The aeolian sedimentary system along the transition between the Qilian Shan and northern Chinese drylands during the late Quaternary

THESIS ABSTRACTresearc

LowFormer: Hardware Efficient Design for Convolutional Transformer Backbones

Research in efficient vision backbones is evolving into models that are a mixture of convolutions and transformer blocks. A smart combination of both, architecture-wise and component-wise is mandatory to excel in the speed-accuracy trade-off. Most publications focus on maximizing accuracy and utilize MACs (multiply accumulate operations) as an efficiency metric. The latter however often do not measure accurately how fast a model actually is due to factors like memory access cost and degree of parallelism. We analyzed common modules and architectural design choices for backbones not in terms of MACs, but rather in actual throughput and latency, as the combination of the latter two is a better representation of the efficiency of models in real applications. We applied the conclusions taken from that analysis to create a recipe for increasing hardware-efficiency in macro design. Additionally we introduce a simple slimmed-down version of Multi-Head Self-Attention, that aligns with our analysis. We combine both macro and micro design to create a new family of hardware-efficient backbone networks called Low-Former. Low Former achieves a remarkable speedup in terms of throughput and latency, while achieving similar or better accuracy than current state-of-the-art efficient backbones. In order to prove the generalizability of our hardware-efficient design, we evaluate our method on GPU, mobile GPU and ARM CPU. We further show that the downstream tasks object detection and semantic segmentation profit from our hardware-efficient architecture. Code and models are available at https://github.com/altair199797/LowFormer

Efficient Feature Extraction for High-resolution Video Frame Interpolation

Most deep learning methods for video frame interpolation consist of three main components: feature extraction, motion estimation, and image synthesis. Existing approaches are mainly distinguishable in terms of how these modules are designed. However, when interpolating high-resolution images, e.g. at 4K, the design choices for achieving high accuracy within reasonable memory requirements are limited. The feature extraction layers help to compress the input and extract relevant information for the latter stages, such as motion estimation. However, these layers are often costly in parameters, computation time, and memory. We show how ideas from dimensionality reduction combined with a lightweight optimization can be used to compress the input representation while keeping the extracted information suitable for frame interpolation. Further, we require neither a pretrained flow network nor a synthesis network, additionally reducing the number of trainable parameters and required memory. When evaluating on three 4K benchmarks, we achieve state-of-the-art image quality among the methods without pretrained flow while having the lowest network complexity and memory requirements overall.Comment: Accepted to BMVC 2022. Code: https://github.com/visinf/fldr-vf

Rematerializing Vision - Contemporary Dis/Embodied Art on the 'War on Terror'.

This inquiry into corporeal experiences of the 'war on terror' is pursued through the lens of contemporary art that, it is argued here, can be seen to innovatively trace war through its corporeal effects. In order to investigate the ways in which contemporary artists are commenting on the pivotal place of the body in war, the thesis examines contemporary artists' responses to the 'war on terror' with a view to the ways in which artists endeavour to render the corporeal experiences of the 'war on terror' intelligible and conceivable for audiences untouched by the violence of war. Specifically, the research project explores artistic strategies that have been utilized by artists from around the globe since 9/11 that can be seen to problematize distanced perception of war. The thesis posits that as their commentary is timely, artists can be seen to critically involve themselves in the representation of the 'war on terror' and to participate in the writing of its narrative. It argues that by drawing on diverse media, a range of venues in and through which to present their work, and unique artistic strategies that raise the body to the centre of attention, artists such as those considered in this thesis can be seen to speak to the body in pain in innovative and thought-provoking works that trouble our ways of seeing and rematerialize vision of the 'war on terror'

Exploring Motives and Strategies in the Production of Knowledge in the University Context by the Example of Academic Career Trajectories

Current research has shown that the combination of implicit and explicit knowledge among various actors is particularly crucial to the production of knowledge and that the characteristics of social relationships and resulting networks impact on how proficienty is acquired transferred absorbed and applied Although investigations have suggested that the actors involved in knowledge production are active and strategic agents who differ considerably in their abilities to incorporate and generate knowledge they are mostly referred to in terms as nodes or black boxes In this regard relationship research has demonstrated that actors differ in terms of motivations and abilities to share information and knowledge Such motives are often strategi

VE-PTP controls blood vessel development by balancing Tie-2 activity

Vascular endothelial protein tyrosine phosphatase (VE-PTP) is an endothelial-specific receptor-type tyrosine phosphatase that associates with Tie-2 and VE-cadherin. VE-PTP gene disruption leads to embryonic lethality, vascular remodeling defects, and enlargement of vascular structures in extraembryonic tissues. We show here that antibodies against the extracellular part of VE-PTP mimic the effects of VE-PTP gene disruption exemplified by vessel enlargement in allantois explants. These effects require the presence of the angiopoietin receptor Tie-2. Analyzing the mechanism we found that anti–VE-PTP antibodies trigger endocytosis and selectively affect Tie-2–associated, but not VE-cadherin–associated VE-PTP. Dissociation of VE-PTP triggers the activation of Tie-2, leading to enhanced endothelial cell proliferation and enlargement of vascular structures through activation of Erk1/2. Importantly, the antibody effect on vessel enlargement is also observed in newborn mice. We conclude that VE-PTP is required to balance Tie-2 activity and endothelial cell proliferation, thereby controlling blood vessel development and vessel size

The archaeal RNA polymerase subunit P and the eukaryotic polymerase subunit Rpb12 are interchangeable in vivo and in vitro

The general subunit of all three eukaryotic RNA polymerases, Rpb12, and subunit P of the archaeal enzyme show sequence similarities in their N-terminal zinc ribbon and some highly conserved residues in the C-terminus. We report here that archaeal subunit P under the control of a strong yeast promoter could complement the lethal phenotype of a RPB12 deletion mutant and that subunit Rpb12 from yeast can functionally replace subunit P during reconstitution of the archaeal RNA polymerase. The ΔP enzyme is unable to form stable open complexes, but can efficiently extend a dinucleotide on a premelted template or RNA on an elongation scaffold. This suggests that subunit P is directly or indirectly involved in promoter opening. The activity of the ΔP enzyme can be rescued by the addition of Rpb12 or subunit P to transcription reactions. Mutation of cysteine residues in the zinc ribbon impair the activity of the enzyme in several assays and this mutated form of P is rapidly replaced by wild-type P in transcription reactions. The conserved zinc ribbon in the N-terminus seems to be important for proper interaction of the complete subunit with other RNA polymerase subunits and a 17-amino-acid C-terminal peptide is sufficient to support all basic RNA polymerase functions in vitro

VE-PTP maintains the endothelial barrier via plakoglobin and becomes dissociated from VE-cadherin by leukocytes and by VEGF

We have shown recently that vascular endothelial protein tyrosine phosphatase (VE-PTP), an endothelial-specific membrane protein, associates with vascular endothelial (VE)–cadherin and enhances VE-cadherin function in transfected cells (Nawroth, R., G. Poell, A. Ranft, U. Samulowitz, G. Fachinger, M. Golding, D.T. Shima, U. Deutsch, and D. Vestweber. 2002. EMBO J. 21:4885–4895). We show that VE-PTP is indeed required for endothelial cell contact integrity, because down-regulation of its expression enhanced endothelial cell permeability, augmented leukocyte transmigration, and inhibited VE-cadherin–mediated adhesion. Binding of neutrophils as well as lymphocytes to endothelial cells triggered rapid (5 min) dissociation of VE-PTP from VE-cadherin. This dissociation was only seen with tumor necrosis factor α–activated, but not resting, endothelial cells. Besides leukocytes, vascular endothelial growth factor also rapidly dissociated VE-PTP from VE-cadherin, indicative of a more general role of VE-PTP in the regulation of endothelial cell contacts. Dissociation of VE-PTP and VE-cadherin in endothelial cells was accompanied by tyrosine phoshorylation of VE-cadherin, β-catenin, and plakoglobin. Surprisingly, only plakoglobin but not β-catenin was necessary for VE-PTP to support VE-cadherin adhesion in endothelial cells. In addition, inhibiting the expression of VE-PTP preferentially increased tyrosine phosphorylation of plakoglobin but not β-catenin. In conclusion, leukocytes interacting with endothelial cells rapidly dissociate VE-PTP from VE-cadherin, weakening endothelial cell contacts via a mechanism that requires plakoglobin but not β-catenin

Local microvascular leakage promotes trafficking of activated neutrophils to remote organs.

Increased microvascular permeability to plasma proteins and neutrophil emigration are hallmarks of innate immunity and key features of numerous inflammatory disorders. Although neutrophils can promote microvascular leakage, the impact of vascular permeability on neutrophil trafficking is unknown. Here, through the application of confocal intravital microscopy, we report that vascular permeability-enhancing stimuli caused a significant frequency of neutrophil reverse transendothelial cell migration (rTEM). Furthermore, mice with a selective defect in microvascular permeability enhancement (VEC-Y685F-ki) showed reduced incidence of neutrophil rTEM. Mechanistically, elevated vascular leakage promoted movement of interstitial chemokines into the bloodstream, a response that supported abluminal-to-luminal neutrophil TEM. Through development of an in vivo cell labeling method we provide direct evidence for the systemic dissemination of rTEM neutrophils, and showed them to exhibit an activated phenotype and be capable of trafficking to the lungs where their presence was aligned with regions of vascular injury. Collectively, we demonstrate that increased microvascular leakage reverses the localization of directional cues across venular walls, thus causing neutrophils engaged in diapedesis to reenter the systemic circulation. This cascade of events offers a mechanism to explain how local tissue inflammation and vascular permeability can induce downstream pathological effects in remote organs, most notably in the lungs

Dissociation of VE-PTP from VE-cadherin is required for leukocyte extravasation and for VEGF-induced vascular permeability in vivo

Artificially stabilizing contacts between VE-cadherin and VE-PTP reduce vascular permeability and leukocyte extravasation in vivo