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Berlin Brandenburg

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  • 1
    Language: English
    In: BMC Neurology, 01 December 2017, Vol.17(1), pp.1-6
    Description: Abstract Background Anterior sacral meningoceles are rare, and usually occur with other malformations of the posterior lower spine. While these are more frequently reported in pediatric cohorts, we report a case in an elderly woman. Case presentation We report on a 71 year-old woman with a recently diagnosed colorectal adenocarcinoma who presented with a severe bacterial meningitis. The cerebrospinal fluid cell count revealed a pleocytosis of 80,000 cells/μl and a severe disturbance of the blood-brain-barrier. Fusobacterium nucleatum was cultured as the causing pathogen. A lumbar MRI showed, in addition to contrast-enhancing meninges as sign of inflammation, a presacral mass. In the next step, the mass was diagnosed as an anterior sacral meningocele connected to the gut. An adequate antibiotic was used to treat the leptomeningitis. The connection between gut and meningocele was closed surgically and the patient recovered well and underwent further treatment of her colorectal adenocarcinoma. Conclusion We report on a case of meningitis with an anterior sacral meningocele that was connected to the gut in a patient with a infiltrative colorectal adenocarcinoma. Anatomic variants have to be considered as rare causes of meningitis with typical intestinal germs.
    Keywords: Meningitis ; Colorectal Carcinoma ; Anterior Sacral Meningocele ; Occult Spinal Dysraphism ; Medicine
    E-ISSN: 1471-2377
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  • 2
    Language: English
    In: Neuroimmunology and Neuroinflammation, July-Sept, 2014, Vol.1(3), p.135
    Description: 〈b〉Journal Title in English: 〈/b〉Neuroimmunology and Neuroinflammation
    Keywords: Cell Receptors -- Properties ; Cancer Metastasis -- Genetic Aspects ; Brain Diseases -- Genetic Aspects ; Genetic Regulation -- Research ; Genetic Research ; Cancer Research
    ISSN: 2347-8659
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  • 3
    In: Brain Pathology, July 2015, Vol.25(4), pp.491-504
    Description: The macrophage migration inhibitory factor () receptor 74 is overexpressed in various neoplasms, mainly in hematologic tumors, and currently investigated in clinical studies. 74 is quickly internalized and recycles after antibody binding, therefore it constitutes an attractive target for antibody‐based treatment strategies. 74 has been further described as one of the most up‐regulated molecules in human glioblastomas. To assess the potential relevance for anti‐74 treatment, we determined the cellular source and clinicopathologic relevance of 74 expression in human gliomas by immunohistochemistry, immunofluorescence, immunoblotting, cell sorting analysis and quantitative polymerase chain reaction (). Furthermore, we fractionated glioblastoma cells and glioma‐associated microglia/macrophages () from primary tumors and compared 74 expression in cellular fractions with whole tumor lysates. Our results show that 74 is restricted to  , while being absent in tumor cells, the latter strongly expressing its ligand . Most interestingly, a higher amount of 74‐positive was associated with beneficial patient survival constituting an independent prognostic parameter and with an anti‐tumoral 1 polarization. In summary, 74 expression in human gliomas is restricted to and positively associated with patient survival. In conclusion, 74 represents a positive prognostic marker most probably because of its association with an 1‐polarized immune milieu in high‐grade gliomas.
    Keywords: Cd 74 ; Glioma ; Immune Polarization ; Mif
    ISSN: 1015-6305
    E-ISSN: 1750-3639
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  • 4
    In: Neurosurgery, 2017, Vol.64(CN_suppl_1 Suppl 1), pp.268-268
    Description: Abstract INTRODUCTION Previous pivotal studies on the influence of extent of resection (EOR) in primary glioblastoma (GBM) have failed to incorporate molecular tumor markers, so the impact of extensive surgical approaches in the light of MGMT methylation and/or IDH mutation status is unclear. METHODS We retrospectively analyzed our prospectively collected database of patients undergoing surgery for newly diagnosed GBM WHO °IV and included only IDH1_R132H wild-type patients. All patients had volumetric assessment of EOR and received adjuvant treatment according to local tumor board recommendation and patient preference. We hypothesized that gross total resection was associated with better outcome. This analysis was approved by our local ethics committee. RESULTS 〉175 patients (median age: 60 years) were included. Median overall survival (OS) was 18.0 months. MGMT promotor methylation was present in 80 patients (45.7%). Complete removal of contrast-enhancing tissue (CRET) was achieved in 104 patients (59.4%). In Cox regression analysis, both MGMT-promoter methylation (HR 1.55; 95% CI, 1.01-2.19; P = 0.013) and CRET (HR 1.48; 95% CI, 1.06-2.07; P = 0.020) were significantly associated with favorable progression-free survival (PFS). Further, both MGMT promotor methylation (HR 2.13; 95% CI, 1.45-3.12; P = 0.0001) and CRET (HR 1.81; 95% CI, 1.24-2.63; P = 0.002) were independently associated with longer OS. No benefit was seen for resections 〈99%. Of other risk factors analyzed, only age (〉60 vs. 〈= 60 years) was significantly associated with PFS (HR 1.60; 95% CI, 1.14-2.24; P = 0.006) and OS (HR 2.19; 95% CI, 1.51-3.19; P 〈 0.0001). No significant outcome differences were observed between non-MGMT methylated patients undergoing CRET, and non-CRET, MGMT methylated patients (PFS: P = 0.726; OS: P = 0.477). CONCLUSION Both CRET and MGMT promotor methylation are independent prognostic factors for improved OS and PFS. Our study incorporates molecular markers and our data highlight the importance of aggressive surgical approaches. If achieved, CRET might compensate for the biological disadvantage of lacking MGMT promotor methylation.
    ISSN: 0148-396X
    E-ISSN: 15244040
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  • 5
    Language: English
    In: Cell Communication and Signaling, Jan 19, 2013, Vol.11(1)
    Description: Background Although ADP-ribosylation has been described five decades ago, only recently a distinction has been made between eukaryotic intracellular poly- and mono-ADP-ribosylating enzymes. Poly-ADP-ribosylation by ARTD1 (formerly PARP1) is best known for its role in DNA damage repair. Other polymer forming enzymes are ARTD2 (formerly PARP2), ARTD3 (formerly PARP3) and ARTD5/6 (formerly Tankyrase 1/2), the latter being involved in Wnt signaling and regulation of 3BP2. Thus several different functions of poly-ADP-ribosylation have been well described whereas intracellular mono-ADP-ribosylation is currently largely undefined. It is for example not known which proteins function as substrate for the different mono-ARTDs. This is partially due to lack of suitable reagents to study mono-ADP-ribosylation, which limits the current understanding of this post-translational modification. Results We have optimized a novel screening method employing protein microarrays, ProtoArrays[R], applied here for the identification of substrates of ARTD10 (formerly PARP10) and ARTD8 (formerly PARP14). The results of this substrate screen were validated using in vitro ADP-ribosylation assays with recombinant proteins. Further analysis of the novel ARTD10 substrate GSK3[beta] revealed mono-ADP-ribosylation as a regulatory mechanism of kinase activity by non-competitive inhibition in vitro. Additionally, manipulation of the ARTD10 levels in cells accordingly influenced GSK3[beta] activity. Together these data provide the first evidence for a role of endogenous mono-ADP-ribosylation in intracellular signaling. Conclusions Our findings indicate that substrates of ADP-ribosyltransferases can be identified using protein microarrays. The discovered substrates of ARTD10 and ARTD8 provide the first sets of proteins that are modified by mono-ADP-ribosyltransferases in vitro. By studying one of the ARTD10 substrates more closely, the kinase GSK3[beta], we identified mono-ADP-ribosylation as a negative regulator of kinase activity. Keywords: ARTD, Posttranslational modification, ADP-ribosyltransferase, PARP10, PARP14, ARTD8, NAD.sup.+, Kinase activity, Regulation
    Keywords: DNA Damage – Analysis ; Enzymes – Analysis ; Recombinant Proteins – Analysis ; Post-Translational Modifications – Analysis
    ISSN: 1478-811X
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  • 6
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  • 8
    Language: English
    In: BMC neurology, 04 July 2015, Vol.15, pp.103
    Description: Hereditary diffuse leukodystrophy with spheroids is a rare type of leukoencephalopathy. Mutations in the colony stimulating factor 1 receptor have recently been identified to be the cause of this microgliopathy. Clinical and radiological presentation can often misguide physicians during the diagnosis of patients with this underdiagnosed disease. We present a 29 year-old woman with a rapid course of hereditary diffuse leukodystrophy with spheroids. She mainly showed cognitive impairment and severe motor dysfunctions. Her MRI showed spotted and confluent hyperintensities of the white matter on T2-weighted images involving the corticospinal tract as well as the corpus callosum. Further, those lesions showed striking restricted diffusion. As this restricted diffusion in all areas showing signs of leukoencephalopathy was so impressive we searched Medline for these terms and got hereditary diffuse leukodystrophy with spheroids as one of the first results. After a comprehensive diagnostic workup and exclusion of other leukoencephalopathies, stereotactic biopsy and genetic testing confirmed the diagnosis. This case points out at two important features of hereditary diffuse leukodystrophy with spheroids being spotted and/or confluent leukoencephalopathy with areas of restricted diffusion. This might help to identify more patients with this underdiagnosed disease. Moreover, the rapid clinical course in our patient raises the question whether the relatively pronounced areas of restricted diffusion are indicative of a more acute progression of the disease.
    Keywords: Magnetic Resonance Imaging ; Receptor, Macrophage Colony-Stimulating Factor -- Genetics
    E-ISSN: 1471-2377
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  • 9
    In: Nature, 2018
    Description: Accurate pathological diagnosis is crucial for optimal management of patients with cancer. For the approximately 100 known tumour types of the central nervous system, standardization of the diagnostic process has been shown to be particularly challenging-with substantial inter-observer variability in the histopathological diagnosis of many tumour types. Here we present a comprehensive approach for the DNA methylation-based classification of central nervous system tumours across all entities and age groups, and demonstrate its application in a routine diagnostic setting. We show that the availability of this method may have a substantial impact on diagnostic precision compared to standard methods, resulting in a change of diagnosis in up to 12% of prospective cases. For broader accessibility, we have designed a free online classifier tool, the use of which does not require any additional onsite data processing. Our results provide a blueprint for the generation of machine-learning-based tumour classifiers across other cancer entities, with the potential to fundamentally transform tumour pathology.
    Keywords: DNA Methylation ; Tumors ; Standardization ; Data Processing ; Classification ; Methylation ; Brain Cancer ; Bioinformatics ; Cancer ; Generalized Linear Models ; DNA Methylation ; Diagnosis ; Tumors ; Genomes ; Classification ; Central Nervous System ; Central Nervous System ; Diagnosis ; Cancer ; Learning Algorithms ; Diagnostic Software ; Data Processing ; Tumors ; Central Nervous System ; Gene Expression ; Standardization ; Classification ; Cancer ; Classifiers ; Classification ; Clinical Trials ; Deoxyribonucleic Acid–DNA ; Probability ; Diagnostic Systems ; Nervous System ; Methylation ; Data Processing ; Tumors ; Data Processing ; Deoxyribonucleic Acid–DNA ; Deoxyribonucleic Acid–DNA ; World Health Organization;
    ISSN: 0028-0836
    E-ISSN: 1476-4687
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  • 10
    Language: English
    In: Neuromuscular Disorders, April 2016, Vol.26(4-5), pp.283-291
    Description: Deposits of the terminal-membrane-attack-complex (MAC) C5b-9 on perfascicular endomysial capillaries are generally regarded as diagnostic hallmark of dermatomyositis (DM). Although the pathophysiology is not clear, C5b-9 deposits on capillaries seem to be associated with microinfarctions and vascular damage. Here, we report on a series of 19 patients presenting with C5b-9 accumulation on endomysial capillaries in the absence of features for DM. To decipher differences in the capillary C5b-9 accumulation pattern between DM and non-DM cases, we assessed the extent of endomysial capillary C5b-9 deposits related to capillary density and extent of myofiber necrosis by immunohistochemistry in 12 DM and 8 control patients. We found similar numbers of C5b-9-positive myofibers in both DM and non-DM C5b-9 cases. The distribution pattern differed as DM cases showed significantly more perifascicular capillary C5b-9 deposits as compared to non-DM cases, which presented stronger endomysial capillary C5b-9 deposits in a diffuse pattern. While total capillary density was not differing, DM patients displayed significantly more C5b-9 necrotic fibers as compared to non-DM C5b-9 . In summary, endomysial capillary C5b-9 deposits are present in a variety of non-DM cases, however with differing distribution pattern. In conclusion, capillary C5b-9 deposits should be assessed critically, taking into consideration the distribution pattern.
    Keywords: C5b-9 ; Microvascular Unit ; Muscle Disease ; Dermatomyositis ; Mhc-I ; Medicine
    ISSN: 0960-8966
    E-ISSN: 1873-2364
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