Contents page

Welcome message by the Dean of Research 4

Welcome message by the Associate Dean 5

Student welcome message 6

Keynote talk 7

Overview Talk Sessions & Poster Walks 8

Abstracts 9 - 28

Acknowledgments 29

Notes 30

Editorial 31

3

Welcome message by the Dean of Research

Dear students,

I am pleased to see the successful continuation of the Munich Medical Student

Science Conference MMS ScienceCon, which combines students’ research projects

from different fields, united by this year’s conference theme "Inspiring curiosity".

These projects show the broad range of medical research and illustrate curiosity-

driven research activities both during medical training and medical practice.

The guiding motto of the Faculty of Medicine and the University Hospital of LMU

Munich is “Top Minds, Best Structures, Strong Networks”.

Top Minds: We aim to attract, support and retain excellent people for research and

education on all levels from student to chair holder, people who maintain their

curiosity and inspire others.

Best Structures: We strive to create efficient structures and processes and to

provide an administration that supports science and scientists to where curiosity

leads them.

Strong Networks: We foster excellent scientific networks and collaborations with

strong internal and external partners that inspire.

The Dean's Office supports these principles by funding students’ research projects

as well as Clinician Scientist programs, which make it possible to follow your

curiosity and link healthcare with first-rate science. In this context, please take a

look at the overview of funding and current calls on the homepage of the Faculty of

Medicine: https://www.med.uni-muenchen.de/intern/forschungsportal/index.html

I thank Dr Canady as well as the whole team organizing the third Munich Medical

Student Science Conference, and I wish you many interesting contributions and

discussions.

Prof. Dr. Stefan Endres

Dean of Research

4

Dear participants of this year’s meeting,

What makes a good scientist? There will be many answers to this. My personal views have been

shaped by having had the privilege of conducting my doctoral thesis work with the late Hans

Thoenen, a neuroscientist from the Swiss Zweisimmen and director at the Max-Planck-Institute in

Martinsried. And it is best said in his own words (all quotations are from his autobiographical sketch

for the Society for Neuroscience, (1)).

„In the biographies of many successful scientists, the wish to become a scientist was already apparent

in their early childhood. Barely out of their diapers, they had their own laboratory and were reading

the biographies of their scientific idols. My laboratory was the natural environment of a mountain

valley in the Swiss Alps.“

So there is hope, even if you have not yet pinned the portraits of great scientists and nobel prize

winners to the wall behind your bed.

„Before I went to school my reading and mathematical abilities were very limited. When I

participated in my first ski race I had a high number that was beyond the limits of my numerical

knowledge so the amused starter had to say, „ Come on Hansi, it’s your turn now.“ I did not shine in

this race. Later on I did much better and won many races in different age categories.“

So, keep trying and, there is life beyond science.

After finishing his studies of medicine in Berne and Innsbruck he took a first laboratory position. „This

first position ended one Christmas morning when I was fired for reasons of „scientific incapability and

insubordination “. The label „incapability“ was based on the fact that I did not find what my boss

wanted. The label of „insubordination“ resulted from my rather undiplomatic way of explaining to

him why I could not satisfy his expectations.“

So, be aware of the non-scientific pressures when shaping your scientific career. With regard to

diplomacy you could probably do better (forgive me, Hans).

His last sentence is „What remains is my gratitude that I have lived in a period of evolution brought

about by a fortunate combination of numerous variables that made such interesting events possible

including our own existence and that I was privileged to become a scientist.“

Nothing more to be said.

Enjoy the meeting.

May the force be with you!

Michael Meyer MD Univ. Prof. of Molecular Neurophysiology Associate Dean Medical Faculty Ludwig-Maximilians-University Munich

(1) http://www.sfn.org/About/History-of-Neuroscience/Autobiographical-ChaptersThe History of Neuroscience in Autobiography, Volume 6Edited by Larry R. SquireISBN: 0-12-538010-1

5

Dear visitors,

Welcome to the Munich Medical Student Science Conference 2019!

The theme of our conference this year is “Inspiring curiosity” – and it refers to our aim to enthuse

more medical students for scientific research. So how do we aspire to reach this goal?

Generally speaking, the earliest time medical students in Germany get involved in any kind of

scientific research is when they decide to finally tackle their MD thesis, starting from third year of

medical school. In order to change this, our faculty has introduced the Undergraduate Research

Opportunity Program (UROP) that gives highly enthusiastic students the opportunity to handle a

research project on their own, starting from first year of medical school !

Some of the presenters today are undergraduate medical students who will not only refer to their

research projects that they have done during their UROP experience, but who will share their

personal experiences as well. While doing one’s first own project, there is a number of problems one

may come across. At first it is difficult to learn the trades of a scientist: culturing cells or bacteria,

running an experiment and evaluating it correctly, quantifying contents of a solution and many more.

But you may also acknowledge how fast these tasks can be acquired. From personal experience I can

tell that writing out your first own paper or scientifically based text brings some difficulties as well.

So now our next question would be how we could gain access to a network of both other medical

students accomplishing more advanced research, and of scientific researchers? To answer this

question, just take a look at our participants: Young students and more experienced scientists from

various fields of research will present their projects today, exchange ideas, share their personal

experience and as we already said: Inspire curiosity! Furthermore, this year’s jury consists of faculty

members and medical students.

Hopefully, some of the posters and talks encourage you to look closer and take part in the

discussions afterwards. Ideally, today’s event will help you to get a better image of medical research

and maybe you find answers to the questions: Which fields of research am I most interested in? How

can I gain more experience in medical research? Where is the interface between clinical medicine

and scientific research? What options do Munich and other German cities offer me?

For further information or any kind of question, feel free to ask members of the organizing team or

contact us via e-mail: mms-sciencecon@med.uni-muenchen.de

Now we wish you an exciting visit!

With kind regards,

Maria Charlotte Brielmaier

Medical student

Team MMS ScienceCon 2019

6

Keynote Talk:

Genomic Medicine - What we can learn from children with rare diseases

Professor Christoph Klein is the Director of the Department of Pediatrics at the Dr. von

Hauner Children‘s Hospital and the co-founder and principal architect of the Care-for-Rare

Foundation. The Care-for-Rare Foundation has been established in order to help children

with rare diseases. Care-for-Rare is Germany’s first foundation solely devoted to this cause.

The foundation pursues its mission “From Discovery to Cure” through targeted sponsorship

of clinical care, research and education.

Christoph Klein studied Philosophy and Medicine at the Universities of Ulm, Harvard and

Munich. Upon subspecialty training in pediatric immunology (Hôpital Necker Enfants

Malades, Paris) and pediatric hematology/oncology (Boston Children’s Hospital, Harvard

Medical School) he held faculty appointments at Harvard Medical School and Hannover

Medical School before being nominated chairman of the Department of Pediatrics and

Adolescent Medicine at LMU.

Professor Klein has made seminal contributions to the understanding of how blood and

immune cells develop and control immunity and tolerance. Together with his team, he has

identified and characterized numerous inherited diseases of the immune system and

developed novel cell- and gene-based therapies. He is a member of many scientific societies

and is the recipient of many national and international awards including the Adalbert Czerny

Prize, the Hector Fellow Prize, the William-Dameshek Prize and the Gottfried Wilhelm Leibniz

Prize.

He will share his vision on how children with rare diseases may be pioneers of a new era of

personalized medicine.

7

Overview Talk Sessions and Poster Walks

Talk Session 1

10:30 am Melina Schlegel Ago2 phosphorylation and Stau2 knockdown in neurons leads to distinct Ago2 protein localisation

10:45 am Maria Charlotte Brielmaier Differentiating PC12 cells and differentiating with TW2B

11:00 am Tim Wiegand Translational Neuroimaging in Mild Traumatic Brain Injury

11:15 am Cecilia Lozano Simon Does Calbindin-D28k affect the intracellular distribution and accumulation of alpha-synuclein in a hippocampal neuronal cell line?

Talk Session 2

1:00 pm Luisa Delius, Lea Merkel Generation and characterization of RanBPM mutants using CRISPR-Cas9

1:15 pm Noemi Vereb Extramuscular manifestations of non-dystrophic myotonia

1:30 pm Felix Stieglmeier Cartography and Evaluation of Native and Decellularized Bovine Pericardium for Use as a Medical Implant

1:45 pm Benedikt Freystetter Multi-Layered Electro-Spun Scaffolds – Development and Examination for Application in Cardiovascular Tissue Engineering

Posters in Room N01.012

Luna Slemann: Simultaneous cuprizone intoxication and active induction of experimental autoimmune encephalomyelitis to study MS lesion development in the forebrain

Eva Riedlinger: Activity-based quantification of neutrophil granule-associated serine proteases

Elene Nikolaishvili, Simone Weber: Investigation of RanBPM and Procaspase 3 as possible interactors with Calbindin

Frederik Lorenz: Effect of Hep7 on the remyelination in the chronic Cuprizone-model

Noah Hirsch: Arteriogenesis – A potential bypass to compensate for arterial occlusion

Mortimer Hladik: Auswertung von 10 Jahren Erfahrung interdisziplinärer Behandlung von geburtstraumatischen Plexusparesen, retrospektiv und prospektive Analyse des Outcomes nach operativer bzw. konservativer Therapie

Posters in Room N01.011

Elena Nikolova: High-speed ventral plane videography is a sensitive tool for detecting subclinical motor changes in EAE mice

Alexander Holzner: Innervation pattern of the medial rectus eye muscles in a monkey after experimentally induced exotropic strabismus by unilateral transection of the trigeminal nerve

Gertraud Stelzer: Professional Identity and Interprofessional Collaboration

Ekaterina Lapteva: Potassium channels in oculomotor nucleus in monkey

Yavor Yakimov, Armin Gruber: Transmembrane protein 119 as a microglial marker in cuprizone model

8

Abstracts

In alphabetical order

8

Differentiating PC12 cells and differentiating with TW2B

Maria Charlotte Brielmaier, Paula Sanchez-Baeza

AG Kerschensteiner, Klinisches Institut für Neuroimmunologie, Ludwig-Maximilians University of Munich

Multiple Sclerosis (MS) is a neuroinflammatory disease of the central nervous system during which demyelination of the axons can lead to irreversibly damaged axonal membranes. The most common symptoms are double vision, blindness, trouble with sensation and coordination and muscle weakness – determined by the location of the lesion. The existence of these symptoms and predisposing genetic factors are reasons to run further medical tests. Furthermore, there are different forms of MS, depending on the frequency of attacks and the disease course which have been categorized: Clinically Isolated Syndrome (CIS), Relapsing-remitting MS (RRMS), Secondary Progressive MS (SPMS), Primary Progressive MS (PMMS).

While the etiology of MS is not fully clear yet, earlier research has proven that the neurons affected by MS show broken axons when the membrane is demyelinated. In order to imitate this process on cells of a PC12 cell line, the aim of the experiment was to differentiate PC12 wild type cells, so that they develop nerve-cell-like extensions. A transfection with TW2B was used to make the PC12 cells fluoresce in the green light channel of a microscope. Different amounts of DNA and other ingredients, varying methods of transfection, as well as variable timings of the differentiation were tested.

The results of our first experiment showed that a concurrent transfection and differentiation of the PC12 cells was quite rare. It could only be achieved with cells that were transfected with 1 μg of TW2B via 3 μl Trans-IT in an undifferentiated cell stage and differentiated later, and the results of the successful transfection and differentiation could only be seen on 1.72% of all the cells on that slide. The highest number of transfected cells could be achieved with cells, which were transfected with 2.5 μg of TW2B via 7.5 μl Trans-IT in an undifferentiated cell stage and differentiated later. 9.00% of these cells could be transfected successfully.

Parallel to this experiment and in another second experiment, we also tried Trans-IT transfections with lower DNA concentrations and transfections via a Calcium-Phosphate precipitation that we performed with self-produced, but also with solutions acquired by purchase. These transfections resulted in such low numbers of transfected and differentiated cells that we would not even count them. There were many possible reasons for the low outcome, such as personal mistakes, but also the characteristics of the PC12 cell line as well.

10

Generation and characterization of RanBPM mutants using CRISPR-Cas9

Luisa Delius, Lea Merkel, Michael Meyer

Molecular Neurophysiology, Meyer Group, Department of Cellular Physiology, Biomedical Center, Ludwig-Maximilians-University of Munich

The aim of our research group is to understand cell biology and physiology of calcium-binding proteins. The focus of our work is on EF hand proteins, a specific class of calcium-binding proteins, amongst them Calbindin-D28k. Questions we address are if Calbindin-D28k interacts with other proteins in situ in cells and what the physiological and pathophysiological significance of specific interactions is. In this context the protein RanBPM attracts our interest. Its co-expression and putative interaction with Calbindin1, especially in the Purkinje neurons of the cerebellar cortex2, make it desirable to get a better knowledge of its many supposed functions. To investigate the physiological role of RanBPM we created null mutants of the RanBPM protein using the CRISPRCas9 technology.

The target genomic locus within the RanBPM gene was selected using the CRISPR Design Tool3. It is located in the first exon around 30bp upstream of the start codon. The homologous 20-nt guide sequence was designed and cloned into the pSpCas9(BB)-2A-puro plasmid for co-expression with Cas9. The completed plasmid (called pLL1) was verified by sequence analysis. PLL1 was then transfected into neuronal HN10e cell lines and into non-neuronal NIH 3T3 cell lines. The first selection was made by exposing the cells to puromycin. The transfected cells were clonally expanded to derive isogenic cell lines with defined mutations4. To detect mutant phenotypes Western Blots and immunostaining using RanBPM-specific antibodies were made. About 42% of the HN10e cell clones and 18% of the NIH 3T3 cell clones were identified as null mutants.

Current work aims at the characterization of the genomic alterations and the functional analysis of the RanBPM null mutants.

Supported by Lehre@LMU

1 Lutz et al., Calbindin D28K interacts with Ran-binding protein M: identification of interacting domains by NMR spectroscopy, DOI: 10.1016/S0006-291X(03)00499-6, 2003 2 Floriani, Carmen. Interaktion Calbindin D-28k - RanBPM: Konfokale Kolokalisations - und Korrelationsanalyse, 2017 3 http://tools.genome-engineering.org 4 Ran et al., Genome engineering using the CRISPR-Cas9 system, DOI:10.1038/nprot.2013.143, 2013

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Multi-Layered Electro-Spun Scaffolds – Development and Examination for Application in Cardiovascular Tissue Engineering

Benedikt Freystetter, Grab M, Hagl C, Thierfelder N

Laboratory for Cardiovascular Engineering, Department of Cardiac Surgery, Ludwig-Maximilians-University of Munich

Aim and Background: Electrospinning has become a very important tool in cardiovascular tissue engineering since it offers the possibility to create scaffolds with adjustable properties. The aim of this study is to create synthetic multi-layered scaffolds mimicking the properties of human heart valves.

Methods: Multi-layered electro-spun scaffolds made of polyurethane (Pellethane® 2363 80AE, Lubrizol Co., Wickliffe, USA) are produced with an electrospinning device developed by the research group. The surface structure and mechanical properties of the scaffolds are assessed with a scanning electron microscope (SEM) and tensile tests respectively. The effects of fiber orientation and multi-layer construction will be compared using mechanical tests. The cytotoxicity of the material is tested over two weeks by adding it to an endothelial cell culture. To show effects of the fiber orientation on cell growth scaffolds with organized and randomly orientated fibers are colonized. Cell vitality and ingrowth behavior will be determined by immune-histochemical staining.

Results: It was possible to create multi-layered scaffolds combining aligned and unaligned layers. By adjusting voltage, temperature and humidity it was possible to control fiber diameter and density, which were evaluated by SEM. Biomechanical evaluation showed high tensile strength parallel to fiber orientation. Biocompatibility assessment of the electro-spun material showed no cytotoxicity after 24, 48 and 72 hours. Preliminary results of colonized scaffolds show differing ingrowth behavior depending on fiber orientation and density.

Conclusion: The multi-layered scaffolds created in this study offer new possibilities in the development of tissue engineered heart valves.

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Arteriogenesis – A potential bypass to compensate for arterial occlusion

Noah Hirsch, Iana Emelianova, Anna Klüver

Walter-Brendel-Centre of Experimental Medicine, Ludwig-Maximilians University of Munich

Cardiovascular occlusive diseases are still the number one cause of death in western countries: Though the human body can build natural bypasses in a process called arteriogenesis, our knowledge about this promising mechanism is still insufficient.

Arteriogenesis is a physiological process, where upon occlusion of an artery a network of preexisting arteriolar collaterals is remodeled to form functional arteries in order to compensate circulation deficiency.

The underlying mechanisms include the shear-stress induced activation and proliferation of endothelial and smooth muscle cells, the degranulation of mast cells, followed by local recruitment and extravasation of leukocytes and subsequent release of cytokines and growth factors.

After surgical procedure comprising the ligation of the femoral artery in a murine hind-limb model, we analyzed the development of arteriogenesis at different time points by using histological methods. Studies were focused on mast cell degranulation, tissue-remodeling macrophages and regulative functions of lymphocytes.

The injection of cobra venom factor (CVF), which initially induces a pronounced complement activation, but ultimately results in decomplementation, was used to investigate the role of the complement system in arteriogenesis and seemed to increase both the luminal diameter of collaterals and the perivascular mast cell count.

The amount of extravasated macrophages (M1 & M2) was also increased at various time points after ligation whereby the biggest changes occurred in the anti-inflammatory M2 subpopulation showing increased amounts at day seven.

Consequently macrophage-polarization towards tissue-remodeling active M2-phenotype (CD68+/MRC1+) seems to be essential in the pathway – regulated by stimulation of M1-phenotype (CD68+/MRC1-). In context of arteriogenesis we found increased numbers of perivascular CD20+ B cells, which may connect the steps between M1 and M2 by secretion of IL10.

In summary, it can be stated that even though there are unanswered questions, arteriogenesis could be a way to receive complete recovery after arterial occlusion without any invasive therapy.

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Auswertung von 10 Jahren Erfahrung interdisziplinärer Behandlung von geburtstraumatischen Plexusparesen, retrospektiv und prospektive Analyse des Outcomes nach operativer bzw. konservativer Therapie

Mortimer M. Hladik1, Elisabeth M. Haas1, Riccardo Giunta1

1 Abteilung für Handchirurgie, Plastische Chirurgie und Ästhetische Chirurgie Campus Innenstadt und Großhadern der Ludwig-Maximilians Universität München

Hintergrund: Die geburtstraumatische Plexusparese tritt mit einer Inzidenz von etwa 0,6-2,5/1000 Geburten auf. Sie ist somit eine seltene Läsion des Neugeborenen, die aber dennoch die Betroffenen in Ihrer Entwicklung und Lebensqualität stark einschränkt. Liegen nur leichte Dehnungsverletzungen vor, können diese mit Hilfe von krankengymnastischen Behandlungen innerhalb weniger Tage bis Wochen vollständig verheilen. Bei ca. 5-10% der Patienten liegen stärkere Dehnungsverletzungen bzw. Abrissverletzungen vor, die einer operativen Behandlung bedürfen. Diese mikrochirurgische Nervenrekonstruktion ist meist verbunden mit einer zuvor gehenden Physiotherapie.

Ziele: Um eine Therapiefindung für den individuellen Patienten zu erleichtern, sollte die konservative mit der operativen Therapie verglichen und damit deren Stellenwert in den heutigen Behandlungsoptionen erhoben werden.

Fragestellung: Zu untersuchen ist die Veränderung der individuellen Bewegungsausmaße, sowie der Lebensqualität nach gegebener Therapie.

Methoden: Literaturrecherche, klinische und operative Erfahrungen der letzten 10 Jahren, körperliche Nachuntersuchungen der bisher behandelten Patienten (ROM, Kraftgrade, Armlänge, usw.), Betreuung aktueller Patienten bei der Indikation, der Operation und den Follow-Up Untersuchungen in den nächsten Jahren, sowie Fragebögen zur Quality of Life

Ergebnisse: Da es sich hierbei um ein Forschungsvorhaben handelt, liegen noch keine Ergebnisse vor.

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Innervation pattern of the medial rectus eye muscles in a monkey after experimentally induced exotropic strabismus by unilateral transection of the trigeminal nerve

Alexander Holzner1, Das V2, Ying H3, May P4, Lienbacher K1, Horn AKE1

¹Anatomisches Institut I, LMU München; 2College of Optometry, University of Houston; 3Boston Eye Care Center, Boston;

4Department of Neurobiology and Anatomical Sciences, University of Mississippi Medical Center

Background: Binocular alignment is essential for normal vision in foveate species. Developmental failure in fusion causes congenital strabismus, whose exact cause is unclear. Current animal models of strabismus involve the disruption of binocular vision during the critical period by wearing prism goggles or eye muscle surgery. Alternatively, the loss of proprioceptive information may lead to strabismus. To test this hypothesis in two weeks old monkeys the ophthalmic trigeminal nerve was cut after exit from the trigeminal ganglion, which led to an exotropic strabismus.

Objective: Since the characteristics of the trigeminal innervation of eye muscles is unlcear, we compared the innervation pattern between the medial rectus muscles (MR) of the operated and non-operated eye. We further compared the quantity of muscle fiber types in the orbital and global layers of both MR.

Method: After sacrifizing and transcardial fixation (4% paraformaldehyde) of the animal, both eyes were removed and shipped to Munich. After dissecting both MR, longitudinal and transverse sections were cut frozen and immunostained for either SNAP-25 or neurofilament or synaptophysin to reveal the complete innervation combined with choline acetyltransferase (ChAT) as marker for motoaxons. Double-immunofluorescence stainings for slow and fast isoforms of myosin heavy chains served to identify non-twitch and twitch muscle fibers.

Result: The quantitative analysis of muscle fiber numbers of both MR did not reveal a significant difference between the operated and non-operated side. The semiautomatic quantitative analysis (Histoquant; 3D Histech) for immunostained nerve fibers showed a trend of less innervation on the lesioned side. With double-immunostaining for ChAT and synaptophysin few non-cholinergic nerve fibers were found including some putative sensory nerve endings.

Conclusion: No significant differences in muscle fiber quantity and innervation were found. In future experiments the quality of the non-cholinergic nerve endings needs to be specified, whether they represent autonomic fibers or trigeminal fibers.

28

Potassium channels in oculomotor nucleus in monkey

Ekaterina Lapteva, Mirjam Seidler, Ümit Mayadali, Karoline Lienbacher, Anja Horn

Institute of Anatomy, Dept. I, Ludwig-Maximilians University of Munich

Background: The oculomotor nucleus (nIII) in the mesencephalon contains functional cell groups for eye movements: motoneurons of singly-innervated twitch muscle fibres (SIF-MNs), motoneurons of multiply-innervated tonic fibres (MIF-MNs) and internuclear neurons (INTs). SIF-MNs correspond to alpha-motoneurons of limb muscles and move the eyes. MIF-MNs target muscle fibers via multiple small nerve endings and may control fine eye alignment during fixation. Non-cholinergic INTs project to the spinal cord, cerebellum, and to the abducens nucleus. SIF-MNs lie within nIII and are ensheathed by aggrecan (ACAN)-positive perineuronal nets (PN) as INTs, whereas MIF-MNs lie in the periphery of nIII and lack PNs.

Objective: Since voltage-gated potassium channels are crucial for neuronal firing characteristics, we investigated the expression pattern of Kv1.1 and Kv3.1b channels in SIF-MNs, MIF-MNs and INTs in nIII of monkey.

Methods: Monkey brainstem was fixed in 4% paraformaldehyde, embedded in paraffin and cut at 5 µm thickness. Parallel series of neighbouring sections through nIII were stained using immunoperoxidase methods with diaminobenzidine with and without Ni-ions as chromogen. Section 1 was immunostained for the simultaneous detection of choline-acetyltransferase (ChAT) and Kv1.1, section 2 for ChAT and ACAN to reveal PNs, and section 3 only for Kv3.1b.

Results: In all investigated cell types Kv1.1 channels were present within the cytoplasm including proximal dendrites, with a weaker immunoreactivity in MIF-MNs compared to SIF-MNs and INTs. Unlike in SIF-MNs and INTs showing a moderate staining, Kv3.1b immunoreactivtiy could not be distinguished from background staining in MIF-MNs.

Conclusion: Recent recordings of MIF- and SIF-MNs in the cat abducens nucleus demonstrated that both groups exhibit a burst-tonic firing pattern, but MIF-MNs with a reduced firing (Hernandez et al., 2019; PNAS 116:3837-3846). In light of these observations our findings indicate that Kv3.1b channels are required for the high frequent burst in SIF-MNs, but not in MIF-MNs.

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Effect of Hep7 on the remyelination in the chronic Cuprizone-model

Frederik Lorenz1, Jiangshan Zhan1, Uta Chrzandowski1, Markus Kipp2

1 Department of Neuroanatomy, Ludwig-Maximilians University of Munich, 80336, Munich, Germany 2 Institute of Anatomy, Medical University of Rostock, 18057, Rostock, Germany

Multiple sclerosis (MS) is defined as a chronic inflammatory disease of the central nervous system (CNS). Histopathological characteristics are demyelination, perivascular infiltration, microgliosis, astrogliosis, and finally a neurodegeneration. In our research we investigated Hep7, a heparan derivative, as a potential drug to induce remyelination. Oligodendrocytes that were previously lesioned will be renewed during this process and thereby forming new myelin sheaths around axons. This supports the regeneration of neuronal function after the lesion. In the presence of low-sulfated heparans (LS-Hep), like Hep7, the development of boundary formations of transplanted glia cells and astrocytes is reduced (Higginson et al., 2012). Binding of specific fibroblast growth factors (FGF) at the FGF-receptor 3b is inhibited by LS-Heps. High-sulfated heparan sulfates (HS-Hep) on the other hand induce increased binding of FGF1 and FGF9 on the FGF-receptor 3b. Cell mingling of astrocytes and glia cells is decreased by the presence of HS-heps. These effects were further examined by the University of Glasgow with in vitro-cultures of oligodendrocytes after Cuprizone-induced demyelination (unpublished data, 2018). We used this data to investigate the effect of Hep7 in vivo. Demyelination was induced with the Cuprizone-model in mice. The results from these experimental conditions contrast with the described effect in the in vitro models regarding remyelination, while further testing points to a possible effect of Hep7 in the recruitment process of immune cells in the corpus callosum.

28

Does Calbindin-D28k affect the intracellular distribution and accumulation of alpha-synuclein in a hippocampal neuronal cell line?

Simon Cecilia Lozano, Michael Meyer

Meyer Group, Department of Cellular Physiology, Biomedical Center, Ludwig-Maximilians University of Munich

Purpose: The formation of Lewy bodies (LB) is characteristical for many neurodegenerative disorders, the most common one being Parkinson´s disease. The main component of LB is aggregated alpha-synuclein (alpha-syn). This 14kDa protein is expressed in the central nervous system, where it is thought to regulate neurotransmitter release in dopaminergic neurons. Alpha-syn is natively unfolded but a number of factors, including raised intracellular calcium levels and oxidative stress, can lead to its aggregation. Studies have shown that Calbindin-D28k (Cb), a calcium binding protein, can inhibit alpha-syn aggregation.

Methods: To study this further we transfected HN10e cells with alpha-syn, two alpha-syn mutants linked to familial Parkinson´s (A30P, A53T) and calbindin, then induced alpha-syn aggregation through KCl treatment. Intracellular distribution was evaluated using immunofluorescence, while quantitative aspects were studied using Western Blot.

Results: Preliminary results indicate a colocalization of the two proteins which could potentially indicate interaction. Furthermore, we observed an unexpected and so far unexplained regulatory influence of calbindin expression which markedly increased the visibility of immunodetection of endogenous alpha-syn.

Conclusion: Current work aims at better understanding the nature and consequences (e.g. for synuclein structure) of colocalization as well as the causes of the calbindin dependent alpha-synuclein signals.

Supported by Lehre@LMU

28

Investigation of RanBPM and Procaspase 3 as possible interactors with Calbindin

Elene Nikolaishvili, Simone Weber, Michael Meyer

Meyer Group, Department of Cellular Physiology, Biomedical Center, Ludwig-Maximilians University of Munich

Calbindin is an EF-handed protein with four Ca2+ binding sites, mostly found in mammalian kidney and brain cells. In those it serves as a Ca2+ buffer and sensor. It is known that cellular Ca2+ levels rise dramatically during apoptosis, thus the possible role of Calbindin in apoptosis has been discussed for long time. Both Procaspase 3, an important effector in apoptosis, and RanBPM, a protein with many known interactors possibly acting as a scaffolding protein, have been suggested to interact with Calbindin, sharing the same binding domain. With our project we tried to verify and further characterize these interactions, which have so far been shown only in non-neuronal cells or in cell free systems, in the neuronal cell line HN10e, the fibroblastic 3T3 cell line an the epithelial MDCK cell line. Using a coimunoprecipitation assay form calbindin-transfected cells we found weak complexes containing calbindin and procaspase 3, but were not able to demonstrate complexes of calbindin and endogenous RanBPM. Thus we succeeded in providing addiotional evidence for an interaction of calbindin with procaspase 3 also in neuronal cell enviroment. We used indirect immunostaining of cultured cells searching for colocalization of the two proteins and change of transfected cells protein expression in comparison to untransfected cells, which does not prove but could give hints to an interaction.

We discovered that cells transfected with calbindin showed lower levels of procaspase 3 or activated caspase3 than control populations after inducing apoptosis with Staurosporin.

During our studies we also noticed that procaspase 3 is mainly localized in nueronal cells nuclei, which to some extent changes during apoptosis. Current work extends the analysis to include pull-down and gel-filtration assays to affirm our recent results.

28

High-speed ventral plane videography is a sensitive tool for detecting subclinical motor changes in EAE mice

Elena Nikolova1, Vladislav Yakimov1, Jiangshan Zhan2, Christoph Schmitz1 and Markus Kipp2

1Department of Anatomy II, Ludwig-Maximilians University of Munich, 80336, Munich, Germany 2Institute of Anatomy, Medical University of Rostock, 18057, Rostock, Germany

Purpose: Experimental Autoimmune Encephalomyelitis (EAE) is the most commonly used animal model for multiple sclerosis (MS). Like MS, EAE is characterized by infiltration of the central nervous system by myelin-reactive immune cells, which leads to myelin degeneration and impaired nerve conduction with functional deficits. Currently, the severity of EAE is evaluated through observation and assessment of motor functions in laboratory animals. This method is subjective and insensitive. In our project, we tested whether gait analysis with high-speed ventral plane videography (i.e. DigiGait™) is superior to currently used standard protocols for the detection of subclinical gait changes.

Methods: EAE was induced in female mice through immunization with MOG35-55 peptide. Starting on the 5th day after immunization, the animals were scored daily using the conventional scoring protocol. Ten of the animals were also tested with the DigiGait™ Imaging System, which conducts gait analysis of laboratory animals using ventral imaging technology1. For that purpose, the animals run on a transparent belt, while a high-speed camera underneath continuously records their gait. The accompanying software generates specific parameters, allowing quantification of the gait. The mice were sacrificed and their brains were histochemically evaluated for the presence of inflammatory infiltrates, visualized by H&E stains. Two independent experiments were performed. The results of the first one were verified in a second independent experiment.

Results: Our analysis revealed that EAE severity was not decreased by the imaging procedure. Furthermore, during the subclinical phase when there was no functional impairment detected by the conventional scoring protocol, the DigiGait™ Imaging System was able to detect alterations in parameters such as swing time and absolute paw angle between the hind paws of EAE mice.

Conclusion: High-speed ventral plane videography (i.e. DigiGait™) is a more sensitive and objective tool to study early gait alterations in EAE mice than the conventional scoring protocol.

References: Vincelette J, Xu Y, Zhang LN, Schaefer CJ, Vergona R, Sullivan ME, et al. Gait analysis in a murine model of collagen-induced arthritis. Arthritis Res Ther. 2007;9:R123.

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Activity-based quantification of neutrophil granule-associated serine proteases

Eva Riedlinger

Institut für Laboratoriumsmedizin der LMU

Objective: Granule-associated serine proteases of immune defense (GASPIDS) are a family of multifunctional proteases that are indispensable for the regular function of the immune system. When excessively released and active, however, GASPIDS contribute to the development of various inflammatory and degenerative disorders. Neutrophils contain large quantities of neutrophil elastase, proteinase 3, cathepsin G and NSP4 (neutrophil serine protease 4) that are stored in azurophilic granules after being activated by the cysteine proteinase cathepsin C. Current immunoassays do not discriminate between the mature, active protease and inactive forms, e.g. the zymogen and protease/inhibitor complexes. Activity-based assays therefore seem to be more appropriate to quantify the active and pathophysiologic relevant form of neutrophil GASPIDS.

Methods: Polymorphonuclear neutrophils were isolated from whole blood samples from healthy volunteers (n=28, age 25 ± 4.4 years) by immunomagnetic depletion. Purity and residual erythrocytes were assessed by cytospin and Harboe spectrophotometric method, respectively. The enzymatic activity of neutrophil elastase, proteinase 3, cathepsin G and cathepsin C was quantified in neutrophil lysates using kinetic assays with fluorogenic and chromogenic peptide substrates.

Results and discussion: Purity of isolated neutrophils was 98 ± 0.45 % of recovered leucocytes. With intra-assay CVs of ≤10%, fluorogenic kinetic assays were better suited to quantify the activity of GASPIDS than chromogenic assays. Protease activity was stable throughout a freeze/thaw cycle and short-term storage at -80°C with recoveries ≥90 %. The assays were linear and selective as verified e.g. using isolated or recombinant proteases and protease inhibitors.These novel activity assays thus appear adequate for quantifying GASPIDS and their activatorcathepsin C in crude neutrophil lysates. Only ~20,000 neutrophils usually present in < 20 µl of wholeblood are sufficient for all measurements. These assays therefore may advance investigations on therole of GASPID in immune defense and inflammatory disorders.

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Ago2 phosphorylation and Stau2 knockdown in neurons leads to distinct Ago2 protein localisation

Melina Schlegel

Biomedical Center Munich, Cell Biology, Ludwig-Maximilians University of Munich

Most posttranscriptional regulation of gene expression is based on interactions of RNA-binding proteins (RBPs) with their target-mRNAs. Argonaute2 (Ago2) is such an RBP and, as part of the RNA induced silencing complex (RISC), is involved in gene silencing. For effective inhibition of expression, Ago2 interacts with small RNAs, i.e. microRNA (miRNA), which guide Ago2 to the target-mRNA. Ago2 is bound by GW proteins that mediate silencing of gene expression by RNA degradation and translational repression. In the cell, Ago2 localizes to processing bodies (P-bodies), but is also found in ribonucleoprotein particles, both in the cell body as well as in distal dendrites of neurons. There are established phosphorylation sites in Ago2, which impact the efficiency of gene silencing by impairing the binding of miRNA, mRNA or GW protein to Ago2. One important phosphorylation cluster at serine/threonine 824:34 impairs mRNA binding, while miRNA binding is not affected. In HEK 293 cells, Ago2 824:34 phosphomutants and -mimics localize to P-bodies and show no difference in localisation compared to wt Ago2. In contrast, the phosphomimic 824:34E Ago2 protein shows strongly reduced localisation to P-bodies in mature neurons, while the number of overall P-bodies is not affected. Furthermore, Ago2 protein localisation is also affected by the RBP Staufen2 (Stau2), which plays an important role in mRNA localisation in cells. When Stau2 was downregulated by shStau2 RNA interference in hippocampal neurons, we detected reduced localisation of Ago2 to P-bodies. Together these data suggest a role of Stau2 in Ago2 recruitment to P-bodies.

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Simultaneous cuprizone intoxication and active induction of experimental autoimmune encephalomyelitis to study MS lesion development in the forebrain

Luna Slemann1, Vladislav Yakimov1, Markus Kipp2

1Institute of Anatomy II, Faculty of Medicine, LMU Munich, Pettenkoferstrasse 11, 80336 München, Germany 2Institute of Anatomy, Rostock University Medical Center, Gertrudenstraße 9, Rostock, 18057, Germany

Objective: Although oligodendrocyte degeneration is a hallmark of multiple sclerosis (MS) lesions, the underlying mechanisms are poorly understood. Oligodendrocyte loss can be mediated either by an aberrant immune response or by metabolic disturbances. Here, we investigated whether the combination of metabolic and immune-mediated oligodendrocyte injury in mice replicates histopathological features of MS lesions.

Methods: Female C57Bl/6 mice were immunized with myelin oligodendrocyte glycoprotein35-55 (MOG35-

55) peptide to generate the formation of myelin-reactive T cells. In parallel, the mice were intoxicatedwith cuprizone to induce metabolic oligodendrocyte injury (i.e., Cup/EAE mice). Animals were thenscored daily for clinical deficits and sacrificed at the peak of the disease. Brains were (immuno-)histochemically evaluated for the presence of inflammatory infiltrates, oligodendrocyte injury,demyelination and glia reactivity.

Results: In spite of its immunosuppressive effects, a synchronous cuprizone intoxication allowed the induction of active experimental autoimmune encephalomyelitis (EAE) by MOG35-55 immunization. Cuprizone intoxication slightly ameliorated the EAE disease course. As a consequence of the cuprizone-induced metabolic oligodendrocyte injury, peripheral immune cell recruitment into the forebrain was triggered in Cup/EAE mice. Those lesions were characterized by the presence of lymphocytes, oligodendrocyte apoptosis, moderate demyelination and microgliosis, closely resembling pattern III MS lesions.

Conclusions: We provide a protocol that allows to study the interplay of metabolic oligodendrocyte pathology and immune cell recruitment in the forebrain, as well as potential factors involved in type III MS lesion development. A better understanding of those factors would result in personalized treatment strategies.

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Professional Identity and Interprofessional Collaboration

Gertraud Stelzer, Prof. M. Siebeck

AG Prof. M. Fischer, DAM, LMU München

Purpose: To understand the role of interpersonal factors on developing professional identity.

Introduction: There is growing evidence that interprofessional collaboration is crucial for patient safety as well as health professional’s satisfaction1,2,3. Coping well with the issues of collaboration is not just a question of competences which one can acquire; it is as well a question of identification4. There are plenty of theories that could serve as a lens to understand identity construction. A core set combines the aspect of social influences, constructivists ideas, and individual differences: Social Identity Theories focus on the interaction processes of individuals5 as well as the interaction of individuals belonging to different groups6. Constructivists believe that we construct our "individual world" by exploring it. Developmental theories focus on individual biography7 and the transformation of the "self" over time8.

Context: The operating theatre serves as a micro-political context where collaboration is indispensable, but communication is often tense, and turnover times are fast. Different identifications and emphases may lead to strained relations9,10.

Methods: I will use interviews and network analysis to explore perceptions and individual coping strategies of collaborative demands. A qualitative analysis of the data could provide insight into the process of professional identity development.

Similarities and differences in professional identity and identity development may help to understand the impact of role models, e.g., scrub nurses and senior surgeons on student´s career choices.

Understanding these processes through which students and trainees develop professional identity will have implications for educational settings11.

I expect that my findings will have implications for how trainees are introduced into and prepared for the operating theatre.

Literature: 1. Khalili H., Orchard, C., Spence Laschinger, H. K., & Farah, R. (2013). An interprofessional socialization framework for developing aninterprofessional identity among health professions students. J Interprof Care, 27(6), 448-453. 2. Joynes V. C. (2018). Defining and understanding the relationship between professional identity and interprofessional responsibility: implications for educating health and social care students. Adv in Health Sci Educ, 23, 133-149. 3. Monrouxe L. V. (2010). Identity, identification and medical education: why should we care? Medical Education, 44, 40-49.4. Ward H., Gum, L., Attrill, S., Bramwell, D., Lindemann, I., Lawn, S., & Sweet, L. (2017). Educating for interprofessional practice: moving fromknowing to being, is it the final peace of the puzzle? BMC Medical Education, 17(5). 5. Mead G. H. (1973). Geist, Identität und Gesellschaft. Frankfurt am Main: Suhrkamp.6. Tajfel H. (1982). SOCAL IDENTITY AND INTERGROUP RELATIONS. Cambridge: Cambridge University Press 7. Erikson E. H. (1973). Identität und Lebenszyklus. Frankfurt am Main: Suhrkamp8. Kegan R. (1994). In over our heads: The mental demands of modern life. Cambridge:Havard Universitiy Press 9. Bleakley A. (2006). A common Body of Care: The Ethics and Politics of Teamwork in the Operating Theater are Inseparable. Journal ofMedicin and Philosophy, 31:3, 305- 322 10. Lingard L. Reznick R., DeVito I., Espin S. (2002). Forming professional identities on the health care team: discursive construction of the „other“ in the operating room. Medical Education, 36:728:734 11. Pratt M. G. Rockmann, K. W., & Kaufmann, J. B. (2006). Constructing Professional Identity: The Role of Work and Identity Learning Cyclesin the Customization of Identity among Medical Residents. The Academy of Management Journal, 49(2), 235-262.

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Cartography and Evaluation of Native and Decellularized Bovine Pericardium for Use as a Medical Implant

Felix Stieglmeier, M. Grab, C. Hagl, N. Thierfelder

Laboratory for Cardiovascular Tissue Engineering, Department of Cardiac Surgery, Ludwig-Maximilians University of Munich

Aim: Today decellularized bovine pericardium is already used for medical implants. It is not yet fully clear, which part of the pericardium is most suitable. Therefore, it is the aim of this study, to find the most appropriate area for that purpose.

Methods: As a first step, bovine pericardia (n=20) were collected from a local slaughterhouse. Subsequently five areas were defined to evaluate their attributes. For the decellularization process, the selected areas were washed in a 3D-printed box with detergents (0,2%SDS/0,2%DS) for 24 hours. The areas were compared before and after decellularization. The thickness of the native pericardia was measured at 140 spots, which were proportionally determinated. Additionally, the fiber alignment was highlighted. Biomechanical properties were determined using tensile tests. The outcome of the decellularization was evaluated by DNA isolation and DAPI staining. To investigate the histology, Picrosirius-, Pentachrome- and HE- staining were used.

Results: Proven by DNA Isolation and DAPI staining, the decellularization was successful on every investigated pericardium. The thickness varied across the pericardia, with one thicker area (native:0.85±0,14mm) and two homogenous thinner areas (native:0.57±0,10mm). Concerning the fiber alignment, no significant orientations could be recorded. The tensile tests showed, that the tensile strength is higher in circumferential direction (native:19,05±7,05N/mm2; DZ:15,81±6,29N/mm2) than in axial direction (native:8,97±4,94N/mm2; DZ:8,08±5,20N/mm2). Additionally, decellularized samples (11.95±2,50N/mm2) and native samples (14.01±3,09N/mm2) are almost equally tensile. It is also noticeable, that areas located near to the basal side of the heart, can handle more tension stress (native:17,29±6,77N/mm2; DZ:13,84±6,55N/mm2) than those, farer away (native:11,77±4,54N/mm2; DZ:9,59±3,44N/mm2). Demonstrated by the histological stainings, the pericardia consist of collagen in every layer and elastic fibers inside the core.

Conclusion: It was possible to find two areas, that were homogenous and simultaneously mechanically loadable. As a result, two homogenous areas located near the basal side of the heart can be recommended as implants and further investigation.

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Extramuscular manifestations of non-dystrophic myotonia

Noemi Vereb

Department of Neurology, Ludwig-Maximilians Univeristy of Munich

Purpose: Myotonia, the involuntary delay in relaxation of muscle contraction, can be caused by different rare disorders of muscular ion channels. These are attributed to gene mutations which lead to modified function of the sodium, chloride, calcium or the potassium channel. In contrast to dystrophic myotonia, with known multisystemic and especially gastrointestinal manifestations, the non-dystrophic myotonia is not yet proved to cause any gastrointestinal complaints. Our intent is to prove the occurrence of gastrointestinal symptoms in patients with non-dystrophic myotonia, hoping to answer the question if those symptoms have an identical origin. Also, with this project we hope to improve the consultation of people with non-dystrophic myotonia.

Methods: To examine this issue, we use an approximately 13 pages questionnaire. This questionnaire is inspired by few older questionnaires and considers feedback from affected patients, so it is highly customized to examine the extramuscular manifestations of people with non-dystrophic myotonia. We hope to reach a collective of 50-60 patients.

Results: This project is only at its beginning, there are no results so far.

Conclusion: Since there is no examination of extramuscular manifestations of patients with non-dystrophic myotonia so far, we hope to be able to pursue the hunch, if myotonia is the reason for gastrointestinal symptoms in both diseases, the dystrophic and non-dystrophic myotonia.

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Translational Neuroimaging in Mild Traumatic Brain Injury

Tim L. T. Wiegand1,2, Nico Sollmann1,2,3,4, Nikolaus Plesnila5,6, Martha E. Shenton1,7,8, Alexander P. Lin1,7, Inga K. Koerte1,2,9,10

1 Psychiatry Neuroimaging Laboratory, Department of Psychiatry, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA; 2 cBRAIN, Department of Child and Adolescent Psychiatry, Psychosomatic and Psychotherapy, Ludwig-Maximilians-University of Munich, Munich, Germany; 3 Department of Diagnostic and Interventional Neuroradiology, Klinikum rechts der Isar, Technische Universität München, Munich, Germany; 4 TUM-Neuroimaging Center, Klinikum rechts der Isar, Technische Universität München, Munich, Germany; 5 Institute for Stroke and Dementia Research, Ludwig-Maximilians University of Munich, Munich, Germany; 6 Munich Cluster for Systems Neurology (Synergy), Munich, Germany; 7 Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA; 8 VA Boston Healthcare System, Brockton Division, Brockton, MA, USA; 9 Department of Psychiatry, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; 10 Graduate School of Systemic Neuroscience, Ludwig-Maximilians University of Munich, Munich, Germany.

Mild traumatic brain injury (mTBI), also referred to as concussion, is the most common type of traumatic brain injury and characterized by a short period of unconsciousness followed by impaired cognitive function. In up to 30% of the cases, patients report persistent symptoms such as anxiety, depression and fatigue. The main challenges of mTBI research include the quest for biomarkers and understanding of patient-specific disease process and outcome of mTBI. In this context, neuroimaging and animal models represents valuable research modalities to address these challenges in a translational perspective. This article aims to review translational neuroimaging findings of magnetic resonance imaging (MRI), MR spectroscopy (MRS), diffusion tensor imaging (DTI) and positron emission tomography (PET). Altogether they allow the assessment of (micro-)structure, biochemistry and functioning of healthy and diseased brains and, to some extent, the comparison of human and animal data. Finally, this article discusses remaining limitations of translational neuroimaging and describes future directions of research that might lead to a better understanding of mTBI.

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Transmembrane protein 119 as a microglial marker in cuprizone model

Yavor Yakimov1, Armin Gruber1, Uta Chrzanowzski1, Markus Kipp2

1Department of Anatomy II, Ludwig-Maximilians-University of Munich, 80336, Munich, Germany 2Institute of Anatomy, Medical University of Rostock, 18057, Rostock, Germany

Purpose: Multiple sclerosis (MS) is a chronic, inflammatory, neurodegenerative disease, which is pathologically characterized by demyelination, microglial activation, astrogliosis and axonal damage. There is a growing body of evidence that the microglia cells play major role not only in demyelination, but also in remyelination of the axons in the brain 1. IBA1 (ionized calcium-binding adapter molecule 1) is one of the most commonly used marker-proteins for visualization of microglial cells. However, IBA1 is expressed not only in microglia cells but in monocytes as well, which poses a great setback. The lack of a specific microglial marker hinders the understanding of the influence, which the microglia cells have on the pathology of the disease. A recently published study has suggested that the transmembrane protein 119 (TMEM119) might serve as a specific microglia-marker2. In our project we investigated whether TMEM119 could be regarded as a specific microglia-marker in the cuprizone model - a commonly used MS animal model.

Methods: Considering that MS is a human disease, we needed a model that represents the different pathophysiological aspects, especially microgliosis, of the disease in animals. In our research we used the neurotoxicant, cuprizone, as such model to investigate the extent of microglial activation in the brain. Four groups of mice were used in our project. The first group served as a control group and was fed with normal chow. The other three groups were fed with 0.25% cuprizone for one, three and five weeks respectively. Brain slices were immunhistochemically stained with specific anti-TMEM119 and anti-IBA1 antibodies so that a comparison could be drawn between them. The slices were then stereologically analyzed and compared.

Results: Our analysis revealed an increase in microglial activity in the anti-IBA1-stained slices compared to the control group, which was evident after 1 week, severe after 3 weeks and most severe after 5 weeks of cuprizone feeding. However, the analysis of the anti-TMEM119-stained slices showed a decrease in the expression of transmembrane protein 119 in corpus callosum.

Conclusion: The aforementioned results suggested that TMEM119 cannot be regarded as a specific microglia-marker in the cuprizone model.

References: 1. O'Loughlin, Madore, Lassmann, Butovsky et al. microglial phenotypes and functions in multiple sclerosis. 2. Satoh, Kino, Asahina, Takitani, Miyoshi, Ishida, Saito et al. TMEM119 marks a subset of microglia in the human brain.

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Acknowledgements

I am happy and proud that this year the MMS ScienceCon takes place for the third time. This

wouldn’t have been possible without the effort and time dedicated by many motivated and

enthusiastic people.

First of all, I owe my deepest gratitude to the Associate Dean, Prof. Michael Meyer for

creating this friendly space where students of all Bavarian medical faculties can come

together to discuss their work and talk about the ups and downs of lab life.

Also, I am very grateful to our Dean of Research, Prof. Stefan Endres for the moral support.

It is my pleasure to thank Prof. Christoph Klein for committing his time and sharing his

expertise in form of this year’s very insightful keynote talk about genomic medicine.

I cordially want to thank all the members of the faculty Jury namely Prof. Anja Horn-Bochtler,

Prof. Michael Meyer, Dr. Matthias Ilmer, and Prof. Ben Aronson, as well as the members of

the student Jury Ms. Anne Eberhart, Mr. Matthias Seifert and Ms. Ayse Gertrude Yenicelik.

Your enthusiasm and constructive feedback is of great value to all the participants.

As always, the most important people at this conference are the students themselves. I want

to thank you all for choosing courage over comfort and for putting your work and yourselves

out there.

I offer my special thanks to Ayse Gertrude Yenicelik, the student coordinator, for her diligence

and her serenity that were crucial for the realization of this event. Also, I want to thank all the

other members of the student team: Ms. Brielmaier, Ms. Delius, Mr. Gruber, Mr. Hirsch, Ms.

Kluever, Ms. Lapteva, Mr. Lorenz, Ms. Lozano Simon, Ms. Merkel, Ms. Nikolaishvili, Ms.

Sleeman, Ms. Weber and Ms. Zahn. Your input helps greatly to improve the ScienceCon year

by year.

The MMS ScienceCon was again generously supported by the Lehre@LMU program and

therefore the BMBF. We appreciate the funding very much.

I want to express my gratitude to Mr. Aumüller and his colleagues for the hands on support

with the poster boards and the building services.

Eventually, I want to thank all guests for their curiosity. I hope you feel encouraged and

inspired.

Yours sincerely,

Dr. Johanna Canady

Coordinator of research promotion

Lehre@LMU Medical Faculty

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Notes

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Fakultät für Medizin

Ludwig-Maximilians-Universität München

Prof. Dr. Michael Meyer

Studiendekan für den 1. Studienabschnitt Humanmedizin

Großhaderner Str. 9

82152 Planegg-Martinsried

Tel: 089-2180-71566

Email: michael.meyer@lrz.uni-muenchen.de

Dr. Johanna Canady

Koordinatorin der Forschungsförderung

Lehre@LMU Medizin

Großhaderner Str. 9

82152 Planegg-Martinsried

Tel: 089-2180-75335

Email: johanna.canady@med.lmu.de

www.mms-sciencecon.med.uni-muenchen.de