TY - THES A1 - Köhler, Olga T1 - Analysen von Bürstenbiopsien oraler Läsionen im Hinblick auf die Expression von GLUT1 und SHH und deren Bedeutung für die Diagnose maligner Transformationen T1 - Analyses of brush biopsies of oral lesions with regard to the expression of GLUT1 and SHH and their importance for the diagnosis of malignant transformations N2 - Prinzipiell ist es möglich, dass sich Plattenepithelkarzinome aus klinisch gesund erscheinender Mundschleimhaut bilden. Allerdings konnte nachgewiesen werden, dass ein hoher Anteil aus bereits langfristig bestehenden Vorläuferläsionen, wie z.B. Leukoplakien und Läsionen, die dem Lichen planus zugeschrieben werden, hervorgeht. Der Expressionsnachweis verschiedener Tumormarker konnte bereits genutzt werden, um den Prozess der Karzinogenese besser zu verstehen und vielversprechende Methoden der Früherkennung zu entwickeln. Die vorliegende Arbeit beschäftigt sich mit der Analyse von immunzytochemisch gefärbten Bürstenbiopsien oraler Läsionen im Hinblick auf die Expression von GLUT1 und SHH und deren Bedeutung für den Prozess der malignen Transformation. Die untersuchte diagnostische Methode erreichte in der vorliegenden Arbeit eine Sensitivität von 80 % und eine Spezifität von 68 % für die Verwendung eines GLUT1-Antikörpers. Für SHH konnte eine Sensitivität von 60 % und eine Spezifität von 96 % ermittelt werden. N2 - In principle, it is possible that squamous cell carcinomas form from seemingly clinically healthy oral mucosa. However, it has been shown that a large proportion results from long-term precursor lesions, such as leukoplakia and lesions attributed to lichen planus. The detection of various tumor markers has already been used to better understand the process of carcinogenesis and to develop promising methods of early detection. The present work deals with the analysis of immunocytochemically stained brush biopsies of oral lesions with regard to the expression of GLUT1 and SHH and their significance for the process of malignant transformation. In the investigated diagnostic method we achieve a sensitivity of 80% and a specificity of 68% for the use of a GLUT1 antibody. For SHH, a sensitivity of 60 % and a specificity of 96 % could be determined. KW - Bürstenbiopsie KW - Plattenepithelcarcinom KW - Leukoplakie KW - Lichen ruber planus KW - Immuncytochemie KW - GLUT1 KW - SHH KW - Immuncytochemie KW - immunocytochemistry Y1 - 2022 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-270368 ER - TY - JOUR A1 - Koepsell, Hermann T1 - Glucose transporters in brain in health and disease JF - Pflügers Archiv - European Journal of Physiology N2 - Energy demand of neurons in brain that is covered by glucose supply from the blood is ensured by glucose transporters incapillaries and brain cells. In brain, the facilitative diffusion glucose transporters GLUT1-6 and GLUT8, and the Na+-D-glucosecotransporters SGLT1 are expressed. The glucose transporters mediate uptake of D-glucose across the blood-brain barrier anddelivery of D-glucose to astrocytes and neurons. They are critically involved in regulatory adaptations to varying energy demandsin response to differing neuronal activities and glucose supply. In this review, a comprehensive overview about verified andproposed roles of cerebral glucose transporters during health and diseases is presented. Our current knowledge is mainly based onexperiments performed in rodents. First, the functional properties of human glucose transporters expressed in brain and theircerebral locations are described. Thereafter, proposed physiological functions of GLUT1, GLUT2, GLUT3, GLUT4, andSGLT1 for energy supply to neurons, glucose sensing, central regulation of glucohomeostasis, and feeding behavior are compiled, and their roles in learning and memory formation are discussed. In addition, diseases are described in which functionalchanges of cerebral glucose transporters are relevant. These are GLUT1 deficiency syndrome (GLUT1-SD), diabetes mellitus, Alzheimer’s disease (AD), stroke, and traumatic brain injury (TBI). GLUT1-SD is caused by defect mutations in GLUT1. Diabetes and AD are associated with changed expression of glucose transporters in brain, and transporter-related energy defi-ciency of neurons may contribute to pathogenesis of AD. Stroke and TBI are associated with changes of glucose transporter expression that influence clinical outcome KW - glucosetransporter KW - brain KW - GLUT1 KW - GLUT2 KW - GLUT3 KW - GLUT4 KW - SGLT1 KW - diabetes KW - Parkinson’s disease KW - stroke Y1 - 2020 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-232746 SN - 0031-6768 VL - 472 ER -