Kompression medizinischer Computertomographie-Bilder mit Hilfe von Optimierungsverfahren

The analysis of clinical use cases suggests that one of the most important aspects in storing and transmitting medical image data still consists in compression with its focus on time-efficiently reducing storage demand while maintaining image quality. Current appliances typically perform compression using common signal processing codecs like described in JPEG or MPEG/ITU-T standards. As such codecs have been designed mostly for compression of camera-captured natural scenes, efficiency can be improved by exploitation of deviating image treatment and image characteristics in medicine. Using a bottom-up approach, this thesis introduces novel techniques both for pixel-wise prediction, mostly used in lossless and high-quality scenarios, as well as for frame-wise prediction, most useful in medium-quality scenarios. Because of diverse image characteristics across modalities, focus is restricted to computed tomography and for frame prediction in particular to dynamic 3-D+t cardiac acquisitions. Apart from traditional approaches, foremostly numerical optimization like linear and nonlinear least-squares but also discrete algorithms are utilized in order to find context region, mean, and variance of predictions, determine local image structures, weight rate versus distortion, identify motion between frames, remove noise from predictors, etc. Backward-adaptive autoregression approaches are thoroughly compared and extended to 3-D images, adaptive context selection and boundary treatment, closed probability distribution estimation, and lots of other procedures in order to make them usable within real codecs like a massively parallel implementation on GPUs or the presented Open Source framework Vanilc. Vanilc's compression ratio is shown to beat all algorithms from literature with implementations available for comparison the author is aware of. Next to alternative developments intended for use with small contexts like Burg or EMP predictors, also a lossy application has been designed, outperforming on the one hand established codecs like HM or VTM at high qualities, while featuring on the other hand a noise removing behavior that in reality even enhances image quality as proven by phantom reconstruction simulations. For medium-quality image compression three deformation compensation methods are proposed to replace block-based compensation in dynamic data evincing heart movements. One of them models physiological 3-D muscle contractions and is again realized in Nvidia CUDA. Together with Vanilc compression of motion information and frequency-filtered combination with axially preceding slices, it surpasses the rate-distortion performance of modern inter predictors like the one realized in HM. A harmonized deformation inversion algorithm for applications like motion-compensated temporal filtering or intermediate image interpolation completes the thesis.Die Analyse klinischer Prozesse legt nahe, dass einer der wesentlichsten Aspekte beim Speichern und Übertragen von medizinischen Bilddaten noch immer in der Kompression besteht, deren Idee eine zeiteffiziente Datenreduktion bei gleichbleibender Bildqualität ist. Aktuelle Geräte komprimieren für gewöhnlich mittels gängiger Signalverarbeitungscodecs, wie sie in JPEG oder MPEG/ITU-T Standards beschrieben sind. Da derartige Codecs vorrangig zur Kompression von Kameraaufnahmen natürlicher Szenen konzipiert wurden, kann deren Effizienz unter Berücksichtigung des unterschiedlichen Umgangs mit und der unterschiedlichen Eigenschaften von Medizinbildern verbessert werden. Die vorliegende Arbeit führt neue Verfahren grundlegend sowohl für pixelweise Prädiktion mit vorrangig verlustfreien und hochqualitativen Anwendungen, als auch für bildweise Prädiktion, nützlich in mittelqualitativen Szenarien, ein. Wegen voneinander abweichenden Eigenschaften verschiedener Bildgebungsverfahren liegt das Augenmerk auf Computertomographie; bezüglich bildweiser Prädiktion insbesondere auf kardiologischen 3-D+t Bewegtbildern. Abseits herkömmlicher Ansätze kommen vor allem numerische Optimierung wie lineare und nichtlineare Methode der kleinsten Quadrate aber auch diskrete Algorithmen zum Einsatz, um Kontextbereich, Mittelwert und Varianz der Prädiktionen sowie lokale Bildstrukturen zu bestimmen, Rate gegen Verzerrung abzuwägen, Bewegung zwischen Bildern zu ermitteln, Rauschen aus Prädiktoren zu entfernen, etc. Rückwärtsadaptive Autoregressionsansätze werden eingehend verglichen and erweitert auf 3-D Bilder, adaptive Kontextwahl und Randbehandlung, geschlossene Wahrscheinlichkeitsverteilungsschätzung und vielerlei andere Verfahren, um sie für echte Codecs wie z. B. eine massiv parallele Implementierung auf GPUs oder das vorgestellte Open Source Framework Vanilc nutzbar zu machen. Es zeigt sich, dass Vanilcs Kompressionsrate alle dem Autor bekannten Algorithmen aus der Literatur, zu denen vergleichsfähige Implementierungen existieren, schlägt. Neben alternativer Entwicklungen wie Burg oder EMP Prädiktor, bestimmt für den Einsatz mit kleinen Kontexten, wurde auch eine verlustbehaftete Anwendung konzipiert, deren Leistung zum Einen die etablierter Codecs wie HM oder VTM für hohe Qualitäten übertrifft und die zum Anderen durch Rauschentfernung die Bildqualität tatsächlich sogar verbessert, wie eine Phantomrekonstruktionssimulation belegt. Für Bildkompression mittlerer Qualität werden drei Methoden zur Vorformungskompensation vorgestellt, um blockbasierte Kompensation bei Herz-Bewegtdaten zu ersetzen. Eine davon stellt physiologische 3-D Muskelkontraktionen nach und ist erneut in Nvidia CUDA umgesetzt. In Verbindung mit Vanilc-komprimierter Bewegungsinformation und frequenzgefilterter Kombination mit axial vorangehenden Schichtbildern übertrifft sie das Raten-Verzerrungs-Ergebnis moderner Inter-Prädiktoren wie dessen aus HM. Ein darauf abgestimmter Algorithmus zur Verformungsumkehr für Anwendungen wie bewegungskompensierte zeitliche Filterung oder Zwischenbildinterpolation rundet die Dissertation ab

Improving HEVC Encoding of Rendered Video Data Using True Motion Information

This paper shows that motion vectors representing the true motion of an object in a scene can be exploited to improve the encoding process of computer generated video sequences. Therefore, a set of sequences is presented for which the true motion vectors of the corresponding objects were generated on a per-pixel basis during the rendering process. In addition to conventional motion estimation methods, it is proposed to exploit the computer generated motion vectors to enhance the ratedistortion performance. To this end, a motion vector mapping method including disocclusion handling is presented. It is shown that mean rate savings of 3.78% can be achieved.Comment: 4 pages, 4 figure

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field

Dichotomy between RIP1- and RIP3-mediated necroptosis in tumor necrosis factor-α-induced shock

Tumor necrosis factor receptor (TNFR) signaling may result in survival, apoptosis or programmed necrosis. The latter is called necroptosis if the receptor-interacting protein 1 (RIP1) inhibitor necrostatin-1 (Nec-1) or genetic knockout of RIP3 prevents it. In the lethal mouse model of TNFα-mediated shock, addition of the pan-caspase inhibitor zVAD-fmk (zVAD) accelerates time to death. Here, we demonstrate that RIP3-deficient mice are protected markedly from TNFα-mediated shock in the presence and absence of caspase inhibition. We further show that the fusion protein TAT-crmA, previously demonstrated to inhibit apoptosis, also prevents necroptosis in L929, HT29 and FADD-deficient Jurkat cells. In contrast to RIP3-deficient mice, blocking necroptosis by Nec-1 or TAT-crmA did not protect from TNFα/zVAD-mediated shock, but further accelerated time to death. Even in the absence of caspase inhibition, Nec-1 application led to similar kinetics. Depletion of macrophages, natural killer (NK) cells, granulocytes or genetic deficiency for T lymphocytes did not influence this model. Because RIP3-deficient mice are known to be protected from cerulein-induced pancreatitis (CIP), we applied Nec-1 and TAT-crmA in this model and demonstrated the deterioration of pancreatic damage upon addition of these substances. These data highlight the importance of separating genetic RIP3 deficiency from RIP1 inhibition by Nec-1 application in vivo and challenge the current definition of necroptosis

Trans-splicing of the mod(mdg4) Complex Locus Is Conserved Between the Distantly Related Species Drosophila melanogaster and D. virilis

The modifier of mdg4, mod(mdg4), locus in Drosophila melanogaster represents a new type of complex gene in which functional diversity is resolved by mRNA trans-splicing. A protein family of >30 transcriptional regulators, which are supposed to be involved in higher-order chromatin structure, is encoded by both DNA strands of this locus. Mutations in mod(mdg4) have been identified independently in a number of genetic screens involving position-effect variegation, modulation of chromatin insulators, apoptosis, pathfinding of nerve cells, and chromosome pairing, indicating pleiotropic effects. The unusual gene structure and mRNA trans-splicing are evolutionary conserved in the distantly related species Drosophila virilis. Chimeric mod(mdg4) transcripts encoded from nonhomologous chromosomes containing the splice donor from D. virilis and the acceptor from D. melanogaster are produced in transgenic flies. We demonstrate that a significant amount of protein can be produced from these chimeric mRNAs. The evolutionary and functional conservation of mod(mdg4) and mRNA trans-splicing in both Drosophila species is furthermore demonstrated by the ability of D. virilis mod(mdg4) transgenes to rescue recessive lethality of mod(mdg4) mutant alleles in D. melanogaster

Tryptophan degradation in multiple trauma patients: survivors compared with non-survivors

International audienceImmune dysfunction in trauma patients is associated with immune system activation and inflammation. Cytokine-inducible enzyme indoleamine 2,3-dioxygenase (IDO) initiates the degradation of the essential aromatic amino acid tryptophan via the kynurenine pathway and could contribute to deficient immune responsiveness. Activated IDO is indicated by an increased kynurenine to tryptophan ratio (kyn/trp). This study investigated whether tryptophan degradation is associated with outcome of patients post trauma. Tryptophan and kynurenine concentrations were measured by HPLC in serum specimens of 15 patients post-trauma during 12-14 days of follow up. Of every patient up to 5 specimens within this observation period were included in this analysis, in total 69 specimens were available. For further comparisons, concentrations of immune activation marker neopterin were measured. Compared to healthy controls, average kyn/trp and kynurenine were increased in patients, and tryptophan concentrations were decreased. During follow-up, increasing kyn/trp and kynurenine concentrations (all p <0.001) were observed, the changes of tryptophan concentrations were not significant. Non-survivors presented with higher kyn/trp and with higher kynurenine concentrations than survivors. Kyn/trp correlated with neopterin (rs = 0.590, p <0.001) concentrations. Data imply that increased tryptophan degradation in patients is due to activated IDO, which most likely represents a result of host defence response. Data support a possible role of IDO in the development of immunodeficiency and death in patients

Dichotomy between RIP1- and RIP3-Mediated Necroptosis in Tumor Necrosis Factor-α-Induced Shock

Tumor necrosis factor receptor (TNFR) signaling may result in survival, apoptosis or programmed necrosis. The latter is called necroptosis if the receptor-interacting protein 1 (RIP1) inhibitor necrostatin-1 (Nec-1) or genetic knockout of RIP3 prevents it. In the lethal mouse model of TNFα-mediated shock, addition of the pan-caspase inhibitor zVAD-fmk (zVAD) accelerates time to death. Here, we demonstrate that RIP3-deficient mice are protected markedly from TNFα-mediated shock in the presence and absence of caspase inhibition. We further show that the fusion protein TAT-crmA, previously demonstrated to inhibit apoptosis, also prevents necroptosis in L929, HT29 and FADD-deficient Jurkat cells. In contrast to RIP3-deficient mice, blocking necroptosis by Nec-1 or TAT-crmA did not protect from TNFα/zVAD-mediated shock, but further accelerated time to death. Even in the absence of caspase inhibition, Nec-1 application led to similar kinetics. Depletion of macrophages, natural killer (NK) cells, granulocytes or genetic deficiency for T lymphocytes did not influence this model. Because RIP3-deficient mice are known to be protected from cerulein-induced pancreatitis (CIP), we applied Nec-1 and TAT-crmA in this model and demonstrated the deterioration of pancreatic damage upon addition of these substances. These data highlight the importance of separating genetic RIP3 deficiency from RIP1 inhibition by Nec-1 application in vivo and challenge the current definition of necroptosis