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Xie, Li

Publications and source records attributed to Xie, Li.

Q-VR: System-Level Design for Future Mobile Collaborative Virtual Reality

High Quality Mobile Virtual Reality (VR) is what the incoming graphics technology era demands: users around the world, regardless of their hardware and network conditions, can all enjoy the immersive virtual experience. However, the state-of-the-art software-based mobile VR designs cannot fully satisfy the realtime performance requirements due to the highly interactive nature of user's actions and complex environmental constraints during VR execution. Inspired by the unique human visual system effects and the strong correlation between VR motion features and realtime hardware-level information, we propose Q-VR, a novel dynamic collaborative rendering solution via software-hardware co-design for enabling future low-latency high-quality mobile VR. At software-level, Q-VR provides flexible high-level tuning interface to reduce network latency while maintaining user perception. At hardware-level, Q-VR accommodates a wide spectrum of hardware and network conditions across users by effectively leveraging the computing capability of the increasingly powerful VR hardware. Extensive evaluation on real-world games demonstrates that Q-VR can achieve an average end-to-end performance speedup of 3.4x (up to 6.7x) over the traditional local rendering design in commercial VR devices, and a 4.1x frame rate improvement over the state-of-the-art static collaborative rendering.

Xie, Chenhao↗

Activation of the CaR-CSE/H2S pathway confers cardioprotection against ischemia-reperfusion injury

Ischemia-reperfusion (I/R) injury is a multifactorial process triggered when an organ is subjected to transiently reduced blood supply. The result is a cascade of pathological complications and organ damage due to the production of reactive oxygen species following reperfusion. The present study aims to evaluate the role of activated calcium-sensing receptor (CaR)-cystathionine γ-lyase (CSE)/hydrogen sulfide (H2S) pathway in I/R injury. Firstly, an I/R rat model with CSE knockout was constructed. Transthoracic echocardiography, TTC and HE staining were performed to determine the cardiac function of rats following I/R Injury, followed by TUNEL staining observation on apoptosis. Besides, with the attempt to better elucidate how CaR-CSE/H2S affects I/R, in-vitro culture of human coronary artery endothelial cells (HCAECs) was conducted with gadolinium chloride (GdCl3, a CaR agonist), H{sub 2}O{sub 2}, siRNA against CSE (siCSE), or W7 (a CaM inhibitor). The interaction between CSE and CaM was subsequently detected. Plasma oxidative stress indexes, H2S and CSE, and apoptosis-related proteins were all analyzed following cell apoptosis. We found that H2S elevation led to the improvement whereas CSE knockdown decreased cardiac function in rats with I/R injury. Moreover, oxidative stress injury in I/R rats with CSE knockout was aggravated, while the increased expression of H2S and CSE in the aortic tissues resulted in alleviated the oxidative stress injury. Moreover, increased H2S and CSE levels were found to inhibit cell apoptotic ability in the aortic tissues after I/R injury, thus attenuating oxidative stress injury, accompanied by inhibited expression of apoptosis-related proteins. In HCAECs following oxidative stress treatment, siCSE and CaM inhibitor were observed to reverse the protection of CaR agonist. Coimmunoprecipitation assay revealed the interaction between CSE and CaM. Taken together, all above-mentioned data provides evidence that activation of the CaR-CSE/H2S pathway may confer a potent protective effect in cardiac I/R injury.

60 APPLIED LIFE SCIENCES↗