Die Deletion von Chromosom 17q bei rezidivierenden Meningeomen

Meningeome gehören zu den häufigsten intrakraniellen Tumoren. Obwohl die Mehrzahl der Meningeome durch eine vollständige Resektion geheilt werden können, weisen bis zu 20 % der Tumore ein aggressives Verhalten mit rascher Tumorprogression beziehungsweise einem Rezidivwachstum auf. Die genetische Analyse von Meningeomen zeigt meist einen normalen Karyotyp oder eine Monosomie von Chromosom 22 als einzige zytogenetische Aberration. Die Tumorprogression und das Rezidivverhalten von Meningeomen sind mit sekundären chromosomalen Verlusten assoziiert. Ziel dieser Arbeit war es, die Rolle der Deletion von Chromosom 17q bei Patienten mit rezidivierenden Meningeomen zu bestimmen. Gegenstand der vorliegenden Arbeit waren alle Patienten, die aufgrund eines Meningeomrezidivs in der Klinik für Neurochirurgie des Universitätsklinikums des Saarlandes zwischen 1999 und 2015 operiert wurden. Aus diesem Kollektiv wurden weiter nur die Patienten ausgewählt, von denen mindestens zwei Tumorproben von unterschiedlichen Operationszeitpunkten vorlagen, um die zytogenetische Progression der Tumore im zeitlichen Verlauf zu untersuchen. Die zytogenetische Untersuchung der Tumorproben erfolgte mittels Fluoreszenz-in-situ-Hybridisierung (FISH) für die Chromosomen 1p, 10, 17q und 22q. Insgesamt wurden 22 Tumorproben (3 Primärtumorproben, 19 Rezidivtumorproben) von sieben Patienten untersucht. In 20/22 (90,1 %) der Tumore konnte eine Deletion von Chromosom 17q detektiert werden. In allen Primärtumorproben war die Deletion von Chromosom 17q ebenfalls nachweisbar. Es zeigte sich im zeitlichen Verlauf kein stetiger An- oder Abstieg des prozentualen Anteils der 17q-Deletion in den Tumorproben der Patienten. Zusammenfassend konnte in der vorliegenden Arbeit erstmals eine Deletion von Chromosom 17q in einem Kollektiv von Patienten mit rezidivierenden Meningeomen mittels Fluoreszenz-in-situ-Hybridisierung gezeigt werden. Deletionen der chromosomalen Region 17q könnten ein frühes Ereignis in der Progression von Meningeomen darstellen. Der Nachweis dieser Deletion könnte in der klinischen Anwendung als potentieller Marker für Malignität und ein erhöhtes Rezidivrisiko bei Meningeomen dienen.Deletion of chromosome 17q in recurrent meningiomas Meningiomas are among the most frequent intracranial tumours. Although the majority of meningiomas can be cured by surgical resection, up to 20 % of the tumours show an aggressive clinical course with tumour recurrence or progressive disease. Cytogenetically, meningiomas frequently harbour a normal karyotype or monosomy of chromosome 22 as the sole anomaly. However, progression of meningiomas is associated with a non-random pattern of secondary losses. The aim of this study was to determine the role of deletions of chromosome 17q in patients with recurrent meningiomas. A total of seven patients underwent repeated surgery for recurrent meningiomas between 1999 and 2015 at the Department of Neurosurgery at the Saarland University Hospital. Patients were included in this study in case tumor samples from two or more different meningiomas of the same patient were available. Fluorescence in situ hybridization (FISH) was performed on interphase nuclei of tumor cells from the tumour samples to evaluate the clonal cytogenetic evolution of recurrent meningiomas. Collectively, 22 biopsies (3 primary tumours, 19 recurrent tumours) from seven patients were examined. In 20/22 (90.1 %) specimens, the tumor samples showed a 17q deletion. The three primary tumors also showed a 17q deletion. In the course of time, there was no steady in- or decrease in the percentage of deletions of chromosome 17q in the patients’ tumors. In conclusion, this is the first report to demonstrate deletion of chromosome 17q via fluorescence-in-situ-hybridization in patients with recurrent meningiomas. Deletion of chromosome 17q could display an early event in meningioma progression. Accordingly, deletion of chromosome 17q might clinically serve as a marker for malignancy and a higher risk for meningioma recurrence

Mobile Technology in the Construction Industry - the Impact on Business Processes in Job Production

Research on mobile technologies has received an increasing attention. However, most of the existing literature focuses on the use of mobile technologies on a managerial level, with technology as an enabler for information and communication exchange. The impact potential and their corresponding functionalities at the operational level have not yet been analyzed. This study addresses this gap. The key objective is the development of a conceptual model to explain how mobile technologies impact business processes in the construction industry on the operational level. Thus, a generic model will be developed on the basis of existing literature, especially the concept of Task-Technology-Fit. It emphasizes how task complexity affects the required effort of individual information access, information capturing as well as the timeliness of information. Then, it will be deduced how mobile technologies affect the forces and relationships in this model. The evaluation of the model shows that there is a strong influence of the reduced effort for accessing information on the process performance if there is a high task complexity. In addition to the new level of analysis (the system user is a worker instead of a manager), a new method of performing the model evaluation is utilized. For this evaluation, a 3D-laboratory experiment is combined with a computer simulation

Neutrophil extracellular traps and delayed cerebral ischemia in aneurysmal subarachnoid hemorrhage

IMPORTANCE: Myeloperoxidase (MPO)-DNA complexes, biomarkers of neutrophil extracellular traps (NETs), have been associated with arterial and venous thrombosis. Their role in aneurysmal subarachnoid hemorrhage (aSAH) is unknown. OBJECTIVES: To assess whether serum MPO-DNA complexes are present in patients with aSAH and whether they are associated with delayed cerebral ischemia (DCI). DESIGN, SETTING, AND PARTICIPANTS: Post-hoc analysis of a prospective, observational single-center study, with de novo serum biomarker measurements in consecutive patients with aSAH between July 2018 and September 2020, admitted to a tertiary care neuroscience ICU. MAIN OUTCOMES AND MEASURES: We analyzed serum obtained at admission and hospital day 4 for concentrations of MPO-DNA complexes. The primary outcome was DCI, defined as new infarction on brain CT. The secondary outcome was clinical vasospasm, a composite of clinical and transcranial Doppler parameters. We used Wilcoxon signed-rank-test to assess for differences between paired measures. RESULTS: Among 100 patients with spontaneous subarachnoid hemorrhage, mean age 59 years (sd ± 13 yr), 55% women, 78 had confirmed aSAH. Among these, 29 (37%) developed DCI. MPO-DNA complexes were detected in all samples. The median MPO-DNA level was 33 ng/mL (interquartile range [IQR], 18–43 ng/mL) at admission, and 22 ng/mL (IQR, 11–31 ng/mL) on day 4 (unpaired test; p = 0.015). We found a significant reduction in MPO-DNA levels from admission to day 4 in patients with DCI (paired test; p = 0.036) but not in those without DCI (p = 0.17). There was a similar reduction in MPO-DNA levels between admission and day 4 in patients with (p = 0.006) but not in those without clinical vasospasm (p = 0.47). CONCLUSIONS AND RELEVANCE: This is the first study to detect the NET biomarkers MPO-DNA complexes in peripheral serum of patients with aSAH and to associate them with DCI. A pronounced reduction in MPO-DNA levels might serve as an early marker of DCI. This diagnostic potential of MPO-DNA complexes and their role as potential therapeutic targets in aSAH should be explored further