiology department)


Professional memberships

2006-2008 The Biochemical Society
2005-2006 Australian Neuroscience Society
2005-2006 Center for Neuroscience- student member
Current Research

Parkinson’s disease (PD) is a severe progressive neurodegenerative disorder characterized by bradykinesia, rigidity and tremor. The hallmark pathological features of PD are loss of dopamine (DA) neurons in the substantia nigra pars compacta (Snpc) and neuronal intracellular Lewy body inclusions. While current therapies alleviate the motor symptoms of PD, they are largely palliative. Although PD is sporadic in the majority of patients, rare familial forms of the disease do exist. To date, early-onset of PD has been linked to mutations in four genes, alpha-synuclein (Polymeropoulos et al., 1997), parkin (Kitada et al., 1998), DJ-1 (Bonifati et al., 2003) and PINK1 (Valente et al., 2004). Recently a gene encoding for LRRK2 (also called dardarin) has been characterized and thought to be responsible for late-onset PD in 5 families from England and Spain (Zimprich et al., 2004; Paisan-Ruiz et al., 2004). LRRK2 is a large protein of 2527 amino acids belonging to a group within the Ras/GTPase superfamily termed ROCO, which includes MASL1, DAPK1 and LRRK1. Several mutations have been described, which are scattered throughout the predicted domains of the LRRK2 protein, G2019S is the most common mutation found in 3-41% of patients with familial PD and 1-2% in sporadic cases.

Though the physiological function of LRRK2 is currently unknown, studies have suggested that it might be implicated in cellular signalling or protein-protein interactions as it contains putative tyrosine kinase like, Ras/GTPase-like, LRR and WD40 domains (Di Fonzo et al., 2005; Singleton, 2005). In order to gain novel insight into the biological function of LRRK2 and to understand how mutations in this protein lead to the pathogenesis of this devastating disorder, it is crucial to study the expression of endogenous and recombinant LRRK2. In the first part of my MSc, specific LRRK2 antibodies were generated, which allowed for the recognition of endogenous LRRK2 in several cell lines and rat tissues. I then employed a combination of Flag-tagged purification of wild-type LRRK2 transiently transfected in HEK 293 cells or immunoprecipitated LRRK2 from brain extract followed by mass spectrometry analysis to identify binding partners for LRRK2. In addition, I analyzed the detail distribution of LRRK1 and LRRK2 mRNA in mouse tissues using RT-PCR. The main findings of our study showed that both genes were expressed throughout the mouse organs with LRRK1 exhibiting widespread distribution and LRRK2 showing relatively important interregional differences in expression level. Protein kinase inhibitors have been used as a tool to dissect the signal pathways involved in LRRK2 and may open up new avenuses for treating PD.


Publications/ Abstracts

1. Surgery for obsessive-compulsive disorder. Nuttin, B., Gabriλls, L., Cosyns, P., van Kuyck, K., Welkenhuysen, M., Luyten, L., Prodanov, D., Ahmed, A. & Das, J, in Deep Brain Stimulation, Oxford University Press: Oxford Neurology Library Pocketbook Series. (Eds Bain, P., Nandi, D., Aziz, Tipu. & Liu, X. 2008.

2. Ahmed, A., Chegini, F., Raghupathi, R. & Gai, W.P (2006). Overexpression of leucine-rich repeat kinase 2 induces degeneration in cell cultures. 26th annual meeting of the Australian Neuroscience Society. 31st January - 3rd February 2006, Sydney, Australia.

Conferences/ workshops attended.

1. Overexpression of leucine-rich repeat kinase 2 induces degeneration in cell cultures. (February, 2006). 26th annual Australian Neuroscience Society, Sydney. (Oral presentation).

2. Overexpression of leucine-rich repeat kinase 2 induces degeneration in cell cultures. (March, 2006). Center for Neuroscience, Flinders Medical Centre, Adelaide (Oral presentation).

3. Overview of endnote - Staff Development and Training Unit, Flinders University, South Australia, 2005.

4. Getting published in scientific journals – Staff Development and Training Unit, Flinders University, South Australia, 2005.

5. Taking control of your career - Staff Development and Training Unit, Flinders University, South Australia, 2005.

6. Top ten tips for time management -Staff Development and Training Unit, Flinders University, South Australia, 2005.

7. The seven habits of highly effective PhD students - Staff Development and Training Unit, Flinders University, South Australia, 2005.

Student Awards

1. Australian Neuroscience Society student travel award, 2006
2. Medical Research Council Research in Capacity Building Area


Computing skills
• Software: Windows 98, Microsoft Word, Minitab, Excel, Power Point

Languages
• Somalian – mother tongue
• Italian – Fluent (won the first prize Italian essay Competition in May 2000, in UK. The competition organiser was Mariolina Freeth).
• French – advanced (passed DELF1)
• English – Fluent
• Spanish- Intermediate
• Dutch- Beginner
Conoscenze
Lingue straniere inglese: 10
francese: 10
spagnolo: 6
   

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