Some of the barriers preventing Virtual Reality (VR) from being widely adopted are the cost and unfamiliarity of VR systems. Here we propose that in many cases the specialized controllers shipped with most VR head-mounted displays can be replaced by a regular smartphone, cutting the cost of the system, and allowing users to interact in VR using a device they are already familiar with. To achieve this, we developed SmartVR Pointer, an approach that uses smartphones as a replacement for the specialized controllers for two essential operations in VR: selection and navigation by teleporting. In SmartVR Pointer a camera mounted on the head-mounted display (HMD) is tilted downwards so that it points to where the user will naturally be holding their phone in front of them. SmartVR Pointer supports three selection modalities: tracker-based,gaze-based, and combined/hybrid. In the tracker-based SmartVR pointer selection we use image-based tracking to track a QR code displayed on the phone screen and them map the phone’s position to a pointer shown within the field of view of the camera in the Virtual Environment. In the gaze-based selection modality the user places the pointer using their gaze and taps on the phone for selection. The combined technique is a hybrid between head-gaze-based interaction in VR and smartphone-based Augmented Reality. It allows the user to control a VR pointer that behaves like a mouse pointer by moving their smartphone to select objects within the virtual environment, and to interact with the selected objects using the smartphone’s touch screen. The touchscreen is used for selection and dragging. SmartVR Pointer is simple and requires no calibration and no complex hardware assembly or disassembly. We demonstrate successful interactive applications of SmartVR Pointer in a VR environment with a demo where the user navigates in the virtual environment using teleportation points on the floor and then solves a Tetris-style key-and-lock challenge.

The homeostasis of cellular calcium is fundamental for many physiological activities, while calcium levels maintain inhomogeneous within cells. During the onset of asthma, epithelial and inflammatory cells secrete platelet derived growth factor (PDGF), inducing proliferation and migration of airway smooth muscle (ASM) to the epidermal layer, narrowing the airway. The regulation of ASM cells by PDGF is closely related to the conduction of calcium signals. In this work, we generated subcellular-targeted FRET biosensors to investigate calcium regulations at different compartments of ASM cells. PDGF-induced cytoplasmic calcium [Ca2+]C increase was attributed from both extracellular calcium influx and endoplasmic reticulum (ER) calcium [Ca2+]ER release, which was partially regulated by PLC-IP3R pathway. Interestingly, removal of extracellular calcium influx led to inhibited ER calcium release, likely through inhibitory effect on calcium-dependent activation of ER ryanodine receptor. Inhibition of L-type calcium channel on plasma membrane, or SERCA pump on ER resulted in both reduced [Ca2+]C and [Ca2+]ER from PDGF stimulation, while IP3R channel inhibition led to reduced [Ca2+]C only. Inhibited SERCA pump caused immediate [Ca2+]C increase and [Ca2+]ER decrease, indicating an active calcium exchange between cytosol and ER storage in resting cells. PDGF-induced calcium at outer mitochondrial membrane sub-region showed similar regulatory response to cytosolic calcium, not influenced by inhibition of mitochondrial calcium uniporter channel. Therefore, our work identified calcium flow pathways among extracellular medium, cell cytosol, and ER by regulatory calcium channels. Particularly, extracellular calcium flow has an essential function to fully activate ER calcium release.

Cell-to-cell distant mechanical communication has been demonstrated by using in-vitro and in-vivo models. However, the molecular mechanisms underlying long-range cell mechanoresponsive interactions remain to be more elucidated. This study further examined the roles of α-Catenin and Piezo in traction force-induced rapid branch assembly of airway smooth muscle (ASM) cells on Matrigel hydrogel containing type I collagen. Our findings demonstrate that siRNA-mediated downregulation of α-Catenin or chemical inhibition of Piezo activity significantly reduced both cell directional movement and branching assembly. In regarding the role of N-cadherin in regulating branch assembly but not directional migration, our results further confirmed that siRNA downregulation of α-Catenin caused a remarked reduction of focal adhesion formation, as assessed by focal Paxillin and Integrin α5 localization. These observations implied that mechanosensitive α-Catenin was involved in both cell-cell and cell-matrix adhesions. Additionally, Piezo showed partial localization with Paxillin in focal adhesions, which was inhibited by α-Catenin downregulation with siRNA. This provides a plausible clue for Piezo mechanosensing traction force in the hydrogel. Collectively, our findings highlight the significance of α-Catenin in regulating cell-matrix interactions along with possible interpretation for Piezo mechanosensation at focal adhesions during cell-cell distant mechanical communication.