Experimental Neuroinflammation Group -ucl Cover Letter
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Research Assistant Cover Letter At Experimental Neuroinflammation Group -UCL
Experimental Neuroinflammation Group -UCL
Neurological deficits in multiple sclerosis (MS) have traditionally been attributed to abnormalities in axonal conduction as a result of demyelination. However
increasing evidence suggests that inflammation alone is sufficient to impair function. Research from the laboratory has revealed that the inflamed CNS suffers from a significant reduction in blood flow
resulting in tissue hypoxia
which in turn leads to mitochondrial dysfunction and the expression of symptoms. We can monitor oxygen gradients across vessels and tissue using different techniques
including
but not limited to
in vivo confocal microscopy and hyperspectral imaging
allowing us to understand oxygen delivery in the inflamed CNS. We aim to examine different models of MS to determine the downstream effects of impaired blood flow and tissue hypoxia
in order to develop rational therapeutic strategies aimed at restoring function by improving tissue perfusion and oxygenation. Skills & Qualifications • Ability to work independently and efficiently. • Strong organizational and task prioritization skills. • Excellent communication skills and proficiency in performing administrative and clerical tasks. • Proficient in general laboratory procedures
techniques
and documentation. • Willingness to learn and adapt to new techniques and technologies. • Fluent in English
Spanish
French
and Catalan. • Proficient in statistical analysis and software such as SPSS
MATLAB
and Python. • Proficient in using various software programs
including Microsoft Office Suite (Word
Excel
PowerPoint). • Advanced knowledge and experience in 3D cell culture techniques. • Skilled in protein isolation
Western Blot
PCR
rt-qPCR
toxicity testing
IHC
Northern Blot
and ELISA. • Proficient in anatomical dissection studies for medical and veterinary purposes. • Experienced in static analysis of behavioral data and microarray data. • Familiarity with electrophysiology
imaging
protein purification
and optical and electron microscopy techniques. • Advanced level proficiency in conducting animal experiments
behavioral experiments
anatomical dissection
and molecular analysis. Education Uskudar University
M.Sc. September 2019-June
2022 Istanbul
Turkey Cumulative GPA:3.78 High Honor Student Master Science in Neuroscience Department of Neuroscience Sciences Thesis: Investigation of TopoII ß Gene Expression in LPS-Induced HMC3 Microglia Cell Line Pamukkale University
B.Sc. September2015-June 2019 Denizli
Turkey Cumulative GPA: 3.0 Honour Student Bachelor of Science in Physical Therapy and Rehabilitation Universitat de Barcelona September2018- June 2019 Barcelona
Spain International Student ERASMUS Study Abroad ProgramHypoxia hypoxia image Particular current interests derive from our discovery that neuroinflammatory lesions can be hypoxic
and sufficiently hypoxic to impair mitochondrial metabolism. This impairment is especially likely in an inflammatory environment containing nitric oxide and superoxide. The hypoxia and energy deficit directly contribute to three of the cardinal features of MS
namely loss of function (symptoms)
demyelination and degeneration. Based on this realisation
our research explores novel protective treatment strategies that we are developing for clinical trial. One approach is to reduce energy demand by partial blockade of sodium channels. This therapy is also effective in dampening the activation of microglial cells (these cells can damage brain tissue)
and we have recently shown the efficacy of one clinically relevant drug in this respect. Therapies based on this new understanding have been examined in recent and ongoing clinical trials in MS and related diseases. Encouragingly
such therapies can be very effective in neuroprotection
and they are also inexpensive and safe for long term administration. Image: Inflamed spinal cord showing strong labelling for hypoxia in the grey matter. Blood Flow Blood flow in vessels indicated by fluorescent streaks Impaired blood flow or hypoperfusion is becoming an increasing focus of our research
as it is likely to be the primary cause of the tissue hypoxia observed in neuroinflammation. Hypoperfusion is well established in MS with reports of reduced flow affecting both grey and white matter. The white matter (composed of myelinated nerve fibres) is particularly vulnerable to disturbances in blood flow
explaining why MS lesions have a predilection to form at sites known to have a vulnerable blood supply. Our evidence is that therapies aimed at maintaining or restoring blood flow improve neurological function and reduce structural damage
with major implications for the way MS is treated. Image: Blood flow in vessels indicated by fluorescent streaks. Long streaks (upper image) show fast flow through normal tissue
and short streaks (lower) show slow flow through inflamed tissue. Mitochondria Mitochondria are of particular interest in our research. In the normal nervous system we have found that mitochondrial trafficking along axons is highly influenced by the level of impulse activity along the axons
which has implications for neurodegenerative disease. In the inflamed nervous system we have discovered that many axonal mitochondria become non-functional
which starves the axons of energy. In fact our evidence is that the energy insufficiency can cause conduction failure (and hence symptoms) and ultimately degeneration. We have also investigated how mitochondria become damaged in diabetic axons
and how this damage contributes to diabetic neuropathy. retinal vasculature Image: Retinal vasculature revealed as a shadow over green fluorescence due to ongoing retinal mitochondrial respiration. excessive superoxide production Image: Excessive superoxide production in inflamed tissue on the left of the spinal cord. Model of the early MS lesion early lesion We have developed and characterised a model of the Pattern III (hypoxic) type of demyelination found in early MS lesions. The model lesion demonstrates the prominent role of innate immune mechanisms in lesion formation. The lesion provides an excellent opportunity to test the efficacy of putative therapeutic agents. Image: Pattern III demyelination (circled)
as occurs in early MS lesions. Model of ‘slow-burning’ neurodegeneration Model of slow-burning neurodegeneration Among our experimental models is a new focal lesion of ‘slow burning’ degeneration of the grey matter
consequent to a neuroinflammatory event. The lesion commences after a short delay following induction and it causes slowly progressive disability that advances hand in hand with progressive neurodegeneration and atrophy of the grey matter. The lesion shares many features with progressive MS
and we are exploring the underlying mechanisms in the belief that this will indicate rational neuroprotective strategies. Image: Grey matter atrophy (left) and mitochondrial failure (asterisk) in a lesion of slowly progressive neurodegeneration. Techniques employed electron microscopy Confocal microscopy to monitor mitochondrial dynamics and membrane potential (a measure of mitochondrial metabolism/health)
blood flow
tissue metabolism and inflammation in real time Electrophysiology to monitor changes in neurological function Light and electron microscopy
including a range of immunohistological methods to determine the metabolic and cellular consequences of inflammation Tissue oxygen monitoring by ratiometric oxygen sensitive fluorescent tracer
optical probe and immunohistochemical methods Near-Infrared Spectroscopy (NIRS) using non-invasive methods to monitor mitochondrial function and tissue oxygenation within the brain Multispectral Imaging for non-invasive monitoring of retinal tissue oxygen concentration Image: Electron microscope image showing a normal myelinated axon (left) and a demyelinated axon (right).Our primary research focus is multiple sclerosis (MS)
an inflammatory demyelinating disease of the brain and spinal cord. MS is typically diagnosed in early adulthood and although the disease course is very variable
it can progress over decades to cause a range of serious neurological deficits
including effects on vision
movement and sensation. The disease is characterized by inflammation within the brain and spinal cord
demyelination (loss of the insulating layer of myelin from around nerve fibres)
and neuronal and axonal degeneration. Each type of pathology causes significant symptoms
by different mechanisms. Our research aims to understand the mechanisms responsible for the disease
in order to arrest them and thereby avoid the production of symptoms even before they have started. Our recent research has focused on the reduction in blood flow through inflamed tissue which reduces the supply of the oxygen needed to maintain function and avoid tissue damage. We have shown that appropriately timed treatments to maintain tissue oxygenation can provide remarkable protection from symptoms and damage. Indeed
we have advanced studies from the earliest laboratory observations of previously unsuspected mechanisms
to devise at least one novel treatment strategy that has been proven effective in neuroprotection in clinical trial. A second major line of research concerns cerebral small vessel disease
which becomes common with ageing
and is a major cause of strokes and dementia. The disease affects arterioles
capillaries and venules and causes a reduction in blood flow
and impaired regulation of blood flow. Our research explores the importance of inadequate tissue oxygenation in causing symptoms and damage
and also the therapeutic value of drugs that promote blood flow and oxygenation in achieving protection of cognitive function and tissue integrity.
By Melike Cansel EREN
[Your Name]
[Address]
[City, State ZIP Code]
[Email Address]
[Today’s Date]
PROF Kenneth Smith,
Experimental Neuroinflammation Group,
UCL,
[Address],
[City, State ZIP Code]
Dear PROF Kenneth Smith,
I am writing to express my interest in the Research Assistant position at the Experimental Neuroinflammation Group at UCL. As a highly motivated and skilled individual with a strong background in neuroscience, I am confident that my skills, experience, and passion make me a perfect fit for this role.
Firstly, I would like to introduce myself. My name is Melike Cansel EREN and I am a Master's student in Neuroscience at Uskudar University in Istanbul, Turkey. Throughout my academic journey, I have maintained a high academic standing with a cumulative GPA of 3.78, making me a High Honor student. I am on track to complete my Master's degree in June 2022 and I am eager to continue my academic and professional growth by joining the Experimental Neuroinflammation Group at UCL.
What excites me about this particular position at your esteemed company is the opportunity to work with cutting-edge technology and techniques to understand the role of inflammation and hypoxia in neurological deficits, specifically in multiple sclerosis (MS). The research conducted by the laboratory, as described in the job description, perfectly aligns with my research interests and my academic background. My Master's thesis focuses on investigating the expression of TopoII β gene in LPS-induced HMC3 microglia cell line, which has given me a deep understanding of the role of inflammation in neurological disorders.
Moreover, I am highly impressed by the range of techniques employed by the laboratory, such as in vivo confocal microscopy, hyperspectral imaging, and electrophysiology, to monitor oxygen gradients and tissue perfusion in the inflamed central nervous system. My proficiency in general laboratory procedures, techniques, and documentation, along with my experience in conducting animal experiments, behavioral experiments, and molecular analysis, make me well-equipped to contribute effectively to the research projects at the Experimental Neuroinflammation Group.
In addition, I am fluent in English, Spanish, French, and Catalan, which will enable me to effectively communicate and collaborate with the diverse team at the laboratory. I am also proficient in statistical analysis and various software programs, including SPSS, MATLAB, and Python, which will be an asset in analyzing and interpreting the data collected during research.
One of the aspects that I admire about the Experimental Neuroinflammation Group is the multidisciplinary approach to research. As a Bachelor of Science in Physical Therapy and Rehabilitation, I have a strong foundation in anatomy and physiology, which has been further strengthened by my experience in conducting anatomical dissection studies for medical and veterinary purposes. I am also skilled in 3D cell culture techniques and protein isolation, Western Blot, PCR, rt-qPCR, toxicity testing, IHC, Northern Blot, and ELISA, which will be valuable in understanding the downstream effects of impaired blood flow and tissue hypoxia in different models of MS.
Furthermore, I am fascinated by the research being conducted by the laboratory on the role of mitochondria in neuroinflammation and neurodegenerative diseases. My Master's thesis has provided me with hands-on experience in monitoring mitochondrial dynamics and membrane potential in an inflamed environment. I am also proficient in using electrophysiology, imaging, protein purification, and optical and electron microscopy techniques, which will be instrumental in investigating the mechanisms underlying neurodegeneration and developing novel therapeutic strategies.
I am confident that my skills and qualifications, coupled with my strong work ethic and ability to work independently, make me a suitable candidate for the Research Assistant position at the Experimental Neuroinflammation Group. I am a quick learner and always willing to learn and adapt to new techniques and technologies. I am also highly organized and possess excellent communication skills, which will enable me to effectively collaborate with other team members and perform administrative and clerical tasks efficiently.
I have attached my resume and transcripts for your review. I would appreciate the opportunity to further discuss my qualifications and learn more about the research being conducted at the Experimental Neuroinflammation Group. Thank you for considering my application.
Sincerely,
[Your Name]