On the Feasibility of Real-Time 3D Hand Tracking using Edge GPGPU Acceleration

This paper presents the case study of a non-intrusive porting of a monolithic C++ library for real-time 3D hand tracking, to the domain of edge-based computation. Towards a proof of concept, the case study considers a pair of workstations, a computationally powerful and a computationally weak one. By wrapping the C++ library in Java container and by capitalizing on a Java-based offloading infrastructure that supports both CPU and GPGPU computations, we are able to establish automatically the required server-client workflow that best addresses the resource allocation problem in the effort to execute from the weak workstation. As a result, the weak workstation can perform well at the task, despite lacking the sufficient hardware to do the required computations locally. This is achieved by offloading computations which rely on GPGPU, to the powerful workstation, across the network that connects them. We show the edge-based computation challenges associated with the information flow of the ported algorithm, demonstrate how we cope with them, and identify what needs to be improved for achieving even better performance.Comment: 6 pages, 5 figure

Disengaged Scheduling for Fair, Protected Access to Fast Computational Accelerators

Today’s operating systems treat GPUs and other computational accelerators as if they were simple devices, with bounded and predictable response times. With accelerators assuming an increasing share of the workload on modern machines, this strategy is already problematic, and likely to become untenable soon. If the operating system is to enforce fair sharing of the machine, it must assume responsibility for accelerator scheduling and resource management. Fair, safe scheduling is a particular challenge on fast accelerators, which allow applications to avoid kernel-crossing overhead by interacting directly with the device. We propose a disengaged scheduling strategy in which the kernel intercedes between applications and the accelerator on an infrequent basis, to monitor their use of accelerator cycles and to determine which applications should be granted access over the next time interval. Our strategy assumes a well defined, narrow interface exported by the accelerator. We build upon such an interface, systematically inferred for the latest Nvidia GPUs. We construct several example schedulers, including Disengaged Timeslice with overuse control that guarantees fairness and Disengaged Fair Queueing that is effective in limiting resource idleness, but probabilistic. Both schedulers ensure fair sharing of the GPU, even among uncooperative or adversarial applications; Disengaged Fair Queueing incurs a 4 % overhead on average (max 18%) compared to direct devic

Regulation of HAX-1 anti-apoptotic protein by Omi/HtrA2 protease during cell death

Omi/HtrA2 is a nuclear-encoded mitochondrial serine protease that has a pro-apoptotic function in mammalian cells. Upon induction of apoptosis, Omi translocates to the cytoplasm and participates in caspase-dependent apoptosis by binding and degrading inhibitor of apoptosis proteins. Omi can also initiate caspase-independent apoptosis in a process that relies entirely on its ability to function as an active protease. To investigate the mechanism of Omi-induced apoptosis, we set out to isolate novel substrates that are cleaved by this protease. We identified HS1-associated protein X-1 (HAX-1), a mitochondrial anti-apoptotic protein, as a specific Omi interactor that is cleaved by Omi both in vitro and in vivo. HAX-1 degradation follows Omi activation in cells treated with various apoptotic stimuli. Using a specific inhibitor of Omi, HAX-1 degradation is prevented and cell death is reduced. Cleavage of HAX-1 was not observed in a cell line derived from motor neuron degeneration 2 mice that carry a mutated form of Omi that affects its proteolytic activity. Degradation of HAX-1 is an early event in the apoptotic process and occurs while Omi is still confined in the mitochondria. Our results suggest that Omi has a unique pro-apoptotic function in mitochondria that involves removal of the HAX-1 antiapoptotic protein. This function is distinct from its ability to activate caspase-dependent apoptosis in the cytoplasm by degrading inhibitor of apoptosis proteins

Effects of acute variation of dialysate calcium concentrations on arterial stiffness and aortic pressure waveform

Background. Abnormal mineral metabolism in chronic kidney disease plays a critical role in vascular calcification and arterial stiffness. The impact of presently used dialysis calcium concentration (DCa) on arterial stiffness and aortic pressure waveform has never been studied. The aim of the present study is to evaluate, in haemodialysis (HD) patients, the impact of acute modification of DCa on arterial stiffness and central pulse wave profile (cPWP)

Increased expression of transcription factor TFAP2α correlates with chemosensitivity in advanced bladder cancer

<p>Abstract</p> <p>Background</p> <p>The standard treatment for patients with advanced transitional cell carcinoma of the bladder is platin based chemotherapy. Only approximately 50% of the patients respond to chemotherapy. Therefore, molecular predictive markers for identification of chemotherapy sensitive subgroups of patients are highly needed. We selected the transcription factor <it>TFAP2α </it>from a previously identified gene expression signature for chemotherapy response.</p> <p>Methods</p> <p><it>TFAP2α </it>expression and localization was assessed by immunohistochemistry using a tissue microarray (TMA) containing 282 bladder cancer tumors from patients with locally advanced (pT2-T4_band N_1-3) or metastatic (M₁) disease. All patients had received cisplatin containing chemotherapy. Furthermore, QPCR analysis of three <it>TFAP2α </it>isoforms was performed on tumor specimens of advanced muscle invasive bladder cancers (T2-4). Using the bladder cell lines T24 and SW780 the relation of <it>TFAP2α </it>and cisplatin and gemcitabine sensitivity as well as cell proliferation was examined using siRNA directed <it>TFAP2α </it>knockdown.</p> <p>Results</p> <p>TFAP2α protein expression was analyzed on a TMA with cores from 282 advanced bladder cancer tumors from patients treated with cisplatin based combinational chemotherapy. <it>TFAP2α </it>was identified as a strong independent predictive marker for a good response and survival after cisplatin-containing chemotherapy in patients with advanced bladder cancer. Strong TFAP2α nuclear and cytoplasmic staining predicted good response to chemotherapy in patients with lymph node metastasis, whereas weak TFAP2α nuclear staining predicted good response in patients without lymph node metastasis. In vitro studies showed that siRNA mediated knockdown of TFAP2α increased the proliferation of SW780 cells and rendered the cells less sensitive to cisplatin and gemcitabine. In contrast to that T24 bladder cells with mutated p53 showed to be more drug sensitive upon TFAP2α depletion.</p> <p>Conclusions</p> <p>High levels of nuclear and cytoplasmic TFAP2α protein were a predictor of increased overall survival and progression free survival in patients with advanced bladder cancer treated with cisplatin based chemotherapy. TFAP2α knockdown increased the proliferation of the SW780 bladder cells and reduced cisplatin and gemcitabine induced cell death. The inverse effect was observed in the <it>TP53 </it>mutated T24 cell line where TFAP2α silencing augmented cisplatin and gemcitabine sensitivity and did not stimulate proliferation.</p