105 research outputs found
Interactive volume visualization of general polyhedral grids
No full textThis paper presents a novel framework for visualizing volumetric data specified on complex polyhedral grids, without the need to perform any kind of a priori tetrahedralization. These grids are composed of polyhedra that often are non-convex and have an arbitrary number of faces, where the faces can be non-planar with an arbitrary number of vertices. The importance of such grids in state-of-the-art simulation packages is increasing rapidly. We propose a very compact, face-based data structure for representing such meshes for visualization, called two-sided face sequence lists (TSFSL), as well as an algorithm for direct GPU-based ray-casting using this representation. The TSFSL data structure is able to represent the entire mesh topology in a 1D TSFSL data array of face records, which facilitates the use of efficient 1D texture accesses for visualization. In order to scale to large data sizes, we employ a mesh decomposition into bricks that can be handled independently, where each brick is then composed of its own TSFSL array. This bricking enables memory savings and performance improvements for large meshes. We illustrate the feasibility of our approach with real-world application results, by visualizing highly complex polyhedral data from commercial state-of-the-art simulation packages. © 2011 IEEE
Flow cytometry.
No full text<p>Specificity and uptake of muJ591:MIRB, muIgG:MIRB, muJ591 and muIgG of prostate cancer cells. A. LNCaP cells presented a shift that showed uptake of the muJ591 and of the conjugate muJ591:MIRB and no uptake for the controls muIgG antibody or muIgG:MIRB antibody conjugate. B. Control DU145 cells did not show uptake.</p
Microscopical detection of TBRF <i>Borrelia</i> in blood films.
No full textMicroscopic images of Giemsa-stained thin blood films (original magnifications ×1’000) showing TBRF Borrelia in a patient suffering from TBRF fever due to Borrelia persica (courtesy of Dr. Veronika Muigg).</p
MUIGG P.: Interactive Visual Analysis of Perfusion Data
No full textAbstract—Perfusion data are dynamic medical image data which characterize the regional blood flow in human tissue. These data have a great potential in medical diagnosis, since diseases can be better discriminated and detected at an earlier stage compared to static image data. The wide-spread use of perfusion data is hampered by the lack of efficient evaluation methods. For each voxel, a time-intensity curve characterizes the enhancement of a contrast agent. Parameters derived from these curves characterize the perfusion and have to be integrated for diagnosis. The diagnostic evaluation of this multi-field data is challenging and time-consuming due to its complexity. For the visual analysis of such datasets, feature-based approaches allow to reduce the amount of data and direct the user to suspicious areas. We present an interactive visual analysis approach for the evaluation of perfusion data. For this purpose, we integrate statistical methods and interactive feature specification. Correlation analysis and Principal Component Analysis (PCA) are applied for dimension reduction and to achieve a better understanding of the inter-parameter relations. Multiple, linked views facilitate the definition of features by brushing multiple dimensions using non-binary and composite brushes. The specification result is linked to all views establishing a focus+context style of visualization in 3D. We discuss our approach with respect to clinical datasets from the three major application areas: breast tumor diagnosis, ischemic stroke diagnosis as well as the diagnosis of the coronary heart disease (CHD). It turns out that the significance of perfusion parameters strongly depends on the individual patient, scanning parameters and data pre-processing. Index Terms—Information Visualization, time-varying data.
Deficiency in mitochondrial metabolism : characterization of SERAC1 and Tafazzin
No full textDie 3-Methylglutaconazidurie (3-MGAuria) ist ein klinischer Phänotyp der auf gewisse mitochondrielle Erbkrankheiten hindeutet und sich durch erhöhte Konzentrationen von 3-Methylglutaconsäure (3-MGA) in Urin und Plasma auszeichnet. In der primären 3-MGAuria wird die Akkumulation dieser organischen Säure durch loss-of-function Mutationen der 3-Methylglutaconyl-CoA-Hydratase verursacht, die als Schlüsselenzym im Leucinabbau bekannt ist. Im Gegensatz dazu sind die Mechanismen der 3-MGA Bildung in anderen Subtypen der 3-MGAurias bisher kaum bis gar nicht bekannt. Zu diesen sekundären 3-MGAurien zählen unter anderem auch das Barth-Syndrom und das MEGDEL-Syndrom, die durch Dysfunktion der entsprechenden Gene TAZ und SERAC1 hervorgerufen werden. Obwohl die Aufklärung der genauen Pathobiochemie dieser beiden Gene noch große Lücken aufweist, gibt es interessante Beobachtungen, dass sie mit funktionellen Veränderungen in der mitochondriellen Lipidzusammensetzung in Verbindung stehen .
Das Ziel meiner Masterarbeit ist es, die Rolle der SERAC1-Mutation und der TAZ-Mutation zu untersuchen, die jeweils im Phosphatidylglycerol- und Cardiolipin Modifizierungsprozess beteiligt sind und durch einen Proteindefekt vermutlich ein mitochondrial metabolisches Ungleichgewicht auslösen. Um diese Hypothese zu untersuchen, etablierte ich einen Citrat-Synthase-Assay, mit dem Defekte im mitochondrialen Stoffwechsel studiert werden können. Diese Methode wurde in Fibroblasten die von MEGDEL- und Barth-Syndrom-Patienten entnommen wurden angewandt. Tatsächlich stellte sich heraus, dass SERAC1-defiziente Zellen eine signifikant reduzierte Citrate Synthase Aktivität aufweisen (p<0,01), wohingegen sich für TAZ defekte Fibroblasten kein signifikanter Unterschied (p<0,34) ergab. Da Fibroblasten jedoch nur einen geringen Mitochondrienanteil aufweisen und somit kein ideales Krankheitsmodell darstellte um mitochonrielle Erkrankungen zu studieren, habe ich darüber hinaus die g3-methylglutaconic aciduria (3-MGAuria) is a clinical phenotype connected to a group of mitochondrial inherited diseases and characterized by increased excretion of 3-methylglutaconic acid in the patient’s urine. The accumulation of this organic acid can be caused by deficiency in 3-methylglutaconyl-CoA hydratase (AUH), which catalyzes a reaction step in leucine catabolism and is directly linked to3-MGA accumulation. AUH deficiency is therefore defined as primary 3-MGAuria. In contrast secondary 3-MGAurias are a group of other genetic disorders that result in 3-MGA accumulation such as the Barth syndrome and MEGDEL syndrome. For these diseases exists so far no valid metabolic mechanism explaining for the occurrence of this phenotype is known. However, most of the affected proteins play an important role in maintaining mitochondrial lipid composition, such as Tafazzine utilized for cardiolipin remodeling and SERAC1, which has been reported to remodel phosphatidylglycerols.
The aim of my master thesis is to characterize SERAC1 and TAZ mutation in different cell lines and study their implication in mitochondrial metabolic deficiency. In order to achieve this, I established a citrate synthase assay, which is a prominent mitochondrial related marker enzyme, and used it to investigate mitochondrial defects in fibroblasts derived from MEGDEL syndrome patients and Barth syndrome patients. The enzyme kinetic results showed significantly reduced citrate activity in SERAC1 human fibroblasts derived from MEGDEL syndrome patients, when compared with control fibroblasts, whereas citrate synthase activity in human fibroblasts derived from Barth syndrome patients was not different to controls. Furthermore, I conducted CRISPR/Cas 9 knock-out experiments in TAZ and SERAC1 in HEK 293T cells, with the aim to establish a suitable in vitro model for studying mitochondrial deficiency in this disease. However, in a first attempt it was not possible to yield homozygous knocsubmitted by Katharina MuiggZusammenfassung in deutscher SpracheMasterarbeit University Innsbruck 201
Deficiency in mitochondrial metabolism : characterization of SERAC1 and Tafazzin
No full textDie 3-Methylglutaconazidurie (3-MGAuria) ist ein klinischer Phänotyp der auf gewisse mitochondrielle Erbkrankheiten hindeutet und sich durch erhöhte Konzentrationen von 3-Methylglutaconsäure (3-MGA) in Urin und Plasma auszeichnet. In der primären 3-MGAuria wird die Akkumulation dieser organischen Säure durch loss-of-function Mutationen der 3-Methylglutaconyl-CoA-Hydratase verursacht, die als Schlüsselenzym im Leucinabbau bekannt ist. Im Gegensatz dazu sind die Mechanismen der 3-MGA Bildung in anderen Subtypen der 3-MGAurias bisher kaum bis gar nicht bekannt. Zu diesen sekundären 3-MGAurien zählen unter anderem auch das Barth-Syndrom und das MEGDEL-Syndrom, die durch Dysfunktion der entsprechenden Gene TAZ und SERAC1 hervorgerufen werden. Obwohl die Aufklärung der genauen Pathobiochemie dieser beiden Gene noch große Lücken aufweist, gibt es interessante Beobachtungen, dass sie mit funktionellen Veränderungen in der mitochondriellen Lipidzusammensetzung in Verbindung stehen .
Das Ziel meiner Masterarbeit ist es, die Rolle der SERAC1-Mutation und der TAZ-Mutation zu untersuchen, die jeweils im Phosphatidylglycerol- und Cardiolipin Modifizierungsprozess beteiligt sind und durch einen Proteindefekt vermutlich ein mitochondrial metabolisches Ungleichgewicht auslösen. Um diese Hypothese zu untersuchen, etablierte ich einen Citrat-Synthase-Assay, mit dem Defekte im mitochondrialen Stoffwechsel studiert werden können. Diese Methode wurde in Fibroblasten die von MEGDEL- und Barth-Syndrom-Patienten entnommen wurden angewandt. Tatsächlich stellte sich heraus, dass SERAC1-defiziente Zellen eine signifikant reduzierte Citrate Synthase Aktivität aufweisen (p<0,01), wohingegen sich für TAZ defekte Fibroblasten kein signifikanter Unterschied (p<0,34) ergab. Da Fibroblasten jedoch nur einen geringen Mitochondrienanteil aufweisen und somit kein ideales Krankheitsmodell darstellte um mitochonrielle Erkrankungen zu studieren, habe ich darüber hinaus die g3-methylglutaconic aciduria (3-MGAuria) is a clinical phenotype connected to a group of mitochondrial inherited diseases and characterized by increased excretion of 3-methylglutaconic acid in the patient’s urine. The accumulation of this organic acid can be caused by deficiency in 3-methylglutaconyl-CoA hydratase (AUH), which catalyzes a reaction step in leucine catabolism and is directly linked to3-MGA accumulation. AUH deficiency is therefore defined as primary 3-MGAuria. In contrast secondary 3-MGAurias are a group of other genetic disorders that result in 3-MGA accumulation such as the Barth syndrome and MEGDEL syndrome. For these diseases exists so far no valid metabolic mechanism explaining for the occurrence of this phenotype is known. However, most of the affected proteins play an important role in maintaining mitochondrial lipid composition, such as Tafazzine utilized for cardiolipin remodeling and SERAC1, which has been reported to remodel phosphatidylglycerols.
The aim of my master thesis is to characterize SERAC1 and TAZ mutation in different cell lines and study their implication in mitochondrial metabolic deficiency. In order to achieve this, I established a citrate synthase assay, which is a prominent mitochondrial related marker enzyme, and used it to investigate mitochondrial defects in fibroblasts derived from MEGDEL syndrome patients and Barth syndrome patients. The enzyme kinetic results showed significantly reduced citrate activity in SERAC1 human fibroblasts derived from MEGDEL syndrome patients, when compared with control fibroblasts, whereas citrate synthase activity in human fibroblasts derived from Barth syndrome patients was not different to controls. Furthermore, I conducted CRISPR/Cas 9 knock-out experiments in TAZ and SERAC1 in HEK 293T cells, with the aim to establish a suitable in vitro model for studying mitochondrial deficiency in this disease. However, in a first attempt it was not possible to yield homozygous knocsubmitted by Katharina MuiggZusammenfassung in deutscher SpracheMasterarbeit University Innsbruck 201
Konstruktion einer Kurzversion des Nijmegen Cochlear Implant Questionnaire (NCIQ) in deutscher Sprache
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Chronic paroxetine treatment modulates the neuronal activation pattern in HAB rats in response to the forced swim test
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