In dieser Arbeit wurde die Kupferoxidebene des Hochtemperatur - Supraleiters Yttrium- Barium-Kupferoxid (YBa2Cu3O6+y) mit Hilfe von Kernmagnetischer-Resonanz (NMR - nucleus magnetic resonance) unter Drücken von bis zu 4.4GPa untersucht. Es wurden 2 dieser Druckzellen gebaut, sie enthielten verschieden stark dotierte Einkristalle. Die Änderungen der Ladungsverteilungen in der Kupferoxidebene abhängig von der Dotierung und vom Druck lagen hierbei im Fokus der Untersuchungen. Motivation dieser Arbeit war es YBa2Cu3O6+y Einkristalle bei höheren Drücken als zuvor mit NMR zu untersuchen. Dabei wurde der alte Rekord von 1.8GPa (Steven Reichardt 2018) auf 4.4GPa erhöht (aktuelle Arbeit). Da sich die Probenkammer in einer Druckzelle stark verformt, muss die Unversehrtheit der Kristalle an jedem Druckpunkt überprüft werden. Dies wurde unter anderem mit Bildern,welche mit dem Mikroskop durch die transparenten Anvils gemacht wurden, überprüft, als auch durch aufwendige Höhenmessungen der Probenkammer mit speziellen Mikroskopen in Verbindung mit einem Piezo-gesteuertem Probentisch. Durch die exakte Vermessung und Positionierung der Einkristalle auf dem Anvil konnte in Verbindung mit den Höhen- und Druchmessermessungen sichergestellt werden, dass sich der Kristall unter hydrostatischen Druckbedingungen befindet und nicht linear entlang der Zellenachse komprimiert wird, was zu einem Brechen oder einer Veränderung der Orientierung hätte führen können. Eine allgemeine Erkenntnis konnte dabei gewonnen werden, über die Stabilität, insbesondere der Höhe der Probenkammer, welche zunimmt mit dem Durchmesser des Culets. Dies ist entgegen des allgemeinen Prinzipes der Miniaturisierung zum erreichen höherer Drücke, für die Planung der Zellenarchitektur für Einkristallmessungen in NMR-Anvilzellen aber wichtig. Weiterhin mussten auch andere wichtige Parameter für NMR Messungen erfüllt werden. Die Architektur der Mikrospule welche in der Probenkammer um den Kristall gelegt wurde, mussten um den Füllfaktor zu maximieren an die Dimensionen der Kristalls angepasst werden. Dazu wurde eine Methode entwickelt um elliptische Mikrospulen von Hand zu wickeln, darin wurden die flachen Kristalle aufrecht platziert. Damit konnte das Signal auf eine annehmbare Intensität gebracht werden um in endlicher Zeit Messungen realisieren zu können. Mit den Messungen an Yttrium-Barium-Kupferoxid Einkristallen unter Druck konnte gezeigt werden, dass mit steigendem Druck sowohl die zunehmende Dotierung der Kupferoxidebene die Position am Sauerstoffatom bevorzugt, als auch eine Ladungsumverteilung in der Kupferoxidebene induziert wird. Weiterhin wurden NMR-Messungen am Indium Kern des Thermoelektrika Silber-Indium-Tellurid unter Druck durchgeführt. 5 verschiedenen Druckzellen wurden gebaut und bei Drücken bis zu 10GPa wurde gemessen. Bis 2.5GPa konnten Spektren aufgezeichnet werden die einen Anstieg des elektrischen Feldgradienten nahelegten. Dieser anstiegt konnte mit Nutationsexperimenten bestätigt werden. Die Echo-Experimente bei 4GPa und 5GPa wiesen einen starken Signalverlust auf und legten eine Quadropolaufspaltung des Zentralübergangs zweiter Ordnung nahe. Über 5GPa wurde kein Signal mehr gefunden. Nach dem Ablassen des Drucks zurück zu Umgebungsbedingungen wurde wieder ein Signal bei der ursprünglichen Frequenz gemessen.:0 Introduction 1 Theoretical Basics, Page 5 1.1 Nuclear Magnetic Resonance (NMR), Page 6 1.2 NMR Setup, Page 14 1.3 Pressure as Parameter, Page 17 1.4 NMR under Pressure, Page 28 2 Samples, Page 31 2.1 Yttrium-Barium-Copper-Oxide, Page 32 2.2 Silver-Indium-Telluride, Page 42 3 Experimental, Page 45 3.1 Spectrometer and Magnet, Page 46 3.2 Evaluation of the Measured Signals,Page 46 3.3 Micro Electronics, Page 47 3.4 Summary of the Chapter, Page 53 4 Sample Chamber Monitoring for single crystal NMR in high pressure cells, Page 55 4.1 Necessity of Sample Chamber Monitoring, Page 56 4.2 Measurements, Page 57 4.3 error consideration, Page 64 4.4 Discussion, Page 65 5 Single Crystal NMR of YBa2Cu3O6+y up to 4.4 GPa, Page 67 5.1 Doping Level and the Critical Temperature, Page 68 5.2 Orientation of the Single Crystal, Page 73 5.3 Discussion, Page 81 6 Silver-Indium-Telluride NMR under pressure, Page 83 6.1 Introduction, Page 84 6.2 Sample, Page 85 6.3 Pressures Cells, Page 85 6.4 Measurments, Page 87 6.5 Discussion, Page 97 7 Summary and Outlook, Page 99 7.1 Summary, Page 100 7.2 Conclusion and Outlook, Page 103 Appendix A Appendix, Page 107 A.1 Spectra, Page 108 Y-6.85 Cell, Page 108 Y-6.5 Cell, Page 113 References 127 / In this work the CuO2-plane of the high temperature superconductor yttrium-bariumcopper-oxide (YBa2Cu3O6+y) is investigated by nuclear magnetic resonance (NMR) under pressures up to 4.4GPa. Two high pressure NMR cells were built and filled with differently doped single crystals. The changes of the charge distribution in the CuO2-plane depending on doping and depending on pressure were the focus of the investigations. The motivation of this work was to extend the NMR measurements of YBa2Cu3O6+y single crystals in NMR anvil cells with pressures not achieved before. The old record (from Steven Reichardt 2018) of YBa2Cu3O6+y single crystals up to 1.8GPa was increased to 4.4GPa with this work. Due to the large deformation of the sample chamber, the integrity of a single crystal has to be checked at every pressure point. This was done by pictures, shot through the transparent anvils as well as height measurements of the sample chamber with a special microscope combined with a piezo controlled table. The exact measurements of the position of the single crystals as well as the height and diameter measurements assured that the single crystal is still in hydrostatic conditions or if it is tilted or pressurized linearly. A general cognizance about the stability of the sample chamber was acquired, especially about the stability of the height, which increases with the diameter of the culet. This is contrary to the general principle of miniaturization to reach higher pressures, if single crystals are of interest. The aim here is to have a stable sample chamber for good measuring conditions for NMR under pressure. Further, other expectations for the parameters of a NMR experiment had to be fulfilled as well. The architecture of a microcoil, which is placed around the crystal in the chamber, had to match the flat crystal shape to increase the filling factor and with this the signal to noise ratio (SNR) of the probe. For this, a method to wind elliptical micro coils by hand under the microscope was developed. Thereby signal intensity could be increased to an acceptable value which allowed more rapid measurements. With the measurements on YBa2Cu3O6+y single crystals under pressure it was shown that increasing pressure increase the hole doping in the CuO2-plane. Furthermore a redistibution of the charges in the CuO2-plane occurs. In a second part of this thesis 115In NMR measurements on the thermoelectric AgInTe2 under pressure up to 10GPa in 5 different cells were preformed. Up to 2.5GPa spectra were recorded which could be explained by an increase of the quadrupole frequency. This increase was verified by a power dependent nutation spectroscopy experiment. The echo experiments of pressures between 3GPa and 5GPa showed a high signal loss and pointed to an increasing disorder and a second order affected central transition of a powder spectrum. No signal was found above 5GPa despite elaborate searches in particular for a possible metallic component. After the pressure release a signal was found again at ambient conditions frequency.:0 Introduction 1 Theoretical Basics, Page 5 1.1 Nuclear Magnetic Resonance (NMR), Page 6 1.2 NMR Setup, Page 14 1.3 Pressure as Parameter, Page 17 1.4 NMR under Pressure, Page 28 2 Samples, Page 31 2.1 Yttrium-Barium-Copper-Oxide, Page 32 2.2 Silver-Indium-Telluride, Page 42 3 Experimental, Page 45 3.1 Spectrometer and Magnet, Page 46 3.2 Evaluation of the Measured Signals,Page 46 3.3 Micro Electronics, Page 47 3.4 Summary of the Chapter, Page 53 4 Sample Chamber Monitoring for single crystal NMR in high pressure cells, Page 55 4.1 Necessity of Sample Chamber Monitoring, Page 56 4.2 Measurements, Page 57 4.3 error consideration, Page 64 4.4 Discussion, Page 65 5 Single Crystal NMR of YBa2Cu3O6+y up to 4.4 GPa, Page 67 5.1 Doping Level and the Critical Temperature, Page 68 5.2 Orientation of the Single Crystal, Page 73 5.3 Discussion, Page 81 6 Silver-Indium-Telluride NMR under pressure, Page 83 6.1 Introduction, Page 84 6.2 Sample, Page 85 6.3 Pressures Cells, Page 85 6.4 Measurments, Page 87 6.5 Discussion, Page 97 7 Summary and Outlook, Page 99 7.1 Summary, Page 100 7.2 Conclusion and Outlook, Page 103 Appendix A Appendix, Page 107 A.1 Spectra, Page 108 Y-6.85 Cell, Page 108 Y-6.5 Cell, Page 113 References 127

Environmental monitoring involves the quantification of microscopic cells and particles such as algae, plant cells, pollen, or fungal spores. Traditional methods using conventional microscopy require expert knowledge, are time-intensive and not wellsuited for automated high throughput. Multispectral imaging flow cytometry (MIFC) allows measurement of up to 5000 particles per second from a fluid suspension and can simultaneously capture up to 12 images of every single particle for brightfield and different spectral ranges, with up to 60x magnification. The high throughput of MIFC has high potential for increasing the amount and accuracy of environmental monitoring, such as for plant-pollinator interactions, fossil samples, air, water or food quality that currently rely on manual microscopic methods. Automated recognition of particles and cells is also possible, when MIFC is combined with deep-learning computational techniques. Furthermore, various fluorescence dyes can be used to stain specific parts of the cell to highlight physiological and chemical features including: vitality of pollen or algae, allergen content of individual pollen, surface chemical composition (carbohydrate coating) of cells, DNA- or enzyme-activity staining. Here, we outline the great potential for MIFC in environmental research for a variety of research fields and focal organisms. In addition, we provide best practice recommendations.

Oomycetes (Stramenopiles, protists) are among the most severe plant pathogens, comprising species with a high economic and ecologic impact on forest ecosystems. Their diversity and community structures are well studied in terrestrial habitats, but tree canopies as huge and diverse habitats have been widely neglected. A recent study highlighted distinct oomycete communities in the canopy stratum compared to the ground region of three temperate deciduous trees (Quercus robur, Tilia cordata, Fraxinus excelsior). While the communities from the two strata were distinct when taking oomycete abundances into account, they were rather similar when only OTU presence/absence was considered. It remains, however, unknown if this homogeneity in the OTU presence also leads to a functional homogenisation among microhabitats within the two strata ground and canopy. In this study, we supplemented functional traits to oomycete communities in the tree microhabitats, which were determined over a time period of 2 years with a metabarcoding approach. Our results showed that even though most oomycetes occurred in all microhabitats, a strong discrepancy between the strata and correspondingly the distribution of oomycete lifestyles could be observed. This pattern was constant over several seasons. Obligate biotrophic species, exclusively feeding on living host tissue, dominated the canopy region, implying tree canopies to be a hitherto neglected reservoir for parasitic protists. OTUs assigned to the genus Hyaloperonospora—parasites highly specialised on hosts that were not sampled—could be determined in high abundances in the canopy and the surrounding air, challenging the strict host dependencies ruled for some oomycetes. Our findings further contribute to the understanding of oomycete ecosystem functioning in forest ecosystems

The demise of retinal ganglion cells (RGCs) is characteristic of diseases of the retina such as glaucoma and diabetic or ischemic retinopathies. Pigment epithelium-derived factor (PEDF) is a multifunctional secreted protein that mediates neuroprotection and inhibition of angiogenesis in the retina. We have studied expression and regulation of two of several receptors for PEDF, patatin-like phospholipase 2 gene product/PEDF-R and laminin receptor (LR), in serum-starved RGC under normoxia and hypoxia and investigated their involvement in the survival of retinal neuronal cells. We show that PEDF-R and LR are co-expressed in RGC and R28 retinal precursor cells. Expression of both receptors was enhanced in the presence of complex secretions from retinal glial (Müller) cells and upregulated by VEGF and under hypoxic conditions. PEDF-R- and LR-knocked-down cells demonstrated a markedly attenuated expression of anti-apoptotic Bcl-2 family members (Bcl-2, Bcl-xL) and neuroprotective mediators (PEDF, VEGF, BDNF) suggesting that both PEDF-R and LR mediate pro-survival effects of PEDF on RGC. While this study does not provide evidence for a differential survival-promoting influence of either PEDF-R or LR, it nevertheless highlights the importance of both PEDF receptors for the viability of retinal neurons.

In systems biology, material balances, kinetic models, and thermodynamic boundary conditions are increasingly used for metabolic network analysis. It is remarkable that the reversibility of enzyme-catalyzed reactions and the influence of cytosolic conditions are often neglected in kinetic models. In fact, enzyme-catalyzed reactions in numerous metabolic pathways such as in glycolysis are often reversible, i.e., they only proceed until an equilibrium state is reached and not until the substrate is completely consumed. Here, we propose the use of irreversible thermodynamics to describe the kinetic approximation to the equilibrium state in a consistent way with very few adjustable parameters. Using a flux-force approach allowed describing the influence of cytosolic conditions on the kinetics by only one single parameter. The approach was applied to reaction steps 2 and 9 of glycolysis (i.e., the phosphoglucose isomerase reaction from glucose 6-phosphate to fructose 6-phosphate and the enolase-catalyzed reaction from 2-phosphoglycerate to phosphoenolpyruvate and water). The temperature dependence of the kinetic parameter fulfills the Arrhenius relation and the derived activation energies are plausible. All the data obtained in this work were measured efficiently and accurately by means of isothermal titration calorimetry (ITC). The combination of calorimetric monitoring with simple flux-force relations has the potential for adequate consideration of cytosolic conditions in a simple manner.

The human genome comprises 8% sequences of retroviral origin, so-called human endogenous retroviruses (HERVs). Most of these proviral sequences are defective, but some possess open reading frames. They can lead to the formation of viral transcripts, when activated by intrinsic and extrinsic factors. HERVs are thought to play a pathological role in inflammatory diseases and cancer. Since the consequences of activated proviral sequences in the human body are largely unexplored, selected envelope proteins of human endogenous retroviruses associated with inflammatory diseases, namely HERV-K18, HERV-K113, and HERV-Fc1, were investigated in the present study. A formation of glycosylated envelope proteins was demonstrated in different mammalian cell lines. Nevertheless, protein maturation seemed to be incomplete as no transport to the plasma membrane was observed. Instead, the proteins remained in the ER where they induced the expression of genes involved in unfolded protein response, such as HSPA5 and sXBP1. Furthermore, low expression levels of native envelope proteins were increased by codon optimization. Cell-free expression systems showed that both the transcriptional and translational level is affected. By generating different codon-optimized variants of HERV-K113 envelope, the influence of single rare t-RNA pools in certain cell lines was demonstrated. The mRNA secondary structure also appears to play an important role in the translation of the tested viral envelope proteins. In summary, the formation of certain HERV proteins is basically possible. However, their complete maturation and thus full biologic activity seems to depend on additional factors that might be disease-specific and await elucidation in the future.

For systems biology, it is important to describe the kinetic and thermodynamic properties of enzyme-catalyzed reactions and reaction cascades quantitatively under conditions prevailing in the cytoplasm. While in part I kinetic models based on irreversible thermodynamics were tested, here in part II, the influence of the presumably most important cytosolic factors was investigated using two glycolytic reactions (i.e., the phosphoglucose isomerase reaction (PGI) with a uni-uni-mechanism and the enolase reaction with an uni-bi-mechanism) as examples. Crowding by macromolecules was simulated using polyethylene glycol (PEG) and bovine serum albumin (BSA). The reactions were monitored calorimetrically and the equilibrium concentrations were evaluated using the equation of state ePC-SAFT. The pH and the crowding agents had the greatest influence on the reaction enthalpy change. Two kinetic models based on irreversible thermodynamics (i.e., single parameter flux-force and two-parameter Noor model) were applied to investigate the influence of cytosolic conditions. The flux-force model describes the influence of cytosolic conditions on reaction kinetics best. Concentrations of magnesium ions and crowding agents had the greatest influence, while temperature and pH-value had a medium influence on the kinetic parameters. With this contribution, we show that the interplay of thermodynamic modeling and calorimetric process monitoring allows a fast and reliable quantification of the influence of cytosolic conditions on kinetic and thermodynamic parameters.

The iliotibial band (ITB) is a suitable scaffold for anterior cruciate ligament (ACL) reconstruction, providing a sufficient mechanical resistance to loading. Hence, ITB-derived fibroblasts attract interest for ligament tissue engineering but have so far not been characterized. This present study aimed at characterizing ITB fibroblasts before, during, and after emigration from cadaveric ITB explants to decipher the emigration behavior and to utilize their migratory capacity for seeding biomaterials. ITB and, for comparison, ACL tissues were assessed for the content of alpha smooth muscle actin (αSMA) expressing fibroblasts and degeneration. The cell survival and αSMA expression were monitored in explants used for cell isolation, monolayer, self-assembled ITB spheroids, and spheroids seeded in polyglycolic acid (PGA) scaffolds. The protein expression profile of targets typically expressed by ligamentocytes (collagen types I–III, elastin, lubricin, decorin, aggrecan, fibronectin, tenascin C, CD44, β1-integrins, vimentin, F-actin, αSMA, and vascular endothelial growth factor A [VEGFA]) was compared between ITB and ACL fibroblasts. A donor- and age-dependent differing percentage of αSMA positive cells could be detected, which was similar in ITB and ACL tissues despite the grade of degeneration being significantly higher in the ACL due to harvesting them from OA knees. ITB fibroblasts survived for several months in an explant culture, continuously forming monolayers with VEGFA and an increased αSMA expression. They shared their expression profile with ACL fibroblasts. αSMA decreased during the monolayer to spheroid/scaffold transition. Using self-assembled spheroids, the migratory capacity of reversible myofibroblastic ITB cells can be utilized for colonizing biomaterials for ACL tissue engineering and to support ligament healing.

While cognitive impairment is common in peripheral diseases such as chronic kidney disease (CKD), mechanistic insights and effective therapies are lacking. Multiple toxins accumulating as a consequence of CKD have been identified, yet the consequences for cellular crosstalk in the brain and the mechanisms underlying the associated neuronal dysfunction remain largely elusive. In the case of CKD, more than 100 uremic toxins have been identified. Renal transplantation largely reverses the cognitive impairment associated with CKD, demonstrating that cognitive impairment in CKD can be reversed. This indicates that pharmaceutical approaches to target cognitive impairment in association with CKD may be feasible. However, it is unlikely that targeting a single toxin will be sufficient to combat neuronal dysfunction associated with peripheral diseases such as CKD, given the large number of toxins involved and since the pattern of accumulating toxins varies among affected patients. Rather than identifying single toxins, identifying a common mechanism inducing neuronal dysfunction and thus impairing cognition may identify new and feasible therapeutic approaches. One commonality of peripheral diseases such as liver or renal failure is sterile inflammation. Sterile inflammation has been linked with neurodegenerative diseases and associated cognitive impairment and inflammasome activation is one hallmark of chronic pathologies in the brain. Mutations in the inflammasome component NLRP3 show clinical manifestations of cryopyrin- associated periodic syndromes (CAPS), which are characterized by skin rash, fever and joint pain. Further, abnormal and constant NLRP3 signaling has been associated with some chronic and degenerative diseases such as Alzheimer’s disease (AD), atherosclerosis, arthritis or cancer. A causative function of the NLRP3 inflammasome for neurodegenerative processes is supported by preclinical studies. These pre-clinical studies used whole body knock out mice to demonstrate that deficiencies of NLRP3, caspase-1 or the primary receptor for IL-1β, IL-1R1, protect mice from neurodegenerative processes. While providing important insights into the role of the NLRP3-inflammasome in neurodegenerative processes, these studies did not identify the relevant cell types in which the inflammasome is activated, the mechanisms underlying inflammasome activation and the consequences thereof, e.g. for intracerebral cross-talk. In addition, whether sterile inflammation triggered by the NLRP3 inflammasome impairs cognition in the setting of primarily peripheral diseases such as CKD remains unknown. To address these open questions, I used a mouse model of CKD, in which I detected NLRP3 inflammasome in brains. Interestingly, despite inflammasome activation in the brain, microglial caspase-1 deficiency did not improve cerebral inflammation and cognition in CKD mice. I identified noncanonical IL-1β maturation in microglia in CKD conditions, which was cathepsin c – caspase-8 mediated. Restoring K+ homeostasis in microglia or genetic inhibition of neuronal IL-1R1 signaling abolished CKD-induced cognitive impairment. Mechanistically, noncanonical IL-1β maturation and secretion from microglia promotes via IL-1R signaling cognitive impairment in neurons. This identifies a molecular mechanism of sterile CNS inflammation and the associated intercellular signaling pathway, which may be therapeutically amendable. Microglial K+ dyshomeostasis and noncanonical microglial IL-1β maturation may be druggable targets in some forms of cognitive impairment.:Content 2 List of abbreviations 5 Graphical abstract 8 2 Introduction 9 2.1 Chronic kidney disease and cognition 11 2.2 Microglia cells 13 2.3 The inflammasome, potassium dyshomeostasis in brain cells and thallium autometallography 15 2.4 Sterile inflammation in neurodegenerative diseases 17 3 Aims of the study 19 4 Materials and Methods 20 4.1 Reagents 20 4.2 Mice 27 4.3 CKD mouse model (5/6 nephrectomy model) 30 4.4 Evans Blue extravasation assay 32 4.5 2-photon microscopy 32 4.6 Analysis of mice 33 4.7 In vivo interventions 33 4.8 Histology and immunohistochemical analysis 34 4.9 Cell culture 34 4.10 Dextran permeability assay 35 4.11 Thallium-AMG (TlAMG), ex vivo and in vitro 36 4.12 Protein extraction and Western blotting 38 4.13 IL-1β ELISA 38 4.14 Reverse Transcriptase Polymerase Chain Reaction (RT–PCR) 38 4.15 Proximity ligation assay (PLA) 39 4.16 Behavioral analysis 39 4.17 Cathepsin c substrate assay 40 4.18 snRNA-Seq 41 4.19 Statistical Analysis 42 5 Results 43 5.1 Chronically impaired renal function leads to cognitive decline 43 5.2 Blood brain barrier (BBB) disruption in chronic kidney disease 44 5.3 Potassium dyshomeostasis in brain cells in CKD 45 5.4 CKD leads to microglia activation 46 5.5 Priming of microglia in CKD depends on potassium dyshomeostasis and its restoration improves cognition in CKD 49 5.6 TRAM34 ameliorates potassium dyshomeostasis and behavior in CKD 51 5.7 Uremia-induced cognitive impairment depends on microglia- neuron crosstalk via IL-1R1 52 5.8 Deciphering the microglial molecular pathway in CKD 56 5.9 Microglia activation in CKD is independent of NLRP3 56 5.10 Microglial IL-1β maturation occurs independently of the NLRP3-Caspase-1 inflammasome in CKD 57 5.11 The role of caspase- 8 in microglia activation in CKD 60 5.12 Lysosomal cathepsin c promotes microglia activation pivotal for caspase-8 activation 62 5.13 Broader implication of the pathway in other chronic peripheric diseases 63 5.14 Microglia inflammasome activation and IL-1β release is sufficient to induce cognitive impairment 64 5.15 Tables 66 6 Discussion 69 7 Summary 75 8 Zusammenfassung 80 9 References 86 10 Declaration about the independent preparation of the work 97 11 Presentation of own contribution 98 12 Curriculum vitae 99 13 Publications 104 14 Acknowledgments 106

Serum levels of apolipoprotein ApoC1 have been described in a number of systemic tumor entities as potential biomarkers, but little is known about ApoC1 in neurosurgical patients. A total of 230 serum samples from 96 patients were analyzed using an ELISA technique. Patient diagnoses comprised 70 glioblastomas WHO IV◦ , 10 anaplastic astrocytomas III◦ , one anaplastic oligodendroglioma III◦ , one oligodendroglioma II◦ , one diffuse astrocytoma II◦ , one pilocytic astrocytoma I◦ , and a single case of a spindle cell tumor without WHO grading, as well as 11 spinal interventions. The mean ApoC1 level of the 230 samples was 132.03 µg/mL (median 86.83, SD 292.91). In the 176 glioblastoma samples, the mean ApoC1 level was 130.0 µg/mL (median 86.23, SD 314.9), which was neither different from the whole group nor from patients with spinal interventions (215.1 µg/mL, median 63.6, SD 404.9). In the postoperative samples, the mean ApoC1 level was significantly lower (85.81 µg/mL) than in the preoperative samples (129.64 µg/mL) and in samples obtained during adjuvant chemotherapy (168.44 µg/mL). While absolute ApoC1 serum levels in a patient do not allow for the distinction between neurosurgical histological entities, future analyses will examine whether the time course of ApoC1 in an individual patient can be related to certain treatment stages.